T

Heart: Key Concepts and Mechanisms

Flow of Blood Through the Heart: valves, timing, and direction

  • Valves ensure one-way flow; all valves (AV valves and semilunar valves) prevent backflow and keep blood moving forward.
  • Common teaching pitfall: flow pictured as a single blob moving through the chambers is misleading; real flow is dynamic with continuous chamber-to-chamber movement.
  • A practical way to study flow: trace a single red blood cell as it travels through the heart (helps follow order, even if the real flow is more complex).
  • Chambers and sequence (overview):
    • Systemic circulation returns deoxygenated blood to the heart, arriving at the right atrium (RA).
    • Coronary veins drain deoxygenated blood from the heart muscle into the coronary sinus, which empties into the RA.
    • Blood passes through the tricuspid valve into the right ventricle (RV).
    • RV blood goes through the pulmonary semilunar valve into the pulmonary trunk → pulmonary arteries → lungs for oxygenation.
    • Oxygenated blood returns from the lungs via the pulmonary veins into the left atrium (LA).
    • Blood passes through the mitral (bicuspid) valve into the left ventricle (LV).
    • LV blood goes through the aortic semilunar valve into systemic circulation.
  • Atrioventricular timing: the atria contract together; the ventricles contract together. Do not imagine independent atrial contraction timing.
  • Equal output requirement: Equal volumes must be pumped to the pulmonary and systemic circuits each cycle; otherwise, congestion occurs (congestive heart failure).
  • Left ventricle vs right ventricle: LV has to push blood to the entire body (high afterload) and is thicker; RV pumps to neighboring lungs (lower afterload).
  • Coronary circulation: Heart muscle requires a constant oxygen supply.
    • Blood supply is via coronary arteries branching off the aorta; the first branches are the coronary arteries near the aorta.
    • The heart drains deoxygenated blood via the coronary sinus into the RA.
    • There is considerable anatomical variation between individuals; some hearts show unusual patterns of coronary supply.
    • Coronary vessels are critical because without oxygen to the myocardium, heart function deteriorates quickly and healing is poor (scar tissue forms).
  • Practical note about imaging: isolating vessels in pictures helps identify arteries and veins, but real hearts often have fat and fat deposition that obscure vessels.
  • Metaphor and caution: tracing a single red blood cell can be helpful but not fully realistic; keep in mind synchronized contraction of both atria and both ventricles.

Cardiac Muscle: structure, metabolism, and functional implications

  • Cardiac muscle is striated but differs from skeletal muscle in key ways:
    • Each cardiac myocyte typically has one nucleus.
    • Intercalated discs connect neighboring cells and contain many gap junctions, promoting electrical coupling.
    • The heart behaves as a syncytium (a functional single unit) because ions pass directly from cell to cell; this enables coordinated contraction.
  • Two kinds of cardiac muscle cells:
    • Contractile cells: perform the actual pumping (work of contraction).
    • Pacemaker cells: self-excitable cells that initiate depolarization and set the rhythm.
  • Pacemaker cells vs contractile cells: both use a similar ion sequence for excitation, but pacing cells have a unique rhythm.
  • Tetany and plateau considerations:
    • Cardiac muscle cannot undergo tetany (rigid, locked contraction) because the plateau phase and ion dynamics prevent sustained, fused contraction.
    • A plateau phase in contractile cells is present and important for effective pumping; calcium influx during plateau prolongs depolarization, giving time for ventricular filling.
  • Metabolic demand:
    • The heart relies almost exclusively on aerobic respiration.
    • It is fatigue-resistant but highly oxygen-dependent; interruption of coronary blood flow for even a few seconds causes tissue damage that can be irreversible.
    • Coronary blood flow is tightly linked to heart rate and contractility (oxygen supply must meet demand).

