Myocardial Infaction

What is it?

MI is defined as the irreversible death or necrosis of myocardial tissue due to an inadequate coronary blood supply. MI is nearly always due to a thrombus in the coronary artery. Irreversible cell death begins within 20 minutes of the cessation of blood flow through the coronary artery.

The amount of damage or necrosis depends on whether the occlusion is complete or partial, the duration of the occlusion, where in the coronary artery the blockage occurred, and the amount of collateral blood flow to the affected area of the myocardium.

ST Segment Elevation
  • Mocardial injury results in ST-segment elevation. Significant elevation is defined as 1 mm (1 small box high on the ECG tracing). or greater in two anatomically contiguous leads (looking at the same area of the heart).
    • Hyperacute T waves are considered an early sign of STEMI and should be treated as a STEMI.
    • Loss of the ST segment as the ST segment and T wave become fused together is another early sign of STEMI.
    • Other causes (beyond MI) for ST segment elevation include left ventricular aneurysm, left ventricle hypertrophy, pericarditis, and ventricular-paced rhythms.
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Symptoms
  • Chest pain (pain lasting longer than 2o minutes is likely an MI)
    • Pressure
    • Tightness
    • Squeezing
    • Heaviness
    • Indigestion
  • Diffusion of Pain
    • Pain may radiate into arm, jaw, shoulders, or back
  • Associated Symptoms
    • Palpitations
    • Dyspnea
    • Nausea/Vomiting
    • Dizziness
  • Pulmonary
    • Dyspnea
    • Cough
    • Crackles
    • Wheezing
Labs
  • Troponin I and Troponin T
    • The troponins are the preferred cardiac biomarkers. They are the most specific markers for cardiac injury because they are part of the cardiac cell’s contractile apparatus and should only be present in the blood when there is damage to the heart muscle itself.
    • Troponin I is less than 0.03 ng/mL
    • Troponin T is less than 0.02 ng/mL
  • CK and CK-MB
    • CK and CK-MB are not as sensitive or specific to cardiac cell injury. CK identifies inflammation of muscles, and the CK-MB isoenzymes is specific for cardiac muscle.
    • CK Males: 55-170 units/L
    • CK Females: 30-135 units/L
    • CK-MB: Less than 10 ng/mL or less than 3% of total CK
  • Myoglobin
    • Myoglobin is a protein released when muscle is damaged. It can be detected very early but is not frequently used in ACS because it isn’t cardiac-specific.
Medical Management
  • Beta blocker, unless contraindicated
    • Slows HR to allow increased diastolic perfusion time improving mycoardial oxygen supply
    • Decrease contractility, which decreases oxygen consumption
    • Decreases the incidence of ventricular dysrhythmias
    • Prevent ventricular remodeling
    • Decreases afterload by causing arterial vasodilation
    • Contraindicated if SBP <90, cardiogenic shock, HB, or severe bradycardia
  • ASA
  • P2y12 receptor inhibitor
    • Plavix, initiated prior to or at the time of PCI
  • ACE inhibitor if EF <40 or (ARB)
    • Reduces remodeling of the myocardium
    • Reduced (preload) and (afterload) and workload of the heart.
  • NTG if ongoing chest pain, HTN, or HF
    • low doses 100-150 mcg/min cause venous dilation (preload) reduction
    • High doses cause arterial vasodilation, slightly reducing (afterload)
  • O2 to maintain spO2 >90%
  • Supplemental oxygenation
    • SPO2 is less than 90%
    • Patient with exhibiting respiratory distress
    • Patient is at high risk for hypoxemia
    • American College of Cardiology (ACC) and the American Heart Association (AHA) guidelinesĀ caution that supplemental oxygen may increase coronary vascular resistance, so administer with caution.
Reperfusion Management
  • Urgent PCI
    • Start Heparin (UFH or LMWH) or bivalirudin
    • GP llb/llla antagonist in selected patients
      • abciximab (Reopro)
      • tirofiban (Aggrastat)
      • eptifbatide (Integrilin)
  • Fibrinolytics
    • Used with in 12 hours of onset, and up to 24 hours. Primarily used when PCI can not be accomblished within target timeframe.
    • Start Heparin (UFH or LMWH)
    • Start P2y12 receptor inhibitor
      • Plavix
    • ASA
  • Urgent CABG
IV Drip Management
  • Nitroprusside (Nipride)
    • Dilates both arterioles and venules, decreasing (preload) and (afterload).
    • May be used in conjunction with dopamine for cardiogenic shock.
  • Milrinone (Primacor)
    • Phosphodiesterase inhibitor, with properties similar to dobutamine
    • Decreases mean pulmonary artery pressure (PAP), and SVR without increasing HR.
  • Dopamine (Intropin)
    • infusion rates of 0 to 10 mcg/kg/min increase (contractility) increasing CO, and variable SVR. HR may increase in patients with low preload.
    • Higher doses are contraindicated as increased SVR will increase myocardial oxygen consumption.
  • Phenylephrine (Neosynephrine)
    • Alpha 1 agonsist, causes arterial vasoconstriction increasing (afterload) without increase in HR.
  • NTG
    • low doses less than 100-150 mcg/min cause venous dilation reducing (preload).
    • higher doses cause arterial vasodilation and a slight reduction in (afterload).