MYOCARDIAL INFARCTION Flashcards
Definition
Necrosis of myocardium due to occlusion of a coronary artery (usually by thrombus following atherosclerotic plaque rupture) —> interruption of blood supply
Pathophysiology of MI
Plaque rupture with subsequent platelet adhesion, aggregation, and thrombus formation + vasoconstriction triggered by thromboxane A2, leading to complete occlusion of the artery and transmural infarction
Pathophysiology of dyspnea in MI/CAD leading to left ventricular failure:
MI —> LV systolic dysfunction —> increased blood in the LV —> increased LV end-diastolic pressure —> back pressures lead to increased LAP —> increased PCWP exceeding oncotic pressure of plasma —> leakage of fluid into the interstitium —> dyspnea
Clinical Features (4)
- Intense sub-sterna chest pain (described as crushing/elephant standing on chest), radiates to neck/jaw/left arm/back, not relieved by rest or nitroglycerin
- Diaphoresis, dyspnea, nausea + vomiting, sense of impending doom, syncope
- May be asymptomatic in elderly/diabetics/post-op pts
- ACS is associated with S4 (ischemia is associated with non-compliance of LV)
Types (2)
- STEMI: Transmural involving entire wall thickness (ST-elevation)
- NSTEMI: Subendocardial involving inner 1/3 (ST-depression)
Diagnosis (3)
- ECG (peaked T waves, Q waves, T-wave inversion, ST elevation-depression)
- Location of the MI is known from the leads showing ST changes:
- II, III, aVF: inferior (right coronary artery)
- I, aVL, V5, V6: lateral (left circumflex artery)
- V1, V2: septal
- V3, V4: anterior
- V1, V2, V3, V4: anteroseptal (left anterior descending artery)
- V1 to V5-V6: anterolateral
- V1 to V6, I, aVL: extensive anterior MI
- Cardiac enzymes (gold standard): Troponin I and T and CK-MB
- Troponin: more sensitive + specific; may be falsely elevated (e.g. vasculitis, drug abuse, myocarditis, pulmonary embolism, sepsis, renal failure)
- CK-MB is useful for detecting recurrent infractions bc it returns to normal levels within 48-72 hours.
Treatment (11)
- Admit to CCU and establish IV access
- Oxygen (if O2 <94%)
- Dual anti-platelet: aspirin + clopidogrel (dual anti platelets are given in ACS, post-stenting and post-CABG. Give dual first 6 months then give aspirin for life)
- Morphine
- Heparin (usually after revascularization/PCI)
- Beta blocker
-Nitrate - Statin
- Immediate revascularization
- PCI (door to balloon <90 minutes): superior to tPA if available
- tPA (door to needle <30 minutes): within 12 hours, preferably 6 hours
- Treatment with ACEI, aspirin, statin, and beta blocker is continued indefinitely
- In NSTEMI, revascularization is not necessary immediately. Patient may be treated initially with LMW heparin or GPIIb/IIIa inhibitors + angioplasty&stenting
Complications (6)
- Heart failure (#1 cause of in-hospital mortality)
- Arrhythmias (#1 cause of death in first few days: ventricular arrhythmias)
- Recurrent MI
- Mechanical complications:
- Free wall rupture
- Inter-ventricular septum rupture
- Papillary muscle rupture (—> mitral regurgitation/new murmur)
- Ventricular pseudoaneurysm/aneurysm
- Acute pericarditis (in 1-3days; treated with aspirin)
- Dressler syndrome (triad of fever, pericarditis + pleuritis, leukocytosis) and is treated with aspirin/ibuprofen (develops after 2 weeks)
- Inferior MI (RCA territory) may be associated with right ventricular infarction, 3rd degree heart block, hypotension and raised JVP with clear lung fields. Check with right lead ECG. Treat with high volume fluid replacement. Nitrates are contraindicated, as vasodilator therapy will worsen the hypotension.
Acute LVH/pulmonary edema after MI is due to: (6)
- Multiple infarcts
- Reccurent infarcts
- Large infarcts
- Acute MR
- Rupture —> VSD
- Pump failure —> cardiogenic shock
Management of Acute pulmonary edema after MI: (7)
- Propped up positioning
- Oxygen
- IV furosemide (loop diuretic but also pulmonary venodilator)
- Morphine (venodilation)
- IV nitrate
- Inotropic support if poor LV function (dobutamine or dopamine)
- Infra-aortic balloon pump as a bridge prior to surgery
