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Cardio > Myocardial infarction > Flashcards

Myocardial infarction Flashcards

1
Q

Myocardial infarction, what is it

A
  • death of the heart muscles due to a lack of blood perfusion
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2
Q

MI, cause, E

A
  • due to blockage of the coronary arteries
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3
Q

Coronary arteries and their supply to the heart tissues

A
  • 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)
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4
Q

What happens after 1min of non-oxygenation to the myocardium, and what happens after 20mins

A
  • 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.
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5
Q

Subendocardial infarct: def

A
  • necrosis of the inner 1/3 of the myocardium
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6
Q

Subendocardial infarct: causes

A
  • 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
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7
Q

Subendocardial infarct: ECG

A
  • NSTEMI: non-ST elevation
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8
Q

Transmural infarct: def

A
  • necrosis of the whole wall thickness of the myocardium
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9
Q

Transmural infarct: cause

A
  • due to complete blockage of the coronary artery for around 3-6 hours
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10
Q

Transmural infarct: ECG

A
  • STEMI: ST-elevation
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11
Q

Symptoms of MI

A
  • 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
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12
Q

Diagnostic tools for MI

A
  • LAB
  • irreversible damage to the heart cells -> will damage their membrane -> proteins and enzymes inside escape -> enters the bloodstream
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13
Q

Which markers are seen through a LAB test after an MI

A
  • 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)
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14
Q

State the different complications of MI

A

.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

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15
Q

Complications of MI: Arrhymias, when can it occur, the different types of arrhytmias that can occur

A
  • 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
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16
Q

Complications of MI: Arrhymias: VF/VT, T

A
  • 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.
17
Q

Complications of MI: II-III degree blocks, T

A
  • T: atropine (0.6 - 1.2 mg IV), consider pacemaker
18
Q

Complications of MI: A-fib, T

A
  • T: BB, heparin (anticoagulant, blood thinner), digoxin, cardioversion if nothing else works
19
Q

Complications of MI: Pericarditis, when can it occur

A
  • can occur 1-3 days after MI

- Necrotic area becomes inflammed and gets invaded by neutrophils -> which can lead to pericarditis.

20
Q

Complications of MI: Pericarditis: ECG + T

A
  • ECG: diffuse ST-elevation + PR interval shortening

- T: ASA (aspirin), other NSAIDS

21
Q

Complications of MI: myocardial rupture, when can it occur, pathomechanism, and which parts

A
  • 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
22
Q

Complications of MI: Heart failure, when can it occur, pathomechanism

A
  • can occur 2 weeks after MI

- pathomechanism: scarring process finishes.

23
Q

Complications of MI: ventricular aneurysm

A

weakened myocardium -> arrhythmia, stasis -> thrombus formation -> risk of embolism

24
Q

Complications of MI: Dressler’s syndrome

A
  • 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
25
Q

MI therapy

A
  • 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
26
Q

MI medications

A
  • 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

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