"

Chapter 7 Selected Diseases and Disorders of the Cardiovascular System

7p22 Myocardial Infarction

Zoë Soon

Myocardial Infarctions and Vascular Complications

Myocardial Infarction (MI) – Pathophysiology & Causes:

Causes:

  • Total occlusion of a coronary artery, most often due to atherosclerotic plaque rupture.
  • Thrombus formation: Clot forms at the plaque site or thrombi break off and lodge downstream.
  • Vasospasm: Sudden constriction (though the exact cause is not fully understood).

Potential Triggers:

  • Plaque rupture or hemorrhage.
  • Thromboembolism: Clot breaking free and occluding distal artery.
  • Vasospasm: Sudden, intense constriction of the vessel.

Progression of Occlusion:

  • Partial occlusion causes angina pectoris (chest pain).
  • Complete occlusion can lead to myocardial infarction (MI), commonly known as a heart attack.

Vascular Damage leads to Dysfunction:

  • Endothelial cell dysfunction:
    • Reduced or lost nitric oxide (NO) production or sensitivity.
    • Endothelial cells may produce less NO upon stimulation, or lose responsiveness to NO, leading to excessive vasoconstriction (spasm).
    • Damaged blood vessels are also susceptible to both arteriosclerosis and atherosclerosis.

Severity of MI:

  • Depends on:
    • Size of the infarct.
    • Location: Anterior wall, lateral wall, apex, etc.
    • Depth: How deep into the myocardium the infarct occurs.

Deeper infarcts and those in critical regions (e.g., LAD artery) cause more damage and worse prognosis.

 

Myocardial Infarction Signs and Symptoms:

  • Chest Pain:
    • Described as heaviness, pressure, burning in the chest.
    • Often radiates to the left arm, shoulder, jaw, or neck.
    • Usually not relieved by rest or nitroglycerin, distinguishing from angina.
    • In women: Nausea and indigestion are common, and symptoms may be less recognizable, risking missed diagnosis.
  • Neurological Signs:
    • Reduced oxygen to the brain causes anxiety, fear, confusion.
    • Possible fainting or altered consciousness.
  • Progression:
    • ECG shows characteristic changes:
      • Early: Abnormal P wave and QRS complex indicate ischemia.
      • Later (hours/days): Elevated ST segmentT wave inversionminimal P wave.
      • Necrosis: Shown by flattened QRS and abnormal T wave.

Diagnosis

  • Blood Tests:
    • Elevated enzymes from necrotic heart cells:
      • Creatine phosphokinase (CPK): Released from damaged muscle.
      • Lactate dehydrogenase (LDH).
      • Aspartate aminotransferase (AST): Indicates tissue injury.
      • Troponins: Highly specific for cardiac damage; elevated with necrosis.
    • Potassium: Elevated due to cell rupture, risking dysrhythmias.
    • White blood cells: Increase as part of inflammatory response.
    • CRP (C-reactive protein): Marker of inflammation.
    • ESR (Erythrocyte Sedimentation Rate): Increased during inflammation and tissue damage.
  • Additional Monitoring:
    • Capillary wedge pressure: Assesses left ventricle function and pressure.

Possible Outcomes:

  • Mortality:
    • About 25% die, mainly from arrhythmiashypoxia, or acidosis.
    • Cardiogenic shock: Inadequate cardiac output leading to organ failure.
  • If survived:
    • Can develop acute or chronic congestive heart failure.
    • Heart becomes less effective at contracting, leading to ongoing deterioration and possible death.

4 Possible Complications:

1.  Cardiac Rupture:

  • Typically occurs 3 to 7 days post-MI.
  • Necrotic, weakened heart tissue may rupture because the dead tissue breaks down.
  • Outcome: Usually fatal due to sudden hemorrhage and cardiac tamponade.

2.  Cardiac Tamponade:

  • Damage near the heart can cause exudate or blood to fill the pericardial sac.
  • Effects:
    • Increased pressure on the heart.
    • Impaired filling during diastole.
    • Reduced stroke volume and cardiac output, leading to shock.
  • Management:
    • Pericardiocentesis: Puncture the sac to aspirate fluid and relieve pressure.
    • Critical to monitor for this complication as it can be fatal.

3.  Emboli & Stroke:

  • Damage tissue can lead to clot formationthrombus.
  • Thrombus dislodgement:
    • Loose pieces (emboli) can travel.
    • Left ventricular MI: Emboli may enter the systemic circulation (e.g., brain) causing stroke.
    • Right ventricular MI: Emboli may travel to lungs causing pulmonary embolism.
  • Timing: Usually occurs 3-7 days after MI as thrombi dislodge.

4.  Acidosis & Hypoxia:

  • Ischemia causes tissues to revert to anaerobic respiration.
  • Produces lactic acid, decreasing blood pH.
  • Acidosis (<7.35):
    • Impairs cellular function, including the myocardium.
    • Can cause organ dysfunction and worse outcomes.
  • Emergency care aims to correct hypoxia and prevent acidosis progression.

Treatment:

Emergency Response (Paramedics):

  1. Provide oxygen: Ensures tissues, especially the brain and heart, receive adequate oxygen.
  2. Pain relief:
    • Analgesics (e.g., opioids) to alleviate severe chest pain (“elephant sitting on the chest”).
    • Reduces stress and sympathetic nervous system activation, which can decrease the heart’s workload.
  3. Anticoagulant and thrombolytic therapy:
    • Anticoagulants: Prevent further clot formation.
    • Thrombolytics: Break up existing clots, especially if embolism caused the MI.

