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Cardiologist

1. Medical disorders of the Cardiovascular system

2. Epidemiology of cardiovascular disorders CVDs are the number 1 cause of death globally An estimated 17.7million people died from CVDs in 2015 (31% of all global deaths) Of these deaths, an estimated 7.4million were due to coronary heart diseases (CADs) 6.7million were due to stroke Over ¾ of CVD deaths take place in low- and middle-income countries Limited access to quality healthcare

3. Epidemiology of cardiovascular disorders Most CVDs can be prevented by addressing behavioral risk factors such as Tobacco use Unhealthy diet Obesity Physical inactivity Harmful use of alcohol

4. Review of CVS Anatomy and physiology Anatomy of the heart Hollow, muscular organ located in mediastinum of thorax Weighs about 300g (can be influenced by age, gender, body weight, physical activity & heart diseases) Composed of 3 layers (endocardium, myocardium, epicardium) Covered by a thin, fibrous layer called pericardium (visceral & parietal pericardium, pericardial space, pericardial fluid/20mL) Has 4chambers - atria, ventricles (diastole/ventricular filling, systole) Has 4valves which permit a unidirectional flow of blood (Atrioventricular & semilunar vlaves )

5. Review of CVS Anatomy and physiology Anatomy of the heart… Coronary arteries – originate from the aorta (branches into two) Heart tissue perfusion occurs during diastole Normal HR of 60-80bpm (normal diastole) allows for optimum myocardial perfusion Increased HR (shortened diastole, less myocardial perfusion) increases risk of myocardial ischemia Coronary veins empty into coronary sinus Myocardium consists of highly connected myocytes (forms a figure of eight pattern from base to apex)

6. Anatomy of the heart

7. Review of CVS Anatomy and physiology Function of the heart Cardiac conduction system generate & transmit electrical impulses to maximize cardiac output CCS mainly consists of 2types of cells ( automaticity , excitability & conductivity ) Nodal cells – SA (60-100) & AV (40-60) Purkinje cells Cardiac action potential initiated by specialized cells of the CCS Refractory period – period between depolarization and repolarization 2phases – effective/absolute & relative refractory periods Changes in refractory periods can cause dysrhythmias

8. Anatomy of the heart

9. Anatomy of the heart

10. Review of CVS Anatomy and physiology Function of the heart Cardiac hemodynamics – blood flows from lower to higher pressure (generated during systole & diastole) Cardiac cycle = one diastole + one systole (of all four chambers) Events occurring in during one heartbeat Diastole begins → pressure in all 4chambers low → blood enters atria & ventricles → SA node generates impulse & transmit → atrial diastole end & atrial systole begin → ventricular filling ends → ventricular systole → AV valves close & SL valves open → stroke volume → AV valves open & SL valves close → diastole

11. Anatomy of the heart

12. Review of CVS Anatomy and physiology Function of the heart Cardiac output – blood pumped by each ventricle during a given period (5L/min) CO = Stroke Volume X Heart Rate CO = 70mL X (60-80)bpm HR is under autonomic control via the vagus nerve (innervates SA node) Also influenced by baroreceptors (via cerebral medulla) SV is determined by 3factors: preload/end-diastolic pressure, afterload & contractility Systemic V ascular Resistance (SVR) - resistance of the systemic BP to left ventricular ejection Pulmonary vascular resistance – resistance of pulmonary BP to right ventricular ejection

13. Review of CVS Anatomy and physiology Function of the heart Contractility – strength of myocardial contraction Increased by catecholamines, medications (digoxin, dobutamine , dopamine) Decreased by hypoxia, acidosis, medications (beta-blockers) Ejection fraction - percentage of the end-diastolic blood volume that is ejected with each heartbeat (55-65%) Measures ventricular function Ejection of fraction of less than 40 indicates heart failure

14. Assessment of the cvs system

15. Health history Ability to recognize cardiac symptoms & the appropriate intervention is essential for effective management (including self-management) Major barriers to seeking prompt medical care Lack of knowledge about the symptoms of heart disease Attributing symptoms to a benign source Denying symptom significance Feeling embarrassed about having symptoms Determine if the patient & involved family members are able to recognize symptoms of an acute cardiac problem

16. Common cardiac symptoms Signs and symptoms experienced by people with CVD are related to Coronary Artery Disease (CAD ) Dysrhythmias & conduction problems Structural, infectious & inflammatory disorders of the heart Complications of CVD e.g. HF, cardiogenic shock

17. Common cardiac symptoms Sign or symptom Possible cardiac problem Chest pain or discomfort Angina pectoris, ACS, dysrhythmias, valvular heart disease Shortness of breath or dyspnea ACS, cardiogenic shock, HF, valvular heart disease Palpitations Tachycardia from a variety of causes, including ACS, caffeine or other stimulants, electrolyte imbalances, stress, valvular heart disease, ventricular aneurysms

18. Common cardiac symptoms Sign or symptom Possible cardiac problem Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver or ascites HF Vital fatigue/vital exhaustion (characterized by feeling unusually tired or fatigued, irritable & dejected) An early warning symptom of ACS, HF, valvular heart disease Dizziness, syncope or changes in level of consciousness Cardiogenic shock, cerebrovascular disorders, dysrhythmias, hypotension, postural hypotension, vasovagal episode

19. Common cardiac symptoms Chest pain Most common symptom associated with heart disease Pain of angina pectoris & MI is due to myocardial hypoxia Types of pain include Angina - retrosternal heavy or gripping sensation with radiation to the left arm or neck that is provoked by exertion & eased with rest or nitrates Acute coronary syndrome - similar pain (as above) at rest Aortic dissection - severe tearing chest pain radiating through to the back Pericarditis pain - sharp central chest pain that is worse with movement or respiration but relieved with sitting forward

20. Common cardiac symptoms Dyspnea Left ventricular failure causes dyspnea due to edema of the pulmonary interstitium & alveoli Lungs become stiff (less compliant) → increase respiratory effort to ventilate lungs Tachypnea is present owing to stimulation of pulmonary stretch receptors Hyperventilation with Cheyne–Stokes respiration occurs in severe HF Orthopnea - breathlessness on lying flat Blood is redistributed from legs to torso → increase in pulmonary blood volume Patient uses an increasing number of pillows to sleep

21. Common cardiac symptoms Dyspnoea Paroxysmal nocturnal dyspnea (PND) – patient is woken from sleep fighting for breath Due to same mechanisms as orthopnea Sensory awareness is reduced whilst asleep (pulmonary edema can become severe ) Central sleep apnea syndrome ( CSAS) – breathing during sleep interspersed with hypopnea or apnea Caused by poor cardiac output → cerebrovascular disease → malfunctioning of respiratory center Symptoms overlap with heart failure

22. Common cardiac symptoms Palpitations - an increased awareness of the normal heart beat or sensation of slow, rapid or irregular heart rhythms Most common arrhythmias felt as palpitations are premature ectopic beats & paroxysmal tachycardias Premature beats - a pause followed by a forceful beat (heart resets itself → longer diastole → longer ventricular feeling) Paroxysmal tachycardia - felt as a sudden racing heart beat Bradycardias - may be appreciated as slow, regular , heavy or forceful beats (may not be sensed at all)

23. Common cardiac symptoms Syncope - a transient loss of consciousness due to inadequate cerebral blood flow Causes Postural (orthostatic) hypotension - a drop in SBP of 20 mmHg or more on standing from a sitting or lying position due to failure of reflex vasoconstriction (fluid depletion, vasodilators) Postprandial hypotension - a drop in SBP of 20 mmHg or more or SBP drops from above 100 mmHg to under 90 mmHg within 2 hours of eating (due to splanchnic pooling of blood ) Obstructive causes (aortic stenosis, pulmonary hypertension ) Syncope due to arrhythmia (profound bradycardia, AV block)

24. Common cardiac symptoms Fatigue - may be a symptom of inadequate systemic perfusion in HF May also be due to poor sleep, side-effect of medication (beta-blockers), electrolyte imbalance (diuretic therapy) & as a systemic manifestation of infection such as endocarditis Peripheral edema HF results in salt & water retention due to renal under-perfusion & consequent activation of RAAS This leads to dependent pitting edema

25. Physical examination of the CVS General examination General well-being Conjunctival pallor Obesity Jaundice Cachexia Clubbing Splinter hemorrhages Cyanosis Central cyanosis - shunting of deoxygenated venous blood into systemic circulation e.g. right-to-left shunting Peripheral cyanosis - peripheral vasoconstriction & stasis of blood in extremities (more peripheral oxygen extraction) e.g. congestive heart failure, circulatory shock

26. Physical examination of the CVS Arterial pulse Pulse rate – 60-80bpm for an adult resting quietly Rhythm - regular except for a slight quickening in early inspiration & a slowing in expiration (sinus arrhythmia) Premature beats ( extrasystole /ectopic beat) – occur as occasional or repeated irregularities superimposed on a regular pulse rhythm Irregularity due to ectopic beats disappears on exercise Intermittent heart block - revealed by occasional beats dropped from an otherwise regular rhythm Atrial fibrillation - produces an irregularly irregular pulse Irregular pattern persists when pulse quickens in response to exercise

27. Physical examination of the CVS Auscultation – S1 – closure of AV valves S2 – closure of semilunar valves S3 – rapid ventricular filling (present in HF) S4 – occurs in late diastole due to atrial contraction One or both (S3 & S4) is described as a gallop Murmurs - due to turbulent blood flow & occur in hyperdynamic states or with abnormal valves

28. Cardiac investigations and laboratory investigations Serum cardiac biomarkers Prolonged ischemic (necrotic) or traumatic myocardial cells release specific enzymes & some proteins Creatine kinase [CK ]) CK isoenzymes Proteins ( myoglobin, troponin T, troponin I ) These substances leak into interstitial spaces of myocardium → lymphatic system → general circulation

29. Cardiac investigations and laboratory investigations Blood Chemistry, Hematology & Coagulation Studies Lipid profile ( c holesterol , triglycerides & lipoproteins ) Brain (B-type) natriuretic peptide (BNP ) C-reactive protein Hemocysteine

30. Cardiac investigations and laboratory investigations Chest X-ray Taken from posterior-anterior position (AP is only used during emergencies) Can be used to assess heart size including changes in specific chambers, pericardial effusion, changes in pulmonary vasculature, calcification, lung fields Electrocardiography Record electrical activity of heart Echocardiography A noninvasive ultrasound Used to measure ejection fraction & examine size shape & motion of cardiac structures

31. Coronary artery disorders

32. Coronary atherosclerosis Arteriosclerosis – narrowing & hardening of arteries Atherosclerosis Arteriolosclerosis Atherosclerosis - an abnormal accumulation of lipid/fatty substances & fibrous tissue in the lining of arterial blood vessel walls These substances block & narrow coronary vessels in a way that reduces blood flow to the myocardium Repetitious inflammatory response to injury of the artery wall → alteration in the structural & biochemical properties of the arterial walls → atherosclerosis

33. Coronary atherosclerosis Pathophysiology Begin as fatty streaks of lipids that are deposited in the intima of the arterial wall Lesions commonly begin early in life (sometimes in childhood) Not all fatty streaks later develop into advanced lesions Genetics & environmental factors are involved in the progression of these lesions Development of atherosclerosis involves an inflammatory response (begins with injury to vascular endothelium) Injury may be initiated by smoking, HPT & other factors Inflammation → attraction of inflammatory cells (monocytes, macrophages) → ingestion of lipids → foam cells → transport lipids into arterial wall Activated macrophages also release biochemical substances → cause further damage, attract platelets & initiate clotting

34. Pathogenesis of atherosclerosis

35. Pathogenesis of atherosclerosis

36. Coronary atherosclerosis Pathophysiology Smooth muscle cells (within vessel wall) proliferate & form a fibrous cap over a core filled with lipid & inflammatory infiltrate Deposits (atheromas / plaques) protrude into lumen of vessel → narrowing & obstruction of blood flow Plaque maybe stable or unstable (depends on degree of inflammation & thickness of fibrous cap) Thick fibrous cap → resist stress of blood flow & vessel movement → relatively stable plaque Thin fibrous cap + ongoing inflammation (growth of lipid core) → reduced resistance to blood flow & vessel movement → rupture of lipid core & hemorrhage into plaque A ruptured plaque is a focus for thrombus formation → obstruction of blood flow → ACS → MI

37. Coronary atherosclerosis Pathophysiology Anatomic structure of coronary arteries makes them particularly susceptible to the mechanisms of atherosclerosis The three major coronary arteries have multiple branches ( a therosclerotic lesions most often form where the vessels branch )

38. Coronary atherosclerosis Pathophysiology Other phenomena (aside coronary atherosclerosis) can also lead to heart diseases characterized by reduced blood flow to heart tissues Vasospasm (sudden constriction or narrowing) of a coronary artery Myocardial trauma Internal or external forces Structural disease Congenital anomalies Decreased oxygen supply ( e.g. from acute blood loss, anemia or low BP) Increased oxygen demand ( e.g . from rapid heart rate , thyrotoxicosis or use of cocaine )

39. Coronary atherosclerosis Clinical manifestations Depends on Location & degree of narrowing of the arterial lumen Thrombus formation Obstruction of blood flow to the myocardium Impediment to blood flow is usually progressive → inadequate blood supply to cardiac muscle cells (myocardial ischemia) Angina pectoris - chest pain related to myocardial ischemia Most common presentation

40. Coronary atherosclerosis Clinical manifestations Irreversible damage & death of myocardial cells may result (decrease in blood supply is great enough, of long enough duration or both) Myocardium undergoes degeneration → replaced by scar tissue → myocardial dysfunction → low cardiac output, HF, sudden cardiac death Other clinical manifestations Shortness of breath (dyspnea) – especially among older patients with a hx of DM or HF Atypical symptoms e.g. weakness, nausea Some patients may be asymptomatic

41. Coronary atherosclerosis Non-modifiable risk factors Family history of CAD Increasing age Gender (men develop CAD at an earlier age than women) Race (higher incidence of heart disease in African than in Caucasians ) Modifiable risk factors Hyperlipidemia (elevated LDLs) Cigarette smoking or tobacco use Hypertension Diabetes mellitus Obesity Physical inactivity Metabolic syndrome (insulin resistance, central obesity, dyslipidemia, high blood pressure, high levels of C-reactive protein, high fibrinogen level) Other diseases (peripheral artery disease, abdominal aortic aneurysm, carotid artery disease ) Psychologic states (depression)

42. Coronary atherosclerosis Prevention Controlling cholesterol abnormalities Periodic monitoring of blood cholesterol levels (fasting lipid profile) Dietary changes (therapeutic lifestyle changes diet, Mediterranean diet, strict vegetarian diet, soluble fiber) Increased physical activity Lipid-lowering medication e.g. statins Promoting cessation of tobacco use (counselling, support groups, medications) Managing hypertension (adherence to treatment regimen) Controlling diabetes mellitus (adherence to treatment regimen)

43. Angina pectoris Angina pectoris - a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest Occurs when myocardial oxygen demand exceeds supply Myocardial oxygen demand increases during physical exertion or emotional stress Severity of symptoms of angina is based on magnitude of precipitating activity & its effect on activities of daily living

44. Angina pectoris Pathophysiology Angina is usually caused by atherosclerotic disease Associated with a significant obstruction of at least one major coronary artery Myocardium extracts a large amount of oxygen from coronary circulation to meet its demands Increased in oxygen demand must be accompanied by an increase in coronary blood flow Blockage in a coronary artery → flow cannot be increased → ischemia

45. Angina pectoris Pathophysiology Factors associated with typical angina pain Physical exertion E xposure to cold ( → vasoconstriction → elevated BP → increased myocardial work & oxygen demand) Eating a heavy meal ( ↑ blood flow to mesenteric area for digestion → ↓ blood supply available to myocardium) Stress or any emotion-provoking situation (release of catecholamines → ↑ BP & ↑ HR → ↑ myocardial workload)

46. Angina pectoris Types of angina Stable angina - predictable & consistent pain that occurs on exertion. Relieved by rest and/or nitroglycerin Unstable angina ( preinfarction angina/crescendo angina) - symptoms increase in frequency & severity. May not be relieved with rest or nitroglycerin Intractable/refractory angina - severe incapacitating chest pain Variant angina ( Prinzmetal’s angina ) - pain at rest with reversible ST-segment elevation. Thought to be caused by coronary artery vasospasm Silent ischemia - objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no pain

47. Angina pectoris Clinical manifestation Myocardial ischemia may produce pain of varying severity or other symptoms Mild indigestion Choking or heavy sensation in the upper chest ranging from discomfort to agonizing pain (may be accompanied by severe apprehension & a feeling of impending death) Anxiety may occur with angina Patient often feels tightness or a heavy choking or strangling sensation that has a viselike, insistent quality Pain is retrosternal but may also be poorly located & radiating to neck, jaw, shoulders & inner aspects upper arms (especially left arm)

48. Angina pectoris Clinical manifestation Other symptoms may also accompany the pain A feeling of weakness or numbness in the arms, wrists & hands Shortness of breath, pallor, diaphoresis Dizziness or lightheadedness Nausea & vomiting Patient with DM may not have severe pain with angina (diabetic neuropathy can blunt nociceptor transmission & dull the perception of pain) Angina pain subsides with rest or administration of nitroglycerin Elderly patients may not exhibit the typical pain profile because of diminished neurotransmitter response Typical presenting complaint in the elderly is dyspnea Symptoms may not be present at all Encourage elderly patients not to ignore chest-pain like symptoms

49. Angina pectoris Assessment & diagnostic findings History & physical examination Electrocardiography Echocardiography C-reactive proteins & other cardiac biomarkers

50. Angina pectoris Medical management Aim at decreasing oxygen demand of the myocardium & increasing oxygen supply Medical intervention Pharmacological therapy Control of risk factors Surgical intervention Reperfusion procedures

51. Angina pectoris Medical management Nitrates (e.g. nitroglycerin) – causes peripheral vasodilation & reduces myocardial workload/oxygen consumption Beta-adrenergic blocking agents (e.g. metoprolol, atenolol) – reduces myocardial oxygen consumption by blocking beta-adrenergic stimulation to the heart Calcium channel blockers (e.g. amlodipine, felodipine , diltiazem) - decrease SA node automaticity & AV node conduction → slower HR & a decrease in the strength of myocardial contraction (negative inotropic effect ) Antiplatelet & anticoagulation therapy Antiplatelets - low dose aspirin, clopidogrel Anticoagulant - heparin Oxygen administration –initiated at onset of chest pain to increase oxygen delivery to myocardium & to reduce pain

52. Angina pectoris Potential complications Acute coronary syndrome & MI Dysrhythmias Heart failure Cardiac arrest Cardiogenic shock

53. Angina pectoris Nursing diagnoses Acute pain related to an imbalance in oxygen supply & demand Decreased cardiac o utput related to reduced preload, afterload, contractility , & heart rate secondary to hemodynamic effects of drug therapy Ineffective cardiac tissue perfusion secondary to CAD as evidenced by chest pain or other prodromal symptoms Anxiety related to chest pain, uncertain prognosis and threatening environment Death anxiety related to cardiac symptoms Deficient knowledge about the underlying disease and approaches to avoiding complications Noncompliance or ineffective management of therapeutic regimen related to failure to accept necessary lifestyle changes

54. Angina pectoris Nursing management Enhancing myocardial tissue perfusion Direct patient to stop all activities & sit or rest in bed in a semi-Fowler’s position when chest pain or prodromal signs of myocardial ischemia (indigestion, nausea, choking, heaviness, weakness or numbess in the upper extremities, dyspnea, dizziness) are felt or experienced to help reduce the oxygen requirements of ischemic myocardium Assess angina pain (determine if it’s typical of patient’s previous experience) Monitor vital signs & observe patient for signs of respiratory distress An ECG may be obtained, scrutinized for ST-segment & T-wave changes

55. Angina pectoris Nursing management Enhancing myocardial tissue perfusion Administer nitroglycerin sublingually & assess patient’s response (relief of chest pain, effect on HR & BP) Repeat nitroglycerin (up to 3doses) if chest pain remains unchanged or lessened but still present (monitor BP, HR and ECG changes each time ) Administer oxygen therapy (2L/minute by nasal cannula) if the patient’s respiratory rate is increased or if oxygen saturation level is decreased If chest pain persist, evaluate patient for acute MI and transfer patient to higher care unit (pain unrelieved within 15minutes should be treated at the nearest ER)

56. Angina pectoris Nursing management Reducing anxiety Encourage patient to verbalize fears and concerns about illness through frequent conversations—conveys to patient a willingness to listen Exploring implications that diagnosis of CAD has for the patient (loss of role in family/community, fear of complications/death) Provide information about the illness, its treatment & methods of preventing its progression Encourage patient to verbalize fears and concerns about illness through frequent conversations (conveys to patient a willingness to listen) Adopt various stress reduction strategies e.g. diversional therapy, guided imagery Address the spiritual needs of patient & family Discuss measures to be taken when an anginal episode occurs Administer prescribed anxiolytics, tranquilizers or sedatives