Electrical conduction system and pacemaker physiology

  • Pacemaker cells initiate depolarization, driving the heartbeat without autonomic input for timing; autonomic input modulates rate and force.
  • The pacemaker potential (intrinsic rhythm) is generated by a continuous, rhythmic depolarization:
    • Step 1: Slow Na+ influx (opening of slow Na+ channels) and closing of K+ channels create a gradual depolarization (pacemaker potential).
    • Step 2: Once threshold is reached, Ca2+ influx via calcium channels triggers depolarization (fast Ca2+ channels open), causing a rapid upstroke.
    • Step 3: Repolarization occurs as Ca2+ channels inactivate and K+ channels remain open, causing K+ efflux and membrane potential restoration toward the negative resting value.
  • Important notes:
    • The pacemaker potential never sits at a flat resting membrane potential; it continuously drifts upward toward threshold.
    • The SA node is the primary pacemaker; the AV node provides a delay to allow atrial contraction and ventricular filling (pause ~0.1 s).
  • Conduction system pathway (the “bundle” of His system):
    • SA node → atrial myocardium (via gap junctions) → AV node (pause ~0.1 s) → AV bundle (bundle of His) in the intraventricular septum → bundle branches (left and right) → Purkinje fibers (subendocardial conducting network) → ventricular walls.
    • The impulse spreads through the atria first, then to the ventricles, coordinating the sequence of atrial contraction followed by ventricular contraction.
  • Autonomic modulation of conduction and pumping:
    • Parasympathetic (vagus nerve, CN X) primarily slows heart rate by acting on SA and AV nodes; resting intrinsic rate ~100 bpm is suppressed to around ~75 bpm by vagal tone.
    • Sympathetic input enhances rate and force, with branches to the SA node, AV node, and ventricles to speed rate and increase contraction strength.
  • Clinical insights on conduction control:
    • If vagus nerve is severed, resting heart rate may rise toward intrinsic rate (around 100 bpm).
    • Autonomic tone adjusts rate and contractility but does not dictate the basic initiation of contraction (pacemaker control).

Action potentials in pacemaker vs contractile cells

  • Pacemaker (auto-rhythmic) cells:
    • Do not have a true resting membrane potential; the pacemaker potential is a slow, continuous depolarization driven by Na+ influx and K+ efflux dynamics.
    • Depolarization primarily due to Ca2+ influx during the action potential (late phase) rather than Na+ for the upstroke.
    • Refractory periods are shorter than in skeletal muscle, enabling the heart to beat repeatedly without fatigue from nervous input.
    • Sequence: slow Na+ influx → threshold → Ca2+ influx → depolarization → Ca2+ channel inactivation and K+ efflux → repolarization.
  • Contractile (working) cells:
    • Have a typical action potential with a rapid phase 0 depolarization due to fast Na+ channels opening.
    • A plateau phase follows due to sustained Ca2+ influx via slow calcium channels, which prolongs depolarization and allows time for ventricular filling.
    • Repolarization occurs as Ca2+ channels inactivate and K+ channels open, returning the cell to resting voltage.
    • The plateau phase length (~0.2 seconds) is much longer than skeletal muscle and is essential for pumping efficiency.
  • Overall sequence consistency:
    • Both cell types use the same core ions (Na+, Ca2+, K+), but the timing and channel types differ (fast vs slow Na+ and Ca2+ channels).

Electrocardiography (ECG/EKG): basics and interpretations

  • Three key waveform components and what they represent:
    • P wave: atrial depolarization and atrial contraction.
    • QRS complex: ventricular depolarization and onset of ventricular contraction.
    • T wave: ventricular repolarization (ventricles relaxing).
  • Important notes about interpretation:
    • Do not rely on ST segments or precise timings for this course; intervals vary with activity and patient state.
    • A normal tracing shows a regular, repeating pattern with one P wave, one QRS, and one T wave per cycle.
    • An absence or abnormality of P waves may indicate a rhythm such as a junctional rhythm (SA node nonfunctional).
  • Example rhythms and what they imply:
    • Junctional rhythm: SA node nonfunctional; P waves are absent; AV node paces at ~40–60 bpm; ventricles still beat, but slower.
    • Second-degree heart block: AV node fails to conduct some SA node impulses; more P waves than QRS complexes (some atrial activity not conducted to ventricles).
    • Ventricular fibrillation: disorganized, chaotic electrical activity in ventricles; rhythm is useless for pumping; requires urgent defibrillation to reset electrical activity.
  • Practical clinical note:
    • In exams, describe rhythms with terminology rather than drawing; e.g., “ventricular fibrillation: chaotic, disorganized action potentials with no effective pumping.”

