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Disorders of Cardiac Function: Anatomy & Physiology Study Guide

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Anatomy & Physiology of the Heart

Cardiac Anatomy

The heart is a muscular organ responsible for pumping blood throughout the body. Its structure and function are essential for understanding cardiac disorders.

  • Chambers: The heart has four chambers: right atrium, right ventricle, left atrium, and left ventricle.

  • Valves: The heart contains four main valves (tricuspid, pulmonary, mitral, aortic) that ensure unidirectional blood flow.

  • Chordae tendineae and papillary muscles: These structures anchor the atrioventricular valves (tricuspid and mitral), preventing prolapse during ventricular contraction.

  • Myocardium: The muscular layer of the heart wall, composed of sarcomeres containing actin and myosin filaments. Contraction is dependent on calcium (Ca2+) influx.

  • Intercalated discs: Specialized connections between cardiac muscle cells that facilitate rapid electrical impulse conduction, allowing the heart to contract as a coordinated unit.

Cardiac Cycle

The cardiac cycle describes the sequence of events in one heartbeat, including systole (contraction) and diastole (relaxation).

  • Systole: Ventricular contraction and ejection of blood. Includes isovolumetric contraction (all valves closed) and ventricular ejection (aortic/pulmonary valves open).

  • Diastole: Ventricular relaxation and filling. Includes isovolumetric relaxation (all valves closed) and ventricular filling (mitral/tricuspid valves open).

  • Heart sounds: S1 (closure of AV valves), S2 (closure of semilunar valves), S3 (rapid ventricular filling), S4 (atrial contraction).

Cardiac Function

Cardiac output (CO) is the volume of blood the heart pumps per minute and is a key indicator of cardiac function.

  • Formula:

  • Normal ranges:

    • CO: 4-6 L/min

    • HR (Heart Rate): 70-100 bpm

    • EF (Ejection Fraction): 55-75%

  • Ejection Fraction (EF): , where SV is stroke volume and LVEDV is left ventricular end-diastolic volume.

  • Preload: The degree of stretch of cardiac muscle fibers at the end of diastole (related to LVEDV).

  • Afterload: The resistance the ventricle must overcome to eject blood.

  • Contractility: The intrinsic strength of cardiac muscle contraction, independent of preload and afterload.

Frank-Starling Mechanism: Increased preload leads to increased stroke volume due to optimal overlap of actin and myosin filaments, up to a physiological limit.

Heart Failure

Definition and Types

Heart failure is a structural or functional disorder of the heart resulting in impaired cardiac output and/or congestion.

  • Systolic dysfunction (HFrEF): Heart failure with reduced ejection fraction (EF < 40%). Impaired contractility.

  • Diastolic dysfunction (HFpEF): Heart failure with preserved ejection fraction (EF > 50%). Impaired ventricular relaxation/filling.

  • Left-sided heart failure: Affects pulmonary circulation, leading to pulmonary congestion.

  • Right-sided heart failure: Affects systemic circulation, leading to peripheral edema.

Common Causes

  • Hypertension

  • Coronary artery disease

  • Myocardial infarction

  • Valvular heart disease

  • Cardiomyopathy

Comparison of Systolic vs. Diastolic Dysfunction

Feature

Systolic (HFrEF)

Diastolic (HFpEF)

Mechanism

Impaired contractility

Impaired relaxation/filling

Ejection Fraction

< 40%

> 50%

Common Causes

Myocardial infarction, cardiomyopathy

Hypertension, LV hypertrophy, fibrosis

Compensatory Mechanisms

In response to decreased cardiac output, the body activates several mechanisms:

  • Neurohumoral activation: Sympathetic nervous system (SNS) increases HR and contractility; renin-angiotensin-aldosterone system (RAAS) increases blood volume and vasoconstriction.

  • Natriuretic peptides (ANP, BNP): Released in response to volume overload; promote natriuresis and vasodilation.

  • Ventricular remodeling: Structural changes in the heart (hypertrophy, dilation) in response to chronic stress.

Clinical Manifestations

  • Left-sided failure: Pulmonary congestion (dyspnea, orthopnea, crackles), decreased CO (fatigue, confusion).

  • Right-sided failure: Peripheral edema, jugular venous distension, hepatomegaly, ascites.

  • Other: Arrhythmias, sudden cardiac death.

Diagnosis

  • BNP levels: <100 pg/mL (unlikely HF), 100-500 pg/mL (uncertain), >500 pg/mL (likely HF).

  • Echocardiography: Assesses ejection fraction, chamber size, wall motion.

  • Chest X-ray: May show cardiomegaly, pulmonary edema.

Treatment

  • ACE inhibitors, ARBs, beta-blockers, aldosterone antagonists

  • Diuretics for fluid overload

  • Inotropes (e.g., digoxin) for contractility

  • Management of underlying causes (e.g., hypertension, ischemia)

Valvular Disorders

Types and Definitions

  • Stenosis: Narrowing of the valve opening, impeding forward flow.

  • Regurgitation: Incomplete valve closure, allowing backward flow (leakiness).

  • Prolapse: Valve inversion into the atrium or ventricle, often leading to regurgitation.

Common Valvular Disorders

Disorder

Pathophysiology

Clinical Features

Aortic Stenosis

Resistance to LV outflow, concentric LV hypertrophy

Angina, syncope, heart failure, systolic murmur

Mitral Stenosis

Impaired LV filling, enlarged LA

Exercise intolerance, pulmonary congestion, diastolic murmur

Aortic Regurgitation

LV volume overload from regurgitant flow

Signs of heart failure, diastolic murmur

Mitral Regurgitation

Papillary muscle/chordae tendineae dysfunction

Heart failure symptoms, systolic murmur

Effects on Ventricular Remodeling

  • Stenosis leads to pressure overload and concentric hypertrophy.

  • Regurgitation leads to volume overload and eccentric hypertrophy.

Pericardial Disorders

Types

  • Pericarditis: Inflammation of the pericardium, often viral in origin (e.g., coxsackievirus).

  • Pericardial effusion: Accumulation of fluid in the pericardial space.

  • Cardiac tamponade: Compression of the heart due to rapid or large pericardial effusion, impairing cardiac filling and output.

Pathophysiology and Clinical Presentation

  • Acute pericarditis: Sharp, pleuritic chest pain relieved by sitting forward; pericardial friction rub; ECG changes (ST elevation, PR depression).

  • Pericardial effusion: Small effusions may be asymptomatic; large or rapidly accumulating effusions can cause cardiac tamponade.

  • Cardiac tamponade: Hypotension, jugular venous distension, muffled heart sounds (Beck's triad), pulsus paradoxus (decrease in systolic BP during inspiration).

Diagnosis and Treatment

  • Diagnosis: Echocardiography, clinical signs, ECG, laboratory markers (elevated WBC, CRP).

  • Treatment: NSAIDs, colchicine, corticosteroids for pericarditis; pericardiocentesis for tamponade; treat underlying cause for chronic effusions.

Summary Table: Key Cardiac Terms

Term

Definition

Preload

Ventricular wall stretch at end-diastole (LVEDV)

Afterload

Resistance to ventricular ejection

Contractility

Intrinsic strength of cardiac contraction

Cardiac Output (CO)

Volume of blood pumped per minute ()

Ejection Fraction (EF)

Fraction of end-diastolic volume ejected per beat ()

Example: In a patient with mitral regurgitation, the left ventricle is subject to volume overload, leading to eccentric hypertrophy and symptoms of heart failure such as dyspnea and fatigue.

Additional info: This guide expands on the provided notes with definitions, clinical context, and summary tables to support exam preparation in Anatomy & Physiology.

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