Circulatory Function FINAL with associated notes.pptx

With notes

1. Circulatory Function Brenda Nabawanuka

2. Outline Control of cardiovascular function Disorders of blood flow and blood pressure Disorders of cardiac function Heart failure and circulatory shock

3. Control of cardiovascular function

4. The Heart Gross structures Musculature-pericardium, fibrous & serous epicardium, visceral serous pericardium, myocardium (heart muscle) Muscle cell (microscopic structures), central nucleus, sarcoplasm, sarcolemma, sarcomere-the contractile unit, intercalated discs Pattern of blood flow through the structures of the heart; atria, ventricles, valves

5. Transition from fetal to pulmonary circulation the umbilical cord is cut systemic vascular resistance is increased pressure in the L side of the heart increases foramen ovale closes breathing is initiated pulmonary vascular resistance falls blood that was shunted through the PDA now goes to the lungs.

6. Fetal (prenatal) circulation. Pulmonary (postnatal) circulation

7. Chambers Right side of Heart Right atrium – the thin-walled atrium, low relative pressure receives blood from superior and inferior vena cava, the coronary sinus and thebesian veins.  The outflow of blood through tricuspid valve. Right ventricle – relatively thin muscle wall, crescent-shaped, papillary muscles, chordae tendineae , low pressure.  Outflow through the pulmonic valve to the pulmonary artery.

8. Chambers Left side of the heart Left atrium, - thicker muscle, medium pressure of blood, inflow of blood through the four pulmonary veins.  Outflow is through the mitral valve. Left ventricle – largest muscle mass, high pressure blood flow, papillary muscles, spring-like pump action.  Outflow of blood through the aortic valve and the aorta.

9. Valves Atrioventricular Valves: Tricuspid – has three leaflets, controlled by papillary muscles; chordate tendineae Mitral valve – two cusps, controlled by papillary muscles and the chordae tendineae Semilunar Valves: Pulmonic valve – three-leaflet valve, formed by fibrous ring, tendinous tubercle midpoint free edges Aortic valve – three leaflets, also formed by fibrous ring, tendinous tubercle midpoint free edges.

10. Vasculature of the Heart Right coronary artery – most branches of this artery anastomose distally with left anterior descending. Left coronary artery – divides into two main branches, left ant. descending and left circumflex artery. Great cardiac vein – largest system, forms coronary sinus, drains left ventricle primarily. Anterior cardiac veins – empty directly into right atrium. Thebesian veins – smallest system, empty into right atrium

11. Conduction System of the Heart SA (Sino-atrial node) Atrial preferential pathways – anterior internodal , middle, posterior internodal AV ( Atrio -ventricular node) Bundle of HIS Left Bundle Branch Right Bundle Branch Purkinje fibres

12. Contractility of Heart Muscle Heart muscle possesses the following properties: Automaticity - pacemaker ability Conductivity - each cell has the ability to conduct impulses Contractility - ability to contract (make each cell shorter or longer) Irritability - each cell has ability to contract on its own, to send impulses to cells without it first being stimulated from another source

13. These properties make the myocardium different from other muscle cells in the body Various factors affect the activity of cardiac muscle   The availability of oxygen, afterload, nervous control, muscle condition Drugs

14. Blood Flow through the heart Physical characteristics important to blood flow : Diameter of the blood vessels Cross-section areas of the chambers and vessels Length of the vessels Quantities of blood: Heart 18% Pulmonary vessels 12% Large arteries 8% Small arteries 5% Arterioles 2% Capillaries 5% Small veins 25% Large veins 25%

15. Velocities of blood flow Directly related to the amount of circulating blood volume and the area of the vessels.  Blood returns to the heart from the general circulation.  Almost 50% of all blood in the body is in the systemic veins of the body.  The small veins usually offer little resistance to blood flow. 

16. The large veins do offer much resistance to the flow of blood to the heart.  The patient who is more active will have better flow of blood back to the heart. With reduced activity, the blood tends to pool in the large vessels and can lead to severe venous stasis.

17. From the right atrium blood flows to the right ventricle and is then propelled into pulmonary circulation.  After blood is aerated with fresh oxygen, it is returned to the left side of the heart into the left atrium

18. From the left atrium The blood is ejected into the left ventricle.  The left ventricle then pumps the blood out of the heart into the general circulation.  The aorta is the first vessel to carry blood, At the same time, the coronary arteries are being fed oxygenated blood to circulate through the heart.