57. Angina pectoris Nursing management Preventing pain Review assessment findings and identify level of activity that causes the patient’s pain or prodromal symptoms Plan activity according to patient’s level of tolerance Alternate activities with rest if patient has pain frequently or with minimal activity

58. Angina pectoris Nursing management Promoting home & community based care Goals of education are to reduce frequency & severity of anginal attacks, delay progress of underlying disease (if possible) & to prevent complications Designed in collaboration with patient & family so that patient & family Understand the illness Identify the symptoms of myocardial ischemia State the actions to take when symptoms develop Discuss methods to prevent chest pain & advancement of CAD

59. Angina pectoris Nursing management Promoting home & community based care Reduce the probability of an episode of anginal pain by balancing rest with activity Participate in a regular daily program of activities that do not produce chest discomfort, shortness of breath, or undue fatigue Follow the prescribed exercise regimen Recognize that temperature extremes (particularly cold) may induce anginal pain (avoid exercise in temperature extremes) Alternate activity with periods of rest

60. Angina pectoris Nursing management Promoting home & community based care Use appropriate resources for support during emotionally stressful times (e.g. counselor, nurse, clergy, physician ) Avoid using medications or any over-the-counter substances ( eg , diet pills, nasal decongestants) that can increase the heart rate and blood pressure without first discussing with a health care provider Stop smoking and other forms of tobacco, and avoid secondhand smoke (because smoking increases the heart rate, blood pressure, and blood carbon monoxide levels ) Follow a diet low in saturated fat, high in fiber, and if indicated, lower in calories

61. Angina pectoris Nursing management Promoting home & community based care Achieve and maintain normal blood pressure Achieve and maintain normal blood glucose levels Take medications, especially aspirin and beta-blockers, as prescribed Carry nitroglycerin at all times; state when and how to use it; identify its side effects Make and keep follow-up appointments. Report increase in symptoms to health care provider

62. Angina pectoris Nursing management Maintaining cardiac output Monitor patient’s response to drug therapy (Vitals, BP, HR, side effects of drugs, ECG) Monitor for signs & symptoms of poor perfusion ( ↓ BP, weak pulse, dizziness, shortness of breath, cool extremities, pallor, diaphoresis) Remove previous nitrate patch before applying new patch (prevents hypotension) & to reapply on different body site Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker & calcium channel blocker therapy (rebound tachycardia, chest pain, HPT) Discuss the need to tailor antianginal drug therapy to the timing of circadian events Report adverse effects to physician

63. Angina pectoris Nursing management Instructing patient on CAD Assess readiness to learn (pain free, shows interest, and comfortable), learning style, cognition & education level Review the chambers of the heart & the coronary artery system , using a diagram of the heart Show patient a diagram of a clogged artery (explain how the blockage occurs) Explain what angina is (a warning sign from the heart that there is not enough blood & oxygen because of the blocked artery or spasm ) Review specific risk factors that affect CAD development & progression (highlight those risk factors that can be modified & controlled to reduce risk)

64. Angina pectoris Nursing management Instructing patient on CAD Discuss the signs & symptoms of angina, precipitating factors & treatment for attacks (Stress to patient the importance of treating angina symptoms at once) Distinguish for patient the different signs & symptoms associated with stable angina versus pre-infarction angina Give patient & family handouts to review & encourage questions for a later teaching session

65. Acute Coronary S yndrome & Myocardial Infarction ACS - an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death (MI ) if definitive interventions do not occur promptly Myocardial infarction (MI) - a dynamic process by which a region of the heart experience a prolonged decrease or cessation in oxygen supply because of insufficient coronary blood flow leading to necrosis of the affected myocardial tissue occurs Spectrum of ACS includes Unstable angina Non-ST segment elevation MI ( NSTEMI) ST-segment elevation MI (STEMI )

66. Acute Coronary S yndrome & Myocardial Infarction Pathophysiology A profound imbalance exists between myocardial oxygen supply & demand within the entire spectrum of ACS Typically plaque rupture → thrombus formation → (complete) occlusion of artery → ( permanent/irreversible) damage to myocardium Area of infarction develops over minutes to hours (time is muscle )

67. Acute Coronary S yndrome & Myocardial Infarction Pathophysiology ECG usually identifies the type & location of the MI The location , evolution & resolution of an MI can be identified & monitored by serial ECG monitoring Classic ECG changes in acute MI T-wave inversion ( represent zone of ischemia) - delayed myocardial repolarization (injured myocardium remains depolarized while adjacent myocardium return to resting state) ST-segment elevation (represent zone of injury) - injured myocardial cells depolarize normally but repolarize more rapidly than normal cells Development of an abnormal Q wave (represent zone of necrosis) - lack of conduction of depolarization current from necrotic tissue

68. ECG changes in ACS

69. Acute Coronary S yndrome & Myocardial Infarction Pathophysiology Unstable angina ( preinfarction angina) Artery is not completely occluded Often due to rupture of an atherosclerotic plaque → reduced blood flow in coronary artery Patient most likely to have an MI without prompt intervention ECG & cardiac biomarkers show no evidence of acute MI

70. Acute Coronary S yndrome & Myocardial Infarction Pathophysiology NSTEMI No definite ECG evidence of acute MI Elevated cardiac biomarkers STEMI ECG evidence of acute MI There is significant damage to the myocardium

71. Acute Coronary S yndrome & Myocardial Infarction Clinical manifestations A previous diagnosis of CAD Some of patients have prodromal symptoms Shortness of breath, indigestion, nausea, anxiety, dizziness Cool , pale, moist skin Heart rate & respiratory rate may be faster than normal About half report no previous symptoms Chest pain Occurs suddenly & continues despite rest & medication (require opioids) May be described as crushing , squeezing or dull Most common presenting complaint

72. Acute Coronary S yndrome & Myocardial Infarction Clinical manifestation The signs & symptoms of MI cannot be distinguished from those of unstable angina in many cases Evolution of the term ACS Prognosis depends on severity of coronary artery obstruction & the presence & extent of myocardial damage

73. Acute Coronary S yndrome & Myocardial Infarction Assessment & diagnostic findings History & physical examination ECG Should be obtained within 10 minutes from the time a patient reports pain or arrives in the emergency department Echocardiogram Used to evaluate ventricular function (ejection fraction) Laboratory tests Cardiac biomarkers - creatine kinase isoenzymes, myoglobin, troponin)

74. Acute Coronary S yndrome & Myocardial Infarction Medical management Goals is to minimize myocardial damage , preserve myocardial function & prevent complications Interventions Analgesics (morphine) Thrombolytic medications (aspirin, heparin) Medications to reduce myocardial oxygen demand & increase oxygen supply (beta-blockers, vasodilators, ACEIs) Oxygen administration Bed rest Percutaneous Coronary Interventions Resolution of pain & ECG changes indicate oxygen demand & supply equilibrium or reperfusion ST is often first to return to normal during recovery

75. Acute Coronary S yndrome & Myocardial Infarction Complications Acute pulmonary edema Heart failure Cardiogenic shock Dysrhythmias & cardiac arrest Pericardial effusion & cardiac tamponade

76. Acute Coronary S yndrome & Myocardial Infarction Nursing diagnoses Acute pain related to myocardial tissue ischemia or damage Ineffective cardiac tissue perfusion related to reduced coronary blood flow Risk for imbalanced fluid volume related to compromised myocardial tissue function Decreased cardiac output related to decreased cardiac contractility & dysrhythmias Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction Death anxiety related to cardiac event Deficient knowledge about post-ACS self-care

77. Acute Coronary S yndrome & Myocardial Infarction Nursing management Relieving pain & other manifestations of ischemia Offer support & reassurance to patient that pain relief is a major priority Perform pain assessment regularly & encourage patient to report increasing pain Administer oxygen by nasal cannula along with other medication Assess vital signs frequently Encourage bed rest in the semi-fowlers or fowlers position

78. Acute Coronary S yndrome & Myocardial Infarction

79. Infectious & inflammatory diseases of the heart

80. Introduction Infectious & inflammatory disease processes may affect any of the 3 layers of the heart Infections are named for the layer of the heart most involved in the infectious process Infective endocarditis (endocardium) Myocarditis (myocardium ) Pericarditis (pericardium ) Rheumatic endocarditis is a unique infective endocarditis syndrome

81. Introduction Diagnosis of infections & inflammatory conditions is made primarily on the basis of Patient’s symptoms Echocardiography Ideal management for all infectious diseases is prevention IV antibiotics are usually necessary once an infection has developed in the heart

82. Rheumatic endocarditis (rheumatic heart disease) Rheumatic endocarditis - an acute, recurrent inflammatory disease that occurs following a g roup A beta-hemolytic streptococcal infection & typically result in damage to the heart (endocardium, myocardium, pericardium) The heart valves are particularly involved → valve leakage/insufficiency and/or obstruction (narrowing or stenosis ) Associated compensatory changes in the size of the chambers of the heart & thickness of the walls may occur Acute rheumatic fever - may develop after an episode of group A beta hemolytic streptococcal infection (pharyngitis)

83. Rheumatic endocarditis (rheumatic heart disease) Acute rheumatic fever - an acute autoimmune disease that occurs as a sequelae of group A beta-hemolytic streptococcal infection Characterized by inflammatory lesions of connective tissue & endothelial tissue Primarily affects the joints & heart Occur 1-5 weeks ( average 3 weeks) after a streptococcal infection of the throat or of the upper respiratory tract Peak incidence occurs in children ages 5-14years

84. Rheumatic endocarditis (rheumatic heart disease) Pathophysiology Rheumatic fever is a sequela to group A beta-hemolytic streptococcal infection Preventable through detection & adequate treatment of streptococcal pharyngitis Connective tissue of the heart, blood vessels, joints & subcutaneous tissues can be affected Lesions in CT are known as Aschoff bodies Localized areas of tissue necrosis surrounded by immune cells

85. Rheumatic endocarditis (rheumatic heart disease) Pathophysiology Heart valves (mainly the mitral valve) are affected → valve leakage or narrowing Swelling & erosion of valve leaflets → vegetation forms in areas of erosion (deposits of fibrin & blood cells) → thickening of valve leaflets, fusion of commissures & chordae tendineae , & fibrosis of papillary muscle Valve leaflets may become calcified → valve leaflets become less mobile → close improperly → regurgitation or stenosis Compensatory changes in chamber sizes & thickness of chamber walls occur Heart involvement (rheumatic pancarditis ) - pericarditis, myocarditis , epicarditis , endocarditis

86. Rheumatic endocarditis (rheumatic heart disease) Clinical manifestation Symptoms of streptococcal pharyngitis (may precede rheumatic symptoms) Sudden onset of sore throat (throat reddened with exudates) Swollen , tender lymph nodes at angle of jaw Headache, fever, abdominal pain (in children) Warm & swollen joints (polyarthritis ) – knees, ankles, elbows, wrist Chorea (irregular , jerky, involuntary, unpredictable muscular movements ) Prolonged PR interval as shown on ECG Heart murmurs - pleural & pericardial rubs Rashes over extensor surfaces of extremities

87. Rheumatic endocarditis (rheumatic heart disease) Diagnosis History & physical examination Throat culture Erythrocyte sedimentation rate, WBC count with differentials, CRP, cardiac biomarkers ECG Echocardiography Cardiac catheterization to evaluate valvular damage & left ventricular function

88. Rheumatic endocarditis (rheumatic heart disease) Medical management Antimicrobial therapy (penicillin is the drug of choice) Analgesics & antipyretics e.g. salicylates Bed rest (to reduce myocardial work load) Anticonvulsants (to manage chorea) e.g. phenobarbitone , diazepam Management of heart failure (beta blockers, ACEIs, diuretics, oxygen, sodium & fluid restriction)

89. Rheumatic endocarditis (rheumatic heart disease) Complications Valvular heart disease Cardiomyopathy Heart failure Atrial arrhythmias Pulmonary & systemic embolism

90. Rheumatic endocarditis (rheumatic heart disease) Nursing diagnoses Hyperthermia related to infectious or inflammatory reactions Decreased c ardiac o utput related to decreased cardiac contractility Activity Intolerance related to joint pain & easy fatigability

91. Rheumatic endocarditis (rheumatic heart disease) Nursing management Maintaining Adequate Cardiac Output Assess for signs & symptoms of acute rheumatic carditis Be alert to patient’s complaints of chest pain, palpitations, and/or precordial “ tightness” Monitor for tachycardia (usually persistent even when patient is asleeps ) or bradycardia Auscultate heart sounds every 4 hours Document presence of murmur or pericardial friction rub

92. Infective endocarditis Infective endocarditis ( IE) - an infection of the endocardial layer of the heart Endocardium - innermost layer of heart & heart valves IE affects the heart valves Treatment of IE with antibiotic therapy has improved the prognosis of the disease

93. Infective endocarditis Classification IE can be classified as Subacute form - typically affects those with pre-existing valve disease & has a clinical course that may extend over months Acute form - typically affects those with healthy valves & manifests as a rapidly progressive illness IE can also be classified based on Cause (e.g . IV drug abuse IE, fungal endocarditis) Site of involvement (e.g . prosthetic valve endocarditis)

94. Infective endocarditis Etiology The most common causative organisms of IE are bacterial Staphylococcus aureus Streptococcus viridans Other possible pathogens include fungi & viruses Rheumatic heart disease was the most common cause of IE (now account for <20%) Main contributing factors to IE Aging ( more than 50% of older people have aortic stenosis) IV drug abuse Use of prosthetic valves U se of intravascular devices resulting in health care–associated infections (MRSA) e.g. indwelling catheters Hemodialysis

95. Infective endocarditis Risk factors Cardiac Conditions Prior endocarditis Prosthetic heart valves Acquired valve disease (e.g . mitral valve prolapse with regurgitation , calcified aortic stenosis) Cardiac lesions (e.g . ventricular septal defect, asymmetric septal hypertrophy) Rheumatic heart disease (e.g . mitral valve regurgitation) Congenital heart disease Pacemakers Marfan’s syndrome Cardiomyopathy Noncardiac Conditions Hospital-acquired bacteremia IV drug abuse Procedure-Associated Risks Intravascular devices (e.g . pulmonary artery catheters ) Dental procedures e.g. extractions Respiratory tract incisions e.g. tonsillectomy

96. Infective endocarditis Pathophysiology IE occurs when blood turbulence within the heart allows causative organism to infect previously damaged valves or other endothelial surfaces Infection may spread locally → damage to valves or their supporting structures → valve dysfunction & dysrhythmias Subsequent invasion of myocardium → HF, sepsis, heart block Vegetations - the primary lesion of IE Consist of fibrin, leukocytes, platelets & microbes Stick to valve surface or endocardium

97. Infective endocarditis Pathophysiology Loss of parts of these fragile vegetations into the circulation results in emboli As many as 50% of patients with IE experience systemic embolization Left-sided heart vegetation move to various organs ( e.g. brain , kidneys, spleen) & to extremities (causing limb infarction) Right-sided heart lesions move to lungs → pulmonary emboli

98. Infective endocarditis Clinical manifestation Mostly nonspecific (low grade fever, chills, weakness , malaise, fatigue, anorexia) Subacute forms of endocarditis - a rthralgias , myalgias , back pain, abdominal discomfort, weight loss, headache, clubbing of fingers Vascular manifestations Splinter hemorrhages (black longitudinal streaks) that may occur in nail beds Petechiae (may result from fragmentation & microembolization of vegetative lesions) - can occur in the conjunctivae, lips , buccal mucosa , palate, ankles , feet, antecubital & popliteal areas Osler’s nodes (painful, tender, red or purple, pea-size lesions ) - may be found on fingertips or toes Janeway’s lesions (flat, painless, small, red spots) - may be seen on the palms & soles Roth’s spots - hemorrhagic retinal lesions

99. Infective endocarditis Clinical manifestations Onset of new or changing murmur Murmurs are usually absent in tricuspid endocarditis because right-sided heart sounds are too low to be heard Aortic & mitral valves are most often affected Heart failure Occurs in up to 80% of patients with aortic valve endocarditis & in approximately 50% of patients with mitral valve endocarditis

100. Infective endocarditis Clinical manifestation Manifestations secondary to embolization Spleen - sharp , left upper quadrant pain, splenomegaly, local tenderness, abdominal rigidity Kidneys - flank pain, hematuria, renal failure Arm & legs - ischemia & gangrene Brain - neurologic damage resulting in hemiplegia, ataxia, aphasia, visual changes, change in the level of consciousness Pulmonary - dyspnea, chest pain, hemoptysis, respiratory arrest

101. Infective endocarditis Diagnosis History & physical examination IV drug abuse, invasive procedures (cardiac, respiratory, dental, genitourinary) New or changed heart murmur Blood culture (drawn from different sites, 30minutes apart) WBC count with differentials, erythrocyte sedimentation rate, CRP levels Echocardiography (to note intracardiac mass or vegetation) Chest X-ray (to detect cardiomegaly) ECG (to detect cardiac block especially AV node block)

102. Infective endocarditis Medical management Prophylactic antibiotic therapy prior to invasive procedures in high risk persons Antibiotics therapy Early valve replacement Management of fever Analgesic/antipyretics Fluids Rest

103. Infective endocarditis Nursing diagnoses Decreased cardiac output related to altered heart rhythm & valvular insufficiency Activity intolerance related to generalized weakness, arthralgia & alteration in oxygen transport secondary to valvular dysfunction Ineffective t issue p erfusion (renal, cerebral, cardiopulmonary, GI , and peripheral) related to interruption of blood flow Hyperthermia related to infectious disease process & potential dehydration Imbalanced n utrition : less t han b ody r equirements related to anorexia Anxiety related to acute illness & hospitalization

104. Infective endocarditis Patient and family education Tell the patient to avoid people with infection, especially upper respiratory tract infection, & to report cold, flu & cough symptoms Stress the importance of avoiding excessive fatigue & the need to plan rest periods before & after activity Good oral hygiene including daily care & regular dental visits is also important Alert physician to prescribed prophylactic antibiotics prior to invasive procedures Teach patients & family to recognize signs & symptoms of potential complications ( e.g. change in mental status, dyspnea, chest pain, unexplained weight gain )

105. Acute pericarditis Pericarditis - a condition caused by inflammation of the pericardial sac (pericardium) Pericardium - composed of inner serous membrane (visceral pericardium) & outer fibrous (parietal) layer Pericardial space - cavity between the two pericardial layers Normally contains 10 - 15mL of serous fluid Functions of the pericardium Serves an anchoring function Provides lubrication to decrease friction during systolic & diastolic heart movements Assists in preventing excessive dilation of heart during diastole The pericardium may be congenitally absent or surgically removed

106. Acute pericarditis Etiology Most often cause of acute pericarditis is idiopathic (unknown) or nonspecific It may be a primary illness or it may develop during various medical & surgical disorders Primary cause Viral (common) - coxsackievirus, HIV, influenza Bacterial (rarely) - streptococci, staphylococci , meningococci, gonococci, mycotic (fungal) Pericarditis may occur after pericardiectomy (opening/removal of the pericardium) following cardiac surgery Pericarditis in the patient with an MI may be described as two distinct syndromes Acute pericarditis -may occur within initial 48 - 72hours after an MI Dressler syndrome (late pericarditis ) - appears 4 - 6 weeks after an MI

107. Acute pericarditis Other causes of pericarditis Disorders of connective tissue - systemic lupus erythematosus, rheumatic fever, rheumatoid arthritis, polyarteritis , scleroderma Hypersensitivity states - immune reactions, medication reactions , serum sickness Disorders of adjacent structures - MI, dissecting aneurysm, pleural & pulmonary disease (pneumonia), tuberculosis Renal failure & uremia Neoplastic disease - metastasis from lung cancer or breast cancer, leukemia Radiation therapy of chest & upper torso (peak occurrence 5-9 months after treatment ) Trauma - chest injury, cardiac surgery, cardiac catheterization, implantation of pacemaker or implantable cardioverter defibrillator (ICD)

108. Acute pericarditis Classification Pericarditis may be Acute Subacute Chronic Alternative classification Adhesive ( constrictive) pericarditis - layers of pericardium become attached to each other & restrict ventricular filling Classification by what accumulates in the pericardial sac - serous (serum), purulent (pus), calcific (calcium deposits ), fibrinous (clotting proteins), sanguinous ( blood) Pericarditis also may be described as exudative or noneffusive

