IndietroDisorders 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.