Mechanical events and the cardiac cycle

  • Systole vs diastole definitions:
    • Systole: period of heart contraction (atrial or ventricular).
    • Diastole: period of heart relaxation (atrial or ventricular).
  • Cardiac cycle: atrial systole/diastole followed by ventricular systole/diastole; most functional focus is on ventricular phases since they eject blood.
  • Key ventricular volume concepts:
    • EDV (end-diastolic volume): maximum ventricular volume after filling (diastole).
    • ESV (end-systolic volume): minimum ventricular volume after contraction (systole).
    • SV (stroke volume): amount of blood ejected per beat; SV = EDV - ESV.
    • The maximum ventricular volume occurs at end-diastole; the minimum at end-systole.
  • Practical calculation checks:
    • If you get a negative SV, you’ve reversed the subtraction; SV must be positive.
  • Cardiac output (how effectively the heart pumps):
    • CO = SV imes HR, where HR is heart rate in beats per minute.
    • Normal resting CO ≈ 5.25 ext{ L/min} (five and a quarter liters per minute).
    • Cardiac output can dramatically increase with exercise, reflecting increased stroke volume and/or heart rate.
  • Heart sounds and auscultation:
    • First heart sound (lubb): closure of AV valves (mitral and tricuspid); softer due to cusps closing.
    • Second heart sound (dub): closure of semilunar valves (aortic and pulmonary); louder or moment of sharper closure.
    • Auscultation locations often include four points: aortic (right 2nd intercostal space), pulmonary (left 2nd intercostal space), mitral (apex, left 5th intercostal space at midclavicular line), and tricuspid (left lower sternal border).
    • In some conditions, valve sounds can separate, but normally the AV valves close together and the semilunar valves close together.

Connections, real-world relevance, and implications

  • Foundational principles tying to anatomy and physiology:
    • The heart operates as two pumps in series (pulmonary and systemic circuits) with equal output to prevent congestion.
    • The heart is a muscular organ that requires a constant, adequate blood supply (oxygen for metabolism); coronary circulation is essential for survival.
    • The conduction system coordinates timing so that atria fill ventricles and ventricles eject blood efficiently; autonomic input modulates rate and force but does not dictate the basic rhythm.
  • Practical implications and scenarios:
    • If the coronary blood supply is interrupted, myocardial tissue dies; lack of oxygen leads to tissue damage and potential heart failure if not rapidly restored.
    • Heart rate and contractility are tightly regulated by parasympathetic and sympathetic inputs to adapt to activity level and stress.
    • Arrhythmias (junctional rhythm, heart blocks, ventricular fibrillation) can have profound clinical consequences and require appropriate intervention (e.g., pacing, defibrillation).
  • Ethical, philosophical, and practical considerations:
    • Understanding the heart’s oxygen dependence underscores the importance of avoiding hypoxia and recognizing risk factors for ischemic heart disease.
    • In clinical settings, patient education about symptoms, early detection, and timely treatment is crucial for preventing fatal outcomes in arrhythmias and heart failure.
  • Quick reference reminders for exam readiness:
    • Stroke volume and cardiac output formulas: SV = EDV - ESV;
      CO = SV imes HR. Normal resting CO ~ 5.25 ext{ L/min}.
    • P wave = atrial depolarization; QRS = ventricular depolarization; T wave = ventricular repolarization.
    • AV node delay helps ensure ventricles fill before contraction (pause ~0.1 s).
    • Pacemaker potential features: no resting membrane potential; slow Na+ influx, then Ca2+ influx to depolarize; repolarization via K+ efflux.
    • Contractile cell plateau phase: slow Ca2+ influx prolongs depolarization to allow ventricular filling before contraction.
    • Tetany does not occur in cardiac muscle; continuous rhythmic contraction is prevented by plateau and repolarization dynamics.

Summary of key clinical takeaways

  • The heart’s timing and flow are governed by valves, the conduction system, and coordinated chamber contraction.
  • Equal output to lungs and body is essential to prevent congestive heart failure.
  • The heart’s blood supply (coronary arteries) is critical for life; the heart muscle cannot survive without oxygen.
  • Heart rhythm abnormalities (junctional rhythm, AV block, ventricular fibrillation) illustrate the importance of the conduction system and the potential need for medical intervention.
  • ECG components provide a window into the electrical activity of the heart, with practical implications for diagnosing rhythm disorders and guiding treatment.
  • The cardiac cycle combines mechanical events (systole/diastole) with electrical events (depolarization/repolarization) and volume changes (EDV, ESV, SV) to produce a synchronized pump.

Key equations to memorize

  • Stroke volume: SV = EDV - ESV
  • Cardiac output: CO = SV imes HR
  • Relationship to diastole/ systole: end-diastolic volume is the maximum ventricular volume; end-systolic volume is the minimum
  • Notable numerical reference: intrinsic SA node rate ≈ 100\ ext{bpm}; vagal influence can reduce to about 75\ ext{bpm}; sympathetic influence increases rate and force