Physiology Lectures 20-25: Cardiac Electrical Activity, Hemodynamics & Heart Sounds

Vocabulary flashcards summarizing major terms and definitions from Physiology Lectures 20-25, covering cardiac electrophysiology, ECG interpretation, hemodynamics, heart sounds, autonomic regulation, and pathophysiology.

SA (Sinoatrial) Node

Primary pacemaker of the heart; initiates the fastest spontaneous action potentials.

Internodal Pathway

Conducting fibers that carry impulses from the SA node to the AV node.

AV (Atrioventricular) Node

Electrical relay station with a built-in delay allowing atrial contraction to finish before ventricular contraction.

Bundle of His

Specialized conduction fibers that transmit impulses from the AV node to the bundle branches.

Left & Right Bundle Branches

Pathways that conduct action potentials down the interventricular septum toward the apex.

Purkinje Fibers

Fast-conducting fibers that distribute depolarization throughout ventricular myocardium.

Electrode (ECG)

A sensor attached to the skin that detects voltage changes caused by cardiac electrical activity.

Lead (ECG)

A pair of electrodes; records the electrical potential difference between them.

Bipolar Limb Lead

Standard limb lead (I, II, III) that measures voltage between two active electrodes.

Lead I

Negative electrode on right arm, positive on left arm.

Lead II

Negative electrode on right arm, positive on left leg.

Lead III

Negative electrode on left arm, positive on left leg.

Beethoven’s Triangle

Relationship: Lead I + Lead III = Lead II (Einthoven’s Law).

Unipolar Lead

Uses one active electrode referenced to a passive central terminal (e.g., aVR, aVL, aVF).

aVR

Augmented limb lead with positive electrode on the right arm.

aVL

Augmented limb lead with positive electrode on the left arm.

aVF

Augmented limb lead with positive electrode on the left leg (foot).

Atria

Upper heart chambers that receive blood from veins.

Ventricles

Lower heart chambers that pump blood into arteries.

Arteries

Blood vessels that carry blood away from the heart.

Veins

Blood vessels that return blood to the heart.

Intercalated Disc

Specialized junction connecting cardiac muscle cells via gap junctions for electrical coupling.

Myogenic

Originating within the muscle itself; describes the heart’s self-generated electrical activity.

ECG / EKG

Surface tracing of the summed electrical activity of all cardiac cells.

Pacemaker Cells

Autorhythmic cells that set heart rate by spontaneous depolarization.

Depolarization (ECG)

Wave of positive charge producing an upward deflection when moving toward a positive electrode.

Repolarization (ECG)

Return to resting potential; produces downward deflection when moving toward a positive electrode.

Dipole

Pair of equal and opposite charges separated by distance; the heart acts as a moving this each beat.

Volume Conductor

Property of body tissues that conduct cardiac electrical signals to the skin surface.

Vector (ECG)

Arrow indicating direction and magnitude of net cardiac electrical activity.

P Wave

ECG deflection representing atrial depolarization (and contraction).

P-R Interval

Time from onset of atrial depolarization to onset of ventricular depolarization; includes AV delay.

QRS Complex

Rapid ventricular depolarization; Q = septal, R = apex-directed mass, S = base depolarization.

S-T Segment

Isoelectric interval when ventricles are fully depolarized (phase 2); baseline on ECG.

T Wave

Ventricular repolarization on ECG.

Left Axis Deviation

Mean QRS axis < 0°; causes include LV hypertrophy, pregnancy, obesity.

Right Axis Deviation

Mean QRS axis > +90°; causes include RV hypertrophy or left ventricular infarction.

First-Degree AV Block

Prolonged PR interval; every P wave followed by QRS.

Second-Degree AV Block Type I (Wenckebach)

Progressive PR prolongation leading to dropped QRS beat.

Second-Degree AV Block Type II

Sudden dropped QRS complexes without prior PR lengthening.

Third-Degree (Complete) AV Block

No association between P waves and QRS complexes; atria and ventricles beat independently.

Atrial Fibrillation

Chaotic atrial activity; no distinct P waves; irregular ventricular rhythm.

Ventricular Fibrillation

No coordinated QRS complexes; fatal without immediate intervention.

Systole

Phase of cardiac muscle contraction and blood ejection.

Diastole

Phase of cardiac muscle relaxation and ventricular filling.

