Myocardial Infarction by PGI Enriquez IM

this is based on harrison's internal medicine

1. ISCHEMIC HEART DISEASE

2. OBJECTIVES DEFINE ACUTE CORONARY SYNDROME AND DIFFERENTIATE NSTEmI FROM STEMI 01 Discuss THE BASIC PATHOPHYSIOLOGY AND CLINICAL MANIFESTATION OF acs 02 DISCUSS THE DIFFERENT MANAGEMENT FOR EACH DISEASE CONDITION 03

3. About the DISEASE 01

4. Introduction Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium

5. PATHOPHYSIOLOGY 02

6. In normal condition The myocardium will control the supply of oxygen-rich blood to prevent underperfusion of myocytes and the subsequent development of ischemia and infarction.

7. MAJOR DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND Myocardial wall tension Myocardial contractility Heart rate

8. pathophysiology

9. PATHOPHYSIOLOGY By reducing the lumen of the coronary arteries, atherosclerosis limits appropriate increases in perfusion when the demand for flow is augmented, as occurs during exertion or excitement. Myocardial ischemia also can occur if myocardial oxygen demands are markedly increased and particularly when coronary blood flow may be limited

10. CORONARY ATHEROSCLEROSIS Epicardial coronary arteries are the major site The major risk factors for atherosclerosis: High levels of plasma low-density lipoprotein Low plasma high-density lipoprotein [HDL] Cigarette smoking Hypertension Diabetes mellitus

11. CORONARY ATHEROSCLEROSIS NORMAL FUNCTIONS Local control of vascular tone Maintenance of an antithrombotic surface Control of inflammatory cell adhesion and diapedesis LOSS OF NORMAL FUNCTIONS Inappropriate constriction Luminal thrombus formation Abnormal interactions between blood cells

12. HISTORY & PHYSICAL EXAMINATION 03

13. TYPICAL PATIENT WITH ANGINA Man >50 years of age Woman >60 years of age CHEST DISCOMFORT Heaviness, pressure, squeezing, smothering, or choking and only rarely as frank pain Levine’s sign ANGINA Crescendo-decrescendo in 2–5 min Radiate to either shoulder and to both arms Radiate to the back, interscapular region, root of the neck, jaw, teeth, and epigastrium

14. Myocardial ischemic discomfort DOES NOT radiate to the trapezius muscles .

15. AUSCULTATION Arterial bruits, a third and/or fourth heart sound Mitral regurgitation. These auscultatory signs are best appreciated with the patient in the left lateral decubitus position.

16. Tenderness of the chest wall, localization of the discomfort with a single fingertip on the chest, or reproduction of the pain with palpation of the chest makes it unlikely that the pain is caused by myocardial ischemia.

17. Acute myocardial infarction 04

18. “The presence of acute myocardial injury detected by abnormal cardiac biomarkers in the setting of evidence of acute myocardial ischemia” ACS ST SEGMENT ELEVATION (STEMI) ACS NON ST SEGMENT ELEVATION (STEMI)

19. NON ST SEGMENT ELEVATION (NSTEMI) 05

20. NSTE-ACS is caused by an imbalance between myocardial oxygen supply and demand resulting from one or more of the following four processes that lead to thrombus formation Disruption of an unstable coronary plaque Coronary arterial vasoconstriction Gradual intraluminal narrowing Increased myocardial oxygen demand

21. DIAGNOSTIC EVALUATION CLINICAL EXAMINATION A ECG B CARDIAC BIOMARKERS C

22. Chest discomfort Occurrence at rest (or with minimal exertion), lasting >10 min Of relatively recent onset (i.e., within the prior 2 weeks) A crescendo pattern Located in the substernal region Radiates to the left arm, left shoulder, and/or superiorly to the neck and jaw History and pe

23. ANGINAL EQUIVALENTS Dyspnea Epigastric discomfort Nausea Weakness pHYSICAL FINDINGS Diaphoresis; pale, cool skin; sinus tachycardia A third and/or fourth heart sound Basilar rales sometimes, hypotension. History and pe

24. New ST-segment depression occurs in about one-third of patients with NSTE-ACS ELECTROCARDIOGRAM

25. CARDIAC BIOMARKERS Specific, sensitive, and the preferred markers of myocardial necrosis. TROPONIN I OR T CKMB Less sensitive alternative Elevated levels of any of these markers distinguish patients with NSTEMI from those with Unstable Angina Temporal rise and fall peaking 12–24 h post onset of symptoms of the plasma concentration of these markers and a direct relationship between the degree of elevation and mortality.

26. TIMI RISK SCORE

27. Treatment Acute phase Focused on the clinical symptoms and stabilization of the culprit lesion(s) Longer-term phase Involves therapies directed at the prevention of disease progression and future plaque rupture/erosion.

28. Treatment ANTI-ISCHEMIC TREATMENT Provide relief and prevention of recurrence of ischemic discomfort Initial treatment: Bed rest Nitrates Beta-Adrenergic blockers Inhaled oxygen ANTITHROMBOTIC THERAPY Antiplatelet and anticoagulant drugs represent the second major cornerstone of treatment.