109. Acute pericarditis Pathophysiology An inflammatory response is the characteristic pathologic finding in acute pericarditis There is an influx of neutrophils, increased pericardial vascularity & eventually fibrin deposition on the epicardium The inflammatory process of pericarditis may lead to an accumulation of fluid in the pericardial sac ( pericardial effusion ) & increased pressure on the heart → cardiac tamponade Frequent or prolonged episodes of pericarditis may also lead to thickening & decreased elasticity of the pericardium or scarring may fuse the visceral & parietal pericardium

110. Acute pericarditis Pathophysiology These changes or conditions restrict the heart’s ability to fill with blood (constrictive pericarditis ) The pericardium may become calcified → further restricting ventricular expansion during ventricular filling (diastole ) With less filling → ventricles pump less blood → decreased cardiac output → signs & symptoms of heart failure Restricted diastolic filling may result in increased systemic venous pressure → peripheral edema & hepatic failure

111. Acute pericarditis Clinical manifestations Pericarditis may be asymptomatic Most characteristic symptom of pericarditis is chest pain or discomfort Usually remains fairly constant May worsen with deep inspiration & when lying down (supine) or turning ( rapid, shallow breaths ) May be relieved with a forward-leaning or sitting position Pain may radiate to the neck , arms or left shoulder (making it difficult to differentiate from angina) Pain also may be located beneath the clavicle, in the neck or in the left trapezius (scapula) region Distinction from angina

112. Acute pericarditis Clinical manifestation Another most characteristic sign of pericarditis is a creaky or scratchy friction rub heard most clearly at the left lower sternal border Friction between the roughened pericar dial & epicardial surfaces Ask patient to hold breathe to distinguish from pleural friction rub Other signs may include Mild fever Increased WBC count Anemia An elevated ESR or C-reactive protein level Nonproductive cough or hiccough Dyspnea & other manifestations of HF May occur as a result of pericardial compression due to constrictive pericarditis or cardiac tamponade

113. Acute pericarditis Complications Two major complications may result from acute pericarditis Pericardial effusion Cardiac tamponade Pericardial effusion - a build-up of fluid in the pericardium Can occur rapidly (e.g . chest trauma) or slowly (e.g . tuberculosis pericarditis ) Large effusions may compress nearby structures Pulmonary tissue compression - cough , dyspnea & tachypnea Phrenic nerve compression - can induce hiccups Compression of the laryngeal tissue – hoarseness of voice Heart sounds are generally distant & muffled (although BP usually is maintained)

114. Acute pericarditis Complications Cardiac tamponade - develops as pericardial effusion increases in volume → compression of heart Speed of fluid accumulation affects severity of clinical manifestations Cardiac tamponade can occur acutely ( e.g. trauma ) or subacutely (e.g . secondary to renal failure , malignancy) Patient may report chest pain, tachycardia, tachypnea & is often confused, anxious & restless Cardiac output decreases as compression increases Dyspnea may be the only clinical manifestation in a patient with slow onset cardiac tamponade

115. Acute pericarditis Diagnosis History & physical examination Echocardiography ( may detect inflammation, pericardial effusion or tamponade , HF) Computer tomographic scan Magnetic resonance imaging ECG (concave ST segment elevation, depressed PR segments) WBC count, CRP, ESR, cardiac biomarkers

116. Acute pericarditis Medical management Aimed at identifying & treating the underlying problem & symptoms Antibiotics (bacterial infections ) NSAIDs (pain & inflammation) Colchicine (for recurrent pericarditis) Corticosteroids Pericardiocentesis Pericardiectomy - surgical removal of the tough encasing pericardium may be necessary to release both ventricles from the constrictive & restrictive inflammation & scarring

117. Acute pericarditis Nursing management Patients with acute pericarditis require pain management with analgesics, positioning & psychological support Patients with chest pain often benefit from education & reassurance that the pain is not due to a heart attack The nurse helps the patient with activity restrictions until the pain & fever subside (to minimize complications) The nurse encourages gradual increases of activity (as the patient’s condition improves) Activity restrictions must be resumed if pain, fever or friction rub reappear The nurse educates the patient & family about a healthy lifestyle to enhance the patient’s immune system

118. Acute pericarditis Nursing management Reducing pain Relief of pain is achieved by rest Chair rest may be more comfortable (sitting upright & leaning forward is the posture that tends to relieve pain) Instruct patient to restrict activity until pain subsides Activities of daily living may be resumed gradually as chest pain & friction rub abate Monitor & record patient’s response to analgesics , antibiotics or corticosteroids Assess patients taking NSAIDs for gastrointestinal adverse effects Bed rest or chair rest is resumed if chest pain & friction rub recur

119. Chronic constrictive pericarditis Etiology & pathophysiology Chronic constrictive pericarditis results from scarring with consequent loss of elasticity of the pericardial sac This involves fibrous scarring, thickening of the pericardium from calcium/fibrin deposition & eventual destruction of pericardial space It usually begins with an initial episode of acute pericarditis Characterized by fibrin/calcium deposition with a clinically undetected pericardial effusion Reabsorption of effusion slowly follows as progression toward the chronic stage occurs Fibrotic , thickened & adherent pericardium encases heart → impairs ability of atria & ventricles to stretch adequately

120. Chronic pericarditis Clinical Manifestations and Diagnostic Studies Manifestations of chronic constrictive pericarditis Occur over time & mimic those of HF & cor pulmonale Decreased CO accounts for many of the clinical manifestations (dyspnea on exertion, peripheral edema, ascites, fatigue, anorexia & weight loss) Most prominent finding on physical examination is jugular venous distention ( JVD) ECG changes are often nonspecific in chronic constrictive pericarditis Heart on chest x-ray may be normal or enlarged (depends on degree of pericardial thickening & presence of a pericardial effusion) Echocardiography - may reveal a thickened pericardium CT & MRI - provide measurement of pericardial thickness & assessment of diastolic filling patterns

121. Chronic pericarditis Medical & nursing management Treatment of choice for chronic constrictive pericarditis is a pericardiectomy

122. Myocarditis Myocarditis - a focal or diffuse inflammation of the myocardium Can cause Heart dilation, thrombi on the heart wall (mural thrombi) Infiltration of circulating blood cells around the coronary vessels & between the muscle fibers Degeneration of the muscle fibers themselves Mortality varies with severity of symptoms Most patients with mild symptoms recover completely Some patients develop cardiomyopathy heart failure

123. Myocarditis Etiology Possible causes include Viruses - Coxsackie A & B viruses (most common etiologic agents) Bacteria Fungi Radiation therapy Pharmacologic & chemical factors Autoimmune disorders (e.g . polymyositis, SLE, Crohn’s diseases) It may also be idiopathic Myocarditis is frequently associated with acute pericarditis, (particularly caused by coxsackie B virus)

124. Myocarditis Pathophysiology Infection of myocardium (causative agent invades myocytes → cellular damage & necrosis) Immune response is activated → cytokines & oxygen free radicals are released → activation of autoimmune response → further destruction of myocytes → cardiac dysfunction It may begin in one small area of the myocardium & then spread throughout the myocardium Degree of myocardial inflammation & necrosis determines degree of interstitial collagen & elastin destruction The greater the destruction, the greater the hemodynamic effect & resulting manifestations Myocarditis has been linked to the development of dilated cardiomyopathy

125. Myocarditis Clinical manifestations Clinical features of myocarditis are variable Ranging from a benign course (without any overt manifestations) to severe heart involvement or sudden cardiac death (SCD) Early systemic manifestations of the viral illness Flu-like symptoms, fever , fatigue, malaise , myalgias , pharyngitis, dyspnea, lymphadenopathy, nausea &vomiting Early cardiac signs appear 7 - 10 days after viral infection Pleuritic chest pain with a pericardial friction rub & effusion (pericarditis often accompanies myocarditis), palpitations Late cardiac signs relate to development of HF Syncope , peripheral edema, angina

126. Myocarditis Diagnosis History & physical examination Cardiac MRI Endomyocardial biopsy ECG WBC count, ESR, CRP, cardiac biomarkers

127. Myocarditis Medical management Antibiotics Bed rest to decrease cardiac workload Bed rest also helps decrease myocardial damage and the complications of myocarditis Treatment of complications e.g. heart failure Immunosuppressive agents Oxygen therapy

128. Myocarditis Prevention Prevention of infectious diseases Appropriate immunizations ( e.g . influenza, hepatitis ) Early treatment (appears to be important in decreasing the incidence of myocarditis)

129. Myocarditis Nursing management Maintaining cardiac output Place patient in a semi-Fowler’s position Space activity & rest periods Provide a quiet environment Carefully monitor medications that increase the heart’s contractility & decrease preload, afterload or both

130. Heart failure

131. Heart failure Heart failure - inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen & nutrients Previously referred to as congestive heart failure Many patients experience pulmonary or peripheral congestion Not all cases of HF are associated with pulmonary congestion HF is currently recognized as a clinical syndrome characterized by signs & symptoms of Fluid overload Inadequate tissue perfusion Fluid overload & decreased tissue perfusion result when the heart cannot generate a CO sufficient to meet the body’s demands

132. Heart failure HF: myocardial disease → a problem with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) This may or may not cause pulmonary or systemic congestion HF is mostly a progressive life-long condition Some cases of HF are reversible (depends on the cause) Managed with lifestyle changes & medications to prevent episodes of acute decompensated heart failure or chronic heart failure Characterized by an increase in symptoms, decreased CO & low perfusion Associated with increased hospitalizations , increased health care costs & decreased quality of life

133. Heart failure Types of heart failure Two major types of HF are identified by assessment of left ventricular functioning (usually by echocardiogram) Systolic heart failure (more common) - an alteration in ventricular contraction (characterized by a weakened heart muscle) Diastolic heart failure (less common type) - characterized by a stiff & noncompliant heart muscle (makes it difficult for the ventricle to fill) Mixed systolic and diastolic failure - seen in disease states such as dilated cardiomyopathy (DCM) Characterized by dilated ventricles that are unable to relax Ejection fractions are extremely low (less than 35%) High pulmonary pressures & biventricular failure

134. Heart failure Ejection fraction (EF) is assessed to help determine the type of HF EF = (amount of blood at end of diastole – amount of blood of at end of systole)/end diastolic volume) *100 Calculate proportion of blood ejected from the ventricle A normal EF = 55-65% of ventricular volume EF is normal in diastolic HF but severely reduced in systolic HF Severity of HF is frequently classified according to the patient’s symptoms Independent of EF A low EF is a hallmark of systolic HF

135. Heart failure Pathophysiology HF results from a variety of cardiovascular conditions (chronic HPT, CAD, valvular disease) → systolic failure, diastolic failure or both Significant myocardial dysfunction usually occurs before the patient experiences signs & symptoms of HF such as shortness of breath, edema or fatigue The body activates neurohormonal compensatory mechanisms as HF develops Attempt by body to cope with HF Failure of compensatory mechanisms is responsible for signs & symptoms that eventually develop

136. Heart failure Pathophysiology Systolic HF → decreased EF Decreased ventricular stretch → sensed by baroreceptors in aortic & carotid bodies → SNS stimulated → epinephrine & norepinephrine released → increase HR & contractility (initially support failing heart → increase CO) + vasoconstriction (kidneys, skin, GIT) → increased myocardial workload & oxygen demand → low cardiac output → HF Low renal perfusion → RAAS activation → increase BP, preload & afterload [ vasoconstriction (catecholamines, angiotension II, endothelin), sodium & water retention, ADH secretion] → fluid volume overload Low cerebral perfusion → ADH secretion from posterior pituitary gland

137. Heart failure Pathophysiology Neurohormonal influences → increase in preload & afterload → increased stress on ventricular wall (of a failing heart) → increase workload of the heart → decreased contractility of myocardial fibers → increase end-diastolic volume → increased stretching of myocardial fibers & increased size of ventricle ( ventricular hypertrophy and/or dilation) → more stress & work on heart One way the heart compensates for the increased workload is to increase the thickness of the heart muscle (ventricular hypertrophy) This is characterized by an abnormal proliferation of myocardial cells (ventricular remodeling) → large & fragile myocardial cells → dies early → ventricular wall erosion → ventricular dilation Compensatory mechanisms initiates a vicious cycle

138. Heart failure Pathophysiology Diastolic HF Increased workload on heart → increased number & size of myocardial cells (i.e. ventricular hypertrophy & altered cellular functioning) → resistance to ventricular filling (increases ventricular filling pressures despite a normal or high blood volume) Less blood in the ventricles → decreased CO Low CO & high ventricular filling pressures → neurohormonal responses

139. Heart failure Counter-regulatory mechanisms Natriuretic peptides are hormones produced by the heart muscle in response fluid overload/increased preload Atrial natriuretic peptide [ ANP] – secreted by atria B rain or B-type natriuretic peptide [BNP ]) – secreted by ventricles 3 main functions Renal - increased GFR, natriuresis , diuresis Cardiovascular - vasodilation, reduced BP Neurohormonal - inhibition of aldosterone, renin & ADH secretion Nitric oxide - to counteract the effects of endothelin Effect of ANP & BNP usually not strong enough to overcome negative effects of other mechanisms

140. Heart failure Etiology Myocardial dysfunction is most often caused by CAD Atherosclerosis of coronary arteries is the primary cause of HF CAD is found in more than 60% of patients with HF Cardiomyopathy (dilated, hypertrophic, restrictive) HPT (increased afterload → left ventricular hypertrophy → decreased compliance of myocardium → decrease filling) Valvular disorders (narrowed valves) Systemic conditions – DM, progressive renal failure, metabolic syndrome, acute illness (e.g. pneumonia with fever & hypoxia, hyperthyroidism, anemia), cardiac dysrhythmias, acidosis, electrolyte abnormalities Medications e.g. antiarrhythmic medications

141. Heart failure Clinical manifestations Clinical manifestations produced by the different types of HF (systolic, diastolic, or both) are similar Does not assists in differentiating the types of HF Signs & symptoms of HF can be related to which ventricle is affected Left-sided heart failure Right-sided heart failure Chronic HF patients may have signs & symptoms of both left & right ventricular failure Biventricular failure

142. Heart failure Clinical manifestations General - fatigue, decreased activity tolerance, dependent edema, weight gain (more than 1.4kg in 3days) Cardiovascular - third heart sound, pallor & cyanosis, jugular venous distension Respiratory - dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, cough on exertion or when supine Cerebrovascular - unexplained confusion or altered mental status, lightheadedness Renal - oliguria & decreased frequency during the day, nocturia Gastrointestinal - anorexia & nausea, enlarged liver, ascites, hepatojugular reflux FACES

143. Heart failure Clinical manifestations (left-sided heart failure) Pulmonary congestion occurs when left ventricle cannot effectively pump blood out of ventricle into aorta & systemic circulation Increased left ventricular end-diastolic blood volume (in HF) → decreased EF → increased left ventricular filling pressure → decreased blood flow from left atrium into left ventricle during diastole Blood volume & pressure in left atrium increases → decrease blood flow from pulmonary vessels → increase pulmonary venous blood volume & pressure → fluid in pulmonary capillaries forced into alveoli & other pulmonary tissue → pulmonary interstitial edema & impaired gas exchange

144. Heart failure Clinical manifestations (left-sided heart failure ) Manifestations of pulmonary congestion Dyspnea (on exertion) Orthopnea Paroxysmal Nocturnal Dyspnea (increased venous return during night rest → pulmonary edema → fluid shift into alveoli → difficulty in breathing) Pulmonary crackles, wheezing/rhonchi Cough (progress from non-productive to productive/frothy, blood stained sputum) Low oxygen saturation levels S 3 or ventricular gallop on auscultation (unusual representation of rapid ventricular filling) Oliguria ( nocturia at night because cardiac workload decreases) Altered digestion Dizziness, light-headedness, confusion, Restlessness, anxiety, tachycardia, palpitations, insomnia, fatigue

145. Heart failure Clinical manifestations (right-sided heart failure) Right ventricle fails → decreased right ventricular ejection → increased venous pressure → JVD & increased capillary hydrostatic pressure throughout venous system → congestion in peripheral tissues & viscera → inadequate removal of catabolic waste products from the tissues

146. Heart failure Clinical manifestations (right-sided heart failure ) Systemic manifestations Edema of the lower extremities (dependent edema) – feet & ankles, worsens when patient sits or stands for long Gradually progress up the legs & thighs & into external genitalia & lower trunk Sacral edema is common for patients on bed rest Pitting edema is common after retention of 4.5kg/4.5L of fluid Hepatomegaly (enlargement of the liver) – venous engorgement of the liver Ascites (accumulation of fluid in the peritoneal cavity) – can cause abdominal respiratory distress Anorexia & nausea (venous engorgement & stasis), weakness, weight gain (due to retention of fluid )

147. Heart failure Diagnosis History & physical examination HF may go undetected until the patient presents with signs and symptoms of pulmonary and peripheral edema Physical signs that suggest HF may also occur with other diseases (renal failure & COPD) Echocardiography – assesses ventricular function, confirms HF Cardiac catheterization & ventriculography – rule out CAD ECG Chest X-ray Cardiac stress testing Laboratory investigations - BNP( key diagnostic indicator/high filling pressure), BUN, creatinine, serum electrolytes, FBC, Urine R/E

148. Heart failure Medical management Overall goals of management of HF are to Relieve patient symptoms Improve functional status & quality of life Extend survival Specific objectives of medical management Eliminate or reduce any etiologic contributory factors e.g. uncontrolled HPT or atrial fibrillation with a rapid ventricular response Optimize pharmacologic & other therapeutic regimens Reduce workload on heart by reducing preload & afterload Promote a lifestyle conducive to cardiac health Prevent episodes of acute decompensated HF Medical management is based on type , severity & cause of HF

149. Heart failure Medical management Managing the patient with HF includes providing comprehensive education & counseling to the patient & family Lifestyle recommendations Restriction of dietary sodium Avoidance of excessive fluid intake , alcohol & smoking Weight reduction (if indicated) Regular exercise

150. Heart failure Medical management Pharmacological therapy Angiotensin Converting E nzyme Inhibitors/ACEIs (Lisinopril, enalapril ) Angiotensin II Receptor Blockers/ARBS (valsartan, candesartan) Hydralazine & isosorbide dinitrate combination Beta-blockers (metoprolol, carvedilol) Diuretics – loop (furosemide), thiazide ( metolazone ), potassium-sparing (spironolactone) Diuretics may be most effective if the patient assumes a supine position for 1 or 2 hours after taking them Digitalis (digoxin) – increases strength of myocardial contraction, slow conduction through AV node Calcium channel blockers – only dihydropyridine calcium channel blockers (amlodipine, felodipine ) are indicated because it causes vasodilation

151. Heart failure Medical management Pharmacological therapy (other drugs) Nesiritide (a BNP made using recombinant technology) – promotes vasodilation Milrinone ( phosphodiesterase inhibitor ) – promote vasodilation Supplemental oxygen administration Non-pharmacological measures Ultrafiltration/ aquapheresis Circulatory assistive devices e.g. intra-aortic balloon pump PCI e.g. CABG for CADs Use of implantable cardioverter defibrillators (for life-threatening dysrhythmias ) Cardiac resynchronization therapy (for left bundle block) Cardiac transplant (for end-stage HF)

152. Heart failure Complications Intractable or refractory heart failure [becomes progressively refractory to therapy (does not yield to treatment )] Cardiac arrhythmias Cardiogenic shock Cardiac arrest Pulmonary infarction, pneumonia & emboli Pleural effusion

153. Heart failure Nursing diagnosis Decreased cardiac o utput related to impaired contractility & increased preload & afterload Impaired gas e xchange related to alveolar edema secondary to elevated ventricular filling pressures Activity intolerance and fatigue related to decreased CO Excess fluid volume related to the HF syndrome Anxiety related to breathlessness from inadequate oxygenation Powerlessness related to chronic illness & hospitalizations Ineffective therapeutic regimen management related to lack of knowledge

154. Heart failure Nursing management Maintaining adequate cardiac output Perform a comprehensive assessment of peripheral circulation (e.g . check peripheral pulses, edema, capillary refill, color & temperature of extremity) to determine circulatory status Note signs & symptoms of decreased cardiac output ( e.g. chest pain, S3, S4, jugular venous distention) to detect changes in status Encourage measures to reduce physical & emotional stress Rest in a semi-recumbent position or in an armchair in a well ventilated environment Keep patient informed of the progress of disease and treatment to allay anxiety & fear Administer prescribed drugs to enhance cardiac function

155. Heart failure Nursing management Improving oxygenation Raise the head end of the bed to reduce venous return & to minimize pulmonary congestion Sit orthopneic patient on side of bed with feet supported by a chair, head & arms resting on an over-the-bed table, & lumbosacral area supported with pillows Auscultate lung fields at least every 4 hours for crackles & wheezes in dependent lung fields (fluid accumulates in areas affected by gravity). Observe for increased rate of respirations (could be indicative of falling arterial pH )