19. Cardiac Output Preload Afterload Contractility Heart Rate Stroke Volume = X Factors that affect Cardiac Output

20. PreLoad The volume of blood/amount of fiber stretch in the ventricles at the end of diastole (i.e., before the next contraction) Fluid volume increases Vasoconstriction (“squeezes” blood from vascular system into heart) Preload decreases with Fluid volume losses Vasodilation (able to “hold” more blood, therefore less returning to heart) The greater the heart muscle fibers are stretched (b/c of increases in volume), the greater their subsequent force of contraction – but only up to a point. Beyond that point, fibers get over-stretched and the force of contraction is reduced Excessive preload = excessive stretch → reduced contraction → reduced SV/CO

21. Cardiac Output

22. Afterload Afterload The resistance against which the ventricle must pump. Excessive afterload = difficult to pump blood → reduced CO/SV Afterload increased with: Hypertension Vasoconstriction Afterload decreased with: Vasodilation

23. contractility Contractility Ability of the heart muscle to contract; relates to the strength of contraction. Contractility decreased with: infarcted tissue – no contractile strength ischemic tissue – reduced contractile strength. Electrolyte/acid-base imbalance Negative inotropes (medications that decrease contractility, such as beta blockers). Contractility increased with: Sympathetic stimulation (effects of epinephrine) Positive inotropes (medications that increase contractility, such as digoxin, sympathomimmetics

24. Neural control of circulatory function

25. Autonomic nerve impulses alter the activities of the S-A and A-V nodes Regulation of the cardiac cycle

26. Summary of long term BP control Cardiac output and BP depend on renal control of extra-cellular fluid volume via: Pressure natriuresis , (increased renal filtration) Changes in: Vasopressin Aldosterone Atrial natiuretic peptide All under the control of altered cardiovascular receptor signaling

27. Arginine Vasopressin (AVP) Enhances water retention Causes vasoconstriction Secretion increased by aortic baroreceptors and atrial sensors

28. Baroreceptor reflex Blood pressure falls Aortic arch Carotid sinus Constriction of veins & arterioles Increased stroke volume Increased heart rate Vasoconstriction Cardiac stimulation Cardiac inhibition Nucleus tractus solitarius Increased peripheral resistance Increased cardiac output Increased blood pressure Neural integration Sensors Effectors

29. Disorders of blood flow and blood pressure

30. Blood Pressure Blood pressure is probably one of the most important measures of the overall cardiovascular system Normal blood pressure is determined by the cardiac output, the velocity, the resistance of the blood vessels Systolic pressure refers to the initial force of contraction of the heart.  Diastolic pressure refers to the pressure of the blood vessels after the initial force of contraction of the heart. 

31. HYPERTENSION Factors Influencing Blood Pressure Blood Pressure = Cardiac Output x Systemic Vascular Resistance

32. Problem Magnitude In Uganda the overall prevalence of 26.4%. Prevalence was highest in the central region at 28.5% Followed by the eastern region at 26.4% Western region at 26.3% Northern region at 23.3%. Prevalence in urban areas was 28.9% , and 25.8% in rural areas. Worldwide prevalence estimates for HTN may be as much as 1 billion. 7.1 million deaths per year may be attributable to hypertension.

33. Definition A systolic blood pressure ( SBP) >139 mmHg and/or A diastolic (DBP) >89 mmHg. Based on the average of two or more properly measured, seated BP readings. On each of two or more office visits.

34. Follow-up based on initial BP measurements for adults* *Without acute end-organ damage www.nhlbi.nih.gov

35. Classification www.nhlbi.nih.gov

36. Prehypertension SBP >120 mmHg and <139mmHg and/or DBP >80 mmHg and <89 mmHg . Prehypertension is not a disease category rather a designation for individuals at high risk of developing HTN.

37. Pre-HTN Individuals who are prehypertensive are not candidates for drug therapy but Should be firmly and unambiguously advised to practice lifestyle modification Those with pre-HTN, who also have diabetes or kidney disease, drug therapy is indicated if a trial of lifestyle modification fails to reduce their BP to 130/80 mmHg or less.

38. Isolated Systolic Hypertension Not distinguished as a separate entity as far as management is concerned. SBP should be primarily considered during treatment and not just diastolic BP. Systolic BP is more important cardiovascular risk factor after age 50. Diastolic BP is more important before age 50.

39. Hypertensive Crises Hypertensive Urgencies: No progressive target-organ dysfunction. (Accelerated Hypertension) Hypertensive Emergencies: Progressive end-organ dysfunction. (Malignant Hypertension) Severe elevated BP in the upper range of stage II hypertension. Without progressive end-organ dysfunction. Examples: Highly elevated BP without severe headache, shortness of breath or chest pain. Usually due to under-controlled HTN.