29. ANTI-ISCHEMIC TREATMENT

30. ANTI-ISCHEMIC TREATMENT

31. ANTITHROMBOTIC THERAPY

32. ANTITHROMBOTIC THERAPY

33. ANTITHROMBOTIC THERAPY EXCESSIVE BLEEDING is the most important adverse effect of all antithrombotic agents Attention: Doses of antithrombotic agents Body weight Creatinine clearance Previous history of excessive bleeding

34. LONG-TERM MANAGEMEnT Risk-factor modification: Smoking cessation Achieving optimal weight Daily exercise Blood-pressure control Following an appropriate diet Control of hyperglycemia Lipid management

35. LONG-TERM THERAPY Beta blockers Lipid lowering therapy (statins at high dose, e.g., atorvastatin 80 mg/d, with ezetimibe if needed to achieve an LDL-C below 70 mg/dL) ACE inhibitors or angiotensin receptor blockers Antiplatelet regimen (combination for one year) low-dose (75–100 mg/d) aspirin P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor)

36. ST-SEGMENT ELEVATION (STEMI) 06

37. STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury. Produced or facilitated by factors: Cigarette smoking, hypertension, and lipid accumulation. The surface of an atherosclerotic plaque becomes disrupted and conditions favor thrombogenesis.

38. The amount of myocardial damage caused by coronary occlusion depends The territory supplied by the affected vessel Whether or not the vessel becomes totally occluded Duration of coronary occlusion Quantity of blood supplied by collateral vessels to the affected tissue Demand for oxygen of the myocardium Endogenous factors Adequacy of myocardial perfusion in the infarct zone when flow is restored

39. DIAGNOSTIC EVALUATION CLINICAL EXAMINATION A ECG B CARDIAC BIOMARKERS C cardiac imaging D

40. history Precipitating factor appears to be present before STEMI Pain is deep and visceral described as heavy, squeezing, or crushing. Central portion of the chest and/or the epigastrium, and, on occasion, it radiates to the arms May radiate as high as the occipital area but not below the umbilicus Radiation of discomfort to the trapezius is not seen in patients with STEMI Weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom.

41. PHYSICAL FINDINGS Anxious and restless, attempting unsuccessfully to relieve the pain by moving about in bed, altering their position, and stretching Pallor associated with perspiration and coolness of the extremities Substernal chest pain persisting for >30 min and diaphoresis Anterior Infarct Sympathetic nervous system hyperactivity (tachycardia and/or hypertension) Abnormal systolic pulsation Inferior Infarct Parasympathetic hyperactivity (bradycardia and/or hypotension)

42. PHYSICAL FINDINGS Fourth and third heart sounds, decreased intensity of the first heart sound, and paradoxical splitting of the second heart sound Transient midsystolic or late systolic apical systolic murmur Pericardial friction rub (transmural STEMI) Carotid pulse is often decreased in volume Temperature elevations up to 38°C Systolic pressure declines by ~10–15 mmHg from the preinfarction state

43. Temporal stages Acute - first few hours to 7 days Healing - 7–28 days) Healed - ≥29 days

44. Most patients initially presenting with ST-segment elevation ultimately evolve Q waves on the ECG Among patients presenting with ischemic discomfort but without ST-segment elevation, if a serum cardiac biomarker of necrosis is detected, the diagnosis of NSTEMI is ultimately made ELECTROCARDIOGRAM

45. Cardiac-specific troponin T (cTnT) and cardiac specific troponin I (cTnI) increase after STEMI to levels many times higher than the upper reference limit Levels of cTnI and cTnT may remain elevated for 7–10 days after STEMI. CK rises within 4–8 h and generally returns to normal by 48–72 h CK may be elevated Skeletal muscle disease or trauma, including intramuscular injection. CARDIAC BIOMARKERS

46. A cute STEMI cannot be distinguished from an old myocardial scar or from acute severe ischemia by echocardiography Early detection of the presence or absence of wall motion abnormalities by echocardiography can aid in management decisions CARDIAC imaging

47. Initial management

48. Recognition of symptoms Rapid development of an emergency medical team Transportation of the patient to a hospital facility Reperfusion therapy Prehospital care

49. Recognition of symptoms Rapid development of an emergency medical team Transportation of the patient to a hospital facility Reperfusion therapy Prehospital care

50. Aspirin is essential in the management of patients with suspected STEMI 160–325-mg tablet in the Emergency Department Followed by daily oral administration of aspirin in a dose of 75–162 mg. When hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction; should then be reassessed to determine if there is a continued need for such treatment. Emergency department

51. Sublingual nitroglycerin can be given safely to most patients with STEMI. Up to three doses of 0.4 mg should be administered at about 5-min intervals Therapy with nitrates should be avoided in patients who present with low systolic arterial pressure (<90 mmHg) or in whom there is clinical suspicion of RV infarction Nitrates should not be administered to patients who have taken a phosphodiesterase-5 inhibitor for erectile dysfunction within the preceding 24 h Control of discomfort