156. Heart failure Nursing management Improving oxygenation Reposition the patient every 2 hours (or encourage the patient to change position frequently) - to help prevent atelectasis & pneumonia Encourage deep-breathing exercises every 1 to 2 hours - to avoid atelectasis Offer small, frequent feedings - to avoid excessive gastric filling & abdominal distention with subsequent elevation of diaphragm that causes decrease in lung capacity Administer oxygen as prescribed

157. Heart failure Nursing management Restoring fluid balance Administer prescribed diuretics Give diuretic early in the morning (nighttime diuresis disturbs sleep ) Keep an accurate intake & output record & balance it every 24hrs Weigh patient daily to determine if edema is being controlled (weight loss should not exceed 0.5 - 1 kg/day Assess for signs of hypovolemia caused by diuretic therapy (thirst, decreased urine output, orthostatic hypotension, weak, thready pulse etc )

158. Heart failure Nursing management Restoring fluid balance Be alert for signs of hypokalemia ( may cause weakening of cardiac contractions & may precipitate digoxin toxicity) Administer potassium supplements as ordered Monitor for pitting edema of lower extremities & sacral area Observe for the complications of bed rest - pressure ulcers (especially in edematous patients), phlebothrombosis , pulmonary embolism Encourage patient to adhere to dietary restrictions

159. Heart failure Nursing management Improving activity tolerance Alter or modify patient’s activities to keep within the limits of his or her cardiac reserve Increase patient’s activities gradually Assist patient with self care activities & remain alert to complains of chest pain Observe the pulse, symptoms & behavioral response to increased activity Relieve nighttime anxiety & provide for rest & sleep

160. Heart failure Nursing management Minimizing powerlessness Assessed for factors that contribute to a sense of powerlessness ( lack of knowledge & lack of opportunities to make decisions, hospital policies may limit the patient’s ability to make decisions e.g. meal times) Particularly so if health care providers & family members behave in controlling ways Patients need to recognize that they are not helpless & that they can influence the direction of their lives & the outcomes of treatment

161. Heart failure Nursing management Minimizing powerlessness Take time to listen actively to patient (encourages patient to express their concerns & ask questions) Provide the patient with decision-making opportunities e.g. encouraging food & fluid choices consistent with the dietary restrictions Assist patient to distinguish between factors that can & cannot be controlled

162. Pulmonary edema

163. Pulmonary edema Pulmonary edema - abnormal accumulation of fluid in the interstitial spaces of the lungs that diffuses into the alveoli Etiology Heart disease (acute left-sided heart failure, MI, aortic stenosis , severe mitral valve disease, hypertension) Circulatory overload (transfusions & infusions) Drug hypersensitivity, allergy, poisoning Lung injuries (smoke inhalation, shock lung, pulmonary embolism , or infarct) Central nervous system injuries (stroke , head trauma) Infection & fever (infectious pneumonia) Postcardioversion , postanesthesia , postcardiopulmonary bypass Renal disease

164. Pulmonary edema Pathophysiology Left ventricular associated pulmonary edema Increased resistance to left ventricular filling → blood volume & pressure buildup in left atrium → blood backs up into pulmonary circulation → blood volume overload in lungs → ineffective lymphatic drainage of excess fluid → increase in hydrostatic pressure → fluid forced out of pulmonary capillaries into interstitial spaces & alveoli → pulmonary edema (flash pulmonary edema) Fluid within alveoli → creation of a diffusion block → severe impairment of gas exchange → hypoxemia Fluid within alveoli mixes with air → classic symptom of pulmonary edema → frothy pink (blood-tinged) sputum Same mechanism responsible for pulmonary edema in renal failure

165. Pulmonary edema Clinical manifestations Restlessness & anxiety (decreased cerebral oxygenation) Confusion stupor may occur later Sudden onset of breathlessness & a sense of suffocation Cold & clammy extremities Cyanosis (peripheral or central) and/or pallor Incessant coughing may occur with the production of foamy sputum Extreme dyspnea & orthopnea (use of accessory muscles of respiration with retraction of intercostal spaces & supraclavicular areas) Precordial pain Breathing is rapid, noisy & moist sounding Significant decrease in oxygen saturation levels

166. Pulmonary edema Diagnosis History & physical examination Chest X-ray (evaluate pulmonary tissue & vessels engorgement) Arterial Blood Gas analysis Echocardiography Cardiac biomarkers Blood culture Renal function test (BUN, creatinine, serum electrolytes)

167. Pulmonary edema Medical management Oxygen therapy Morphine (reduces peripheral resistance, venous return & anxiety) Diuretics (furosemide, metolazone ) Vasodilators (IV nitroglycerine, IV nitroprusside) IV nesiritide

168. Pulmonary edema Complications Dysrhythmias Respiratory failure Right ventricular failure (lower extremity edema, ascites, pleural effusion, hepatomegaly)

169. Pulmonary edema Nursing diagnoses Impaired Gas Exchange related to excess fluid in the lungs Anxiety related to sensation of suffocation and fear

170. Pulmonary edema Nursing management Improving Oxygenation Give oxygen in high concentration to relieve hypoxia & dyspnea , to keep oxygen saturation >94% or patient’s baseline Take steps to reduce venous return to the heart. Place patient in upright position; head and shoulders up, feet and legs hanging down to favor pooling of blood in dependent portions of body by gravitational forces and to decrease venous return Give morphine in small, titrated intermittent doses (IV) as ordered Morphine usually is not given if pulmonary edema is caused by stroke or occurs with chronic pulmonary disease or cardiogenic shock Watch for excessive respiratory depression and hypotension Administer prescribed diuretics & keep an accurate intake & output chart Administer prescribed vasodilators and other drugs

171. Pulmonary edema Nursing management Decreasing Anxiety Stay with patient & display a confident attitude Explain to patient in a calm manner all therapies administered & the reason for their use Inform patient & family of progress toward resolution of pulmonary edema Allow time for patient and family to voice concerns and fears

172. Cardiogenic shock

173. Cardiogenic shock Cardiogenic shock - occurs when decreased CO leads to inadequate tissue perfusion & initiation of the shock syndrome Failure of the heart to pump blood adequately to meet the oxygenation needs of the body Heart muscle loses its contractile power It most commonly occurs in association with and as a direct result of acute myocardial infarction (AMI) It is the most common cause of death in the post-AMI patient (about 5-10 % of AMI patients develop cardiogenic shock )

174. Cardiogenic shock Etiology MI causing extensive damage (40% or greater) to left ventricular myocardium is the most common cause Other conditions which can precipitate cardiogenic shock End-stage cardiomyopathy Severe valvular dysfunction Drug toxicities Infection Cardiac tamponade Ventricular aneurysm

175. Cardiogenic shock Pathophysiology Impaired contractility → marked reduction in CO & ejection fraction → lack of blood & oxygen to heart as well as other vital organs (brain & kidneys) → damage to myocardium → further decline in contractile power → heightened inability of heart to provide blood & oxygen to vital organs

176. Cardiogenic shock Clinical manifestations Confusion, restlessness, mental lethargy (due to poor perfusion of brain ) Low systolic blood pressure (90 mm Hg or 30 mm Hg less than previous levels ) Oliguria - urine output less than 30 mL/hour for at least 2hours (due to decreased perfusion of kidneys ) Cold, clammy skin (blood is shunted from peripheral circulation to perfuse vital organs) - profoundly diaphoretic with mottled extremities Weak, thready peripheral pulses, fatigue, hypotension (due to inadequate CO ) Dyspnea, tachypnea, cyanosis (increased left ventricular pressures result in elevation of left atrial & pulmonary pressures, causing pulmonary congestion )

177. Cardiogenic shock Clinical manifestations Dysrhythmias (due to lack of oxygen to heart muscle ) Sinus tachycardia (as a compensatory mechanism for a decreased CO ) Chest pain (due to lack of oxygen & blood to heart muscle) Decreased bowel sounds (due to paralytic ileus from decreased perfusion to GI tract ) Metabolic acidosis due to increased lactate production & reduced clearance (caused by anaerobic metabolism & liver dysfunction)

178. Cardiogenic shock Diagnosis History & physical examination Chest x-ray - pulmonary vascular congestion Renal function test (BUN, creatinine, serum electrolytes) BNP levels ECG - reveals an acute injury pattern consistent with an AMI Echocardiography - ventricular wall motion, valvular dysfunction, tamponade

179. Cardiogenic shock Medical management Goals in the treatment of cardiogenic shock include Correcting the underlying problem Reducing any further demand on the heart Improving oxygenation & restoring tissue perfusion Revascularization Thrombolytics

180. Cardiogenic shock Medical management Standard pharmacological therapy for a failing heart may need to be discontinued or decreased as it may exacerbate systolic hypotension Positive inotropic drugs (epinephrine, dopamine, dobutamine , amrinone , milrinone ) Vasodilator therapy Diuretic therapy Beta-blockers ACEIs or ARBs Circulatory assist devices e.g. intra-aortic balloon pump

181. Cardiogenic shock Complications Neurologic impairment/stroke Acute respiratory distress syndrome Renal failure Cardiopulmonary arrest Dysrhythmia Ventricular aneurysm Multiorgan dysfunction syndrome Bowel ischemia Limb ischemia

182. Cardiogenic shock Nursing diagnoses Decreased Cardiac Output related to impaired contractility due to extensive heart muscle damage Impaired Gas Exchange related to pulmonary congestion due to elevated left ventricular pressures Ineffective Tissue Perfusion (renal, cerebral, cardiopulmonary, GI , and peripheral) related to decreased blood flow Anxiety related to intensive care environment and threat of death .

183. Cardiogenic shock Nursing management Improving cardiac output Establish continuous ECG monitoring to detect dysrhythmias which increase myocardial oxygen consumption Monitor hemodynamic parameters continually e.g. BP, cardiac index, cardiac output Be alert to adverse responses to drug therapy Keep an accurate intake and output chart and balance it every 24hrs Obtain daily weight and stay alert to complains of chest pain

184. Cardiogenic shock Nursing management Improving Oxygenation Monitor rate & rhythm of respirations every hour Auscultate lung fields for abnormal sounds (coarse crackles indicate severe pulmonary congestion) every hour; notify the doctor Evaluate arterial blood gas (ABG) levels & correlate with oxygen saturation Administer oxygen therapy to increase oxygen tension and improve hypoxia Elevate head of bed 20 to 30 degrees as tolerated (may worsen hypotension) to facilitate lung expansion Reposition patient frequently to promote ventilation & maintain skin integrity Observe for frothy pink sputum & cough (may indicate pulmonary edema); report immediately

185. Cardiogenic shock Nursing management Maintaining Tissue Perfusion Perform a neurologic check every hour using the Glasgow Coma Scale Report changes immediately Obtain BUN & creatinine blood levels and monitor urine output to evaluate renal function Auscultate for bowel sounds every 2 hours Evaluate character, rate, rhythm & quality of arterial pulses every 2 hours Monitor temperature every 2 to 4 hours Use soft foot & elbow protectors to prevent skin breakdown

186. Cardiogenic shock Nursing management Relieving Anxiety Stay alert for & evaluate signs of increasing anxiety and/or new-onset anxiety for a physiologic cause before treating with anxiolytics Explain equipment & rationale for therapy to patient & family (Increasing knowledge assists in alleviating fear & anxiety) Encourage patient to verbalize fears about diagnosis & prognosis Explain sensations patient will experience before procedures & routine care measures Offer reassurance & encouragement Provide for periods of uninterrupted rest & sleep Assist patient to maintain as much control as possible over environment and care Utilize social worker or pastoral care for support

187. thromboembolism

188. Thromboembolism (Decreased mobility + impaired circulation) in cardiac disorders → development of intracardiac & intravascular thrombosis Intracardiac thrombi are especially common in patients with atrial fibrillation Atria do not contract forcefully & blood flows slowly & turbulently → increase likelihood of thrombus formation Intracardiac thrombi are detected by an echocardiogram Treated with anticoagulants e.g. heparin, warfarin

189. Thromboembolism Pulmonary embolism Most common thromboembolic problem among patients with HF Blood clots may form in deep veins of legs & embolize to pulmonary vasculature → mechanically obstruct pulmonary vessels → blood supply to sections of lung is cut of → life-threatening embolic event Emboli can cause hypoxic vasoconstriction & release of inflammatory mediators in pulmonary vessels → right heart failure & respiratory failure Clinical indicators of pulmonary embolism can vary but typically include dyspnea, tachypnea, chest pain, hemoptysis, tachycardia & symptoms of DVT Diagnostic tests often include a chest x-ray, ventilation-perfusion lung scan , CT scan Anticoagulant therapy is the mainstay of treatment

190. Cardiac arrest

191. Cardiac arrest Cardiac arrest - occurs when the heart ceases to produce an effective pulse & circulate blood It may be caused by a cardiac electrical event (dysrhythmia ) such as Ventricular fibrillation Progressive profound bradycardia Asystole (when there is no heart rhythm at all) It may also occur when electrical activity is present but there is ineffective cardiac contraction or circulating volume [ pulseless electrical activity (PEA)] Can be caused by hypovolemia ( e.g. excessive bleeding ), hypoxia, hypothermia, hyperkalemia , massive pulmonary embolism, myocardial infarction & medication overdose ( e.g . beta-blockers, calcium channel blockers ) Cardiac arrest may also follow respiratory arrest

192. Cardiac arrest Clinical manifestations Consciousness , pulse & blood pressure are lost immediately Ineffective respiratory gasping may occur Pupils of the eyes begin dilating within 45 seconds Seizures may or may not occur The risk of irreversible brain damage & death increases with every minute from the time that circulation ceases Interval varies with the age & underlying condition of the patient

193. Cardiac arrest Emergency management: C ardiopulmonary resuscitation Activate basic life support e.g. call the Emergency M edical Service & initiate CPR Cardiopulmonary resuscitation (CPR) provides blood flow to vital organs until effective circulation can be reestablished CPR should be performed for 2minutes under the following situations before the activation of EMS Near drowning , drug or medication overdose, respiratory arrest

194. Cardiac arrest Emergency management: Cardiopulmonary resuscitation Assessment and intervention for the patient with cardiac arrest includes utilization of the ABCD protocol ABCDs of basic CPR include a irway, b reathing, c irculation & d efibrillation Airway - opening & maintaining an airway Breathing - providing artificial ventilation by rescue breathing if spontaneous respirations are absent or inadequate Circulation - promoting artificial circulation by external cardiac compression when there is no pulse. A dministering medications ( e.g . epinephrine for asystole ) Defibrillation with standard defibrillator or automatic external defibrillator (AED) for ventricular tachycardia & ventricular fibrillation If patient is placed on a monitor using multifunction pads (found on most defibrillators) & ECG shows ventricular fibrillation or patient is unresponsive with ventricular tachycardia Immediate defibrillation rather than CPR is the treatment of choice

195. Cardiac arrest Emergency management: Cardiopulmonary resuscitation In the case of ventricular fibrillation or the patient who is unresponsive with ventricular tachycardia CPR is performed initially only if the defibrillator is not immediately available Survival rate decreases for every minute that defibrillation is delayed There is little chance of survival if patient is not defibrillated within 10 minutes

196. Cardiac arrest Maintaining airway & breathing Remove any obvious material in the mouth or throat Open the airway using a head-tilt chin-lift maneuver Look, listen & feel for air movement Insert an oropharyngeal airway if available & indicated Provide two rescue ventilations using a bag-mask or mouth-mask device An obstructed airway should be suspected when the rescuer cannot give the initial ventilations Heimlich maneuver or abdominal thrusts should be administered to relieve the obstruction

197. Cardiac arrest Maintaining airway & breathing Ventilate patient every 5-6seconds if first rescue ventilations meet little or no resistance An endotracheal intubation is frequently performed by a physician, nurse anesthetist, or respiratory therapist during a resuscitation procedure (if patient is in hospital) Resuscitation bag device is then connected directly to the endotracheal tube (ET) There is an inherent risk of unrecognized esophageal intubation or dislodgement of the ET Tracheal intubation must be confirmed Direct visualization of the ET passing through the vocal cords into trachea Auscultation of breath sounds or observation of bilateral chest expansion Use of end-tidal carbon dioxide detector Chest X-rays are not very reliable

198. Cardiac arrest Restoring circulation Assess carotid pulse (after ensuring ventilation) Provide external cardiac compressions if no pulse is detected Chest compressions are initiated & arrangement put in place to obtain a defibrillator Compressions are performed with the patient on a firm surface e.g. floor or a cardiac board Rescuer (facing the patient’s side) places the heel of one hand in the center of the chest between the nipples & positions the other hand on top of the first hand Fingers should not touch the chest wall Using the force of body weight while keeping the elbows straight, rescuer presses quickly downward from the (rescuer’s) shoulder area to deliver a forceful compression to the victim’s lower sternum about 3.8 to 5 cm (1.5 to 2 in) toward the spine Chest compression rate is approximately 100 times per minute A compression to ventilation ratio of 30 to 2 is recommended without pause for ventilations

199. Cardiac Dysrhythmias

200. Cardiac Dysrhythmias Normal heart rate & rhythm is required for the heart to efficiently pump oxygenated blood & vital nutrients required to maintain optimal systemic function Cardiac dysrhythmias – disturbances in regular heart rate and/or rhythm due to change in automaticity and/or electrical conduction Dysrhythmias may result from disturbances in the formation or conduction (or both) of electrical impulses within the heart Arrhythmias & dysrhythmias are used interchangeably Dysrhythmias are named according to the Site of origin of the impulse Mechanism of formation or conduction involved

201. Cardiac Dysrhythmias Dysrhythmias may arise from the Sinoatrial (SA) node (sinus bradycardia or tachycardia) Anywhere within the atria or ventricles (known as ectopy or ectopic beats) Some may be benign & asymptomatic whereas other dysrhythmias are life-threatening Dysrhythmias may be detected by change in pulse , abnormality on auscultation of heart rate or ECG wave form abnormality Treatment is based on frequency & severity of symptoms produced Continuous cardiac monitoring is indicated for potentially life-threatening dysrhythmias

202. Cardiac Dysrhythmias Normal electrical conduction Electrical impulse that stimulates & paces the cardiac muscle normally originates in the SA node (sinus node) An area located near the superior vena cava in the right atrium Electrical impulse occurs at a rate of 60 to 100 times a minute in the adult The electrical impulse quickly travels from sinus node through the intermodal tract & atria to atrioventricular (AV ) node This process is known as conduction Electrical stimulation of muscle cells of atria causes them to contract Structure of AV node slows electrical impulse transmission Gives atria time to contract & fill ventricles with blood (atrial kick)

203. Cardiac Dysrhythmias Electrical impulse then travels very quickly through bundle of His to right & left bundle branches & the Purkinje fibers (located in ventricular muscle) Electrical stimulation of muscle cells of ventricles in turn causes mechanical contraction of ventricles ( systole) Ventricular cells repolarize & ventricles then relax (diastole ) Electrical impulse causes mechanical contraction of heart muscle that follows it transmission/conduction Electrical stimulation - depolarization Mechanical contraction - systole Electrical relaxation/absence of impulse - repolarization Mechanical relaxation - diastole

204. Identifying Cardiac Rhythms Sites of Origin Sinus (SA) node Atria Atrioventricular (AV) node or junctional Ventricles Mechanisms of Formation or Conduction Normal ( idio ) rhythm Bradycardia Tachycardia Flutter Fibrillation Premature complexes/contractions Conduction blocks

205. Cardiac Dysrhythmias The electrocardiogram Electrical impulse that travels through the heart can be viewed by means of electrocardiography The end product is an electrocardiogram – a graphical record of electrical activities within the heart Each phase of the cardiac cycle is reflected by specific waveforms on the screen of a cardiac monitor or on a strip of ECG graph paper An ECG is obtained by slightly abrading the skin with a clean dry gauze pad & placing electrodes on body at specific areas Electrodes come in various shapes & sizes but they all have 2 components An adhesive substance that attaches to the skin to secure the electrode in place A substance that reduces the skin’s electrical impedance & promotes detection of the electrical current

206. Cardiac Dysrhythmias The electrocardiogram The number & placement of electrodes depend on the type of ECG needed Most continuous monitors use 2-5 electrodes (usually placed on limbs & chest ) These electrodes create an imaginary line (called a lead) that serves as a reference point from which the electrical activity is viewed A lead is like an eye of a camera (looks only at the electrical activity directly in front of it) ECG waveforms that appear on the paper or cardiac monitor represent the electrical current in relation to a lead A change in the waveform can be caused by A change in the electrical current (where it originates or how it is conducted) or A change in the lead

