Myocardial Ischemia: Causes and Effects

• Ischemia occurs when myocardial perfusion is compromised due to an imbalance between myocardial oxygen supply and demand.

Oxygen Supply and Demand

• Oxygen supply depends on coronary vessel lumen size, ventricular wall compressibility, and diastolic time.
• Oxygen demand depends on myocardial contractility, heart rate, and ventricular wall stress (influenced by preload and afterload).

Causes and Pathophysiology of Ischemia

• Blockage in the coronary artery and coronary artery spasm can cause ischemia.
• Increased demand not met by increased supply results in supply ischemia.
• Ischemia can occur even at rest if the supply is insufficient due to blockage or spasm.
• Ischemia is reversible if blood flow is restored before permanent damage.
• Untreated ischemia leads to injury, apoptosis, or necrosis (cell death).

Effects and Metabolic Shift of Ischemia

• Ischemia occurs within 10 seconds of blood flow interruption.
• Depressed contractility occurs within 1 minute.
• Necrosis occurs within 20 minutes if blood flow is not restored.
• Aerobic metabolism produces 36 ATP molecules and efficient waste removal (CO2, H2O).
• Anaerobic metabolism produces 2 ATP molecules and toxic pyruvic and lactic acids.

Consequences of Inadequate ATP

• Inefficient sodium-potassium pump
• Cell membrane alterations
• Can lead to edema, arrhythmias, cell death, and impaired myocardial contraction.

Impact of Cell Death

• Reduced ventricular muscle available for contraction (hypokinesis or akinesis).
• Decreased ventricular compliance and elasticity.
• Reduced cardiac output.
• Incomplete ventricular emptying.
• Activation of the sympathetic nervous system.

Acute Coronary Syndrome (ACS)

• ACS starts with plaque rupture in a coronary artery, leading to myocardial infarction if perfusion isn't restored quickly.
• Includes unstable angina, non-ST elevation MI, and ST elevation MI.

Atherosclerosis

• Atherosclerosis involves plaque buildup in arteries, leading to ischemia.
• Key steps: endothelial injury, inflammation, fatty streak formation, plaque development, and plaque rupture leading to thrombosis.

Myocardial Infarction (MI) Symptoms

• Shortness of breath and chest tightness.
• Intense and prolonged chest pain.
• Nausea and Fainting.
• Intense sweating and pain in left shoulder, arm, jaw, and back.

Unstable Angina

• Disrupts a vulnerable or unstable atherosclerotic plaque.
• This leads to transient episodes of vessel occlusion
• Symptoms are unpredictable and cannot be controlled by medication or rest.
• Often shows ST segment depression and T wave inversion during pain and usually negative cardiac enzymes.

Non-ST Elevation Myocardial Infarction (Non-STEMI)

• Necrosis of myocardial tissue, but it doesn't involve the full thickness.
• A thrombus forms, partially occluding the lumen.
• Symptoms: Severe and abrupt pain; difficulty obtaining pain relief.
• Often shows ST segment depression and T wave inversion
• Positive for cardiac biomarkers.

ST Elevation Myocardial Infarction (STEMI)

• Complete arterial occlusion results in necrosis of the full thickness of the ventricle.
• Symptoms: Severe and abrupt pain; difficulty obtaining pain relief.
• Shows ST elevation and Elevated cardiac biomarkers.

Cardiac Biomarkers

• Creatinine Kinase (CK) shows heart, brain, skeletal muscles rises 3-6 hours post-infarction, peaks 12-24 hours.
• CKMB, troponin T & Troponin I are used to detect specificity in the heart to identify MI diagnosis.

ECG Changes

• Normal ECG: Shows a p wave, a q wave, an r wave, an s wave, and a t wave.
• The QRS complex represents ventricular depolarization.
• Ischemia: Depicted by ST depression or inverted T waves.
• Injury: Depicted by ST elevation.
• Infarct: Depicted by pathological Q waves.

Zones of Myocardial Infarction

• Zone of Infarct: Cell death and necrosis eventually replaced by scar tissue.
• Zone of Injury: Myocardial cells are damaged but still viable.
• Zone of Ischemia: Perfusion is decreased, but cells remain viable.

Collateral Circulation and Ventricular Remodeling

• Angiogenesis: Formation of new blood vessels to bypass blockages.
• Collateral Circulation: New blood vessels restore flow to the myocardial tissue.
• Ventricular Remodeling: Regeneration of myocardial tissue.

Myocardial Infarction (MI) Study Guide

• Pain: Lactic acid buildup or myocardial stretching.
• Sympathetic stimulation and catecholamine release.
• Dysrhythmias: Anaerobic metabolism during ischemia leads to insufficient ATP.
• Nausea and vomiting: Reflex stimulation of vomiting centers by pain fibers.

Diagnosis and Assessment

• Diagnosis based on thorough history, risk factor identification
• Physical assessment, 12-lead or 15-lead ECG, cardiac enzyme detection, echocardiogram.
• ECG: Identifies changes indicating myocardial infarction.
• Cardiac Enzymes: Detect cellular injury and Echocardiogram: Assesses myocardial damage.

