myocardial infarction

myocardial infarction

1. MYOCARDIAL INFARCTION PRESENTED BY- SAM MATHEW STAFF NURSE DH –ED

2. Objectives Define and understand the epidemiology of MI’s and how they are classified Will be able to identify the risk factors associated with MI’s Will be able to recognize signs and symptoms of MI and what the appropriate interventions are. Understand the treatment options available to treat MI. Nursing responsibilities Follow up care

3. DEFINITION . Myocardial infarction is a disease condition which is caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus .

4. Epidemiology MI’s are the leading cause of death in the United States, affecting one in five men and one in six women. 450,000 people in the US die from coronary disease each year.

5. MI Classifications MI’s can be subcategorized by anatomy and clinical diagnostic information. Anatomic Transmural -  atherosclerosis involving a major coronary artery, it is usually as a result of complete occlusion of the artery in addition on ECG ST elevation and q waves are seen(STEMI )( epicardium,myo,endocardium ) Subendocardial - small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. It is particularly susceptible to ischemia,in addition to ST depression is seen on ecg (NSTEMI) Diagnostic ST elevations (STEMI)- ECG must show new ST elevation in two or more  adjacent ECG leads or new LBBB , it must be greater than 2 mm in leads V2 and V3 or greater than 1 mm in all other leads. non ST elevations (NSTEMI)- ST segment depression ≥0.5mm or dynamic T-wave inversion with pain or discomfort , and cardio specific proteins troponin are rises in blood in NSTEMI.

6. CORONARY ARTERIES OF HEART

7. Tunica Intima T. Adventitia Tunica media plaques Thrombus Atherosclerosis –is a narrowing of the arteries caused by a buildup of plaque

8. ETIOLOGY WELCOME

9. NON-MODIFIABLE RISK FACTORS MODIFIABLE RISK FACTORS ETIOLOGY

10. NON-MODIFIABLE RISK FACTORS

11. AGE: More than 40 years . FAMILY HISTORY: Myocardial infarction can be inherited from parents to children. GENDER: Myocardial infarction is 3 times more in men than women.

12. MODIFIABLE RISK FACTORS

13. HIGH BLOOD CHOLESTROL LEVEL LOW DENSITY LIPOPROTEIN (LDL) DANGEROUS HIGH DENSITY LIPOPROTEIN (HDL) LIPIDS (LIPOPROTIENS)

14. HYPERTENSION High blood pressure our arteries are designed to pump blood at a certain pressure. If that pressure is exceeded, the walls of the arteries will be damaged . injury to endothelial lining , atherosclerosis narrowed & thickened arterial walls risk of M.I.

15. SMOKING Smoking can damage the walls of your arteries.( toxic substances in cigarette) Atherosclerosis narrowed & thickened arterial walls Risk of M.I.

16. PHYSICAL INACTIVITY Improper lipid metabolism LDL level increases Starts accumulating in blood vessels Risk of M.I.

17. OBESITY More lipids are produced LDL level increases Atherosclerosis Risk of M.I.

18. DIABETES MELLITUS Diabetes increases the risk of MI because it increases the rate of atherosclerotic progression and adversely affects the lipid profile Risk of having M.I.

19. STRESS Release stress hormones like adrenaline, noradrenaline , and cortisol increase in heart rate, and elevated blood pressure it’s causing damage over time to all your blood vessel That damage increases the risk of plaque buildup in coronary arteries or can even cause a rupture of plaque MI The way you handle stress also matters. If you respond to it in unhealthy ways -- such as  smoking , overeating,or not  exercising  -that makes matters worse.

