Cardiac Action Potentials, EKG Interpretation, and Autonomic Regulation — Study Notes

Action Potentials in the cardiac conduction system

  • The discussion picks up from depolarization of pacemaker cells and the conduction system, focusing on how action potentials (APs) are generated and how they propagate through the heart.
  • Pacemaker sites and inherent rates:
    • SA node, AV node, and other conduction locations have different inherent rates largely due to differences in sodium leakage (ion leak) across their membranes.
    • The SA node leaks ions fastest, reaches threshold fastest, and depolarizes quickest relative to the AV node and other sites.
    • The AV node and other locations have slower leakiness (slower intrinsic rate) than the SA node.
  • Calcium dynamics:
    • Calcium influx occurs during depolarization and contributes to the pacing and conduction process. Calcium entry is discussed in the context of the second system/phase (the second program) and relates to the rate of depolarization.
  • The observed electrical signal on the heart is not from a single cell but from the entire heart muscle (myocytes) acting together; the EKG is a summated signal from all myocytes via surface electrodes.
  • If the SA node depolarizes, atrial depolarization occurs, which is reflected on the surface ECG as the P wave (atrial depolarization).
  • The typical EKG waveform:
    • P wave: atrial depolarization
    • QRS complex: ventricular depolarization
    • T wave: ventricular repolarization
    • Atrial repolarization occurs during the QRS complex (often referred to as the TA wave) but is not visible on standard ECG because ventricular electrical activity dominates.
  • The spreading of the action potential is over the whole heart muscle, not just within one cell; the ECG represents the amalgamated electrical output of all cardiac cells.
  • Terminology to connect cellular events to ECG:
    • Phase zero: depolarization
    • Phase one: initial repolarization
    • Phase two: calcium plateau, prolongs the action potential duration and allows contraction and blood ejection
    • Phase three: repolarization
    • Phase four: resting membrane potential (or leak dynamics depending on location)
  • Questions often arise about what’s wrong in an ECG trace: reading the pattern helps identify conduction problems (e.g., lack of a P wave indicates atrial depolarization failure).

The ECG and what it represents

  • The surface ECG records electrical activity generated across the heart, not just in one location.
  • The electrode setup captures the aggregate electrical activity as the heart beats.
  • When the SA node initiates depolarization, atria contract first (P wave); then AV node conduction slows the impulse, allowing atria to fully contract before the ventricles are activated.
  • The AV node slows conduction to coordinate atrial and ventricular contraction; the signal is then transmitted to the ventricles where it speeds up again through the AV junction and Purkinje system.
  • If there is a problem in ventricular depolarization, the QRS complex will reflect that change (e.g., widening). If the atria fail to depolarize, there would be missing or abnormal P waves.

Action potential durations by tissue type

  • Cardiac conduction system (including SA and AV nodes) AP duration: approximately 200 ms200\,\text{ms}.
  • Cardiac muscle cell AP duration: roughly 300–400 ms300\text{--}400\,\text{ms}.
  • Nerve AP duration: approximately 3 ms3\,\text{ms}.
  • These differences explain why cardiac conduction is much slower than neural conduction, yet faster than static muscle-only conduction in some contexts; the heart needs slower, controlled propagation for synchronization and effective pumping.

Phases of the cardiac action potential and their significance

  • Phase zero (depolarization): rapid upstroke due to Na+ (and Ca2+ dynamics) influx in non-pacemaker cells; in pacemaker cells, Ca2+ influx can contribute to the upstroke.
  • Phase one (initial repolarization): brief repolarization after the upstroke.
  • Phase two (plateau): sustained depolarization due to Ca2+ influx balancing K+ efflux; this plateau significantly prolongs the AP and, consequently, the contraction duration.
  • Phase three (repolarization): restoration of the resting membrane potential as K+ efflux outpaces Ca2+ influx.
  • Phase four (resting potential): the cell is ready to fire again; in pacemaker cells, phase four involves gradual depolarization (leak) leading to threshold.
  • The plateau phase (phase two) is critical for allowing enough time for the ventricles to fill and for the myocardium to generate a forceful contraction.