40. Hypertensive Urgencies Severe elevated BP in the upper range of stage II hypertension. Without progressive end-organ dysfunction. Examples : Highly elevated BP without severe headache, shortness of breath or chest pain. Usually due to under-controlled HTN.

41. Hypertensive Emergencies Severely elevated BP (>180/120mmHg). With progressive target organ dysfunction. Require emergent lowering of BP. Examples : Severely elevated BP with: Hypertensive encephalopathy Acute left ventricular failure with pulmonary edema Acute MI or unstable angina pectoris Dissecting aortic aneurysm

42. Types of Hypertension Primary HTN: also known as essential HTN. accounts for 95% cases of HTN. no universally established cause known. Secondary HTN: less common cause of HTN ( 5%). secondary to other potentially rectifiable causes.

43. Causes of Secondary HTN Common Intrinsic renal disease Renovascular disease Mineralocorticoid excess Sleep Breathing disorder Uncommon Pheochromocytoma Glucocorticoid excess Coarctation of Aorta Hyper/hypothyroidism

44. Complications of Prolonged Uncontrolled HTN Changes in the vessel wall leading to vessel trauma and arteriosclerosis throughout the vasculature Complications arise due to the “target organ” dysfunction and ultimately failure. CVS (heart and blood vessels Kidneys Nervous system Eyes Damage to the blood vessels can be seen on fundoscopy .

45. Atherosclerosis

46. Effects On CVS Ventricular hypertrophy, dysfunction and failure. Arrhythmias Coronary artery disease, Acute MI Arterial aneurysm, dissection, and rupture. Effects on the kidneys Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease. Ischemic kidney disease especially when renal artery stenosis is the cause of HTN

47. Effect on the nervous system Stroke, intracerebral and subarachnoid hemorrhage. Cerebral atrophy and dementia Effect on the eyes Retinopathy, retinal hemorrhages and impaired vision. Vitreous hemorrhage, retinal detachment Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction

48. Retina Normal and Hypertensive Retinopathy Normal Retina Hypertensive Retinopathy A: Hemorrhages B: Exudates (Fatty Deposits) C: Cotton Wool Spots (Micro Strokes) A B C

49. Patient Evaluation Objectives (1) To assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment (2) To reveal identifiable causes of high BP (3) To assess the presence or absence of target organ damage and CVD

50. (1) Cardiovascular Risk factors Hypertension Cigarette smoking Obesity (body mass index ≥30 kg/m2) Physical inactivity Dyslipidemia Diabetes mellitus Microalbuminuria or estimated GFR <60 mL/min Age (older than 55 for men, 65 for women) Family history of premature cardiovascular disease (men under age 55 or women under age 65)

51. (2) Identifiable Causes of HTN Sleep apnea Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushing’s syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease

52. (3) Target Organ Damage Heart Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure Brain Stroke or transient ischemic attack Chronic kidney disease Peripheral arterial disease Retinopathy

53. Disorders of cardiac function

54. Ductus Arteriosus An opening in fetal circ. between the pulmonary artery (PA) and aorta ( Ao ). In fetal circulation, most of the blood bypasses the lungs and returns to systemic circulation by way of the PDA (PA to Ao ). In transition to pulmonary circulation, the PDA constricts over 10-15hrs; permanent closure should occur by 3wks of age, UNLESS SATURATION REMAINS LOW

55. Image

56. Hypoxemia in the infant Below 95% pulse oximetry. Cyanosis results from hypoxemia Perioral cyanosis indicates central hypoxemia Acrocyanosis does not.

57. Response to Hypoxemia Acute: HR increases Chronic: bone marrow produces more RBC to increase the amount of Hgb available for oxygen transport. Hct >50 is called polycythemia. Increased blood viscosity increases risk of thromboembolism.

58. Cardiac Functioning 2 requirements are high the first few weeks of life Normally, HR increases to provide adequate oxygen transport Infant has little cardiac output reserve capacity Cardiac output depends almost completely on HR until the heart is fully developed (age 5 yr ).

59. Compliance in the infant In infancy, muscle fibers are less developed and organized Results in less functional capacity or less compliance Less compliance means the infant is unable or less able to distend or expand the ventricles to achieve an increase stroke volume in order to compensate for increased demands.

60. Severe Hypoxemia children respond with bradycardia cardiac arrest generally results from prolonged hypoxemia related to respiratory failure or shock in adults, hypoxemia usually results from direct insult to the heart. therefore, in children, bradycardia is a significant warning sign of cardiac arrest. appropriate Rx for hypoxemia reverses bradycardia.