207. Cardiac Dysrhythmias Obtaining an Electrocardiogram Electrodes are attached to cable wires which are connected to an ECG machine A standard 12-lead ECG 10 electrodes (6 on chest & 4 on limbs ) are placed on the body Limb electrodes provide first six leads: leads I, II, III, aVR , aVL & aVF Limb electrodes are usually placed on areas that are not bony & that do not have significant movement To prevent interference from electrical activity of skeletal muscle A standard 12-lead ECG reflects the electrical activity primarily in the left ventricle Six chest electrodes are applied to chest at very specific areas & provide the V or precordial leads (V1 - V6 )

208. Cardiac Dysrhythmias Interpreting the Electrocardiogram ECG waveforms are printed on graph paper that is divided by light & dark vertical & horizontal lines at standard intervals Time & rate are measured on the horizontal axis of the graph Amplitude or voltage is measured on the vertical axis ECG waveform moves toward the top of the paper - positive deflection ECG moves toward the bottom of the paper - negative deflection

209. Cardiac Dysrhythmias Waves, Complexes & Intervals ECG waveforms P wave - represents electrical impulse starting in the sinus node & spreading through the atria ( atrial depolarization ) QRS complex - represents ventricular depolarization (atrial repolarization also occurs) T wave - represents ventricular repolarization ( resting state) U wave - thought to represent repolarization of the Purkinje fibers Sometimes seen in patients with hypokalemia (low potassium levels ), HPT or heart disease May be mistaken for an extra P wave (especially if taller)

210. Cardiac Dysrhythmias Waves, Complexes & Intervals ECG segments & intervals PR interval - measured from the beginning of the P wave to the beginning of the QRS complex & represents the time needed for sinus node stimulation, atrial depolarization & conduction through the AV node before ventricular depolarization ST segment - represents early ventricular repolarization (lasts from the end of the QRS complex to the beginning of the T wave ) Beginning of the ST segment is usually identified by a change in the thickness or angle of the terminal portion of the QRS complex It is analyzed to identify whether it is above or below the isoelectric line (a sign of cardiac ischemia) QT interval - represents the total time for ventricular depolarization & repolarization (measured from the beginning of the QRS complex to the end of the T wave)

211. Cardiac Dysrhythmias Waves, Complexes & Intervals ECG segments & intervals TP interval - measured from the end of the T wave to the beginning of the next P wave (an isoelectric period) PP interval - measured from the beginning of one P wave to the beginning of the next PP interval is used to determine atrial rhythm & atrial rate RR interval - measured from one QRS complex to the next QRS complex RR interval is used to determine ventricular rate & rhythm

212. Waves, Complexes & Intervals

213. Cardiac Dysrhythmias Sinus Tachycardia Etiology Sympathetic nerve fibers which act to speed up excitation of the SA node are stimulated by underlying causes such as Anxiety , exercise, fever, shock, drugs & chemical substances ( catecholamines , atropine, aminophylline, caffeine, nicotine, alcohol), altered metabolic states (faster e.g. hyperthyroidism, fever), electrolyte disturbances Wave of impulse is transmitted through normal conduction pathways The rate of sinus stimulation is simply greater than normal (rate exceeds 100 beats/minute )

214. Cardiac Dysrhythmias Sinus Tachycardia Analysis Rate: 100 - 150 beats/minute Rhythm : RR intervals are regular P wave : present for each QRS complex, normal configuration, and each P wave is identical or may be buried in previous T wave PR interval : falls between 0.12 and 0.20, or 0.16 seconds. P wave may be hidden in preceding T wave in rapid rates QRS complex : normal in appearance, one follows each P wave T wave : follows each QRS complex & is positively conducted QT interval: <0.48 seconds

215. Cardiac Dysrhythmias Sinus Tachycardia Management Treatment is directed toward elimination of the cause rather than the dysrhythmia Urgency is dependent on effect of rapid heart rate on coronary artery filling time to prevent cardiac ischemia Administration of oxygen & normal saline solution should be considered as initial treatment Beta-blockers & calcium channel blockers are rarely used to reduce the HR

216. Cardiac Dysrhythmias Sinus Bradycardia Etiology The parasympathetic fibers (vagal tone) are stimulated & cause the sinus node to slow Underlying causes: Drugs e.g. calcium channel blockers, amiodarone, beta-blockers Altered metabolic states (lower) such as hypothyroidism, sleep, athletic states The process of aging (causes increasing fibrotic tissue scarring of the SA node) Vagal stimulation e.g. vomiting, bearing down (defecation), suctioning, severe pain, extreme emotions

217. Cardiac Dysrhythmias Sinus Bradycardia Etiology Underlying causes Certain cardiac diseases such as acute MI (especially inferior wall MI), increased intracranial pressure The H’s (hypovolemia, hypoxia, hydrogen ion (acidosis), hypokalemia or hyperkalemia, hypoglycemia, and hypothermia) & T’s (toxins, tamponade, tension pneumothorax, thrombosis) The wave of impulse is transmitted through the normal conduction pathways The rate of sinus stimulation is simply less than normal (less than 60 beats/minute )

218. Cardiac Dysrhythmias Sinus Bradycardia Analysis Rate: <60 beats/minute Rhythm : RR interval is regular P wave : present for each QRS complex, normal configuration, and each P wave is identical PR interval: falls between 0.12 & 0.18 seconds QRS complex : normal in appearance, one follows each P wave T wave : follows each QRS and is positively conducted

219. Cardiac Dysrhythmias Sinus Bradycardia Management Urgency of treatment depends on effect of slow rate on maintenance of CO Shortness of breath, acute alteration of mental status, angina, hypotension, ST-segment changes or premature ventricular complexes Decreased exercise capacity, fatigue, unexplained confusion or memory loss may occurs as a result of sinus dysfunction among patients older than 50yeras Atropine 0.5 mg IV push blocks vagal stimulation to the SA node & therefore accelerates heart rate Can be given every 3 - 5 minutes to a maximum total dose of 3 mg Dopamine or epinephrine are alternatives if atropine is ineffective If bradycardia persists a pacemaker may be required Sinus bradycardia is common in athletic individuals & does not require treatment

220. Cardiac Dysrhythmias Sinus a rrhythmia Occurs when the sinus node creates an impulse at an irregular rhythm The rate usually increases with inspiration & decreases with expiration Non-respiratory causes include heart disease & valvular disease (but these are rare) Sinus arrhythmia has the following characteristics Ventricular and atrial rate: 60 to 100 in the adult Ventricular and atrial rhythm: Irregular QRS shape and duration: Usually normal, but may be regularly abnormal T wave: Normal and consistent shape; always in front of the QRS PR interval: Consistent interval between 0.12 and 0.20 seconds Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated

221. Cardiac Dysrhythmias Premature Atrial Contraction (premature atrial complex or atrial premature beat) - an electrical impulse starts in the atrium before the next normal impulse of the sinus node Etiology May occur in the healthy heart (usually idiopathic & benign) A pulse deficit may exist (a difference between the apical & radial pulse) Patient may say “My heart skipped a beat” In the diseased heart Premature atrial contractions ( PACs) may cause ischemia & a resultant irritability in the atria PACs may increase in frequency & be the precursor of more serious dysrhythmias May be caused by electrolyte abnormalities, hypoxia, MI, heart failure, acid-base disturbances, anxiety, caffeine, alcohol, nicotone

222. Cardiac Dysrhythmias Premature Atrial Contraction The wave of impulse of the PAC originates within the atria & outside the sinus node P wave will be present (because the impulse originates within the atria) But P wave will also be different in appearance as compared with those beats originating within the sinus node The impulse traverses the remainder of the conduction system in a normal pattern The QRS complex is identical in configuration to the normal sinus beats

223. Cardiac Dysrhythmias Premature Atrial Contraction Analysis Rate : may be slow or fast Rhythm : will be irregular, caused by the early occurrence of the PAC P wave : will be present for each normal QRS complex (the P wave of the premature contraction will be distorted in shape) PR interval : may be normal but can also be shortened, depending on where in the atria the impulse originated The closer the site of atrial impulse formation to the atrioventricular [ AV] node , the shorter the PR interval will be QRS complex : within normal limits because all conduction below the atria is normal T wave : normally conducted

224. Cardiac Dysrhythmias Premature Atrial Contraction Management Generally requires no treatment if laboratory values are normal PACs should be monitored for increasing frequency (more than 6 PACs require treatment) May herald a worsening disease state or the onset of more serious dysrhythmias e.g. atrial fibrillation Treatment is directed towards the cause

225. Cardiac Dysrhythmias Paroxysmal Atrial Tachycardia Etiology Syndrome of mitral valve prolapse Ischemic CAD Excessive use of alcohol, cigarettes, caffeine Drugs e.g. digoxin is a frequent cause An ectopic atrial focus captures the rhythm of the heart & is stimulated at a very rapid rate The impulse is conducted normally through the conduction system so the QRS complex usually appears within normal limits The rate is often so rapid that P waves are not obvious but may be “buried” in the preceding T wave

226. Cardiac Dysrhythmias Paroxysmal Atrial Tachycardia Analysis Rate : between 150 and 250 beats/minute Rhythm : regular P wave : present before each QRS complex (however , the faster the rate , the more difficult it becomes to visualize P waves) PR interval : usually not measurable QRS complex : will appear normal in configuration & within 0.06 to 0.10 seconds T wave : will be distorted in appearance as a result of P waves being buried in them

227. Cardiac Dysrhythmias Paroxysmal Atrial Tachycardia Management Treatment is directed first to slowing the rate & second, to reverting the dysrhythmia to a normal sinus rhythm Reducing the rate may be accomplished by having the patient perform a Valsalva maneuver (stimulates the vagus nerve to slow the heart) A Valsalva maneuver may be done by having the patient gag or “bear down” as though attempting to have a bowel movement The doctor may choose to perform carotid massage

228. Cardiac Dysrhythmias Paroxysmal Atrial Tachycardia Management Adenosine is the drug of choice for paroxysmal atrial tachycardia associated with hypotension, chest pain or shortness of breath IV beta-adrenergic blockers (e.g. esmolol ) may also be used Calcium channel blockers ( e.g . verapamil) are effective in reverting this dysrhythmia Beware of hypotension especially in the volume-depleted patient If drug therapy is ineffective, elective cardioversion can be used

229. Cardiac Dysrhythmias Atrial Flutter - defect in atrium causes a rapid, regular atrial rate (usually between 250 - 400 beats/minute) Etiology Occurs with atrial stretching or enlargement (as in AV valvular disease ), MI, heart failure, COPD, open heart surgery, repair of congenital cardiac defects, thyrotoxicosis An ectopic atrial focus captures the rhythm in atrial flutter & fires at an extremely rapid rate (200 - 400 beats/minute) with regularity Conduction of the impulse through the conduction system is normal (thus QRS complex is unaffected)

230. Cardiac Dysrhythmias Atrial Flutter An important feature of this dysrhythmia is that the AV node sets up a therapeutic block which disallows some impulse transmission This can produce a varying block or a fixed block (i.e. sometimes the AV node will transmit every second flutter wave, producing a 2:1 block, or the rhythm can be 3:1 or 4:1) If the AV node were to conducted 1:1, then the outcome would be a ventricular rate of also 250 - 400 beats/minute ( → rapid patient deteriorate)

231. Cardiac Dysrhythmias Atrial Flutter Analysis Rate : atrial rate between 250 & 400 beats/minute (ventricular rate will depend on degree of block but usually between 75-150beats/minute) Rhythm : regular or irregular (depending on kind of block e.g . 2:1, 3:1 or a combination ) P wave : typical P wave not present (instead , it is replaced by a saw-toothed pattern that is produced by rapid firing of atrial focus) These waves are also referred to as “ F” waves PR interval : not measurable QRS complex : normal configuration & normal conduction time T wave : present but may be obscured by flutter waves

232. Cardiac Dysrhythmias Atrial Flutter Management Urgency of treatment depends on ventricular response rate & resultant symptoms (too rapid or slow a rate will decrease CO) Chest pain, shortness of breath & low blood pressure Vagal stimulation or administration of adenosine – slows down sympathetic stimulation A calcium channel blocker (e.g. diltiazem) may be used to slow AV nodal conduction Use with caution in the patient with HF, hypotension or concomitant beta-adrenergic blocker therapy)

233. Cardiac Dysrhythmias Atrial Flutter Management Digoxin may be used An IV beta-adrenergic blocker (e.g. esmolol ) may also be used Atrial flutter will typically respond to cardioversion if drug therapy is unsuccessful Electrophysiologic studies & subsequent ablation therapy are highly effective because ectopic focus is usually readily identified

234. Cardiac Dysrhythmias Atrial Fibrillation - an uncoordinated atrial electrical activation that causes a rapid, disorganized & uncoordinated twitching of atrial musculature Etiology Fibrotic changes associated with the aging process, acute MI, CAD, HPT, valvular diseases & digoxin preparations may cause atrial fibrillation Inflammatory or infiltrative diseases (e.g. myocarditis, pericarditis), DM, hyperthyroidism, obesity Fluid shifts in body ( i.e . after hemodialysis or surgery ) Multiple atrial foci fire impulses at rapid & disorganized rates The atria are not depolarized effectively Thus there are no well-formed P waves Instead , the baseline between QRS complexes is filled with a “wiggly ” line that is described as fine or coarse

235. Cardiac Dysrhythmias Atrial Fibrillation If the atrial rate is rapid enough, the line will appear almost flat The atria are said to be firing at rates of between 300 & 500 times per minute Atrial fibrillation may be described as controlled if the ventricular response is 100 beats/minute or less The dysrhythmia is uncontrolled if the rate is above 100 beats/minute Atrial fibrillation may be transient - starting & stopping suddenly & occurring for a very short time ( paroxysmal dysrhythmia ) It may also be persistent - requiring treatment to terminate the rhythm or to control the ventricular rate Lack of consistency in describing the pattern of atrial fibrillation has led to use of numerous labels ( e.g . acute, chronic , paroxysmal, persistent, permanent) and difficulty in comparative assessment of treatments

236. Cardiac Dysrhythmias Atrial Fibrillation Analysis Rate : atrial fibrillation is usually immeasurable because fibrillatory waves replace P waves (300-600beats/minute) ventricular rate may vary from bradycardia to tachycardia; depends on ability of AV node to conduct atrial impulses (often 120-200beats/minute) Rhythm : classically described as an “irregular irregularity” P wave : replaced by fibrillatory waves (sometimes called “little f ” waves ) PR interval : not measurable QRS complex : a normally conducted complex T wave : normally conducted P:QRS ratio – many to 1

237. Cardiac Dysrhythmias Atrial Fibrillation Management Atrial fibrillation has been associated with an increased risk of stroke and premature death Controlled atrial fibrillation of long-standing duration requires no treatment as long as the patient is experiencing no untoward effects Most cardiologists agree that reversion of long-standing atrial fibrillation is hazardous because of the potential for a thrombus to be dislodged from the atria at the time of reversion Uncontrolled atrial fibrillation (ventricular responses of 100 beats/minute or greater) is treated with beta-adrenergic blocker or calcium channel blockers to control rate at rest and activity If the atrial fibrillation is of recent onset, the cardiologist may choose to revert the rhythm to a sinus rhythm

238. Cardiac Dysrhythmias Atrial Fibrillation Management Digoxin is a second-line drug for rate control because it only controls rate at rest Cardioversion for recent-onset atrial fibrillation may be required starting with low amounts of biphasic electrical current (100 to 200 joules ) Chronic anticoagulation therapy may be warranted to prevent microemboli

239. Cardiac Dysrhythmias Premature Ventricular Contraction/complex - an impulse that starts in a ventricle & is conducted through the ventricles before the next normal sinus impulse Etiology Can occur in healthy people, especially with intake of caffeine, nicotine or alcohol May be caused by acute MI, other forms of heart disease, pulmonary diseases, electrolyte disturbances, metabolic instability & drug abuse The wave of impulse originates from an ectopic focus ( foci) within the ventricles at a rate faster than the next normally occurring beat Normal conduction pathway is bypassed Configuration of the premature ventricular contraction (PVC) is wider than normal & is distorted in appearance PVCs may occur in regular sequence with normal rhythm; every other beat ( bigeminy ), every third beat ( trigeminy ) & so forth Patient may feel nothing or may say that the heart “skipped a beat”

240. Cardiac Dysrhythmias Premature Ventricular Contraction Analysis Rate: may be slow or fast Rhythm : will be irregular because of the premature firing of the ventricular ectopic focus P wave : will be absent because the impulse originates in the ventricle, bypassing the atria & AV node PR interval : not measurable QRS complex : will be widened greater than 0.12 second, bizarre in appearance when compared with normal QRS complex The QRS of a PVC is commonly referred to as having a “ sore thumb ” appearance T wave : the T wave of the PVC is usually deflected opposite to the QRS P:QRS ratio: 0:1; 1:1 etc

241. Cardiac Dysrhythmias Premature Ventricular Contraction Management PVCs are usually the precursors of more serious ventricular dysrhythmias Effect of a PVC depends on its timing in the cardiac cycle and how much blood was in the ventricles when they contracted Initial treatment is aimed at correcting the cause The following conditions involving PVCs require prompt & vigorous treatment, especially if the patient is symptomatic or unstable: PVCs occurring at a rate exceeding six per minute Occur as two or more consecutively PVCs fall on the peak or down slope of the T wave (period of vulnerability) Are of varying configurations, indicating a multiplicity of foci

242. Cardiac Dysrhythmias Premature Ventricular Contraction Management Standard treatment (historically) for PVCs has been lidocaine IV Amiodarone is now the preferred drug due to lidocaine’s risk for toxicity Lidocaine toxicities include confusion and slurred speech It should be used with caution in older adults & in those with liver disease Amiodarone toxicities include pulmonary fibrotic changes, hypothyroidism & liver dysfunction Atropine may be chosen to accelerate the heart rate & eliminate ectopic beats in conditions where ventricular premature beats occur in conjunction with a bradydysrhythmia Atropine should be used with caution with acute MI The injured myocardium may not be able to tolerate the accelerated rate Electrolyte infusions may also be needed to treat PVCs e.g. magnesium sulfate in acute MI

243. Cardiac Dysrhythmias Ventricular Tachycardia - three or more PVCs in a row, occurring at a rate exceeding 100 bpm Etiology Occurs with: Acute MI, cardiomyopathy Syndromes of accelerated rhythm that deteriorate (e.g . Wolff-Parkinson-White syndrome ) Metabolic acidosis, especially lactic acidosis Electrolyte disturbance Toxicity to certain drugs, such as digoxin or isoproterenol

244. Cardiac Dysrhythmias Ventricular Tachycardia A life-threatening dysrhythmia that originates from an irritable focus within the ventricle at a rapid rate An emergency because the patient is usually (although not always) unresponsive & pulseless Because the ventricles are capable of an inherent rate of 40 beats/minute or less A ventricular rhythm at a rate of 100 beats/minute may be considered tachycardia Manifestations of VT depends on ventricular rate & severity of ventricular dysfunction

245. Cardiac Dysrhythmias Ventricular Tachycardia Analysis Rate : usually between 100 and 220 beats/minute Atrial rate depends on the underlying rhythm (e.g. sinus rhythm ) Rhythm : usually regular but may be irregular (may be monomorphic or polymorphic) P wave : not present PR interval : not measurable QRS complex : broad, bizarre in configuration, widened greater than 0.12 seconds T wave : usually deflected opposite to the QRS complex P:QRS ratio: d ifficult to determine, but if P waves are apparent , there are usually more QRS complexes than P waves

246. Cardiac Dysrhythmias Ventricular Tachycardia Management Ventricular tachycardia (VT) less than 30 seconds is called non-sustained VT VT more than 30 seconds is sustained VT & requires immediate treatment Medications are the initial treatments if the patient has a pulse & is hemodynamically stable Amiodarone IV bolus can be given to halt the dysrhythmia (suitable for both stable & unstable VTS) Other potential medications that may be used (if amiodarone fails) include lidocaine & procainamide If patient becomes hemodynamically unstable; unconscious & without a pulse Defibrillation or synchronized cardioversion are the preferred interventions

247. Cardiac Dysrhythmias Ventricular Tachycardia Management Purpose of cardioversion/defibrillation Abolish all abnormal electrical activity & allow intrinsic cardiac rhythm the opportunity to restart VT may be refractory to drug therapy under some circumstances Non-pharmacologic treatments e.g. endocardial resection, aneurysmectomy , antitachycardia pacemakers, cryoablation , automatic internal defibrillators, catheter ablation

248. Cardiac Dysrhythmias Ventricular Tachycardia Polymorphous VT or torsades de pointes (twisting of the points) An atypical form of VT which occurs as a result of consequence of drug therapy ( e.g . quinidine therapy) or electrolyte imbalance e.g. hypomagnesemia Torsades de pointes is characterized by a QT interval prolonged to greater than 0.60 second Varying R-R intervals Polymorphous QRS complexes

