Cardiac Electrophysiology and Circulation – Study Notes
Cardiac Myocytes: Contractile vs Noncontractile (Pacemaker) Cells
All cardiac myocytes are attached to one another via gap junctions, enabling spread of electrical activity across the heart.
Contractile cardiac muscle cells (ventricular myocytes) are responsible for pumping action; noncontractile pacemaker cells are still cardiac myocytes but do not contract.
Pacemaker cells include the SA node, AV node, bundle of His, bundle branches, and Purkinje fibers; the same action potential can occur in these nodal cells, but they fire spontaneously and with different frequency.
Pacemaker and contractile cells are interconnected; calcium from pacemaker cells diffuses through gap junctions into contractile myocytes, altering voltage to trigger depolarization in the contractile cells.
In contractile cells, voltage changes are initiated by calcium entering through gap junctions from a neighboring nodal cell, which then opens voltage-gated sodium channels in the contractile cell, causing rapid depolarization.
The initial depolarization in contractile cells is caused by a rapid influx of sodium (through fast Na extsuperscript{+}) channels; this depolarization then propagates along the cell membrane to activate adjacent Na extsuperscript{+} channels.
Potassium channels are voltage-gated and begin to open as the membrane depolarizes; potassium efflux contributes to repolarization.
The key difference in triggering potassium channel opening is the magnitude of voltage change: the calcium influx from the nodal cell is not enough by itself to open these K extsuperscript{+} channels in the same way that the sodium influx is; the sodium-driven depolarization provides the voltage change that opens voltage-gated K extsuperscript{+} channels.
Plateau formation in contractile cells
During plateau (Phase 2), L-type calcium channels open around a threshold of about -20\,\text{mV}, allowing Ca extsuperscript{2+} influx.
At the plateau, slow K extsuperscript{+} channels remain open, and calcium influx counters potassium efflux, keeping the membrane potential from rising too much.
Calcium entering the cell and potassium leaving the cell both carry positive charges, so their simultaneous activity creates the plateau.
Eventually, L-type Ca extsuperscript{2+} channels close and slow K extsuperscript{+} channels continue to drive repolarization.
Resting membrane potential in ventricular (contractile) myocytes is about V_{rest}\approx -90\ \text{mV}.
Resting membrane potential in SA node (pacemaker cells) is about V_{rest}\approx -60\ \text{mV} due to the presence of leaky Na extsuperscript{+} and Ca extsuperscript{2+} channels.
Action potential in contractile ventricular myocytes
Phase 0 (upstroke): opening of fast Na extsuperscript{+} channels; rapid Na extsuperscript{+} influx.
Phase 1 (initial depolarization): closure of fast Na extsuperscript{+} channels and a small efflux of K extsuperscript{+} through open K channels.
Phase 2 (plateau): opening of L-type Ca extsubscript{2+} channels leading to Ca extsuperscript{2+} influx; K extsuperscript{+} channels are closing/less active, which prevents early repolarization.
Phase 3 (final repolarization): closing of L-type Ca extsubscript{2+} channels and opening of slow K extsuperscript{+} channels, causing K extsuperscript{+} efflux and return toward resting potential.
Phase 4 (resting): maintained until next action potential.
Action potential in SA node (pacemaker cells)
Phase 4: slow pacemaker potential due to slow entry of Na extsuperscript{+} and Ca extsuperscript{2+} (leaky channels).
Phase 0: rapid influx of Ca extsuperscript{2+} causing depolarization (no fast Na extsuperscript{+} upstroke like ventricular cells).
Phase 3: repolarization due to cessation of Ca entry and ongoing K extsuperscript{+} efflux;
Resting membrane potential in SA node about V_{rest}^{SA}\approx -60\ \text{mV}.
Side-by-side differences between SA node and ventricular myocytes
Resting potential: SA node V{rest}^{SA}\approx -60\ \text{mV} vs ventricular myocyte V{rest}\approx -90\ \text{mV}.
Upstroke: SA node primarily Ca extsuperscript{2+} influx (slower, less steep) vs ventricular fast Na extsuperscript{+} influx (fast, steep).
Plateau: present in ventricular myocytes (Phase 2) due to Ca extsuperscript{2+} influx and K extsuperscript{+} efflux; absent in SA node.
Repolarization: Phase 3 in SA node is more gradual than in ventricular myocytes.
Phase 4 behavior: ventricular myocytes have a stable resting phase; SA node shows slow diastolic depolarization (automaticity).
Conceptual points about coupling and conduction
Pacemaker (noncontractile) cells are interlinked with contractile myocytes via gap junctions.
Calcium moving from nodal cells into contractile cells via gap junctions initiates voltage changes that open Na extsuperscript{+} channels in the contractile cells.
The same general action potential shape can occur in SA node, AV node, bundle branches, and Purkinje fibers, but firing frequency and magnitude differ.