61. Pulmonary Artery Hypertension Irreversible condition that results from R sided heart circulation being overloaded and therefore shunting excessive blood to the lungs. Overloads the R side of the heart, overloads the pulmonary system causing increased pulmonary vascular resistance (life threatening).

62. Obstructive Congenital Defects Due to abnormally small pulmonary vessels Which restrict flow of blood, so the heart hypertrophies to work harder to provide the blood flow to organs. However, CO increases initially but eventually hypertrophied muscle becomes ineffective. Initially R sided failure, progressing to L sided and eventual bilateral failure

63. CHF in the infant Can be subtle Good assessment skills are a must Tires easily, especially during feeding Initial weight loss Diaphoresis, irritability, frequent infection.

64. CHF in older children Exercise intolerance Dyspnea Abdominal pain or distention Peripheral edema.

65. Symptoms of progressive disease Tachycardia, tachypnea, pallor or cyanosis, F/G/R, cough, crackles. Fluid volume overload: periorbital and facial edema, JVD, hepatomegaly, ascites. Increased weight gain, bounding pulses, edema of dependent body parts.

66. Cardiomegaly Occurs at the heart attempts to maintain CO If CHF is not adequately treated, precursors of Cardiogenic Shock arise: cyanosis, weak peripheral pulses, cool extremities, hypotension, heart murmurs Clarification: not all heart murmurs are heralding cardiogenic shock.

67. Congenital Heart Disease (CHD) Refers to a defect in the heart, great vessels or persistence of a fetal structure Occurs in 1% live births Higher incidence in still births and aborted fetuses Incidence has declined over past 25 yrs d/t technological advances in intrauterine assessment, surgical techniques and intensive care

68. Factors that increase risk for having a child with CHD Family hx of CHD Maternal age >35yr Coexisting maternal disease: DM, collagen vascular disease, PKU Exposure to teratogens or rubella infection

69. CHD Most CHD develop during first 8 wks of gestation Usually result of combined genetic and environmental interaction Fetal exposure to drugs: phenytoin & lithium Maternal viral infections: rubella Maternal metabolic disorders: DM, PKU Maternal complications of pregnancy i.e. increased age, antepartum bleeding

70. CHD etiologies cont. genetic factors: familial patterns chromosomal abnormalities: most common is Down’s syndrome with 40% occurrence rate of CHD. defects are divided into cyanotic and acyanotic (in pure form).

71. Acyanotic Heart Defects Constitutes the majority of heart defects in children Two types: obstructive and non-obstructive Obstructive: PS, AoS , Coarc . Non-obstructive: PDA, ASD, AV canal (endocardial cushion) defect, VSD.

72. Cyanotic Heart Defects Generally caused by a valvular or vascular formation ex: Tetralogy of Fallot , Transposition, hypoplastic LV, tricuspid atresia, pulmonary atresia, truncus arteriosus, and total anomalous venous return.

73. Acyanotic ; non-obstructive lesions PDA ASD AV canal VSD

74. Pathophysiology of Acyanotic , non-obstructive CHD openings in the septal wall cause a L to R shunt oxygenated blood mixes with deoxygenated blood volume overload to the pulmonary system can cause CHF PHT occurs d/t chronic volume overload to the lungs if uncorrected.

75. Patent Ductus Arteriosus common; 9-12% of all CHD persistent fetal structure when the PDA remains open, blood is shunted from the Aorta to the Pulmonary artery, therefore increasing blood flow to the lungs: L to R. bounding pulses, dyspnea, tachypnea, FTT. at risk for frequent URI and endocarditis, CHF. continuous systolic murmur and thrill palpable.

76. PATENT DUCTUS ARTERIOSUS

77. Treatment of a PDA surgical ligation; transcatheter closure >18mos of age. Indomethacin may stimulate closure in premies Prostaglandin helps to keep the PDA open until surgical correction is optimal. left untreated, LVH, pulmonary hypertension (PHT) and vascular obstructive disease develop.

78. Atrial Septal Defect; ASD opening in the atrial shunting L to R shunting accounts for 6-10% of CHD small to moderate size may go undiagnosed until preschool years or later sx of large ASD: CHF, tiring easily, poor growth soft systolic murmur heard in pulmonic space; wide S2 split.

79. ATRIAL SEPTAL DEFECT

80. Treatment of ASD Echo shows RV overload and shunt size C- xray and EKG may be normal unless a large shunt surgery to close or a patch via catheter during Cardiac Cath. atrial arrhythmias can be a late sign or associated with a large ASD involving conduction system in the septum

81. FIGURE 26–7 A , Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect (VSD). B , Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when a thrombus forms in the mass of fabric and wire. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

82. Atrioventricular Canal: Endocardial Cushion Defect accounts for 4-5% of CHD partial or complete ASD/VSD with some degree of involvement of mitral/tricuspid valves variable associated with Down’s syndrome severity of sx depends on degree of mitral regurgitation. sx in infants: CHF, tachypnea, tachycardia, FTT, increased URI, systolic murmur.