249. Cardiac Dysrhythmias Ventricular Tachycardia Polymorphous VT or torsades de pointes (twisting of the points) It is important to diagnose polymorphous VT (as treatment differs from monomorphic VT) Treatment of choice is administration of magnesium sulfate 1 g IV over 5 to 60 minutes If the patient loses consciousness & pulse Defibrillation Ventricular pacing to override the ventricular rate (capture the rhythm) is also an acceptable treatment Procainamide should be avoided because its effect is to prolong the QT interval (suitable only for stable VTs)

250. Cardiac Dysrhythmias Ventricular Fibrillation - a rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles ( n o atrial activity is seen on the ECG ) Etiology Occurs in acute MI, acidosis, cardiomyopathies, valvular heart diseases, electrolyte disturbances, untreated VTs, electrical shock, proarrhythmic medications ( sotalol , amiodarone, terfenadine , thioridazine ) The ventricles are firing chaotically at rates that exceed 300 beats/minute, resulting in ineffective impulse conduction CO ceases, absence of an audible heartbeat, patient loses pulse, respirations, BP & consciousness Must be reversed immediately or the patient will die from cardiac arrest

251. Cardiac Dysrhythmias Ventricular Fibrillation Analysis Rate : not measurable because of absence of well-formed QRS complexes (usually more than 300bpm) Rhythm : chaotic P wave : not present QRS complex : bizarre, chaotic, no definite contour T wave : not apparent

252. Cardiac Dysrhythmias Ventricular Fibrillation Management The only treatment for ventricular fibrillation is immediate defibrillation Defibrillate at 120 - 200 joules with a biphasic defibrillator Epinephrine or vasopressin are first-line drugs after defibrillation ( because these drugs may make the fibrillation more vulnerable to defibrillation) Unsuccessful defibrillation may be a result of lactic acidosis (treatable with sodium bicarbonate ) Check adequacy of the high-quality CPR being performed: 100 compressions/minute

253. Cardiac Dysrhythmias Atrioventricular Block - AV blocks occur when the conduction of the impulse through the AV nodal or His bundle area is decreased or stopped The PR interval is assessed for the possibility of an AV block Etiology May be caused by ischemia or inferior wall MI , valvular diseases, cardiomyopathies, medications (digoxin, CCBs, beta-blockers), hypothyroidism, increased vagal tone (athletic tone, coughing, sleep, suctioning ) or Stokes-Adams syndrome AV block due to increased vagal stimulation is accompanied by sinus bradycardia Impaired tissue at the level of AV node prevents timely passage of the wave of impulse through conduction system AV node block may be temporary & resolve on its own or it may be permanent & require permanent pacing Other blocks may result in decreased heart rate ( → decrease in perfusion to vital organs e.g. brain , heart, kidneys, lungs, skin )

254. Cardiac Dysrhythmias Atrioventricular Block First-degree AV block Impulse is transmitted normally but it is delayed at the level of the AV node All atrial impulses are conducted through the AV node into the ventricles at a rate slower than normal PR interval exceeds 0.20 second s Second-degree AV block Two types of second-degree AV block Second-degree type 1 ( Mobitz 1 Wenckebach ) Second-degree type 2 ( Mobitz 2)

255. Cardiac Dysrhythmias Atrioventricular Block Analysis ( f irst-degree AV block ) Rate : usually normal but may be slow Rhythm : regular P wave : present for each QRS complex, identical in configuration PR interval : prolonged to greater than 0.20 seconds QRS complex : normal in appearance & between 0.06 and 0.10 seconds T wave : normally conducted

256. Cardiac Dysrhythmias Atrioventricular Block Second-degree type 1 ( Mobitz 1 or Wenckebach ) Block occurs above the AV node There is an increase in delay of electrical impulse (increasing PR interval) with every beat until one P wave fails to conduct & is not followed by a QRS complex (beat is dropped) Because the AV node is not depolarized by the blocked atrial impulse, the AV node has time to fully repolarize, so that the next atrial impulse can be conducted within the shortest amount of time Usually a temporary & benign dysrhythmia (seldom requires intervention/pacing unless ventricular rate is slow & patient is unstable)

257. Cardiac Dysrhythmias Atrioventricular Block Second-degree type 2 ( Mobitz 2) Block occurs below AV node in bundle of His or bundle-branch system Atria & ventricles are discharging impulses but the activity bears no relationship to each other There is a sudden failure to conduct an atrial impulse to the ventricles without a delay of the PR interval

258. Cardiac Dysrhythmias Atrioventricular Block Analysis (second-degree AV block) Rate : usually normal Rhythm : may be regular or irregular P wave : present but some may not be followed by a QRS complex A ratio of two, three, or four P waves to one QRS complex may exist PR interval: varies in Mobitz I ( Wenckebach ), usually lengthens until one is not conducted; constant in Mobitz II, but not all P waves conducted T wave : normally conducted

259. Cardiac Dysrhythmias Atrioventricular Block Third-degree AV block or complete heart block Electrical impulse is completely blocked from the SA node to AV node An independent pacemaker in the ventricles takes over at a much slower rate than the atria & are firing independently of each other Having two impulses stimulate the heart results in a condition called AV dissociation

260. Cardiac Dysrhythmias Atrioventricular Block Analysis (third-degree AV block) Rate : atrial rate is measured independently of ventricular rate ; the ventricular rate is usually very slow Rhythm : each independent rhythm will be regular, but they will bear no relationship to each other P wave : present but no consistent relationship with the QRS PR interval : not really measurable QRS complex : depends on the escape mechanism ( i.e . AV node will have normal QRS, ventricular will be wide & the rate will be slower ) T wave : normally conducted

261. Cardiac Dysrhythmias Atrioventricular Block Management Treatment of heart blocks depends on the effect the prevailing rate is having on CO First-degree AV block usually requires no treatment Second-degree AV block (type 1 & 2) may require treatment if the ventricular rate falls too low to maintain effective CO Mobitz type 2 is more serious than Mobitz type 1 Treatment is often aimed at increasing the heart rate

262. Cardiac Dysrhythmias Atrioventricular Block Management Third-degree AV block usually requires intervention Some patients may be able to tolerate third-degree block for a length of time Transcutaneous pacing should be employed in the emergent situation while transvenous pacing is being set up Atropine may be given while awaiting the pacemaker (but it must be remembered that the effect of atropine is to block vagal tone and the vagus acts on the sinus node) Because the AV node is the culprit in heart block, atropine may not be helpful

263. Cardiac Dysrhythmias Nursing diagnoses Decreased cardiac output Anxiety related to fear of the unknown Deficient knowledge about the dysrhythmia and its treatment

264. Cardiac Dysrhythmias Monitoring and managing dysrhythmia Regularly evaluates the patient’s blood pressure, pulse rate & rhythm, rate & depth of respirations, and breath sounds to determine the dysrhythmia’s hemodynamic effect The nurse also asks the patient about episodes of lightheadedness, dizziness or fainting as part of the ongoing assessment Obtain a 12-lead ECG, continuously monitor the patient & analyze rhythm strips to track the dysrhythmia Administer prescribed antiarrhythmic medications, observe for the therapeutic & adverse reactions Monitor patient’s response to exercise (ventricular rate) The 6-minute walk test (distance covered, pre- & post-exercise heart rates) Assess for factors that contribute to the dysrhythmia e.g . oxygen deficits, acid-base & electrolyte imbalances , caffeine, nonadherence to the medication regimen

265. Cardiac Dysrhythmias Minimizing anxiety Stay with the patient & provides assurance of safety & security while maintaining a calm & reassuring attitude Seek the patient’s view of the events & discusses the emotional response to the dysrhythmia Encouraging verbalization of feelings & fears, providing supportive or empathetic statements & assisting the patient to recognize feelings of anxiety, anger or sadness Emphasize successes with the patient to promote a sense of self-management of the dysrhythmia e.g. onset of therapeutic effects of medication help the patient develop a system to identify possible causative, influencing , and alleviating factors e.g . keeping a diary

266. HYPERTENSION

267. Hypertension Introduction A systolic blood pressure greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg based on the average of two or more accurate blood pressure measurements taken during two or more contacts with a health care provider Normal BP - less than 120/80 mmHg Prehypertension - 129/80 to 89 mmHg Hypertension - 140/90 mm Hg or higher The higher either the systolic or diastolic pressure the greater the health risk ( stroke, heart attack, heart failure, cardiovascular death )

268. Classification of blood pressure for adults age 18 & older BP classification Systolic BP (mmHg) Diastolic BP (mmHg) Normal <120 <80 Prehypertension 120–139 80–89 Stage 1 hypertension 140–159 90–99 Stage 2 hypertension ≥ 160 ≥ 100

269. Hypertension Classification of hypertension Primary/essential/idiopathic hypertension Represent 90-95% of hypertensive cases Main reason for elevation in BP cannot be identified Secondary hypertension Represent 5-10 % of hypertensive cases Elevated BP due to an identifiable or specific causes e.g. narrowing of renal arteries, renal parenchymal disease, coarctation of the aorta, cushing syndrome, pregnancy, drugs (NSAIDs, oral contraceptives, sympathomimetics )

270. Hypertension Etiology Essential hypertension - has a multifactorial etiology Genetic factors Fetal factors (low birth weight is associated with subsequent high BP) Race or ethnicity (more common & severe in B lacks than Caucasians) Increasing age (very common between 30 – 60years) Accumulation of atherosclerotic plaque, fragmentation of arterial elastins Increased collagen deposits, impaired vasodilation Isolated systolic hypertension usually occurs

271. Hypertension Etiology Environmental factors Inactive or sedentary lifestyles High alcohol intake High sodium intake High intake of saturated fat (dyslipidemia) Use of oral contraceptives & other drugs such as NSAIDs Obesity Insulin resistance Increased stress levels (physical & emotional ) Metabolic syndrome Other diseases (CAD, metabolic syndrome, DM) NB: Cigarette smoking is not a cause

272. Hypertension Pathophysiology BP = CO X PR Changes in BP are associated with a change in cardiac output and/or peripheral resistance Hypertension occurs when an anomaly with the control systems that monitor & regulate BP develop

273. Hypertension Pathophysiology Hypertension may occur as a result of one or more of the following Increased sympathetic nervous system activity (related to autonomic nervous system dysfunction) Increased renal reabsorption of sodium, chloride & water (related to genetic variations in pathways by which kidneys deal with sodium) Elevated activity of the r enin-angiotensin-aldosterone system (expansion of ECF compartment & increased peripheral resistance) Decreased vasodilation of arterioles (related to a dysfunction of the vascular endothelium) Resistances to the action of insulin (association between hypertension , hypertriglyceridemia, type 2 DM & obesity)

274. Hypertension Pathophysiology Hypertension is associated with an increased risk of atherosclerosis & diabetes mellitus Prolonged elevation of BP → damage to blood vessels → loss of elasticity & compliance → weak vessels → compromised blood delivery to target organs (brain , heart, kidneys, eyes) Common complications of a prolonged & uncontrolled hypertension Myocardial infarction Heart failure Renal failure Stroke Impaired vision

275. Hypertension Clinical manifestations Hypertension clinically can be viewed as A sign - used to monitor hemodynamic stability A risk factor - atherosclerotic heart diseases or A disease - major contributor to cardiac, cerebrovascular, renal & peripheral vascular diseases Sometimes referred to as the “silent killer” Usually symptomless Physical examination may not reveal any abnormalities other than an elevated BP Hypertension on the basis of one BP reading only when the BP is ≥ 210/120 mmHg Presence of signs & symptoms often indicate vascular damage (related to specific organ)

276. Hypertension Clinical manifestations Cardiac manifestations - chest pain (angina or MI), left ventricular hypertrophy, edema, cardiac arrest Renal manifestations - elevated BUN & creatinine, nocturia Cerebrovascular manifestation - weakness , alteration in vision or speech, dizziness, temporary paralysis on one side (hemiplegia ) Retinal manifestations - hemorrhages, periorbital edema, cotton wool spots (infarcts)

277. Hypertension Other common clinical manifestations Headaches Sweating Breathlessness Dizziness Blurred vision Vertigo(light headedness ) Tinnitus(ringing/buzzing sound in ears) Confusion Increased irritability Seizures Transient paralysis Stupor/sleepiness Severe vomiting Epistaxis Chest pains Fatigue/general weakness Palpitations.

278. Hypertension Diagnosis Thorough health history & physical examination (risk assessment & classification) Assessment of target organ damage Routine investigations Urinalysis Blood chemistries (estimations of sodium, potassium, fasting glucose) Lipoprotein/cholesterol levels Renal function test (BUN & creatinine levels) Electrocardiogram Echocardiogram

279. Hypertension Medical management Main goal To prevent complications & death by achieving & maintaining BP at 140/90 mmHg or lower Lower goal pressure of 130/80 mmHg for people with diabetes mellitus or chronic kidney disease Optimal management plan is inexpensive , simple & causes least possible disruption in the patient’s life Management of hypertension is divided into Pharmacological interventions Non-pharmacological interventions

280. Hypertension Non-pharmacological interventions - lifestyle modifications Weight loss if obese Reduction in alcohol & sodium intake Smoking cessation Reduction in dietary saturated fat & cholesterol Reduced intake of coffee & other caffeinated beverages Increased consumption of fruits , vegetables & low-fat dairy products Intake of daily recommended allowances of calcium, potassium & magnesium Regular physical activity

281. Hypertension Pharmacological interventions Diuretics e.g . furosemide, chlorothiazide , spironolactone Adrenergic agents e.g. methyldopa, propranolol Vasodilators e.g Hydralazine, nitroprusside Angiotensin-converting enzyme inhibitors e.g. lisinopril Angiotensin II receptor blockers e.g. losartan, candesartan Calcium channel blockers e.g. Nifedipine

282. Hypertension Nursing diagnoses Noncompliance with medication regimen & lifestyle changes Readiness for Enhanced Self-health Management related to control of hypertension & prevention of target organ disease Deficient knowledge regarding the relation between the treatment regimen and control of the disease process

283. Hypertension Nursing management Improving cooperation & compliance Assess patient’s cooperation towards redirecting lifestyle in accordance with guidelines of therapy; acknowledge associated difficulty & provide support & encouragement Develop a plan of instruction for medication self-management Convenient schedule Awareness of brand names & generic names Stress the fact that there may be no correlation between high BP & symptoms

284. Hypertension Nursing management Improving cooperation & compliance Regular follow-up is important to prevent complications & reduce more serious health care interventions in the future Assess for & try to eliminate side effects of medication regimen Anorexia, fatigue, nausea, or lightheadedness often occur during the first few days or weeks Orthostatic hypotension, constipation, cough, ankle swelling, sexual dysfunction Adverse effects or deteriorating hypertension (fainting, palpitations, dyspnea, headaches) Dose may be reduced or drug changed

285. Hypertension Nursing management Encouraging self-management Explain the meaning of high BP, risk factors & their influences on cardiovascular , cerebral & renal systems Stress that there can never be total cure, only control, of essential hypertension (emphasize the consequences of uncontrolled hypertension) Instruct the patient regarding proper method of taking BP Determine recommended dietary plans & provide dietary education as appropriate Educate patient about factors that may affect BP, such as dehydration , diarrhea, and other illnesses, so BP should be monitored closely and treatment adjusted Encourage the patient to keep follow-up appointments as directed

286. Hypertensive crisis Two classes of hypertensive crisis Hypertensive emergency - BP is extremely elevated (more than 180/120 mm Hg) & must be lowered immediately (not necessarily to less than 140/90 mm Hg) to halt or prevent damage to the target organs Often associated with hypertension of pregnancy, acute myocardial infarction, dissecting aortic aneurysm & intracranial hemorrhage Goal of treatment is to reduce BP by up to 25% within first one hour, then a goal of 160/100 mmHg within the next 6hours Exceptions are ischemic stroke (no benefit from immediate BP reduction) & dissecting aortic aneurysm (lower systolic pressure of 100 mmHg if patient can tolerate) Treated with rapid-acting medications (nitroprusside, nicardipine , fenoldopam , enalaprilat , nitroglycerin) & normal saline (volume replacement) Hypertensive urgency- BP is very elevated but there is no evidence of impending or progressive target organ damage Include elevated BP associated with severe headaches, nosebleeds or anxiety Can be treated with fast acting oral agents e.g. beta blockers, ACE inhibitors

287. Hypertensive crisis May occur under one or more of the following circumstances Undiagnosed hypertensive states Poorly controlled hypertension Abrupt cessation of antihypertensive medication Extremely close hemodynamic monitoring of the patient’s BP & cardiovascular status is required during treatment of hypertensive emergencies & urgencies

288. Other vascular disorders

289. Arteriosclerosis and Atherosclerosis Arteriosclerosis Most common disease of the arteries (occurs throughout the arterial system) A term used to describe the “hardening of the arteries” It involves a diffuse process whereby muscle fibers & endothelial lining of the walls of small arteries & arterioles become thickened A normal part of the aging process Atherosclerosis Involves a different process affecting the intima of large & medium-sized arteries Changes consist of accumulation of lipids, calcium, blood components, carbohydrates & fibrous tissue on the intimal layer of the artery These accumulations are referred to as atheromas or plaques

290. Arteriosclerosis and Atherosclerosis Atherosclerosis is a generalized disease of the arteries When it is present in the extremities, it is usually present elsewhere in the body The pathologic processes of arteriosclerosis & atherosclerosis differ Rarely does one occur without the other

291. Arteriosclerosis and Atherosclerosis Risk factors Modifiable risk factors Nicotine use (tobacco smoking or chewing) Diet (contributing to hyperlipidemia ) Hypertension Diabetes mellitus Obesity Stress Sedentary lifestyle Elevated C-reactive protein Hyperhomocysteinemia Non-modifiable Risk Factors Age Gender (female more prone) Familial predisposition/genetics (positive family history of CVDs)

292. Arteriosclerosis and Atherosclerosis Pathophysiology Most common direct results of atherosclerosis in arteries include Narrowing (stenosis) of the lumen Obstruction by thrombosis Aneurysm Ulceration Rupture Indirect manifestations include Malnutrition (of the distal organ/tissues) Subsequent fibrosis of the organs that the sclerotic arteries supply with blood

293. Arteriosclerosis and Atherosclerosis Pathophysiology Atherosclerosis can develop at any point in the body but certain sites are more vulnerable Regions where arteries bifurcate or branch into smaller vessel Proximal lower extremity - distal abdominal aorta, common iliac arteries, superficial femoral arteries Any artery distal to knee The exact cause of atherosclerosis is not well known The reaction-to-injury theory is widely accepted Prolonged hemodynamic forces (shearing stresses, turbulent blood flow), irradiation, chemical exposure, chronic hyperlipidemia → vascular endothelial cell injury → increase aggregation of platelets & monocytes at site of injury → smooth muscle cells migrate & proliferate → matrix of collagen & elastic fibers form

294. Arteriosclerosis and Atherosclerosis Pathophysiology Atherosclerotic lesions are of two types Fatty streaks Fibrous plaque Fatty streaks Yellow & smooth, protrude slightly into the lumen of the artery Composed of lipids & elongated smooth muscle cells These lesions have been found in the arteries of people of all age groups including infants It is not clear whether fatty streaks predispose a person to the formation of fibrous plaques or whether they are reversible They do not usually cause clinical symptoms .