Fourth Universal Definition of MI

• Myocardial injury: Detectable elevation in cardiac troponin
• Myocardial infarction: Acute myocardial injury with acute myocardial ischemia.
• Pathophysiological MI definition: Myocardial cell death due to prolonged ischemia.

Immediate Non-Pharmacological Interventions

• Immediate Transfer: To an acute care facility via EMS (911) and supplemental oxygen.
• 12-Lead ECG: Identifies infarcted ventricle area and potential culprit coronary artery.
• Continuous Cardiac Rhythm Monitoring: Observes changes in rhythm.
• Vital Signs Monitoring: Assesses cardiac output.
• Bed Rest: Conserves energy, reduces cardiac demand and Blood Tests: Cardiac biomarkers.

Medications for Heart Failure

• Morphine: Pain management and vasodilation.
• Oxygen: Supplements oxygen supply.
• Nitroglycerin: Vasodilation, decreased afterload/myocardial oxygen demand.
• Aspirin: Prevents platelet aggregation.
• Beta Blockers: Reduced myocardial oxygen demand.
• Heparin: Accelerates antithrombin action.
• Glycoprotein IIb/IIIa Inhibitors: Decreases thrombus formation.
• ACE Inhibitors: Prevent angiotensin I to II conversion and ARBs: Prevent angiotensin from binding to receptors.
• Statins: Inhibit cholesterol synthesis.

Consequences of MI and Healing

• Consequences of MI and healing depend on infarct location and size.
• Enzyme Release: Damaged myocardial cells release cardiac enzymes.
• Leukocyte and Neutrophil Invasion: Enzyme release breaks down necrotic tissue.
• Scar Formation (Week 3): Fibrous connective tissue replaces necrotic tissue.
• Wall Motion Abnormalities: Hypokinetic.

What is Heart Failure?

• Heart failure is a complex clinical syndrome.
• The heart's inability to pump blood adequately.
• Heart failure is a syndrome with symptoms of cardiac abnormality.

Causes of Heart Failure

• Valve disease and inflammatory processes.
• Cardiomyopathy and uncontrolled hypertension.

Epidemiology of Heart Failure

• Approximately 500,000 people live with heart failure in Canada.
• 50,000 new cases are identified annually.
• Annual mortality rate: 5-50%.

Myocardial Changes and Systemic Effects

• Decreased cardiac output causing reduced stroke volume.
• Fluid leakage from capillaries increases hydrostatic pressure.

Left-Sided Heart Failure

• Fluid leaks into lung tissue (pulmonary edema).
• Right-Sided Heart Failure: Fluid leaks into the liver, jugular vein, and peripheral tissues.
• Altered tissue perfusion and pulmonary congestion.
• Gas exchange impairment (hypoxia) and dyspnea.
• Cough with frothy pink sputum and paroxysmal nocturnal dyspnea.

Right-Sided Heart Failure

• Blood isn't effectively ejected, increasing pressure on the right side of the heart.
• Peripheral tissue congestion (liver, gastrointestinal tract).

Summary Table: Left vs. Right Heart Failure

Types of Heart Failure

• Left-sided failure affects the left ventricle and right-sided failure affects the right ventricle.

Systolic vs. Diastolic Heart Failure

Compensatory Mechanisms

• Activation of the sympathetic nervous system causes peripheral vasoconstriction.
• Renin-Angiotensin-Aldosterone System (RAAS) preserve fluid volume.
• Endothelin causes vasoconstriction.
• Atrial Natriuretic Peptide releases stretch receptors.

Diagnosis of Heart Failure

• History of risk factors and physical exam.
• Lab Tests: Reduce glomerular filtration rate, elevated liver enzymes.
• Chest X-Ray: Detects enlarged heart.
• Echocardiography: Assesses heart structure and function.
• Ventricularography: Assesses left ventricular systolic dysfunction.

Clinical Manifestations of Heart Failure

• Left-Sided Heart Failure: Pulmonary congestion and reduced organ perfusion.
• Right-Sided Heart Failure: Peripheral congestion.
• Chronic Heart Failure: Fatigue, dyspnea, and edema.

Treatment of Heart Failure aims to:

• Decrease preload (intravascular volume).
• Decrease afterload also reduce heart rate and blood pressure.

Medications for Heart Failure

• Afterload Reduction: Nasirotide and Spironolactone.
• Improving Gas Exchange: Morphine and Supplemental Oxygen.
• Increasing Cardiac Contractility: Digoxin/Dobutamine/Milrinone/Aminone.
• Reducing Anxiety: Morphine and Non-Pharmacological Measures.

Beta-Blocker Generations

• First Generation: Propranolol
• Second Generation (ẞ1 selective): Metoprolol, Atenolol, Bisoprolol
• Third Generation (ẞ and a blockers): Carvedilol