Heart Physiology Key Concepts Flashcards

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Troponin

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Troponin is a regulatory protein complex in cardiac muscle fibers that controls actin-myosin interactions during contraction. Elevated troponin levels in blood indicate cardiac muscle cell injury or death, as occurs after a myocardial infarction. Troponin can also rise with severe exertion, inflammation, pulmonary embolism, or renal failure.

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Cardiac muscle

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Cardiac muscle is the specialized, involuntary muscle tissue that makes up the myocardium of the heart. Cells are striated, branched, usually have one or two centrally located nuclei, and are connected by intercalated discs to coordinate contraction. Cardiac muscle has high mitochondrial content and requires continuous oxygen and ATP supply.

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Intercalated discs

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Intercalated discs are specialized cell junctions that join ends of cardiac muscle fibers and electrically and mechanically couple cells. They contain gap junctions for rapid ion flow and desmosomes for mechanical stability. These discs increase conduction speed and synchronize contraction across the myocardium.

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Sarcolemma

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The sarcolemma is the cell membrane of a cardiac muscle fiber that propagates action potentials. It surrounds the fiber and interfaces with the extracellular environment to allow ion fluxes that initiate contraction. The sarcolemma also forms T-tubules which help transmit depolarization into the cell interior.

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Sarcoplasmic reticulum

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The sarcoplasmic reticulum (SR) is the specialized smooth endoplasmic reticulum in muscle cells that stores calcium ions needed for contraction. In cardiac muscle, SR calcium release and extracellular calcium influx both contribute to contraction strength. Proper SR function is essential for timely relaxation and reuptake of Ca$^{2+}$.

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Myofibrils

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Myofibrils are bundles of thick (myosin) and thin (actin) protein filaments arranged in repeating sarcomeres that give muscle its striated appearance. In cardiac fibers, myofibrils generate the contractile force when cross-bridge cycling occurs. Striations reflect the organized banding pattern of these filament assemblies.

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Contractile cells

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Contractile cells make up about 99% of cardiac muscle fibers and are responsible for generating force and pumping blood. They depolarize in response to electrical stimuli from autorhythmic cells and undergo excitation–contraction coupling. Their action potentials have a characteristic prolonged plateau that lengthens contraction.

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Autorhythmic cells

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Autorhythmic cells are the ~1% of cardiac muscle fibers that are self-excitable and generate the heartbeat without nervous input. They form the intrinsic conduction system (SA node, AV node, bundle branches, Purkinje fibers) and initiate and distribute impulses to contractile cells. These cells have unstable resting potentials called pacemaker potentials that spontaneously depolarize.

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Cardiac mitochondria

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Cardiac muscle fibers have abundant mitochondria (about 30% of cell volume) to meet high ATP demands. This high mitochondrial density enables sustained aerobic metabolism and continuous contraction. Consequently, the heart is highly sensitive to oxygen deprivation.

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Cardiac action potential

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The cardiac action potential in contractile cells begins with rapid depolarization from fast Na$^+$ influx, followed by a prolonged plateau due to slow Ca$^{2+}$ influx, and ends with repolarization from K$^+$ efflux. The plateau phase extends the refractory period and lengthens contraction compared to skeletal muscle. This sequence prevents tetany and ensures coordinated heartbeats.

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Plateau phase

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The plateau phase is a prolonged period of membrane depolarization in cardiac contractile cells caused primarily by slow Ca$^{2+}$ influx balanced by reduced K$^+$ efflux. It maintains positive membrane potential and prolongs contraction, enabling effective ejection of blood. The plateau also lengthens the refractory period to prevent summation of contractions.

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SA node

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The sinoatrial (SA) node is the primary pacemaker of the heart located in the right atrium that normally sets the sinus rhythm at about 60–100 beats per minute. Its autorhythmic cells generate pacemaker potentials that spread across the atria, causing atrial depolarization and contraction. The SA node initiates the electrical sequence of the cardiac cycle.