20. PATHOPHYSIOLOGY

21. How a Heart Attack Happens

22. Cholesterol deposition within the wall of the main artery This deposited cholesterol ultimately forms a plaque in the wall of the artery called atherosclerotic plaque. Atherosclerotic plaque formation is a long term process, required many years to establish. Sometimes this plaque may rupture or erode,it leads to activate clotting mechanism so platelet aggregation and fibrin deposition, which lead to formation of an occlusive thrombus in a coronary artery. This occlusive thrombus completely block a coronary artery and interrupts blood supply to part of the myocardium (heart muscle), It lead to irreversible changes and death of myocardial cells, and ultimately ST-segment elevation myocardial infarction develops. PATHOPHYSIOLOGY

23. CLINICAL MANIFESTATIONS Chest pain due to a lack of blood and oxygen supply of the heart muscle Characteristics: Severe, immobilizing chest pain. Usually prescribed as heaviness, pressure, tightness, burning. Location : Substernal , Retrosternal or Epigastric . Radiation: It may radiate to neck, jaw, arm or back . Duration: Lasts for 20 minutes or more. PAIN

24. Cardiovascular- Initially the BP and pulse may be elevated. Later, BP will drop due to decreased cardiac output. palpitation. Jugular veins may become distended and have obvious pulsations.

25. CONTD….. Respiratory- Respiratory symptoms occur when the damaged the heart muscle limits the pumping action of the left ventricle, causing acute left heart failure and consequent lung congestion. Shortness of breath Dyspnea / Tachypnea Crackles Pulmonary edema

26. Gastrointestinal- Nausea Vomiting Stimulation of vomiting center by severe pain causes nausea & vomiting FEVER It is due to inflammatory process caused by Myocardial cell death.

27. In response to pain and the blood flow abnormalities that result from dysfunction of the heart muscle SYMPATHETIC NERVOUS SYSTEM STIMULATION Increased catecholamine releases .(adrenal medulla) Diaphoresis (perfuse sweating Cold & clammy skin (“cold sweat”). Integumentary system ( Skin) c ool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities

28. Genitourinary- Hypoperfusion to the kidneys leads to decrease renal perfusion pressure which is required to maintain glomerular filteration rate in the kidney Decrease GFR leads to decrease urinary output Urine output ( Oliguria ): 30ml/HR or <400ml/day. Myocardial damage Failure of the pump action of the heart, resulting in reduced cardiac output

29. CONTD….. Neurogenic - due to inadequate blood flow to the brain Light- headedness Headache V isual Disturbances Altered speech Altered motor functions Altered level of consciousness

30. CONTD….. Psychosocial- Fear feeling Pt. may deny that anything is wrong

31. LOOK WHO IS SLEEPING?

32. DIAGNOSTIC TESTS

33. ASSESSMENT/DIAGNOSTIC FINDINGS It is generally based on presenting symptoms, ECG and laboratory test results. Patient history-it includes Description of presenting symptoms History of previous illness, family health history

34. CONTD….. Electrocardiogram- ECG provides information that assists in diagnosing acute MI. The classic ECG changes are- ST segment elevation ST depression T wave inversion Abnormal Q wave

35. RECOGNITION OF ECG TIPS REMEMEBER - SALI S- SEPTAL MI- V1 V2 A -ANTERIOR WALL MI - V3 V4 L- LATERAL WALL MI - V5 V6-1-AVL I- INFERIOR WALL MI- 11-111-AVF POSTERIOR WALL MI- ST V1-V3,ST V7-V9

36. S A L I

37. CORONARY ARTERIES OF HEART LATERAL MI ANTERIOR OR SEPTUM INFERIOR MI

38. SERUM CARDIAC MARKERS CK-MB (ENZYME) TROPONINE-T (PROTEIN) cardiac enzymes are proteins that are released into the blood by dying heart muscles.

39. CK-MB- increases 3-6 hrs after onset of chest pain, peaks in 12-18 hrs & return to normal within 3-4 days. Cardiac troponin T- increases 4-6 hrs after MI & persists for 2 weeks Full blood count: WBC (white blood cell) count is usually elevated. ESR (Erythrocyte sedimentation rate) and CRP (C-reactive protein) may also elevate. CHEST X-RAY To detect cardiomegaly .