Conduction velocity and pathways

  • Whole-heart conduction is faster along specialized pathways (His-Purkinje system) than through the muscle-to-muscle cell connections (myocyte-to-myocyte). This coupling accounts for differences in activation timing and QRS duration.
  • The AV node deliberately slows conduction to allow ventricular filling; after AV node, conduction speeds up at the AV junction/HIS-Purkinje system to synchronize ventricular contraction.
  • When conduction velocity is slow, waveforms become wider on the ECG (e.g., wider QRS) due to longer time for the ventricles to depolarize.
  • Cell-to-cell conduction through myocytes is inherently slower than rapid conduction in specialized pathways; this is why pacing and conduction blocks can alter ECG morphology and heart rhythm.

Drug mechanisms and their clinical implications

  • Sodium channel blockers (antiarrhythmic drugs): slow the leak of Na+ into cells, reducing the rate of spontaneous depolarization in pacemaker tissue and slowing conduction; used to treat tachyarrhythmias but can have side effects like fatigue and reduced cardiac output.
  • Calcium channel blockers: slow calcium influx, producing slower conduction and rate control; can reduce heart rate and also slow AV nodal conduction, affecting the plateau phase and overall contractility.
  • Sympathomimetics (adrenergic agonists) increase sympathetic tone:
    • Positive chronotropy: increases heart rate
    • Positive dromotropy: increases conduction velocity
    • Positive inotropy: increases contractility
    • These effects can raise cardiac output but may raise oxygen demand and blood pressure; autonomic balance is key in maintaining stable hemodynamics.
  • Parasympathomimetic effects (via the vagus) slow heart rate and conduction (negative chronotropy and negative dromotropy).
  • The balance between sympathetic and parasympathetic tone determines resting heart rate and responsiveness to activity. The intrinsic rate of SA node is about 110 bpm110\ \text{bpm} if the heart were completely isolated from autonomic influence; resting heart rate in a real person is typically 60–70 bpm60\text{--}70\ \text{bpm} due to parasympathetic tone.
  • Practical implications:
    • If the heart rate is excessively fast (e.g., at rest), it might reflect high leakiness at the SA node or reduced parasympathetic/overactive sympathetic tone; interventions may include drugs that block Na+ channels or modulate calcium channels to slow the rate.
    • Side effects of antiarrhythmic drugs include fatigue and reduced cardiac output; drugs may also affect the speed of conduction and contractility, requiring careful monitoring.

Autonomic regulation and reflexes

  • Baroreceptor reflex (carotid baroreceptors): detect blood pressure changes and regulate heart rate via a reflex arc involving the medulla and the vagus nerve.
    • If blood pressure is too high, baroreceptors trigger a response that increases parasympathetic output to slow heart rate; the overall equation for blood pressure is:
    • extBloodpressure=extHeartrate×Stroke volume×Systemic vascular resistanceext{Blood pressure} = ext{Heart rate} \times \text{Stroke volume} \times \text{Systemic vascular resistance}
  • The heart is under constant autonomic regulation:
    • Inherent heart rate would be around 110 bpm110\ \text{bpm} if the heart were completely autonomous.
    • At rest, parasympathetic (vagal) tone dominates, reducing heart rate to ~60–70 bpm60\text{--}70\ \text{bpm}.
    • Upon activity, sympathetic tone increases, raising heart rate, conduction velocity, and contractility; parasympathetic tone decreases in proportion to the activity level.
  • Illustrative analogy (balloon): squeezing a balloon (ventricle) increases pressure; relaxing the ventricle lowers pressure. This analogy helps illustrate how forward contraction and relaxation affect pressures and stroke volume.
  • The autonomic system’s modulation of heart rate and conduction velocity is central to both normal physiology and pathophysiology, including tachyarrhythmias and bradyarrhythmias.

Reading the ECG: practical reasoning and problem-solving

  • The lecture emphasizes being able to identify what is wrong in an ECG, even if the exact terminology isn’t known yet.
  • Key diagnostic cues:
    • Absence or abnormal timing of the P wave suggests atrial depolarization issue.
    • Abnormal QRS duration or morphology suggests ventricular depolarization problems, possibly conduction block or abnormal conduction pathways.
    • The presence or absence of a TA wave (atrial repolarization) is usually masked by the larger ventricular activity within the QRS complex.
  • Conceptual takeaway:
    • The presence of a P wave indicates atrial depolarization; the QRS complex indicates ventricular depolarization; the T wave indicates ventricular repolarization. Changes in timing or morphology reflect conduction disturbances, autonomic tone changes, or drug effects.