295. Arteriosclerosis and Atherosclerosis Pathophysiology Fibrous plaque White to white-yellow, protrude in various degrees into the arterial lumen (completely obstructing it sometimes ) Composed of smooth muscle cells, collagen fibers, plasma components & lipids These plaques are found predominantly in the abdominal aorta, coronary , popliteal & internal carotid arteries Believed to be progressive lesions

296. Arteriosclerosis and Atherosclerosis Pathophysiology Gradual narrowing of the arterial lumen stimulates development of collateral circulation Collateral circulation arises from preexisting vessels that enlarge to reroute blood flow around a hemodynamically significant stenosis or occlusion Collateral flow allows continued perfusion to the tissues It is often inadequate to meet increased metabolic demand and ischemia subsequently occurs

297. Arteriosclerosis and Atherosclerosis Clinical Manifestations May affect entire vascular system or one segment of the vascular tree Manifestations are based on area affected Brain ( cerebroarteriosclerosis ) - TIA, stroke, vision disturbances Heart (coronary artery disease [CAD ]) - angina , MI, heart failure GI tract (aortic occlusive disease, aortic aneurysm & mesenteric ischemia) - abdominal pain, unintentional weight loss, lower back pain Kidneys (renal artery stenosis) - renal insufficiency, poorly HPT Extremities (peripheral arterial disease [PAD ]) - intermittent claudication (pain in a muscle associated with exercise caused by lack of oxygen to the muscle), pain at rest, tissue loss (with or without presence of infection or gangrene ), embolic events Decreased or absent pulses; bruits

298. Arteriosclerosis and Atherosclerosis Prevntion Dietary modification Lipid-lowering drugs Exercises Control of hypertension Discontinue or minimize nicotine use

299. Arteriosclerosis and Atherosclerosis Diagnosis Arteriography of involved area (may show stenosis & increased collateral circulation) Computed tomography (CT) scan Magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA ) Noninvasive testing of the vascular system Duplex studies Sequential Doppler studies Pulse volume resistance Anklebrachial index (ABI

300. Arteriosclerosis and Atherosclerosis Medical management Lifestyle modification Lipid-lowering medications Anticoagulants/ antiplatelets Antihypertensives Surgical intervention Inflow procedures - improve blood supply from aorta into femoral artery Outflow procedures - improve blood supply to vessels below the femoral artery Atherectomy , embolectomy, thrombectomy , endarterectomy Radiological interventions Arteriogram & angioplasty (percutaneous transluminal angioplasty) Specific treatment for end-organ dysfunction

301. Arteriosclerosis and Atherosclerosis Nursing diagnosis Ineffective peripheral tissue perfusion related to compromised circulation Chronic pain related to impaired ability of peripheral vessels to supply tissues with oxygen Risk for impaired skin integrity related to compromised circulation Deficient knowledge regarding self-care activities

302. Arteriosclerosis and Atherosclerosis Nursing management Improving peripheral a rterial c irculation Position affected part below the level of the heart Assist patient with walking or other moderate or graded isometric exercises that may be prescribed to promote blood flow & encourage development of collateral circulation Instruct patient to walk to the point of pain, rest until the pain subsides & then resume walking so that endurance can be increased as collateral circulation develops Exercises are not recommended for patients with leg ulcers, cellulitis , gangrene, or acute thrombotic occlusions Discourage standing still or sitting for prolonged periods.

303. Arteriosclerosis and Atherosclerosis Nursing management Promoting vasodilation and p reventing v ascular compression Application of warmth to promote arterial flow & instruction to the patient to avoid exposure to cold temperatures which can cause vasoconstriction Ensure adequate clothing & warm temperature to protect the patient from chilling If chilling occurs a warm bath or drink is helpful A hot water bottle or heating pad may be applied to the patient’s abdomen, causing vasodilation throughout the lower extremities Discourage use of tobacco products Encourage avoidance of constrictive clothing and accessories Encourage avoidance of crossing the legs Administer vasodilator medications and adrenergic blocking agents as prescribed

304. Arteriosclerosis and Atherosclerosis Nursing management Relieving Pain Promote increased circulation Administer analgesic agents as prescribed Use other adjunct approaches to pain management

305. Arteriosclerosis and Atherosclerosis Nursing management Maintaining Tissue Integrity Instruct in ways to avoid trauma to extremities Encourage wearing protective shoes & padding for pressure areas (wear new shoes for short period of time & inspect feet for signs of injury) Encourage meticulous hygiene: bathing with neutral soaps, applying lotions & carefully trimming nails Caution to avoid scratching or vigorous rubbing Promote good nutrition (adequate intake of vitamins A & C, protein, zinc) & control of obesity

306. Arteriosclerosis and Atherosclerosis Nursing management Promoting Home and Community-Based Care Include family/significant others in teaching program. Provide written instructions about foot care, leg care, and exercise program. Assist to obtain properly fitting clothing, shoes , and stockings. Refer to self-help groups as indicated, such as smoking cessation clinics or stress management, weight management, and exercise program .

307. Peripheral Arterial Occlusive Disease Peripheral arterial occlusive disease (also known as peripheral artery disease or PAD) A form of arteriosclerosis in which the peripheral arteries become blocked Obstructive lesions are predominantly confined to segments of the arterial system extending from the aorta below the renal arteries to the popliteal artery Chronic occlusive arterial disease occurs much more frequently than does acute (which is the sudden & complete blocking of a vessel by a thrombus or embolus)

308. Peripheral Arterial Occlusive Disease Arterial insufficiency of the extremities occurs most often in men & is a common cause of disability The legs are most frequently affected Upper extremities may be involved The age of onset & severity are influenced by the type & number of atherosclerotic risk factors Distal occlusive disease is frequently seen in patients with diabetes mellitus and in elderly patients

309. Peripheral Arterial Occlusive Disease Clinical manifestations The hallmark symptom is intermittent claudication This pain may be described as persistent, aching, cramping, boring or inducing fatigue/weakness that occurs with the same degree of exercise/activity It is relieved with rest Pain commonly occurs in muscle groups distal to the area of stenosis or occlusion Patient may have a decreased ability to walk the same distance as previously or may notice increased pain with ambulation Patient experiences rest pain as arterial insufficiency becomes severe It may be so excruciating and unresponsive to opioids (may be disabling)

310. Peripheral Arterial Occlusive Disease Clinical manifestations This pain is associated with critical ischemia of the distal extremity Ischemic rest pain is usually worse at night & often wakes the patient Elevating the extremity or placing it in a horizontal position increases the pain whereas placing the extremity in a dependent position reduces the pain Some patients sleep with the affected leg hanging over the side of the bed Some patients sleep in a reclining chair in an attempt to prevent or relieve the pain A sensation of coldness or numbness in the extremities may accompany intermittent claudication & is a result of reduced arterial flow Unequal pulses between extremities or the absence of a normally palpable pulse Bruits may be auscultated with a stethoscope Nails may be thickened & opaque Skin may be shiny, atrophic & dry with sparse hair growth

311. Peripheral Arterial Occlusive Disease Diagnosis History & physical examination CW Doppler ABIs Treadmill testing for claudication Duplex ultrasonography

312. Peripheral Arterial Occlusive Disease Medical management Planned exercises Weight reduction & cessation of tobacco use Pentoxifylline - increases erythrocyte flexibility, lowers blood fibrinogen concentrations, and has antiplateleteffects Cilostazol - vasodilator that inhibits platelet aggregation Antiplatelet agents e.g. aspirin, clopidogrel Statin therapy Surgical interventions Endarterectomy Bypass graft Amputation

313. Peripheral Arterial Occlusive Disease Nursing management Maintaining circulation An adequate circulating blood volume should be established and maintained Checked & compared pulses, color & temperature, capillary refill, & sensory & motor function of the affected & unaffected extremities Record initially every 15 minutes & then progressively longer intervals as the patient status becomes stable Disappearance of a pulse that was present may indicate thrombotic occlusion of the graft Monitor ABI at least once every 8 hours for the first 24 hours & then once each day until discharge (not usually assessed with pedal artery bypasses )

314. Peripheral Arterial Occlusive Disease Nursing management Monitoring & managing potential complications Continuously monitor urine output, central venous pressure, mental status, & pulse rate & volume (permits early recognition & treatment of fluid imbalances) Be alert for signs of overt and covert blood loss Encourage avoidance of leg crossing & prolonged dependent positioning of the affected extremity Exercises and cautious limb elevation may be used to reduced edema

315. Upper extremity arterial occlusive disease Arterial occlusions occur less frequently in the upper extremities (arms ) than in the legs & cause less severe symptoms Collateral circulation is significantly better in the arms Arms also have less muscle mass & are not subjected to the workload of the legs

316. Upper extremity arterial occlusive disease Clinical manifestations Stenosis & occlusions in the upper extremity result from atherosclerosis or trauma Stenosis usually occurs at the origin of the vessel proximal to the vertebral artery (setting up the vertebral artery as the major contributor of flow) Patient typically complains of Arm fatigue & pain with exercise (forearm claudication) Inability to hold or grasp objects ( e.g . combing hair, placing objects on shelves above the head) Difficulty driving ( occassionally )

317. Upper extremity arterial occlusive disease Clinical manifestations Patient may develop a “subclavian steal” syndrome Characterized by reverse flow in the vertebral & basilar artery to provide blood flow to the arm This syndrome may cause vertebrobasilar (cerebral) symptoms, including vertigo, ataxia , syncope, or bilateral visual changes Other manifestations Coolness & pallor of the affected extremity , decreased capillary refill A difference in arm blood pressures of more than 20 mmHg

318. Thromboangiitis obliterans ( Buerger’s disease) Buerger’s disease - characterized by recurring inflammation of the intermediate & small arteries & veins of the lower & upper extremities It is differentiated from other vessel diseases by its microscopic appearance In contrast to atherosclerosis Buerger’s disease is believed to be an autoimmune vasculitis that results in occlusion of distal vessels Atherosclerosis may accompany Buerger’s disease It results in thrombus formation & segmental occlusion of the vessels

319. Thromboangiitis obliterans ( Buerger’s disease) Buerger’s disease occurs most often in men between 20 & 35 years of age It has been reported in all races & in many areas of the world There is considerable evidence that heavy smoking or chewing of tobacco is a causative or an aggravating factor

320. Thromboangiitis obliterans ( Buerger’s disease) Clinical manifestations Pain is the outstanding symptom of Buerger’s disease Generally bilateral & symmetric with focal lesions (superficial thrombophlebitis may be present) Pain is relieved by rest Aggravated by emotional disturbances, nicotine or chilling Patient complains of foot cramps especially of the arch ( instep claudication) after exercise Pain may also be described as burning Cold sensitivity of the Raynaud type is found in half the patients & is frequently confined to the hands Digital rest pain is constant (characteristics of the pain do not change between activity & rest)

321. Thromboangiitis obliterans ( Buerger’s disease) Physical signs include Intense rubor (reddish-blue discoloration) of the foot Absence of pedal pulse (but with normal femoral & popliteal pulses) Radial & ulnar artery pulses are absent or diminished (if upper extremities are involved) Paresthesias may develop Definite redness or cyanosis of the part appears when the extremity is in a dependent position Color changes may progress to ulceration & ulceration with gangrene eventually occurs

322. Thromboangiitis obliterans ( Buerger’s disease) Diagnosis History & physical examination Segmental limb blood pressures are taken to demonstrate the distal location of the lesions or occlusions Duplex ultrasonography is used to document patency of the proximal vessels and to visualize the extent of distal disease Contrast angiography

323. Thromboangiitis obliterans ( Buerger’s disease) Medical management Treatment of Buerger’s disease is essentially the same as that for atherosclerotic PAD Main objectives are to Improve circulation to the extremities Prevent the progression of the disease Protect the extremities from trauma & infection Treatment of ulceration & gangrene is directed toward minimizing infection & conservative debridement of necrotic tissue Vasodilators are rarely prescribed (cause dilation of only healthy vessels → diversion of blood away from partially occluded vessels)

324. Raynaud’s phenomenon Raynaud’s phenomenon - a form of intermittent arteriolar vasoconstriction that results in coldness, pain & pallor of the fingertips, toes or nose There are two forms of this disorder Primary or idiopathic Raynaud’s (Raynaud’s disease) - occurs in the absence of an underlying disease Secondary Raynaud’s (Raynaud’s syndrome) - occurs in association with an underlying disease Usually a CT disorder e.g. SLE, rheumatoid arthritis, scleroderma Other underlying causes – trauma, obstructive arterial lesions Symptoms may result from a defect in basal heat production that eventually decreases the ability of cutaneous vessels to dilate Symptoms may be mild (so that treatment is not required) Secondary Raynaud’s is characterized by vasospasm & fixed blood vessel obstructions that may lead to ischemia, ulceration & gangrene

325. Raynaud’s phenomenon Epidemiology Episodes may be triggered by emotional factors or by unusual sensitivity to cold It occurs more frequently in cold climates & during the winter Raynaud’s phenomenon is most common in women between 16 - 40years of age Prognosis for patients with Raynaud’s phenomenon varies Some slowly improve Some become progressively worse & others show no change Potential complications (ulceration, gangrene & amputation) are uncommon unless an underlying arterial occlusive disease is present

326. Raynaud’s phenomenon Clinical Manifestations Manifestations tend to be bilateral & symmetric (may involve both toes & fingers) Classic clinical picture reveals pallor (due to sudden vasoconstriction) Skin then becomes bluish/cyanotic (due to pooling of deoxygenated blood during vasospasm) A red color ( rubor ) is produced when oxygenated blood returns to the digits after the vasospasm stops E xaggerated reflow of blood (hyperemia ) immediately follows vasodilation Rebound circulation (reactive hyperemia, rewarming) Characteristic sequence of color change of Raynaud’s phenomenon is described as white, blue & red Numbness , tingling & burning pain may occur as color changes occur

327. Raynaud’s phenomenon Medical Management Avoidance of trigger & aggravating factors Protection of fingers & toes with warm mittens ( not gloves ) & warm boots in cold weather Longer-acting calcium channel blockers are frequently used to prevent or reduce vasospasm Nitroglycerin or sympatholytics e.g. reserpine, guanethidine , prazosin Antiplatelet agents (to prevent total occlusion) e.g. aspirin dipyridamole Sympathectomy Removal of sympathetic ganglia or division of their branches

328. Raynaud’s phenomenon Nursing diagnoses Risk for peripheral n eurovascular d ysfunction related to vasospastic process Acute p ain related to arteriolar vasoconstriction & hyperemia

329. Raynaud’s phenomenon Nursing Management Teach patient to avoid situations that may be stressful or unsafe Minimize exposure to cold (teach patient to wear layers of clothing, hats, mittens & boots when outdoors during cold seasons) Ensure adequate warming or heating of all habitable areas during cold seasons including vehicles Advise patient that episode may be terminated by placing hands (or feet) in warm water Encourage patient to avoid all forms of nicotine Nicotine gum or patches used to help people quit smoking may induce attacks Caution patients to handle sharp objects carefully to avoid injuring their fingers Inform patient about postural hypotension that may result from medication side effects e.g. calcium channel blockers

330. Aneurysms An aneurysm is a localized sac or dilation formed at a weak point in the wall of the artery It may be classified by its shape or form Most common forms of aneurysms are Saccular aneurysm - projects from only one side of the vessel Fusiform aneurysm - an entire arterial segment becomes dilated Very small aneurysms due to localized infection are called mycotic aneurysms Aneurysms are serious because it can rupture → hemorrhage & death

331. Types of aneurysms

332. Aneurysms Aneurysms may form as the result of: Atherosclerosis Heredity Infection Trauma Immunologic conditions False aneurysms ( pseudoaneurysm ) are associated with trauma to the arterial wall Blunt trauma or trauma associated with arterial punctures for angiography and/or cardiac catheterization

333. Aneurysms Etiologic Classification of Arterial Aneurysms Infectious (mycotic) - bacterial, fungal, spirochetal infections Pregnancy-related degenerative - nonspecific, inflammatory variant Anastomotic ( postarteriotomy ) & graft aneurysms - Infection, arterial wall failure, suture failure, graft failure

334. Thoracic aortic aneurysm Occurs from the aortic arch to the level of the diaphragm Thoracic area is the most common site for a dissecting aneurysm Approximately 85% of all cases of thoracic aortic aneurysm are caused by atherosclerosis Occur most frequently in men between the ages of 40 - 70 years About one third of patients with thoracic aneurysms die of rupture of the aneurysm

335. Thoracic aortic aneurysm Clinical Manifestations Symptoms are variable & depend on How rapidly the aneurysm dilates How the pulsating mass affects surrounding intrathoracic structures Some patients are asymptomatic Pain is the most prominent symptom in some cases Usually constant & boring May occur only when the person is supine

336. Thoracic aortic aneurysm Clinical Manifestations Other conspicuous pressure symptoms Dyspnea (due to pressure of aneurysm sac against trachea, main bronchus or lung) Cough (frequently paroxysmal & with a brassy quality) Hoarseness, stridor or weakness or complete loss of voice ( aphonia ) [pressure against laryngeal nerve] Dysphagia (difficulty in swallowing) [due to impingement on esophagus by aneurysm ]

337. Thoracic aortic aneurysm Diagnosis History & physical assessment - related to aneurysm sac compression of large veins Superficial veins of chest , neck or arms become dilated Edematous areas on chest wall and cyanosis Pressure against the cervical sympathetic chain can result in unequal pupils Chest x-ray Computed tomographic angiography Transesophageal echocardiography (TEE )

338. Thoracic aortic aneurysm Medical Management Controlling blood pressure & correcting risk factors Systolic pressure is maintained at approximately 100 - 120 mmHg with a beta-blocker e.g. esmolol , metoprolol Antihypertensives such as hydralazine & sodium nitroprusside may also be used Surgical intervention Goal is to repair aneurysm & restore vascular continuity with a vascular graft (endovascular grafts) May be done percutaneously or through open surgical repair Percutaneous interventions associated less complications (paraplegia, CVA), morbidity & mortality

339. Abdominal aortic aneurysm Most common cause of abdominal aortic aneurysm is atherosclerosis More common among Caucasians Affects men four times more often than women Most prevalent in elderly patients Most abdominal aneurysms occur below the renal arteries ( infrarenal aneurysms ) Eventual outcome of an untreated abdominal aneurysm may be rupture & death

340. Abdominal aortic aneurysm Pathophysiology All aneurysms involve a damaged media layer of the vessel May be caused by congenital weakness, trauma or disease It tends to enlarge after its development Risk factors include Genetic predisposition Tobacco use Hypertension (more than half of patients with aneurysms have HPT)

341. Abdominal aortic aneurysm Clinical Manifestations It may be asymptomatic Only about 40% of patients have symptoms Common complains Feeling of heart beating in abdomen when lying down Feeling an abdominal mass Feeling of abdominal throbbing Thrombus formation → embolism → occlusion of major or small distal vessels → cyanosis & mottling of toes

342. Abdominal aortic aneurysm Diagnosis History & physical examination Most important diagnostic indication of an abdominal aortic aneurysm is a pulsatile mass in the middle & upper abdomen About 80% of these aneurysms can be palpated A systolic bruit may be heard over the mass Duplex ultrasonography or Computed tomographic angiography Used to determine the size, length & location of the aneurysm

343. Abdominal aortic aneurysm Medical Management Pharmacologic therapy Close blood pressure monitoring [an association between increased diastolic BP (above 100 mm Hg) and aneurysm rupture] Antihypertensive agents e.g. diuretics , beta-blockers, ACE inhibitors, angiotensin II receptor antagonists, calcium channel blockers Surgical management Vessel resection & bypass graft insertion Transluminal placement & attachment of a sutureless aortic graft prosthesis across the aneurysm

344. Abdominal aortic aneurysm Nursing Management Nursing assessment is guided by Anticipating a rupture Recognizing that patient may have cardiovascular, cerebral , pulmonary & renal impairment from atherosclerosis Assess the functional capacity of all organ systems Promptly implement medical therapies designed to stabilize physiologic function Observe for signs of impending rupture [severe back or abdominal pain) Indications of a rupturing abdominal aortic aneurysm include constant, intense back pain, falling blood pressure & decreasing hematocrit A retroperitoneal rupture of an aneurysm may result in hematomas in the scrotum, perineum, flank or penis

345. Other aneurysms Aneurysms may also arise in peripheral vessels (most often as a result of atherosclerosis) Subclavian artery, renal artery, femoral artery & most frequently popliteal artery Aneurysm produces a pulsating mass & disturbs peripheral circulation distal to it Pain & swelling develop because of pressure on adjacent nerves & veins Diagnosis is made by duplex ultrasonography & CTA to determine the size, length & extent of the aneurysm Arteriography may be performed to evaluate the level of proximal and distal involvement

346. Other aneurysms Medical Management Surgical repair is performed with replacement grafts or endovascular repair using a stent-graft or wall graft

347. Other aneurysms Nursing Management Put patient who had undergone endovascular repair in the supine position for the first 6 hours after surgery Head of bed may be elevated up to 45 degrees after 2 hours Make provision for the patient to use a bedpan in the immediate postoperative phase while on bed rest An indwelling urinary catheter may also be used to minimize mobility Monitor and report any signs of postimplantation syndrome Typically begins within 24 hours of stent-graft placement Characterized by a spontaneously occurring fever, leukocytosis & occasionally transient thrombocytopenia

348. Other aneurysms Nursing Management Monitor vital signs every 15 minutes & then at progressively longer intervals if the patient’s status remains stable The access site (usually the femoral or iliac artery) is assessed when vital signs & pulses are monitored Assess for bleeding, pulsation, swelling, pain, hematoma formation Report to the surgeon any skin changes of the lower extremity, lumbar area or buttocks which may signify embolization (extremely tender, irregularly shaped, cyanotic areas) & any changes in vital signs, pulse quality, bleeding, swelling, pain or hematoma Notify the surgeon of persistent coughing, sneezing, vomiting, or systolic blood pressure greater than 180 mm Hg (because of increased risk of coughing)