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AV node

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The atrioventricular (AV) node delays impulses arriving from the atria by about 0.1 s before transmitting them to the ventricles. This delay allows atrial contraction to complete ventricular filling. The AV node can act as a secondary pacemaker if the SA node fails, producing a slower junctional rhythm.

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AV bundle

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The AV bundle (Bundle of His) is a band of autorhythmic conduction fibers that transmits impulses from the AV node into the interventricular septum and toward the ventricles. It forms the pathway that connects atrial and ventricular electrical activity. The bundle then splits into left and right bundle branches.

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Bundle branches

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Bundle branches are the left and right extensions of the AV bundle that conduct impulses down the interventricular septum toward the apex. They ensure coordinated depolarization of both ventricles. From the branches, impulses spread to Purkinje fibers and ventricular myocardium.

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Purkinje fibers

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Purkinje fibers are specialized conducting cardiac muscle fibers that rapidly distribute the impulse throughout the ventricular myocardium. They depolarize contractile cells of the ventricles and stimulate papillary muscles to tense chordae tendineae. Their fast conduction helps synchronize ventricular contraction from apex to base.

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Pacemaker potential

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The pacemaker potential is the slow, spontaneous depolarization of autorhythmic cell membranes that occurs between action potentials. It is driven by gradual Na$^+$ and Ca$^{2+}$ influx until threshold is reached, triggering an action potential. This intrinsic property underlies automaticity of the SA and other pacemaker tissues.

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Intrinsic conduction

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The intrinsic conduction system is the network of autorhythmic cardiac cells (SA node, AV node, AV bundle, bundle branches, Purkinje fibers) that generates and conducts electrical impulses through the heart. It ensures coordinated timing of atrial and ventricular contractions without requiring neural input. Pathologies of this system can cause arrhythmias or heart block.

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Electrocardiogram

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An electrocardiogram (ECG or EKG) is a surface recording that reflects the composite electrical activity of the heart from autorhythmic and contractile cells. It displays characteristic waves and intervals (P wave, QRS complex, T wave, PQ/PQ interval, ST segment, QT interval) used to assess conduction and rhythm. ECG timing corresponds to electrical events that precede mechanical contraction.

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P wave

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The P wave on an ECG represents atrial depolarization initiated by the SA node. Atrial depolarization is closely followed by atrial contraction (atrial systole) and contributes to ventricular filling. Abnormal P waves can indicate atrial enlargement or ectopic pacemakers.

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QRS complex

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The QRS complex corresponds to ventricular depolarization and occurs just before ventricular contraction. It is normally a sharp, large deflection because ventricular muscle mass is large. Atrial repolarization occurs during the QRS but is obscured by the large ventricular signal.

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T wave

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The T wave on an ECG represents ventricular repolarization and occurs as the ventricles relax. It follows the QRS complex and marks the beginning of ventricular diastole. Abnormal T waves can indicate ischemia, electrolyte disturbances, or other ventricular pathologies.

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Cardiac cycle

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The cardiac cycle comprises all mechanical and blood flow events during one complete heartbeat, including systole (contraction/ejection) and diastole (relaxation/filling). Electrical events (ECG) precede and trigger mechanical events. A full cycle normally takes less than one second at resting heart rates.

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Systole

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Systole is the phase of the cardiac cycle when the heart muscle contracts and ejects blood from the chambers. Atrial systole contributes to ventricular filling, while ventricular systole ejects blood into the pulmonary trunk and aorta. Valve closures and openings (AV close = LUB, SL open) accompany systolic events.

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Diastole

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Diastole is the relaxation phase of the cardiac cycle when chambers fill with blood. Ventricular diastole includes isovolumetric relaxation followed by passive and active ventricular filling. The diastolic interval between the T wave and the next P wave represents chamber relaxation.