52. Morphine is a very effective analgesic for the pain associated with STEMI. Routinely administered by repetitive (every 5 min) intravenous injection of small doses (2–4 mg) Side effects: reduced cardiac output and arterial pressure, diaphoresis and nausea, bradycardia or advanced degrees of heart block INTRAVENOUS BETA BLOCKERS are also useful in the control of the pain of STEMI. These drugs control pain effectively in some patients, presumably by diminishing myocardial O2 demand Metoprolol, 5 mg every 2–5 min for a total of three doses Then, oral regimen of 50 mg every 6 h for 48 h, followed by 100 mg every 12 h Control of discomfort

53. Angioplasty and/or stenting without preceding fibrinolysis More effective than fibrinolysis in opening occluded coronary arteries Associated with better short-term and long-term clinical outcomes Primary percutaneous coronary intervention

54. If no contraindications are present (see below), fibrinolytic therapy should ideally be initiated within 30 min of presentation Tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK), and reteplase (rPA) tPA - 15-mg bolus followed by 50 mg intravenously over the first 30 min, followed by 35 mg over the next 60 min Streptokinase - 1.5 million units (MU) intravenously over 1 h rPA - double-bolus regimen consisting of a 10-MU bolus given over 2–3 min, followed by a second 10-MU bolus 30 min later. TNK - a single weight-based intravenous bolus of 0.53 mg/kg over 10 s FIBRINOLYSIS

55. Clear contraindications History of cerebrovascular hemorrhage Nonhemorrhagic stroke or other cerebrovascular event within the past year Marked hypertension >180/110 at any time during the acute presentation Suspicion of aortic dissection, Active internal bleeding Hemorrhage is the most frequent and potentially the most serious complication. FIBRINOLYSIS

56. Hospital phase management Activity Bed rest for the first 6–12 h In the absence of complications, patients should be encouraged, under supervision, to resume an upright posture by dangling Their feet over the side of the bed and sitting in a chair within the first 24 h. Diet Receive either nothing or only clear liquids by mouth For the first 4–12 h ≤30% of total calories as fat and have a cholesterol content of ≤300 mg/d. Complex carbohydrates should make up 50–55% of total Calories High in potassium, magnesium, and Fiber, but low in sodium Bowel management A bedside commode rather than a bedpan • diet rich in bulk, and the routine use of a stool softener Sedation Withstand the period of enforced inactivity with tranquility. Diazepam (5 mg), oxazepam (15–30 mg), or lorazepam (0.5–2 mg), given three to Four times daily

57. ASPIRIN is the standard antiplatelet agent for patients with STEMI. The standard anticoagulant agent used in clinical practice is UNFRACTIONATED HEPARIN (UFH) Antithrombotic agents

58. Improves the myocardial O2 supply-demand relationship, decreases pain, reduces infarct size, and decreases the incidence of seriou ventricular arrhythmias. Specifically contraindicated: Patients with heart failure or severely compromised LV function, heart block, orthostatic hypotension, or a history of asthma BETA-ADRENOCEPTOR BLOCKERS

59. ACE inhibitors reduce the mortality rate after STEMI Mechanism: reduction in Ventricular remodeling after infarction Risk of CHF Angiotensin receptor blockers (ARBs) should be administered to STEMI patients who are intolerant of ACE inhibitors and who have either clinical or radiologic signs of heart failure. INHIBITION OF THE RENIN-ANGIOTENSIN- ALDOSTERONE SYSTEM

60. Long-term treatment with an antiplatelet agent (usually aspirin) after STEMI is associated with a 25% reduction in the risk of recurrent infarction, stroke, or cardiovascular mortality ACE inhibitors or ARBs and, in appropriate patients, aldosterone antagonists should be used indefinitely by patients with clinically evident heart failure, a moderate decrease in global ejection fraction, or a large regional wall motion abnormality to prevent late ventricular remodeling and recurrent ischemic events. The chronic routine use of oral beta-adrenoceptor blockers for at least 2 years after STEMI is supported by well-conducted, placebo controlled trials. Evidence suggests that warfarin lowers the risk of late mortality and the incidence of reinfarction after STEMI Secondary prevention

61. Ventricular dysfunction After STEMI, the left ventricle undergoes a series of changes in shape, size, and thickness in both the infarcted and noninfarcted segments. (ventricular remodeling) Generally precedes the development of clinically evident CHF in the months to years after infarction. Hemodynamic assessment Pump failure is now the primary cause of in-hospital death from STEMI Pulmonary rales and S3 and S4 gallop sounds; Pulmonary congestion; Elevated LV filling pressure and elevated pulmonary artery pressure complications

62. Hypovolemia may be secondary to previous diuretic use, and/or to vomiting associated with pain or medications. Cardiogenic Shock Patients who develop cardiogenic shock have severe multivessel coronary artery disease with evidence of “piecemeal” necrosis extending outward from the original infarct zone. Arrhythmias Mechanism: autonomic nervous system imbalance, electrolyte disturbances, ischemia, and slowed conduction in zones of ischemic myocardium complications

63. Recurrent chest discomfort Pericarditis Thromboembolism Left ventricular aneurysm complications

64. THANK YOU!