Myocardial infarction Flashcards
Myocardial infarction, what is it
- death of the heart muscles due to a lack of blood perfusion
MI, cause, E
- due to blockage of the coronary arteries
Coronary arteries and their supply to the heart tissues
- LAD: Left anterior descending, supplies ant wall + septum of anterior left ventricle (40-50% of cases)
- LCA: Left circumflex artery, supplies lateral wall of the left ventricle (15-20% of cases)
- RCA: Right coronary artery, supplies posterior wall, post septum, and papillary muscles of the left ventricle (30-40% of cases)
What happens after 1min of non-oxygenation to the myocardium, and what happens after 20mins
- after 1 min: the area becomes ischemic, and the muscle ability to contract becomes severely reduced. Potentially reversible
- after 20-40 mins: Irreversible. Becomes a zone of necrosis.
Subendocardial infarct: def
- necrosis of the inner 1/3 of the myocardium
Subendocardial infarct: causes
- blockage for a temporary moment of the coronary artery with return of blood flow
- severe atherosclerosis
- hypotension
- anything that leads to poor perfusion
- seen in Stable angina, and unstable angina
Subendocardial infarct: ECG
- NSTEMI: non-ST elevation
Transmural infarct: def
- necrosis of the whole wall thickness of the myocardium
Transmural infarct: cause
- due to complete blockage of the coronary artery for around 3-6 hours
Transmural infarct: ECG
- STEMI: ST-elevation
Symptoms of MI
- chest pain/pressure radiating to the left arm/jaw (organ low perfusion)
- diaphoresis (sweating) (sympathetic response from the body trying to keep the heart working harder to preserve the blood pressure)
- nausea
- fatigue
- dyspnea
Diagnostic tools for MI
- LAB
- irreversible damage to the heart cells -> will damage their membrane -> proteins and enzymes inside escape -> enters the bloodstream
Which markers are seen through a LAB test after an MI
- Troponin T and I: elevates 2-4h after the infarct, peaks around 48h, stay elevated for 7-10 days. Troponin I is the most specific marker
- CK-MB: elevates 2-4h after the infarct, peaks around 24h, stay elevated for 48h. Useful to diagnose re-infarction, which can occur 48h after the first one (10% of cases)
State the different complications of MI
.0-24h after MI: arrhythmias, cardiogenic shock
.1-3 days after MI: Pericarditis
.3-14 days after MI: myocardial rupture
. after 2 weeks: heart failure
others: Dressler’s syndrome, recurrent MI, Unstable angina
Complications of MI: Arrhymias, when can it occur, the different types of arrhytmias that can occur
- occurs 0-24h after MI
- life-threatening
- occurs due to damaged of the cells conducting the electrical signals
- Ventricular fibrillation (VF)/Ventricular tachycardia (VT),
- II-III degree blocks
- A-fib
Complications of MI: Arrhymias: VF/VT, T
- Ventricular fibrillation (VF)/Ventricular tachycardia (VT), can lead to sudden death.
- T:
.Perform an immediate cardioversion/defibrillation (if pulseless),
.BB,
.ICD (implantable cardioverter defibrillator) should be considered.
Complications of MI: II-III degree blocks, T
- T: atropine (0.6 - 1.2 mg IV), consider pacemaker
Complications of MI: A-fib, T
- T: BB, heparin (anticoagulant, blood thinner), digoxin, cardioversion if nothing else works
Complications of MI: Pericarditis, when can it occur
- can occur 1-3 days after MI
- Necrotic area becomes inflammed and gets invaded by neutrophils -> which can lead to pericarditis.
Complications of MI: Pericarditis: ECG + T
- ECG: diffuse ST-elevation + PR interval shortening
- T: ASA (aspirin), other NSAIDS
Complications of MI: myocardial rupture, when can it occur, pathomechanism, and which parts
- can occur 3-14 days after MI
- pathomechanism: macrophages then invade the tissue -> healing process begins with formation of new granulation tissue, at this phase it is most at risk of myocardial rupture
- mitral papillary rupture -> acute regurgitation -> pulmonary oedema
- ventricular septal rupture -> systolic murmur and thrill
- free wall rupture -> cardiac tamponade and loss of BP
Complications of MI: Heart failure, when can it occur, pathomechanism
- can occur 2 weeks after MI
- pathomechanism: scarring process finishes.
Complications of MI: ventricular aneurysm
weakened myocardium -> arrhythmia, stasis -> thrombus formation -> risk of embolism
Complications of MI: Dressler’s syndrome
- a post myocardial infarct complication, occurs when there’s an autoimmune response to myocardial antigen which results in pericarditis.
- can occur month after the AMI
- whereas fibrinous pericarditis occurs 1-3 days later
MI therapy
- lifesaving treatments that can be done immediately following an MI
- fibrinolytic therapy: medications to destroy fibrin and blood clot
- angioplasty: to open arteries
- percutaneous coronary intervention: stent implantation in the coronary to physically open the blood vessels
MI medications
- antiplatelets: ASA (aspirin)
- anticoagulants: Heparin
- Nitrates: vasodilator -> lowers the preload
- Beta Blockers: slows HR and cardiac demand
- Pain medication
- Statins: to improve patient’s lipid profile
- “STAR”: Streptokinase, Tenecteplase, Alteplase, Releplase, are the 4 most common fibrinolytics used for MI