Additional Treatments:

  1. Treat dysrhythmias and hypertension:
    • Use medications like digoxin (for contractility), beta blockerscalcium channel blockersalpha blockers.
  2. Address heart failure:
    • Use medications to reduce load, manage blood pressure, and normalize heart rate.

Surgical Intervention Procedures:

  • Coronary interventions:
    • Catheter-based delivery: Thrombolytics, balloons, and stents.
      • Angioplasty: Balloon inserted via catheter to open blocked arteries; sometimes followed by placement of a stent.
      • Laser therapy: To remove or reduce plaque.
    • Bypass surgery (CABG): Creating new pathways around blocked arteries.
  • Plaque removal: Can be performed via laser, balloon, or stent insertion depending on location.

Tools:

  • Defibrillators: Automated external defibrillators (AEDs) are accessible in public places and gyms; easy for laypersons to operate.

Other Organ Systems Affected by Vascular Occlusion:

  1. Brain (Stroke):
    • TIA (Transient Ischemic Attack): A mini-stroke caused by partial occlusion of cerebral arteries.
    • Full occlusion: Leads to cerebrovascular accident or stroke — an ischemic stroke.
  2. Peripheral arteries (Aneurysm and Peripheral Vascular Disease):
    • Damage and narrowing of arteries (e.g., in the aorta) cause aneurysm formation:
      • Bulging of arterial wall due to damage and calcium deposits.
      • Brittle and susceptible to rupture.
      • Rupture of the aorta is often fatal due to massive internal bleeding.
    • Other arteries (e.g., iliac arteries):
      • Can develop peripheral vascular disease.
      • Usually affects legs and feet.
      • Occlusion leads to ischemia, tissue death, gangrene, and possibly amputation.

Signs and Symptoms of Peripheral Vascular Disease:

    • Muscle pain and fatigue:
      • Occurs during activity (exercise) when muscles demand more oxygen.
    • Nerve symptoms:
      • Tingling, numbness, burning sensations due to oxygen deprivation.
    • Pulse weakness or absence:
      • Reduced blood flow results in weak or absent pulses in affected limbs.
    • Physical signs:
      • Cyanosis: Bluish skin.
      • Paleness: Reduced blood flow.
      • Dry skin, less hair growth, thickened nails (clues of chronic ischemia).
      • Slow healing of wounds due to poor tissue maintenance.

Prevention and Management of Arterial Disease:

  • Prevention is key:
    • Maintain a healthy diet low in saturated fats, trans fats, cholesterol, and salt.
    • Engage in regular exercise to help control weight and improve vascular health.
  • Control Diabetes:
    • Adherence to medications and blood glucose management to prevent vascular damage.
  • Weight Management:
    • Avoid obesity as it contributes to high lipid levels and increased cardiovascular risk.
  • Lipid Control:
    • Use anticoagulants and platelet inhibitors if at risk for thrombosis or thromboembolism.
  • Lifestyle Changes:
    • Stop smoking: Significantly reduces the formation of atherosclerotic plaques.
  • Leg Care:
    • Maintain dependent positions (legs below the heart) to improve perfusion.
    • Proper foot hygiene and wound care to prevent infections.
  • Interventional Procedures:
    • Vasodilators: Medications to improve blood flow.
    • Surgical options include:
      • Coronary artery bypass grafting (CABG): Restores blood flow around blocked arteries.
      • Angioplasty: Balloon dilatation to open narrowed vessels.
      • Endarterectomy: Surgical removal of plaque from vessels.

Lifestyle Adjustments:

  • Exercise regularly.
  • Healthy diet.
  • Stress reduction.

Summary:

Occlusions in arteries can cause localized tissue ischemia in the heart, brain, or limbs, leading to serious conditions such as MI, stroke, aneurysm rupture, or limb gangrene. Recognizing symptoms like pain during activity, skin changes, and slow wound healing is vital to early diagnosis and intervention, preventing catastrophic outcomes.

Prevention of artery disease involves lifestyle modifications, proper disease management, and surgical interventions when necessary. Myocardial infarctions are typically caused by plaque rupture and thrombus formation, with vasospasm also contributing. Damaged endothelium reduces NO availability, leading to increased constriction and risk of infarction. The extent of myocardial damage depends on the size and location of the occlusion.

Myocardial infarction presents with characteristic chest pain, ECG changes, and elevated cardiac enzymes indicating cell death. Early diagnosis and treatment are crucial to prevent fatal arrhythmias, shock, or heart failure. Post-infarction, the heart’s compromised ability can cause long-term dysfunction, emphasizing the importance of timely intervention.

Complications after MI include heart wall rupture, pericardial tamponade, and emboli formation leading to stroke or pulmonary embolism. Acidosis from tissue hypoxia further exacerbates organ failure risks. Rapid intervention and close monitoring are essential to prevent these potentially fatal outcomes.

Treatment of MI involves rapid oxygenation, pain management, clot dissolution, and mechanical intervention with angioplasty, stents, or bypass surgery. Long-term management includes lifestyle changes and medications to support the heart and prevent recurrent events. Early intervention and use of devices like defibrillators can save lives

License

Icon for the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License

7p22 Myocardial Infarction Copyright © by Zoë Soon is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, except where otherwise noted.

Share This Book