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Ventricular filling

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Ventricular filling occurs during ventricular diastole when AV valves are open and blood flows from atria into ventricles. About 80% of filling is passive; atrial systole contributes the remaining ~20%. End-diastolic volume (EDV) is the maximum ventricular volume at the end of filling.

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Isovolumetric contraction

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Isovolumetric contraction is the early phase of ventricular systole when ventricles contract with all valves closed so volume remains constant and pressure rises. This phase follows AV valve closure (LUB) and precedes opening of semilunar valves. It readies ventricular pressure to exceed arterial pressure for ejection.

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Isovolumetric relaxation

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Isovolumetric relaxation is the early phase of ventricular diastole following ventricular repolarization when ventricles relax with all valves closed so volume stays constant. The semilunar valves close (DUB) due to arterial backflow, and ventricles decrease pressure without volume change. It precedes AV valve opening and passive filling.

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End-diastolic volume

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End-diastolic volume (EDV) is the blood volume in a ventricle at the end of ventricular filling (end of diastole). It represents the precontraction volume that contributes to preload and influences stroke volume via the Frank–Starling mechanism. A typical EDV is around 120 ml in a healthy adult.

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End-systolic volume

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End-systolic volume (ESV) is the amount of blood remaining in a ventricle after systole (after ejection). It reflects residual volume determined by contractility and afterload; a typical ESV is about 50 ml. Stroke volume equals EDV minus ESV.

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Stroke volume

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Stroke volume (SV) is the volume of blood ejected by one ventricle with each heartbeat and is given by the equation $$SV = EDV - ESV$$. For example, with EDV $\approx120\,$ml and ESV $\approx50\,$ml, SV $\approx70\,$ml per beat. SV is a key determinant of cardiac output.

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Cardiac output

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Cardiac output (CO) is the volume of blood pumped by each ventricle per minute and is calculated by $$CO = SV \times HR$$. For example, with $SV=70\,$ml and $HR=80\,$bpm, $$CO = 70\,\text{ml} \times 80\,\text{bpm} = 5600\,\text{ml/min} = 5.6\,\text{L/min}$$. CO indicates overall heart performance and matches total blood volume flow per minute.

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Preload

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Preload refers to ventricular wall stretch at the end of diastole, primarily determined by venous return and EDV. Increased preload enhances stroke volume through the Frank–Starling mechanism because greater stretch yields stronger contraction. Excessive preload, however, can stress the heart.

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Afterload

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Afterload is the pressure the ventricles must overcome to eject blood into the arteries and is primarily determined by arterial blood pressure and vascular resistance. High afterload reduces ejection and increases ESV, lowering stroke volume. Chronic high afterload (e.g., hypertension) increases cardiac workload.

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Contractility

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Contractility is the intrinsic strength of cardiac muscle contraction at a given preload and afterload, influenced by Ca$^{2+}$ availability and sympathetic stimulation. Increased contractility lowers ESV and raises stroke volume. Positive inotropic agents (e.g., epinephrine) increase contractility.

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Sympathetic nervous system

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Sympathetic innervation increases heart rate and contractile force via cardiac accelerator nerves and circulating catecholamines like epinephrine. Sympathetic activity raises SA node firing and enhances contractility, increasing cardiac output during stress or exercise. It also reduces ESV by increasing ejection.

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Parasympathetic nervous system

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Parasympathetic (vagal) activity decreases heart rate by reducing SA and AV node firing via the vagus nerve (CN X). It has little direct effect on ventricular contractility but slows conduction and prolongs AV nodal delay. Parasympathetic dominance lowers cardiac output during rest.

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Vagus nerve

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The vagus nerve (cranial nerve X) carries parasympathetic fibers to the heart, primarily innervating the SA and AV nodes to decrease heart rate. Stimulation from the cardioinhibitory center in the medulla reduces pacemaker firing. Vagal tone helps maintain resting heart rate below intrinsic sinus rates.

