Electrical Activity of the Heart and Cardiac Electrophysiology

Flashcards on the electrophysiology of the heart, components of the conducting system, cardiac action potentials, ion channels, autonomic nerve effects, and refractory periods based on lecture notes.

Conducting Cells

Specialized cardiac muscle cells that do not contract, but generate and conduct action potentials throughout the heart to make up its conducting system.

Contractile Cells

Working cardiac muscle cells that contract and develop force responsible for pumping blood.

Sinoatrial Node (SA Node)

The primary pacemaker of the heart located in the right atrium that initiates cardiac action potentials and exhibits the highest intrinsic firing frequency.

Atrioventricular Node (AV Node)

A conducting component that slows impulse propagation to create an AV delay of $0.1\,\text{seconds}$, allowing time for ventricular filling, and acting as a secondary pacemaker if the SA node fails.

Bundle of His

The specialized conducting pathway carrying action potentials from the atria to the ventricles; it is the only electrical connection between atria and ventricles.

Purkinje Fibers

The continuation of the bundle branches within the working ventricular myocardium; they are the fastest conducting component of the entire cardiac conducting system.

Park At Ventura Avenue

A mnemonic for remembering the order of cardiac tissue conduction velocity from fastest to slowest: Purkinje system > Atrial muscle > Ventricular muscle > AV node.

Fast Response Action Potential

The type of action potential generated by working contractile myocardial cells, characterized by a rapid Phase 0 depolarization and a prominent plateau phase.

Slow Response Action Potential

The type of action potential characteristic of SA and AV nodal pacemaker cells, defined by an unstable resting phase (Phase 4) and slow upstroke.

Phase 0 (Rapid Depolarization)

The phase in ventricular muscle cells caused by the opening of voltage-gated sodium channels and a fast inward $\text{Na}^+$ current, bringing the membrane potential to $+20\,\text{mV}$.

Phase 1 (Initial Brief Repolarization)

The brief early repolarization phase caused by the inactivation of fast voltage-gated sodium channels and outward $\text{K}^+$ current.

Phase 2 (Plateau Phase)

The prolonged stable depolarization phase at roughly $0\,\text{mV}$ where slow inward $\text{Ca}^{2+}$ current through L-type calcium channels balances outward $\text{K}^+$ current.

Phase 3 (Rapid Repolarization)

The phase caused by the closure of voltage-gated $\text{Ca}^{2+}$ channels and strong outward $ contest {K}^+$$ current via delayed rectifier potassium channels, restoring the potential to RMP.

Phase 4 (Resting Phase)

The stable resting membrane potential period ($-90\,\text{mV}$) in contractile cells during which voltage-gated $\text{Na}^+$ and $\text{Ca}^{2+}$ channels remain closed while delayed rectifier $\text{K}^+$ channels finish closing.

Inward Rectifying Potassium Channels ($I_{K1}$)

Potassium channels open at resting potentials that close during depolarization and the plateau phase, reopening during repolarization.

Delayed Rectifying Potassium Channels ($I_K$)

Voltage-gated potassium channels that open slowly late in the plateau phase to drive Phase 3 rapid repolarization and close slowly into Phase 4.

Pacemaker Potential (Prepotential)

The gradual Phase 4 depolarization in SA node cells from $-65\,\text{mV}$ to threshold, caused by decreased $\text{K}^+$ conductance, inward funny $\text{Na}^+$ current ($I_f$), and T-type $\text{Ca}^{2+}$ channel influx.

Positive Chronotropic Effect

An increase in heart rate, such as that mediated by sympathetic norepinephrine binding to $\beta_1$ receptors, raising cAMP and speeding up Phase 4 depolarization in the SA node.

Positive Dromotropic Effect

An increase in the velocity of impulse conduction through the AV node, resulting in a shortened AV delay.

Negative Chronotropic Effect

A decrease in heart rate, such as that mediated by parasympathetic acetylcholine binding to $M_2$ muscarinic receptors, decreasing cAMP and slowing Phase 4 slope in the SA node.

Negative Dromotropic Effect

A decrease in conduction velocity through the AV node, prolonging the AV delay.

Propranolol

A beta-adrenergic receptor antagonist (beta blocker) that decreases heart rate and slows AV nodal conduction velocity.

Atropine

A muscarinic receptor antagonist that blocks parasympathetic action on the heart, resulting in an increased heart rate.

Absolute Refractory Period (ARP)

The duration during a cardiac action potential when no second stimulus can trigger a new action potential, preventing tetanic contraction and ensuring intermittent pumping action.