349. Varicose veins Varicose veins ( varicosities) - abnormally dilated, tortuous, superficial veins caused by incompetent venous valves Most commonly occurs in Lower extremities (especially in the saphenous veins) Lower trunk It can also occur elsewhere in the body such as esophagus or rectum (esophageal varices & hemorrhoidal veins) when flow or pressure is abnormally high It is most common in women & in people whose occupations require prolonged standing (salespeople , hair stylists, teachers , nurses, ancillary medical personnel, construction workers) Incidence tends to increase with increasing age Varicose veins are rare before puberty

350. Varicose veins Types of varicosities Primary varicose veins - unilateral or bilateral dilation & elongation of saphenous veins Deeper veins are normal Process is irreversible Secondary varicose veins - result from obstruction of deep veins Telangiectasias (spider veins) - dilated superficial capillaries, arterioles & venules They may be cosmetically unattractive but do not pose a threat to circulation

351. Varicose veins Predisposing factors: Hereditary weakness of vein wall or valves. Long-standing distention of veins brought about by Pregnancy Obesity Prolonged standing Advanced age - loss of tissue elasticity

352. Varicose veins Pathophysiology A reflux of venous blood in the veins results in venous stasis Hydrostatic pressure & vein weakness increases → vein wall become distended → asymmetric dilation → some of the valves become incompetent (valve cusp do not meet or prolapse) → increased backup pressure passed into the next lower segment of the vein The combination of vein dilation & valve incompetence produces the varicosity Symptoms may not be present if only superficial veins are involved The person may be troubled by the appearance of the varicosities

353. Varicose veins Pathophysiology A hereditary weakness of the vein wall may contribute to the development of varicosities It commonly occurs in several members of the same family Pregnancy may cause varicosities due to hormonal effects related to decreased venous outflow, increased pressure by the gravid uterus & increased blood volume

354. Varicose veins Clinical Manifestations Symptoms may include Dull aches, muscle cramps (nocturnal cramps are common), increased muscle fatigue in the lower legs, increased pain during menstruation Ankle edema, a feeling of heaviness of the legs Disfigurement due to large, discolored, tortuous leg veins When deep venous obstruction results in varicose veins → patient may develop the signs & symptoms of chronic venous insufficiency → edema , pain, pigmentation & ulcerations Increased susceptibility to injury & infection

355. Varicose veins Diagnosis History & physical examination Duplex ultrasound scan (identifies anatomic site of reflux & provides a quantitative measure of the severity of valvular reflux ) Air plethysmography (measures the changes in venous blood volume) Venography (not routinely performed to evaluate for valvular reflux) Injection of a radiopaque contrast agent into the leg veins so that the vein anatomy can be visualized by x-ray studies during various leg movements

356. Varicose veins Prevention The patient should avoid activities that cause venous stasis Wearing socks that are too tight at the top or that leave marks on the skin Crossing the legs at the thighs Sitting or standing for long periods Encourage patient to change position frequently, elevate the legs when they are tired & get up to walk for several minutes of every hour to promote circulation Graduated compression stockings (especially knee-high stockings) are useful Encourage the overweight patient to begin a weight reduction plan

357. Varicose veins Medical Management Ligation and stripping Surgery for varicose veins requires that the deep veins be patent & functional Saphenous vein is ligated high in the groin (where the saphenous vein meets the femoral vein) & divided An incision is made 2 - 3 cm below the knee (after the vein is ligated) & a metal or plastic wire is passed the full length of the vein to the point of ligation The wire is then withdrawn, pulling ( removing, stripping ) the vein as it is removed Pressure application & limb elevation minimize bleeding during surgery

358. Varicose veins Medical Management Thermal Ablation - a nonsurgical approach using thermal energy Sclerotherapy Injection of an irritating chemical into a vein to produce localized phlebitis & fibrosis → obliterates lumen of vein Sclerosing is palliative rather than curative Treatment may be performed alone for small varicosities or may follow vein ablation, ligation or stripping

359. Nursing Diagnoses Impaired t issue i ntegrity related to chronic changes & postoperative inflammation Acute Pain related to surgical incisions or inflammation

360. Varicose veins Nursing Management Bed rest following recovery from sedation is discouraged & patient is encouraged to become ambulatory as soon as possible Instruct patient to walk every hour for 5-10 minutes while awake for the first 24 hours if he or she can tolerate the discomfort Walking & activity should be encouraged as much as can be tolerated Graduated compression stockings are worn continuously for about 1 week after vein stripping Standing & sitting are discouraged Nurse assists the patient to perform exercises & move the legs The foot of the bed should be elevated

361. Varicose veins Nursing Management Promoting Comfort & Understanding Administer prescribed analgesic agents to help the patient move the affected extremities more comfortably Inspect dressings for bleeding, particularly at the groin, where the risk of bleeding is greatest Remain alert for reported sensations of “pins & needles” (indication of inadequate circulation) & hypersensitivity to touch in the involved extremity [may indicate a temporary or permanent nerve injury resulting from surgery (saphenous vein & nerve are close to each other in the leg)] Patient may shower after the first 24 hours Instruct patient to dry the incisions well with a clean towel using a patting technique rather than rubbing Patient may also be instructed to dry the area using a blow-dryer Avoid a pplication of skin lotion until the incisions are completely healed to avoid infection

362. Varicose veins Nursing Management Promoting Comfort & Understanding Instruct patient to apply sunscreen or zinc oxide to the incisional area prior to sun exposure (hyperpigmentation of the incision, scarring, or both may occur) A burning sensation in the injected leg may be experienced for 1 or 2 days if the patient underwent sclerotherapy Encourage the use of a mild analgesic medication as prescribed & walking to provide relief Promoting Home & Community-Based Care Long-term venous compression is essential after discharge Patient needs to obtain adequate supplies of graduated compression stockings or elastic bandages. Exercise of the legs is necessary An individualized plan of exercise should be developed in consultation with patient & health care team

363. Lymphedema, lymphangitis and lymphadenitis Lymphedema - swelling of the tissues (particularly in the dependent position ) produced by an obstruction to the lymph flow in an extremity This results in excessive accumulation of fluid ( composed of high-molecular-weight proteins ) in the interstitial space Lymphangitis - an acute inflammation of lymphatic channels Most commonly arises from a focus of infection in an extremity The infectious organism is a usually hemolytic streptococcus The characteristic red streaks that extend up the arm or the leg from an infected wound outline the course of the lymphatic vessels as they drain Lymphadenitis – inflammation of lymph nodes Lymph nodes become enlarged , red & tender (acute lymphadenitis) Lymph nodes may also become necrotic & form an abscess ( suppurative lymphadenitis) Commonly involved lymph nodes - groin , axilla or cervical region

364. Lymphedema, lymphangitis and lymphadenitis Pathophysiology and Etiology Lymphedema It may be caused or aggravated by radiation therapy, trauma, cancer, morbid obesity or surgery involving the lymph tissue (particularly radical mastectomy) It may also be associated with varicose veins & chronic thrombophlebitis Lymphatic obstruction caused by a parasite ( filaria ) is most frequently seen in the tropics Classified as primary (congenital malformations/ lymphedema praecox ) or secondary (acquired obstruction) Swelling in extremities occurs due to an increased quantity of lymph fluid that results from an obstruction of lymphatics Obstruction may be in both the lymph nodes & lymphatic vessels Chronic swelling → frequent bouts of acute infection (high fever, chills, increased residual edema) → subcutaneous tissue eventually becomes fibrotic , impairing vascular flow & oxygen transfer to tissues

365. Lymphedema, lymphangitis and lymphadenitis Pathophysiology and Etiology Lymphangitis Most commonly caused by infection in an extremity The pooled protein-rich lymph fluid creates a good medium for growth of bacteria & fungi The characteristic red streak extending up an arm or leg from the infected wound outlines the course of the lymphatics as they drain Recurrent lymphangitis is typically associated with lymphedema

366. Lymphedema, lymphangitis and lymphadenitis Clinical Manifestations Lymphedema : edema may be massive and is usually firm Especially marked when the extremity is in a dependent position Edema is initially soft & pitting Edema becomes firm, nonpitting & unresponsive to treatment as the condition progresses Lymphangitis Displays characteristic red streaks that extend up an arm or leg from an infection that is not localized and that can lead to septicemia. Produces general symptoms (high fever, chills) Produces local symptoms (local pain, tenderness, swelling along involved lymphatics) Produces local lymph node symptoms [enlarged , red, tender (acute lymphadenitis )] Produces an abscess [necrotic , pus-producing ( suppurative lymphadenitis)]

367. Lymphedema, lymphangitis and lymphadenitis Diagnosis History & physical examination Check feet for tinea pedis (athlete’s foot) - a common cause of bacterial entry into skin & lymphatics Lymphangiography (outlines lymphatic system) Lymphoscintigraphy (reliable alternative to lymphangiography using radioactive colloid material; detects obstruction or inflammation CT or MRI

368. Lymphedema, lymphangitis and lymphadenitis Medical management Lymphedema Bed rest with leg elevation Active & passive exercises Lymphedema therapy Massage to help move fluid & myofascial release to break up fibrotic tissue Compression garments to help squeeze the fluid out of tissues (medical-grade stockings or pneumatic compression) Diuretics - usually not effective & can worsen edema Surgery Excision of affected subcutaneous tissue & fascia with skin grafting Transfer of superficial lymphatics to deep lymphatic system by buried dermal flap Complications include flap necrosis, hematoma, abscess under flap, cellulitis

369. Lymphedema, lymphangitis and lymphadenitis Medical management Lymphangitis Administer antibiotics. Treat affected extremity by rest, elevation & application of hot, moist dressings Incise & drain if necrosis & abscess formation occur Treat tinea pedis (if present)

370. Lymphedema, lymphangitis and lymphadenitis Complications Abscess formation (rare with lymphangitis ) Firm , nonpitting lymphedema unresponsive to treatment (congenital lymphedema, called lymphedema praecox). Elephantiasis secondary to parasitaemia ( filariasis ) - chronic fibrosis of subcutaneous tissue & chronic swelling of the extremity Septicemia

371. Lymphedema, lymphangitis and lymphadenitis Nursing diagnosis Risk for impaired s kin i ntegrity related to edema and/or inflammation Acute p ain related to tissue injury secondary to surgical procedure

372. Lymphedema, lymphangitis and lymphadenitis Nursing management Maintaining Skin Integrity Apply elastic bandages or prescription compression stockings (after acute attack with lymphangitis ) Advise the patient to rest frequently with affected part elevated (each joint higher than the preceding one) Make sure the patient cleans in crevices of skin if edema has caused skin folds Administer diuretics as prescribed to control excess fluid Give antibiotics or antifungals as prescribed Recommend isometric exercises with extremity elevated Suggest moderate sodium restriction in diet Observe postoperatively for signs of infectio n

373. Lymphedema, lymphangitis and lymphadenitis Nursing management Relieving Pain Postoperatively Encourage comfortable positioning and immobilization of affected area Administer or teach patient to administer analgesics, as prescribed; monitor for adverse effects. Use bed cradle to relieve pressure from bed covers

374. Lymphedema, lymphangitis and lymphadenitis Nursing management Patient Education and Health Maintenance Instruct patient on proper application of compression garments. Encourage compliance with therapy, which often involves frequent rewrapping of compression bandages, exercise, & massage for several months. Advise patient to avoid trauma to extremity. Instruct patient to use lotions that are free of perfumes, which may irritate skin. Advise patient to practice good hygiene to avoid superimposed infections . Instruct patient about the signs & symptoms of infection to report to health care providers Instruct patient to inspect feet & legs daily for evidence of skin breakdown, particularly between toes, & to look for tinea pedis

375. Cellulitis Cellulitis is the most common infectious cause of limb swelling Cellulitis can occur as a single isolated event or a series of recurrent events It is sometimes misdiagnosed as recurrent thrombophlebitis or chronic venous insufficiency Pathophysiology Cellulitis occurs when an entry point through normal skin barriers allows bacteria to enter & release their toxins in the subcutaneous tissues

376. Cellulitis Clinical Manifestations Acute onset of swelling, localized redness & pain Redness may not be uniform & often skips areas Systemic signs of fever, chills & sweating Regional lymph nodes may also be tender & enlarged

377. Cellulitis Medical Management Antibiotic therapy (oral or IV) The key to preventing recurrent episodes of cellulitis lies in adequate antibiotic therapy for the initial event & in identifying the site of bacterial entry Cracks & fissures that occur in the skin between the toes must be examined as potential sites of bacterial entry Other locations include drug use injection sites, contusions , abrasions, ulceration, ingrown toenails, and hangnails .

378. Cellulitis Nursing Management Instruct patient to elevate the affected area above heart level & apply warm, moist packs to the site every 2 to 4 hours Patients with sensory & circulatory deficits (such as those caused by diabetes & paralysis) should use caution when applying warm packs because burns may occur It is advisable to use a thermometer or have a caregiver ensure that the temperature is not more than lukewarm Education should focus on preventing a recurrent episode The patient with peripheral vascular disease or diabetes mellitus should receive education or reinforcement about skin & foot care

379. Lymphoma Lymphomas - malignant disorders of the reticuloendothelial system that result in an accumulation of dysfunctional, immature lymphoid-derived cells These tumors usually start in lymph nodes but can involve lymphoid tissue in the spleen, GI tract ( e.g . the wall of the stomach ), liver or bone marrow Lymphomas are often classified according to the origin of the predominant malignant cell & degree of cell differentiation (well differentiated, poorly differentiated or undifferentiated) Lymphomas can be broadly classified into two categories Hodgkin lymphoma Non-Hodgkin lymphoma (NHL )

380. Hodgkin Lymphoma Hodgkin lymphoma - originates in the lymphoid system & involves predominantly lymph nodes It accounts for about 12% of all lymphomas More common in men than women & has two peaks of incidence One in the early 20s & the other after 50 years of age Disease occurrence has a familial pattern First-degree relatives have a higher-than-normal frequency of disease (but the actual incidence of this pattern is low) No increased incidence for nonblood relatives ( e.g. spouses) has been documented Hodgkin lymphoma is seen more commonly in Patients receiving chronic immunosuppressive therapy ( e.g . for renal transplant) Veterans of the military who were exposed to the herbicide Agent Orange

381. Hodgkin Lymphoma Pathophysiology Hodgkin lymphoma (unlike other lymphomas) is unicentric in origin in that it initiates in a single node Spreads by contiguous extension along the lymphatic system The malignant cell of Hodgkin lymphoma is the Reed-Sternberg cell (a gigantic tumor cell that is morphologically unique & is thought to be of immature lymphoid origin) It is the pathologic hallmark & essential diagnostic criterion The tumor is very heterogeneous & may actually contain few Reed-Sternberg cells Repeated biopsies may be required to establish the diagnosis The cause of Hodgkin lymphoma is unknown A viral etiology is suspected Fragments of the Epstein-Barr virus have been found in some Reed-Sternberg cells (precise role of this virus in the development of Hodgkin lymphoma remains unknown)

382. Hodgkin Lymphoma Clinical Manifestations Hodgkin lymphoma usually begins as a painless enlargement of one or more lymph nodes on one side of the neck The individual nodes are painless & firm but not hard The most common sites for lymphadenopathy are the cervical, supraclavicular & mediastinal nodes (involvement of iliac or inguinal nodes or spleen is much less common) A mediastinal mass may be seen on chest x-ray (occasionally the mass is large enough to compress the trachea & cause dyspnea) Pruritus is common (it can be extremely distressing & the cause is unknown) Some patients experience brief but severe pain after drinking alcohol (usually at the site of the tumor & the cause is unknown)

383. Hodgkin Lymphoma Clinical Manifestations All organs are vulnerable to invasion by tumor cells (symptoms result from compression of organs by the tumor ) Pulmonary infiltrates - cough and pulmonary effusion Hepatic involvement or bile duct obstruction- jaundice Splenomegaly or retroperitoneal adenopathy - abdominal pain Skeletal involvement - bone pain Herpes zoster infections are common “B symptoms” - a cluster of constitutional symptoms has important prognostic implications (common in advanced disease) Fever (without chills), drenching sweats (particularly at night) & unintentional weight loss of more than 10% of body weight

384. Hodgkin Lymphoma Clinical Manifestations A mild anemia is the most common hematologic finding Leukocyte count may be elevated or decreased Platelet count is typically normal (unless the tumor has invaded the bone marrow & suppressing hematopoiesis) Erythrocyte sedimentation rate (ESR) & serum copper level are used by some clinicians to assess disease activity

385. Hodgkin Lymphoma Diagnosis History & physical assessment (assess for B symptoms) Excisional lymph node biopsy Finding of the Reed-Sternberg cell A chest x-ray & a CT scan of the chest, abdomen & pelvis (to identify the extent of lymphadenopathy within these regions) Bone marrow biopsy Laboratory tests (FBC , platelet count, ESR & liver & renal function studies)

386. Hodgkin Lymphoma Medical Management The general goal in the treatment of Hodgkin lymphoma is cure Chemotherapy (doxorubicin, bleomycin, vinblastine ) & radiation therapy

387. Hodgkin Lymphoma Nursing management Potential development of a second malignancy should be addressed with the patient when treatment decisions are made It is also important to tell patients that Hodgkin lymphoma is often curable The nurse should encourage patients to reduce other factors that increase the risk of developing second cancers (use of tobacco & alcohol, exposure to environmental carcinogens, excessive sunlight) Screening for late effects of treatment is necessary The nurse should provide education about relevant self-care strategies disease management

388. Hodgkin Lymphoma Potential Long-Term Complications of Therapy for Hodgkin Lymphoma Table

389. Non-Hodgkin Lymphomas Non-Hodgkin lymphomas (NHLs) - a group of malignancies of lymphoid tissue arising from T or B lymphocytes or their precursors It includes both indolent & aggressive forms Most NHLs involve malignant B lymphocytes (only 5% involve T lymphocytes) The lymphoid tissues involved are largely infiltrated with malignant cells Spread of these malignant lymphoid cells occurs unpredictably True localized disease is uncommon Lymph nodes from multiple sites may be infiltrated [as may sites outside the lymphoid system ( extranodal tissue)]

390. Non-Hodgkin Lymphomas Types of Non-Hodgkin’s lymphomas include Chronic lymphocytic leukemia or small lymphocytic lymphoma Follicular lymphoma Diffuse large B-cell lymphoma Primary cutaneous B-cell lymphoma

391. Non-Hodgkin Lymphomas Etiology No common etiologic factor has been identified Increased incidence of NHL has been observed under these conditions People with immunodeficiencies or autoimmune disorders Patients receiving immunosuppression for organ transplant Viral infections (including Epstein-Barr virus and HIV) Exposure to pesticides, solvents, dyes or defoliating agents (including Agent Orange) History of Helicobacter gastritis (for gastric B-cell lymphoma) History of Hodgkin’s lymphoma History of radiation therapy Family history, male gender, white ethnicity Diet high in meats & fat

392. Non-Hodgkin Lymphomas Clinical Manifestations Symptoms are highly variable (reflecting the diverse nature of the NHLs) Lymphadenopathy is most common - painless enlargement of lymph nodes (generally unilateral cervical or supraclavicular ) Lymphadenopathy may wax & wane with indolent types of NHLs Early-stage disease - may be virtually absent or very minor Lymphadenopathy becomes distinctly noticeable as disease advances B symptoms (fever, drenching night sweats & unintentional weight loss ), pruritus Lymphomatous masses can compromise organ function Respiratory distress ( mediastinal masses), renal dysfunction (abdominal masses), abdominal discomfort , nausea, early satiety, anorexia & weight loss(splenomegaly )

393. Non-Hodgkin Lymphomas Diagnosis Incisional or excisional lymph node biopsy to detect type F BC , bone marrow aspirate & biopsy to detect bone marrow involvement CT scan of the chest, abdomen & pelvis with oral & intravenous contrast PET with CT scan to detect deep nodal involvement Liver function tests, liver scan to detect liver involvement Hepatitis B testing is recommended due to risk of reactivation Lumbar puncture to detect CNS involvement (for some lymphoma types) Surgical staging (laparotomy with splenectomy, liver biopsy, multiple lymph node biopsies )

394. Non-Hodgkin Lymphomas Medical Management Radiation therapy Chemotherapy Monoclonal antibodies Radioimmune therapy Hematopoietic stem cell transplant

395. Non-Hodgkin Lymphomas Nursing diagnosis Risk for infection related to altered immune response secondary to lymphoma & leukopenia caused by chemotherapy or radiation therapy

396. Non-Hodgkin Lymphomas Nursing diagnosis Minimizing Risk of Infection Care for patient in protected environment with strict handwashing observed Avoid invasive procedures, such as urinary catheterization if possible Assess temperature and vital signs, breath sounds, LOC, and skin and mucous membranes frequently for signs of infection Notify health care provider of fever greater than 38.3 ° C or change in condition Obtain cultures of suspected infected sites or body fluids

397. Non-Hodgkin Lymphomas

398. Non-Hodgkin Lymphomas

399. Non-Hodgkin Lymphomas