40. ECHOCARDIOGRAM PURPOSE: it is useful to assess the ability of heart muscles to contract & relax. It is done to evaluate ventricular function by checking ejection rate. CT & MEGNATIC RESONANCE IMAGING (MRI) PURPOSE: To detect site & extent of myocardial cells.

41. ANGIOGRAPHY Angiography is used to detect abnormalities,including narrowing ( stenosis ) or blockages in the blood vessels (called occlusions). This is done by injecting a radio-opaque  contrast agent  into the blood vessel this dye makes the coronary arteries visible on x-ray pictures. This helps doctors see blockages in the arteries.

42. MANAGEMENT GOALS Restoration of the balance between the oxygen supply and demand to prevent further ischemia Pain relief Prevention and treatment of any complications that may arise

43. Chest pain suggestive of ischemia Vital signs 12 lead ECG Obtain initial cardiac enzymes electrolytes , cbc lipids, bun/ cr , glucose, coags CXR Immediate assessment within 10 Minutes Establish diagnosis Read ECG Identify complicatio -ns Assess for reperfusion Initial labs and tests Emergent care History & Physical Cardiac monitoring IV access Morphine Oxygen<94% Nitrates Aspirin

44. STEMI vs. NSTEMI

45. MEDICAL MANAGEMENT

46. ANTIPLATELET DRUG (D ecrease platelet aggregation and inhibit thrombus formation) Aspirin (160 to 325mg) slows the  blood 's clotting action by reducing the clumping of platelets Clopidogrel (300mg) -works by blocking platelets from sticking together and prevents them from forming harmful clots. It is an antiplatelet drug. DRUG THERAPY

47. ANALGESIC: NITRATES . Sublingual Nitroglycerine- Nitrates act as a vasodilator and relief pain ,Total 3 doses (can repeat 3-5mts if no contraindication)-use only SBP ˃ 90mmhg heart rate 50-100/ mt Morphine Sulphate . produces central nervous system analgesia. Produce venodilation (it helps to reduce left ventricular preload and oxygen demand)

48. BETA ADRENERGIC BLOCKERS ( Propanolol ) it inhibit SNS stimulation of heart. reduces both heart rate & contractility CALCIUM CHANNEL BLOCKERS ( Verapamil , Nifedipine ) It causes coronary artery vasodilatation & decreases myocardial contractility. Increases blood supply to myocardium & decreases O 2 demand of myocardium. ANTI COAGULATION THERAPY ( pre vent the formation of blood clots) LMWH-ENOXAPARIN UNFRACTIONED HEPARIN

49. ACE Inhibitors These medicines lower bloodpressure and reduce the strain on your heart. They also help slow down further weakening of the heart muscle. Eg:enalapril , captopril

50. FIBRINOLYTIC THERAPY TIME OF ADMINISTRATION: Thrombolytics are given to the patient upto 12 hours of onset of chest pain but for best results it should be given within 1 hr after onset of chest pain. ACTION: These will dissolve & do lysis of thrombus in coronary artery. We are using metalyse for thrombloysis If STEMI is present, the goal is to achieve a door- to –drug time of 30 min & a door-to –balloon time of within 90 min. Indicated for patients with STEMI MI’s.

51. Absolute & relative contraindications for thrombolytic therapy Absolute contraindications- Any prior ICH Ischemic stroke within 3 months Known structural cerebral vascular lesion Known malignant intracranial neoplasm Active bleeding Significant closed head trauma within past 3 months

52. Relative contraindications- History of chronic, severe, poorly controlled hypertension Severe uncontrolled hypertension on presentation History of prior ischemic stroke >3months Dementia Pregnancy Active peptic ulcer Current use of anticoagulants, the higher the INR the greater the risk

53. Angioplasty During angioplasty, a thin, flexible tube with a balloon on  the end is threaded through a blood vessel to the blocked coronary artery. Then,the balloon is inflated to push the plaque against the wall of the artery.This widens the inside of the artery,restoring blood flow. Also a small mesh tube called a stent may be put in the artery to help keep it open.Some stents are coated with medicines that help prevent the artery from becoming blocked again. SURGICAL MANAGEMENT

54. PTCA ( Percutaneous Transluminal Coronary Angioplasty)

55. ATHERECTOMY With Atherectomy the plaque is shaved off using a type of rotational blade.

56. CORONARY ARTERY BYPASS GRAFT (CABG) A form of bypass surgery that can create new routes around narrowed and blocked coronary arteries , permitting increased blood flow to deliver oxygen and nutrients to the heart muscle.  Coronary artery bypass graft  is an option for selected groups of patients with significant narrowings and blockages of the heart arteries. The bypass graft for a CABG can be a vein from the leg or an inner chest-wall artery.

