Disorders of Cardiac Function

Introduction

Cardiac function disorders, particularly those affecting coronary circulation, are a major focus in Anatomy & Physiology and clinical medicine. This guide covers the mechanisms, clinical presentations, and management of ischemic heart disease (IHD) and acute coronary syndromes (ACS), emphasizing the balance between myocardial oxygen supply and demand.

Coronary Artery Disease

Overview

• Coronary artery disease (CAD) is characterized by impaired blood flow in the coronary arteries, most commonly due to atherosclerosis.

• CAD can manifest as ischemic heart disease (IHD) or acute coronary syndromes (ACS).

Classification of Ischemic Heart Disease and Acute Coronary Syndromes

• Stable IHD (Angina): Predictable chest pain with exertion, relieved by rest or nitroglycerin.

• Variant Angina (Vasospastic, Prinzmetal’s): Chest pain due to transient coronary artery spasm, often at rest.

• Unstable IHD (Angina): New or worsening chest pain, not relieved by rest, may progress to myocardial infarction.

• Non-ST Elevated Myocardial Infarction (NSTEMI): Partial thickness infarction, no ST elevation on EKG.

• ST Elevated Myocardial Infarction (STEMI): Full thickness (transmural) infarction, ST elevation on EKG.

Ischemic Heart Disease

Pathophysiology

• IHD results from an imbalance between oxygen supply and oxygen demand in myocardial tissue.

• Most cases are related to atherosclerosis, which restricts coronary blood flow.

Oxygen Supply & Demand

Determinants

• Myocardial tissue extracts approximately 75% of the oxygen supplied.

Regulation of Coronary Blood Flow

Mechanisms

• Coronary blood flow primarily occurs during diastole (when the heart relaxes).

• Vasoconstriction is mediated by the sympathetic nervous system (SNS) and endothelin.

• Vasodilation (increased flow, up to 4-5x) is mediated by adenosine, nitric oxide (NO), and hypoxia.

• Increased heart rate (HR) reduces diastolic filling time, potentially decreasing coronary perfusion.

Additional info: The left main coronary artery and its branches (left anterior descending, left circumflex, right coronary artery) are most commonly affected by atherosclerosis.

Clinical Presentation of Ischemic Heart Disease

Stable Angina

• Chest pain described as squeezing or suffocating, typically substernal or precordial, may radiate to neck, jaw, shoulder, or arm.

• Pain is usually triggered by exertion or emotional stress and relieved by rest or nitroglycerin.

• Duration is typically 2-5 minutes.

• May be confused with gastroesophageal reflux (heartburn).

Unstable Angina

• New onset or worsening chest pain, more severe, not relieved by rest or nitroglycerin.

• Pain may last longer (up to 10 minutes or more) and can progress to ACS.

STEMI/NSTEMI

• STEMI: Severe, crushing chest pain, not relieved by nitroglycerin; may be associated with nausea, vomiting, anxiety, tachycardia, diaphoresis, and a sense of impending doom.

• NSTEMI: Similar symptoms but less pronounced; EKG changes may show ST depression or T wave inversion.

Diagnosis of IHD/ACS

Laboratory Testing

• Troponins (I and T) are proteins released from infarcted myocardial cells.

• Troponin levels rise within hours of infarction and remain elevated for 7-10 days.

• High sensitivity and specificity for myocardial injury.

• Normal: < 0.4 ng/mL; MI: > 0.4 ng/mL.

Pathophysiology of Myocardial Infarction

Types of Infarction

• STEMI: Transmural (full thickness) infarction due to complete coronary artery occlusion.

• NSTEMI: Subendocardial (partial thickness) infarction due to partial occlusion.

Ventricular Remodeling

• Infarcted tissue thins and dilates; non-infarcted tissue hypertrophies to preserve stroke volume (SV).

• Impaired cardiac function is more severe with STEMI.

Treatment of IHD/ACS

Goals and Strategies

• Treat underlying risk factors: hypertension, hyperlipidemia, lifestyle modification.

• Improve oxygen supply: supplemental O2, RBC transfusion, nitrates (nitroglycerin, isosorbide dinitrate), coronary vasodilation.

• Surgical intervention: stent placement, coronary artery bypass graft (CABG), balloon angioplasty.

• Pharmacologic therapy: antiplatelet agents (aspirin, clopidogrel, ticagrelor), anticoagulants (heparin, low-molecular weight heparin), tissue plasminogen activator (for STEMI only).

• Decrease O2 demand: beta-blockers (reduce heart rate and contractility), calcium channel blockers (verapamil, diltiazem).

Coronary Stent and CABG

• Coronary stent: A device placed in the coronary artery to keep it open after angioplasty.

• Coronary artery bypass graft (CABG): Surgical procedure to restore blood flow by bypassing blocked arteries using grafts.

Summary Table: Types of Angina and Myocardial Infarction

Key Equations

• Oxygen Delivery to Myocardium:

• Arterial O2 Content:

Additional info: [Hb] = hemoglobin concentration (g/dL); SaO2 = arterial oxygen saturation; PaO2 = partial pressure of oxygen in arterial blood.

Conclusion

Understanding the pathophysiology, clinical presentation, and management of ischemic heart disease and acute coronary syndromes is essential for students of Anatomy & Physiology. The balance between myocardial oxygen supply and demand underlies the development and treatment of these disorders.