Summary of key terms
Myocyte: muscle cell; contractile vs noncontractile (pacemaker) distinctions.
Gap junctions: intercellular connections permitting ion flow and electrical coupling.
L-type Ca extsubscript{2+} channels: responsible for the plateau phase in contractile cells, open near V\approx -20\ \text{mV}.
Phase numbering (in contractile cells): Phase 0 = upstroke (fast Na extsuperscript{+}); Phase 1 = initial depolarization (K extsuperscript{+} efflux); Phase 2 = plateau (Ca extsuperscript{2+} in, K extsuperscript{+} out); Phase 3 = repolarization (Ca extsuperscript{2+} closes, K extsuperscript{+} out); Phase 4 = resting.
Blood Vessels and Circulation: Introduction
The left ventricle pumps blood through the aortic valve into the aorta (an artery).
Arteries typically carry oxygenated blood to tissues; a notable exception is the pulmonary artery, which carries deoxygenated blood to the lungs.
Arteries branch into arterioles, which feed into capillary beds where exchange with tissues occurs.
Capillaries drain into venules, which merge into veins.
Veins return blood to the heart: inferior vena cava (from the body below the diaphragm) and superior vena cava (from the head/neck and upper body).
Coronary veins drain the heart muscle into the coronary sinus, which empties into the right atrium.
Pulmonary circuit (exception to the usual artery/vein oxygenation rule)
The pulmonary trunk divides into left and right pulmonary arteries; these arteries carry oxygen-poor, CO extsubscript{2}-rich blood to the lungs.
In the lungs, alveolar gas exchange occurs: oxygen diffuses from the alveoli into the blood, and CO extsubscript{2} diffuses from blood into the alveoli to be exhaled.
Oxygenated blood returns from the lungs to the left atrium via four pulmonary veins (two from each lung: two on the right and two on the left).
Bronchial arteries are part of the systemic circulation that supply oxygenated blood to the lung tissue itself, separate from the pulmonary circuit.
In systemic circulation, veins typically carry oxygen-poor blood back toward the heart while arteries carry oxygen-rich blood away; the pulmonary circuit reverses this pattern.
Quick recap of key pathways
LV → aortic valve → aorta → arteries → arterioles → capillaries → venules → veins → right atrium (via superior/inferior vena cavae and coronary sinus).
Pulmonary circulation: right atrium → right ventricle → pulmonary valve → pulmonary trunk → left/right pulmonary arteries → lungs (gas exchange) → four pulmonary veins → left atrium.
Practical Implications and Connections
Understanding the differences between contractile and pacemaker cells explains how the heart maintains rhythm (automaticity) and force generation (contractility).
The plateau phase in ventricular action potentials ensures a longer refractory period, preventing tetany and coordinating heart rhythm with contraction.
The heart’s electrical system relies on intercellular coupling via gap junctions; disruption can lead to arrhythmias.
The pulmonary circuit’s unique pattern (arteries carry deoxygenated blood) is essential for gas exchange and systemic oxygen delivery.
Knowledge of arterioles, capillaries, venules, and veins underpins how blood flow is regulated and how oxygen delivery and waste removal occur at the tissue level.
Formulas and Key Numerical References
Resting membrane potential: V_{rest}^{Vent} \approx -90\ \text{mV}
Resting membrane potential (SA node): V_{rest}^{SA} \approx -60\ \text{mV}
Plateau and Ca extsuperscript{2+} threshold: V_{threshold}^{Ca} \approx -20\ \text{mV}
Plateau involves simultaneous Ca extsubscript{2+} influx and K extsuperscript{+} efflux; outcomes depend on channel timing.
Plateau explanation: if Ca extsubscript{2+} channels did not open or K extsuperscript{+} channels did not stay open, the action potential would not plateau and would resemble a neuron-like spike.
Connections to Foundational Principles
Ion channel dynamics (voltage-gated channels) determine phases of the action potential and how quickly depolarization and repolarization occur.
The electrochemical gradients drive ions from regions of higher to lower concentration, influencing membrane potential changes.
Gap junctions enable direct electrical coupling between cells, enabling synchronized cardiac activity.
Gas exchange principles underlie pulmonary circulation: diffusion of O extsubscript{2} into blood and diffusion of CO extsubscript{2} into alveolar air.
Notes on Terminology
Myocyte: muscle cell; contractile vs noncontractile (pacemaker) refers to capability to contract.
Pacemaker cells are noncontractile but still myocytes and are capable of automaticity due to their ionic conductances.
Arteries vs veins: arteries carry blood away from the heart (usually oxygenated); veins carry blood toward the heart (usually deoxygenated); pulmonary vessels are exceptions (pulmonary arteries carry deoxygenated blood; pulmonary veins carry oxygenated blood).
If you have questions or want to review specific segments (e.g., phase-by-phase tracings or the exact ion channel timing), we can zoom in on those parts or compare your own notes against this summary.