83. Treatment of AV Canal surgery during infancy to prevent PHT patches placed over septal defects; mitral valve replacement arrhythmias and mitral valve insufficiency occur post/op no difference between short term survival rates in infants with or without Down’s syndrome.

84. Ventricular Septal Defect; VSD opening in the ventricular septum shunts L to R; increases pulmonary blood flow most common: accounts for 20% CHD only 15% large enough to generate symptoms: tachypnea, dyspnea, FTT, reduced fluid intake, CHF, PHT. systolic murmur ; LLSB most small VSD close spontaneously

85. Treatment of VSD if no sx CHF or PHT, treatment is conservative surgical patching during infancy if FTT closure by transcatheter device during Cardiac Cath for some defects: prophylaxis for infective endocarditis is required high risk for surgical repair in first few months of life

86. Acyanotic ; obstructive lesions PS AoS Coarctation of the Aorta

87. Pathophysiology of Acyanotic , obstructive CHD narrowing across the valves causes pressure overload and hypertrophy of the closest ventricle child will have a murmur some experience fatigue and exercise intolerance d/t inability to increase CO many are asymptomatic and grow normally older children: exercise induced dizziness and syncope: requires immediate attention

88. Pulmonary Stenosis: PS narrowing of the pulmonary valve or valvular area obstructs flow to the PA increases pre-load; results in RVH second most common CHD accounts for 8-12% of CHD systolic murmur with fixed split S2 in Pulmonic area.

89. Treatment of PS dx usually made at birth with murmur auscultated C- xray may show heart enlargement EKG may demonstrate RVH echo provides information regarding pressure gradient across the valve may dilate during Cardiac Cath using balloon valvuloplasty or valvular replacement lifelong endocarditis prophylaxis is required

90. Aortic Stenosis: AoS narrowing of the aortic valve; obstructs blood flow to systemic circulation accounts for 3-6% of CHD; progressive during childhood often associated with bicuspid rather than normal tricuspid aortic valve. asymptomatic, grow normally; BP wnl but may have a narrow pulse pressure systolic murmur; thrill in Ao ; chest pain. after exercise.

91. Treatment of AoS C- xray and EKG are usually normal if mild echo can reveal number of valve leaflets, pressure gradient across the valve, and size of the aorta. surgical valvuloplasty or dilated with balloon during cardiac cath. valvular replacement requires lifelong SBE prophylaxis

92. Coarctation of the Aorta narrowing or obstruction of descending Ao . obstructs systemic blood flow accounts for 5-8% CHD grow normally but constriction is progressive lower BP in LE and higher in UE, neck, head. pulse weak or absent in LE; full/bounding in UE

93. COARCTATION OF AORTA

94. Treatment of Coarctation of the Aorta EKG shows LVH c- xray reveals enlargement and pulmonary venous congestion and constricted aorta balloon dilation in cardiac cath or surgical resection/anastomosis/patch. risks of reoccurrence, persistent HTN in adulthood, 20% develop post- coarctectomy syndrome (abdominal pain and distention). SBE prophylaxis needed.

95. Cyanotic Heart Defects Tetralogy of Fallot Transposition of the Great Vessels caused by malformation or a combination of defects that prevent adequate level of oxygenation R to L shunt occurs resulting in chronic hypoxemia and cyanosis.

96. Pathophysiology of Cyanotic Heart Disease P0 2 is lower than normal; PC0 2 rises hypoxemia becomes progressively worse as respiratory center overreacts and increased respiratory effort increased respiratory effort attempts to increase P0 2 at risk for thromboembolism d/t hypoxemia causing polycythemia

97. Clinical Manifestations of Cyanotic Heart Disease chronic hypoxemia causes fatigue, clubbing, exertional dyspnea, delayed milestones, tire easily with feeding, reduced growth, CHF Hyper-cyanotic (hypoxic) spells: increased rate and depth of respiration, increased cyanosis, increased HR, pallor and poor perfusion, agitation and irritability.

98. Tetralogy of Fallot combination of four defects pulmonary stenosis: degree determines severity VSD over-riding of the aorta(the aorta is positioned directly over a ventricular septal defect, instead of over the left ventricle) RVH accounts for 10% of CHD elevated R sided pressures: R to L shunt xray : boot shaped heart d/t RVH risk for metabolic acidosis and syncope.