Connections to foundational principles and real-world relevance

  • Foundational ion channel physiology underpins cardiac conduction: Na+ leak, Ca2+ influx, and K+ efflux determine phase transitions and pacing.
  • The impulse travels through a hierarchy: SA node → atrial conduction → AV node (slows) → AV junction/HIS-Purkinje system (speeds up) → ventricular myocardium.
  • Real-world relevance includes management of arrhythmias with antiarrhythmic drugs, rate control in tachycardias, and understanding the effects of autonomic modulation on heart rate and contractility.

Summary of practical takeaways

  • The SA node is the fastest depolarizing pacemaker due to higher Na+ leak; this sets the baseline heart rate, but autonomic tone can override this intrinsic rate.
  • The AV node slows conduction to allow atrial contraction and ventricular filling, then conduction resumes quickly through the His-Purkinje system to coordinate ventricular contraction.
  • ECG interpretation relies on recognizing P waves (atrial depolarization), the QRS complex (ventricular depolarization), and the T wave (ventricular repolarization); atrial repolarization occurs during the QRS but is typically hidden.
  • Action potentials in the heart are relatively slow compared to nerves (cardiac AP ~200 ms200\ \text{ms} for conduction system, 300–400 ms300\text{--}400\ \text{ms} for muscle cells, ∼3 ms\sim 3\ \text{ms} for nerves).
  • Pharmacology can alter conduction and rate via Na+ channel blockers or Ca2+ channel blockers; these drugs have therapeutic benefits and potential side effects, including fatigue and reduced cardiac output.
  • Autonomic regulation via the baroreflex and vagus/sympathetic influences determines resting heart rate and responses to stress or exercise; intrinsic rate is ~110 bpm110\ \text{bpm}, but resting rates are typically lower due to parasympathetic tone.

Key equations and numerical references

  • Cardiac conduction system AP duration: textconduction≈200  mst_{ ext{conduction}} \approx 200\ \,\text{ms}
  • Cardiac muscle cell AP duration: textmuscle≈300–400  mst_{ ext{muscle}} \approx 300\text{--}400\ \,\text{ms}
  • Nerve AP duration: textnerve≈3  mst_{ ext{nerve}} \approx 3\ \,\text{ms}
  • Inherent SA node rate (isolated): HRextinherent≈110 bpmHR_{ ext{inherent}} \approx 110\ \text{bpm}
  • Resting heart rate (typical, with autonomic influence): HRextrest≈60–70 bpmHR_{ ext{rest}} \approx 60\text{--}70\ \text{bpm}
  • Cardiac output concept (blood pressure relationship): BP=HR×SV×SVR\text{BP} = \text{HR} \times \text{SV} \times \text{SVR} (where HR = heart rate, SV = stroke volume, SVR = systemic vascular resistance)
  • Cardiac phases summary:
    • Phase 0: Depolarization
    • Phase 1: Initial repolarization
    • Phase 2: Plateau (Ca2+ influx) prolongs AP and contraction
    • Phase 3: Repolarization
    • Phase 4: Resting membrane potential (pacemaker diastolic depolarization in some cells)

Hypothetical scenarios for study consistency

  • If SA node leakiness increases (faster spontaneous depolarization), resting heart rate may rise unless compensatory autonomic adjustments occur. This can manifest as tachycardia on ECG and symptoms of reduced filling time.
  • If AV node conduction slows excessively, there may be a delay between atrial contraction and ventricular contraction, visible as altered PR interval on ECG.
  • If Na+ channels are blocked (class I antiarrhythmic), the rate of spontaneous depolarization and conduction velocity decrease, potentially stabilizing a tachyarrhythmia but risking a slower heart rate and reduced output.
  • If the sympathetic system dominates (e.g., during exercise), heart rate and contractility increase (positive chronotropy and inotropy), improving cardiac output to meet metabolic demands.

Questions to test understanding (quick checks)

  • What does a missing P wave indicate about atrial depolarization, and how would that affect the ECG interpretation?
  • Why is the AV node slower than other conduction pathways, and what effect does that have on the timing of atrial and ventricular contractions?
  • How do Na+ channel blockers and Ca2+ channel blockers differ in their impact on conduction and heart rate?
  • How does the autonomic nervous system shift the heart from resting to active states in terms of HR, conduction velocity, and contractility?
  • Why is atrial repolarization not clearly visible on a standard ECG, and when does it occur?