57. COMPLICATIONS Dysrrythmia s - Damaged heart muscle disrupts electrical signals and produces arrhythmia in which heartbeat may be too fast, too slow or irregular like VF,VT,AF Cardiogenic shock-   It may develop after the large territory heart muscle damage. It leads to failure of the pumping action of the heart. The end results are very low blood pressure with an inadequate supply of oxygen rich blood to vital organs most significantly the brain, kidneys and heart Heart failure- It occurs slowly over time after an attack in which the heart cannot pump enough blood to meet the body’s demand Embolism . sometimes thrombus may dislodged from heart and may cause stroke (if reach in the brain) or ischemic limb (if reach in the limb)

58. mechanical complications It is due to tear or rupture of infarcted heart muscle. It includes- Severe mitral regurgitation – it is due to rupture of papillary muscle(l eakage of blood backward through the mitral valve from left ventricle to lt atrium ) Cardiac tamponade – it is due to rupture of ventricle. Right heart failure – it is due to rupture of interventricular septum. Late complications: These develop after one week of attack and include: Dressler’s syndrome- This syndrome is characterized by fever, pleuritis and percarditis . It is caused by an autoimmune reaction to damage heart muscle

59. Nursing diagnosis Acute pain R/T myocardial ischemia resulting from coronary artery occlusion Outcome- the client will experience improved comfort as evidenced by dec . in pain rating scale. Interventions- assess characteristics of pain Assess respiration, BP, heart rate with each episode of chest pain. Obtain 12 lead ECG on admission & on each episode of chest pain. Monitor respond to drug therapy. Limit visitors. As morphine as ordered. Administer nitrates as ordered.

60. Ineffective tissue perfusion R/T thrombus in coronary artery Outcome- the client will demonstrate improved cardiac tissue perfusion as evidenced by dec . rating of pain. Interventions- provide bed rest. Administer oxygen as prescribed. Administer thrombolytics . Monitor ST segments.

61. Dysrrhythmias R/T electrical instability or irritability secondary to infarcted tissue Outcome- the client will have no dysrrythmias as evidenced by normal sinus rhythm. Interventions- teach client & family about need for continous monitoring. Assess apical heart rate. Give antidysrrythmic agents as ordered. Monitor effects of antidysrrythmics . Monitor serum K levels. Maintain patent IV line. Monitor ST segments & document changes.

62. Risk for bleeding R/T coagulopathies with thrombolytic therapy. Powerlessness R/T a near-death experience & anticipated lifestyle changes. Anxiety & fear R/T hospital admission & fear of death. Risk for constipation R/T bed rest, pain medications & NPO or soft diet. Ineffective health maintenance R/T MI & implications for lifestyle changes. Risk for activity intolerance R/T an imbalance b/w oxygen supply & demand.

63. Health education Proper medication compliance (right dose and right time) Perform exercise Do not smoke follow the diet plan Maintain a healthy weight Manage your stress signs and symptoms to be reported to physician

64. Conclusion :   MI is a life threatening disease caused by many factors. Health education must be given to the patients with predisposing or risk factors to prevent it. Early diagnosis is also very important for saving the life of the patient. “ prevention is better than cure ”

65. REFERENCE Mosby’s Comprehensive Review of Nursing Dolores F.Saxton,Patricia M.Nugent. The Lippincott Manual of Nursing Practice https://en.wikipedia.org/wiki/Myocardial_infarction