99. TETRALOGY OF FALLOT

100. Treatment of TOF total repair is done by 6 mo if cyanotic spells surgery is not necessarily curative, but most have improved quality of life and improved longevity residual problems: arrhythmias and RV dysfunction lifelong SBE required

101. Transposition of the Great Arteries: TGA position of the PA and Ao are switched life threatening at birth; cyanosis, hypoxia, acidosis cyanosis does not improve with 02 admin survival depends upon a patent DA and foramen ovale accounts for 5% of CHD may be associated with an ASD or VSD

102. TRANSPOSITION OF THE GREAT VESSELS

103. Treatment of TGA prostaglandin E1 used to keep PDA open until palliative procedure corrective surgery (artery switch) usually performed by 1 wk of age balloon atrial septostomy during cardiac cath may be used to open foramen ovale survival depends upon surgery; risk for arrhythmia, SBE, RV failure, sudden death.

104. Pulmonary Artery Hypertension: PHT increased load to the lungs causes pulmonary vascular changes in an attempt to decrease the blood flow inflammation, hypertrophy of the pulmonary vessels and fibrosis develop pulmonary venous hypertension develops and leads to R to L shunting, with R sided heart function impaired. life threatening: irreversible

105. GENERAL S & S of CHD in INFANTS AND CHILDREN INFANTS : Dyspnea Difficulty feeding Stridor, choking spells Pulse rate over 200 FTT Heart murmurs Frequent URI’s Anoxic attacks CVA CHILDREN: Exercise intolerance Increased BP Poor physical development Heart murmurs Cyanosis Recurrent URI Clubbing fingers/toes squatting

106. Valvular Heart Disease STENOSIS: heart valve that does not open properly REGURGITATION: leaking heart valves

107. Heart failure and circulatory shock

108. Congestive Heart Failure

109. Types of Heart Failure Low-Output Heart Failure Systolic Heart Failure: decreased cardiac output Decreased Left ventricular ejection fraction Diastolic Heart Failure: Elevated Left and Right ventricular end-diastolic pressures May have normal LVEF High-Output Heart Failure Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism , beriberi, carcinoid, anemia Often have normal cardiac output Right-Ventricular Failure Seen with pulmonary hypertension, large RV infarctions.

110. Causes of Low-Output Heart Failure Systolic Dysfunction Coronary Artery Disease Idiopathic dilated cardiomyopathy (DCM) 50% idiopathic (at least 25% familial) 9 % mycoarditis (viral) Ischemic heart disease, perpartum , hypertension, HIV, connective tissue disease, substance abuse, doxorubicin Hypertension Valvular Heart Disease Diastolic Dysfunction Hypertension Coronary artery disease Hypertrophic obstructive cardiomyopathy (HCM) Restrictive cardiomyopathy

111. Clinical Presentation of Heart Failure Due to excess fluid accumulation: Dyspnea (most sensitive symptom) Edema Hepatic congestion Ascites Orthopnea, Paroxysmal Nocturnal Dyspnea (PND) Due to reduction in cardiac output: Fatigue (especially with exertion) Weakness

112. Cardiomegaly

113. Pulmonary vessel congestion

114. Pulmonary Edema due to Heart Failure

115. Classification of Heart Failure New York Heart Association (NYHA) Class I – symptoms of HF only at levels that would limit normal individuals. Class II – symptoms of HF with ordinary exertion Class III – symptoms of HF on less than ordinary exertion Class IV – symptoms of HF at rest

116. Classification of Heart Failure ACC/AHA Guidelines Stage A – High risk of HF, without structural heart disease or symptoms Stage B – Heart disease with asymptomatic left ventricular dysfunction Stage C – Prior or current symptoms of HF Stage D – Advanced heart disease and severely symptomatic or refractory HF

117. Chronic Treatment of Systolic Heart Failure Correction of systemic factors Thyroid dysfunction Infections Uncontrolled diabetes Hypertension Lifestyle modification Lower salt intake Alcohol cessation Medication compliance Maximize medications Discontinue drugs that may contribute to heart failure (NSAIDS, anti- arrhythmics , calcium channel blockers)

118. Management of Refractory Heart Failure Inotropic drugs: Dobutamine , dopamine, milrinone , nitroprusside, nitroglycerin Mechanical circulatory support: Intra-aortic balloon pump Left ventricular assist device (LVAD) Cardiac Transplantation A history of multiple hospitalizations for HF Escalation in the intensity of medical therapy A reproducable peak oxygen consumption with maximal exercise (VO2max) of < 14 mL/kg per min. (normal is 20 mL/kg per min. or more) is relative indication, while a VO2max < 10 mL/kg per min is a stronger indication.