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Cardio centers

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Cardioacceleratory and cardioinhibitory centers in the medulla oblongata integrate autonomic input to regulate heart rate and contractility. The cardioacceleratory center increases sympathetic output to raise heart rate and force, while the cardioinhibitory center increases vagal output to lower heart rate. These centers respond to baroreceptor and higher brain inputs.

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Heart sounds

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Heart sounds (LUB–DUB) are produced by valve closures: LUB (first sound) is from AV valve closure at systole onset, and DUB (second sound) is from semilunar valve closure at diastole onset. Auscultation locations over specific intercostal spaces help identify valve function. Extra or abnormal sounds can indicate valve disease.

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AV valves

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Atrioventricular (AV) valves (tricuspid and mitral/bicuspid) separate atria from ventricles and prevent backflow during ventricular contraction. They open during diastole to allow ventricular filling and close during isovolumetric contraction to create the first heart sound (LUB). Papillary muscles and chordae tendineae anchor valve leaflets to prevent prolapse.

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Semilunar valves

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Semilunar (SL) valves (aortic and pulmonary) guard the exits of the ventricles into the aorta and pulmonary trunk and prevent arterial backflow. They open during ventricular ejection and close when arterial pressure exceeds ventricular pressure, producing the second heart sound (DUB). SL valve dysfunction alters ejection and arterial pressures.

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Papillary muscles

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Papillary muscles are conical projections of ventricular myocardium that attach to AV valve leaflets via chordae tendineae. During ventricular contraction they tense the chordae to prevent valve prolapse into the atria. Their coordinated activation ensures AV valve competence under pressure.

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Arrhythmia

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An arrhythmia is any irregularity in heart rhythm due to abnormal impulse formation or conduction in the intrinsic conduction system. Arrhythmias range from benign premature beats to life-threatening rhythms that impair cardiac output. Diagnosis and management rely on ECG patterns and hemodynamic impact.

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Fibrillation

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Fibrillation is a chaotic, disorganized rhythm where cardiac muscle fibers contract asynchronously, severely impairing effective pumping. Atrial fibrillation increases stroke risk and reduces atrial contribution to ventricular filling; ventricular fibrillation is life-threatening and requires immediate defibrillation. Defibrillators deliver shocks to reset the electrical state and restore organized rhythm.

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PVCs

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Premature ventricular contractions (PVCs) are early ventricular depolarizations originating from ectopic ventricular foci, causing an abnormal QRS and compensatory pause. Occasional PVCs may be benign, but frequent or multifocal PVCs can compromise cardiac efficiency and signal underlying pathology. They appear as wide, bizarre QRS complexes on ECG without preceding P waves.

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Heart block

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Heart block refers to impaired conduction from atria to ventricles due to AV node or bundle branch dysfunction. Degrees vary: first-degree prolongs PR interval, second-degree shows dropped beats (more P waves than QRS), and third-degree (complete) dissociation causes independent atrial and ventricular rhythms. Severe blocks often require pacemaker therapy.

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Bradycardia

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Bradycardia is a persistent heart rate below 60 beats per minute that can reduce tissue perfusion if severe. It may result from high vagal tone, hypothermia, conduction system disease, or certain medications. Some well-conditioned athletes have benign bradycardia; symptomatic cases may need intervention.

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Tachycardia

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Tachycardia is a persistent heart rate above 100 beats per minute that may reduce filling time and precipitate ischemia or fibrillation. Causes include fever, anxiety, sympathetic stimulation, hypovolemia, or arrhythmogenic foci. Management depends on cause and hemodynamic effect.

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Defibrillator

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A defibrillator delivers an electrical shock to the heart to depolarize a critical mass of myocardium simultaneously and terminate chaotic rhythms like ventricular fibrillation or pulseless ventricular tachycardia. The shock allows the intrinsic conduction system (ideally SA node) to regain control and restore organized rhythm. Timely defibrillation greatly improves survival in cardiac arrest.