Cardiac Anatomy and Function

Cardiac Anatomy and Function

• The heart is a muscular pump located in the mediastinum, enclosed by the pericardium.
• It has three layers: epicardium, myocardium, and endocardium.
• It beats over 86,000 times daily, circulating approximately 6000 liters of blood.
• The heart has four chambers (two atria and two ventricles) separated by valves and functions as two independent, connected sides.
• The right side is a low-pressure system with low oxygen and outflow to the lungs.
• The left side is a high-pressure system with high oxygen and outflow to the body.
• Blood pumped by both sides per unit time is equal.

Rules of Cardiac Pathology

• Increased cardiac workload demands higher blood supply.
• Prolonged exposure to increased volume or pressure leads to cardiac muscle enlargement (hypertrophy).
• In adults, cardiac growth may outpace blood supply increase.
• Excessive hypertrophy can result in ventricular dilation and dysfunction.
• Cardiac structural disease increases electrical instability and arrhythmia risk.

Congestive Heart Failure (CHF)

• CHF is a symptom complex, not a specific disease, indicating inadequate blood flow to meet body demands or insufficient pumping of returning blood.
• Symptoms arise from forward failure (reduced tissue blood flow) causing fatigue, renal insufficiency, and hypoxia, and reverse failure (venous return backup) leading to edema.
• Right-sided CHF manifests as peripheral edema, ascites, pleural effusions, and stasis dermatitis.
• Left-sided CHF presents as pulmonary edema with dyspnea, cough, hemoptysis, paroxysmal nocturnal dyspnea, and orthopnea.
• Causes include hypertension, valvular disease, ischemic heart disease, and cardiomyopathies (left-sided); and left-sided failure, lung disease (cor pulmonale), and congenital heart disease (right-sided).

CHF Progression

• Compensation involves increased sympathetic tone (increased contractility and preload), aldosterone release (fluid retention), and hypertrophy (increased pumping power).
• Decompensation occurs when compensation fails, leading to ventricular dilation, reduced pumping efficiency, and an S3 heart sound.
• A dilated heart is electrically unstable.

Cor Pulmonale

• Lung disease-induced heart disease primarily affecting the right ventricle.
• Elevated pulmonary circulation pressure causes right ventricular hypertrophy, dilation, and failure.
• Predisposing disorders: lung diseases, pulmonary vessel diseases, chest movement disorders, and pulmonary arteriolar constriction disorders; chronic obstructive pulmonary disease is the most common cause.

Ischemic Heart Disease

• Myocardial damage due to inadequate blood supply to meet demand.
• Most often caused by coronary artery occlusion from atherosclerosis (coronary artery disease).
• Other causes include hypovolemia, emboli, drugs, infection, etc.
• Damaged endocardium promotes thrombus formation and potential thromboembolism.
• Large transmural anteroseptal infarcts can lead to ventricular aneurysms.
• Papillary muscle dysfunction may result in post-infarct regurgitation.

Clinical Features of Acute Myocardial Infarction (AMI)

• Angina lasting over 30 minutes (some are silent).
• Dyspnea, tachycardia, diaphoresis, acute congestive heart failure, and cardiogenic shock (usually with >40% LV involvement).
• Arrhythmias.
• EKG changes: Q waves (old AMI), ST-segment elevation (acute MI), and T-wave inversion.
• Cardiac enzyme elevations (Troponin I is most specific) showing a defined sequence/timeframe.

Chronic Ischemic Heart Disease

• Progressive myocardial damage due to moderate-to-severe atherosclerosis over years.
• May be punctuated by AMIs.
• Leads to progressive heart failure, a common cause of heart transplantation.
• Features: dilation of all cardiac chambers, myocardial fibrosis, and hypertrophy.

Sudden Cardiac Death

• Death within 24 hours of symptom onset, often without preceding symptoms or a clear cause.
• Often attributed to a sudden arrhythmia that prevents adequate cardiac output.