119. Acute Decompensated Heart Failure Cardiogenic pulmonary edema is a common and sometimes fatal cause of acute respiratory distress. Characterized by the transudation of excess fluid into the lungs secondary to an increase in left atrial and subsequently pulmonary venous and pulmonary capillary pressures.

120. Acute Decompensated Heart Failure Causes: Acute MI Rupture of chordae tendinae /acute mitral valve insufficiency Volume Overload Transfusions, IV fluids Non-compliance with diuretics, diet (high salt intake) Worsening valvular defect Aortic stenosis

121. Decompensated Heart Failure Symptoms Severe dyspnea Cough Clinical Findings Tachypnea Tachycardia Hypertension/Hypotension Crackles on lung exam Increased JVD S3, S4 or new murmur

122. Decompensated Heart Failure Treatment Strict I’s and O’s, daily weights Oxygen, mechanical ventilation if needed Loop diuretics (Lasix) Morphine Vasodilator therapy (nitroglycerin) Nesiritide (BNP) – can help in acute setting, for short term therapy

123. Shock

124. Definition of Shock Inadequate oxygen delivery to meet metabolic demands Results in global tissue hypoperfusion and metabolic acidosis Shock can occur with a normal blood pressure and hypotension can occur without shock

125. Understanding Shock Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery Sympathetic nervous system NE, epinephrine, dopamine, and cortisol release Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) Renin-angiotensin axis Water and sodium conservation and vasoconstriction Increase in blood volume and blood pressure

126. Understanding Shock Cellular responses to decreased systemic oxygen delivery ATP depletion → ion pump dysfunction Cellular edema Hydrolysis of cellular membranes and cellular death Goal is to maintain cerebral and cardiac perfusion Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms

127. Global Tissue Hypoxia Endothelial inflammation and disruption Inability of O 2 delivery to meet demand Result: Lactic acidosis Cardiovascular insufficiency Increased metabolic demands

128. Multiorgan Dysfunction Syndrome (MODS) Progression of physiologic effects as shock ensues Cardiac depression Respiratory distress Renal failure DIC Result is end organ failure

129. Approach to the Patient in Shock History Recent illness Fever Chest pain, SOB Abdominal pain Comorbidities Medications Toxins/Ingestions Recent hospitalization or surgery Baseline mental status Physical examination Vital Signs CNS – mental status Skin – color, temp, rashes, sores CV – JVD, heart sounds Resp – lung sounds, RR, oxygen sat, ABG GI – abd pain, rigidity, guarding, rebound Renal – urine output

130. Shock Do you remember how to quickly estimate blood pressure by pulse? 60 80 70 90 I f you palpate a pulse, you know SBP is at least this number.

131. End Points of Resuscitation Goal of resuscitation is to maximize survival and minimize morbidity Use objective hemodynamic and physiologic values to guide therapy Goal directed approach Urine output > 0.5 mL/kg/ hr CVP 8-12 mmHg MAP 65 to 90 mmHg Central venous oxygen concentration > 70%

132. Persistent Hypotension Inadequate volume resuscitation Pneumothorax Cardiac tamponade Hidden bleeding Adrenal insufficiency Medication allergy

133. Types of Shock Hypovolemic Septic Cardiogenic Anaphylactic Neurogenic Obstructive

134. Hypovolemic Shock

135. Hypovolemic Shock Non-hemorrhagic Vomiting Diarrhea Bowel obstruction, pancreatitis Burns Neglect, environmental (dehydration) Hemorrhagic GI bleed Trauma Massive hemoptysis AAA rupture Ectopic pregnancy, post-partum bleeding

136. Hypovolemic Shock ABCs Establish 2 large bore IVs or a central line Crystalloids Normal Saline or Lactate Ringers Up to 3 liters PRBCs O negative or cross matched Control any bleeding Arrange definitive treatment

137. Evaluation of Hypovolemic Shock CBC ABG/lactate Electrolytes BUN, Creatinine Coagulation studies Type and cross-match As indicated CXR Pelvic x-ray Abd /pelvis CT Chest CT GI endoscopy Bronchoscopy Vascular radiology

138. Septic Shock

139. Sepsis Two or more of SIRS criteria Temp > 38 or < 36 C HR > 90 RR > 20 WBC > 12,000 or < 4,000 Plus the presumed existence of infection Blood pressure can be normal!

140. Septic Shock Sepsis Plus refractory hypotension After bolus of 20-40 mL/Kg patient still has one of the following: SBP < 90 mm Hg MAP < 65 mm Hg Decrease of 40 mm Hg from baseline

141. Pathogenesis of Sepsis Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.

142. Septic Shock Clinical signs: Hyperthermia or hypothermia Tachycardia Wide pulse pressure Low blood pressure (SBP<90) Mental status changes Beware of compensated shock! Blood pressure may be “normal”

143. Cardiogenic Shock

144. Cardiogenic Shock Signs: Cool, mottled skin Tachypnea Hypotension Altered mental status Narrowed pulse pressure Rales, murmur Defined as: SBP < 90 mmHg CI < 2.2 L/m/m 2 PCWP > 18 mmHg

145. Etiologies What are some causes of cardiogenic shock ? AMI Sepsis Myocarditis Myocardial contusion Aortic or mitral stenosis, HCM Acute aortic insufficiency

146. Pathophysiology of Cardiogenic Shock Often after ischemia, loss of LV function Lose 40% of LV clinical shock ensues CO reduction = lactic acidosis, hypoxia Stroke volume is reduced Tachycardia develops as compensation Ischemia and infarction worsens

147. Treatment of Cardiogenic Shock Goals- Airway stability and improving myocardial pump function Cardiac monitor, pulse oximetry Supplemental oxygen, IV access Intubation will decrease preload and result in hypotension Be prepared to give fluid bolus

148. Anaphylactic Shock

149. Anaphylactic Shock Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement IgE mediated Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure Not IgE mediated occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation.

150. Anaphylactic Shock What are some symptoms of anaphylaxis? First- Pruritus, flushing, urticaria appear Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse

151. Anaphylactic Shock Risk factors for fatal anaphylaxis Poorly controlled asthma Previous anaphylaxis Reoccurrence rates 40-60% for insect stings 20-40% for radiocontrast agents 10-20% for penicillin Most common causes Antibiotics Insects Food

152. Anaphylactic Shock- Diagnosis Clinical diagnosis Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems Look for exposure to drug, food, or insect Labs have no role

153. Neurogenic Shock

154. Neurogenic Shock Occurs after acute spinal cord injury Sympathetic outflow is disrupted leaving unopposed vagal tone Results in hypotension and bradycardia Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)

155. Neurogenic Shock Loss of sympathetic tone results in warm and dry skin Shock usually lasts from 1 to 3 weeks Any injury above T1 can disrupt the entire sympathetic system Higher injuries = worse paralysis

156. Neurogenic Shock- Treatment A,B,Cs Remember c-spine precautions Fluid resuscitation Keep MAP at 85-90 mm Hg for first 7 days Thought to minimize secondary cord injury If crystalloid is insufficient use vasopressors Search for other causes of hypotension For bradycardia Atropine Pacemaker

157. Obstructive Shock

158. Obstructive Shock Tension pneumothorax Air trapped in pleural space with 1 way valve, air/pressure builds up Mediastinum shifted impeding venous return Chest pain, SOB, decreased breath sounds No tests needed! Rx: Needle decompression, chest tube

159. Obstructive Shock Cardiac tamponade Blood in pericardial sac prevents venous return to and contraction of heart Related to trauma, pericarditis, MI Beck’s triad: hypotension, muffled heart sounds, JVD Diagnosis: large heart CXR, echo Rx: Pericardiocentisis

160. Obstructive Shock Pulmonary embolism Virscow triad: hypercoaguable , venous injury, venostasis Signs: Tachypnea, tachycardia, hypoxia Low risk: D-dimer Higher risk: CT chest or VQ scan Rx: Heparin, consider thrombolytics

161. Obstructive Shock Aortic stenosis Resistance to systolic ejection causes decreased cardiac function Chest pain with syncope Systolic ejection murmur Diagnosed with echo Vasodilators (NTG) will drop pressure! Rx: Valve surgery

162. Pregnancy Physiological edema Renin and aldosterone activity are increased by estrogens, progesterone and prostaglandins, leading to increased fluid and electrolyte retention. Physiological anemia The total plasma volume is increase in higher percentage in comparison to RBC which result in hemodilution

163. Decrease blood pressure Increase cardiac output leads to decreased arterial blood pressure by 10%, therefore resistance to flow must be decreased. In addition this can be result in decrease in systemic vascular resistance, particularly in the peripheral vessels. The decrease begins at 5 weeks' gestation, reaches a nadir in the second trimester (a 21% reduction) and then gradually rises as term approaches

164. Supine hypotensive syndrome The enlarging uterus compresses both the inferior vena cava and the lower aorta when the woman lies in supine position. This reduces venous return to the heart this condition happen in 10% of pregnant women. Sign of supine hypotension hypotension, bradycardia, dizziness, light-headedness .