Isovolumic Ventricular Contraction

Early systole; pressure rises with all valves closed; produces S1 sound.

Ventricular Ejection

Semilunar valves open; blood expelled; ventricular pressure exceeds arterial.

Isovolumic Relaxation

Early diastole; semilunar valves close (S2); pressure falls with no volume change.

Afterload

Resistance the ventricle must overcome to eject blood (e.g., aortic pressure).

Preload

Myocardial stretch at end-diastole; approximated by EDV or EDP.

End-Diastolic Volume (EDV)

Volume of blood in ventricle just before systole.

End-Systolic Volume (ESV)

Volume of blood remaining in ventricle after ejection.

Stroke Volume (SV)

EDV – ESV; blood ejected per heartbeat.

Ejection Fraction (EF)

EF = (SV / EDV) × 100%; indicator of ventricular performance.

Cardiac Output (CO)

CO = SV × HR; mL of blood pumped per minute.

Stroke Work (SW)

SW = Ventricular pulse pressure × SV; work done per beat.

Frank-Starling Law

Increased EDV stretches sarcomeres, raising contractile force and SV.

Contractility

Intrinsic strength of myocardium independent of preload and afterload; modulated by Ca²⁺ and SNS.

Positive Inotropic Agent

Substance (e.g., NE, digitalis) that increases contractility and SV.

Negative Inotropic Agent

Substance (e.g., ischemia, β-blocker) that decreases contractility.

Bowditch (Treppe) Effect

Direct effect where increased HR enhances Ca²⁺ cycling and slightly raises contractility.

Ventricular Compliance

Ease with which ventricles fill; reduced increases diastolic pressure for a given volume.

Hydrostatic Pressure

Force exerted by a fluid at rest against vessel walls.

Vasoconstriction

Decrease in vessel radius; increases resistance and pressure.

Vasodilation

Increase in vessel radius; decreases resistance and pressure.

Poiseuille’s Law

Flow (Q) ∝ ΔP / R; resistance inversely ∝ radius⁴, directly ∝ viscosity and length.

Series Circuits (Vasculature)

Add individual resistances; yield higher total resistance.

Parallel Circuits

Add reciprocals of resistances; lower total resistance; allow localized flow control.

Pulse Pressure

Difference between systolic and diastolic pressure (LV or systemic).

Heart Sound S1

Closure of mitral and tricuspid (AV) valves; start of systole.

Heart Sound S2

Closure of aortic and pulmonic valves; start of diastole.

Heart Sound S3

Early diastolic sound from rapid ventricular filling; normal in youth, pathologic in older adults.

Heart Sound S4

Late diastolic sound caused by atrial contraction into a stiff ventricle; indicates low compliance.

Systolic Murmur

Occurs between S1 and S2; due to semilunar stenosis or AV regurgitation.

Diastolic Murmur

Occurs between S2 and S1; due to AV stenosis or semilunar regurgitation.

Continuous Murmur

Heard in both systole and diastole; classic for patent ductus arteriosus (PDA).

Stenosis (Valve)

Failure to open fully; causes turbulent forward flow and ejection murmurs.

Regurgitation (Valve)

Failure to close completely; allows backward flow and holosystolic/diastolic murmurs.

Sympathetic Cardiac Innervation

Preganglionic fibers synapse in stellate ganglia; postganglionic fibers release NE onto β1 receptors.

Parasympathetic Cardiac Innervation

Vagus nerve fibers release ACh on M2 receptors in SA/AV nodes and atria.

Right Stellate Ganglion

Sympathetic outflow with greater chronotropic (HR) influence.

Left Stellate Ganglion

Sympathetic outflow with stronger inotropic (contractility) influence.

Right Vagus Nerve

Predominantly slows SA node firing (HR).

Left Vagus Nerve

Primarily slows AV nodal conduction.

β1-Adrenergic Receptor

GPCR that increases cAMP → PKA → enhanced Ca²⁺ entry, SR uptake, and contractility.

M2 Muscarinic Receptor

GPCR that decreases cAMP and opens K⁺ channels, slowing HR and AV conduction.

Funny Current (I_f)

Na⁺/K⁺ inward current in pacemaker cells; slope increased by cAMP to speed HR.

Accentuated Antagonism

Parasympathetic effects are more pronounced when sympathetic tone is high.

Aortic Valve Stenosis

Narrowed aortic valve; raises LV pressure required to open valve and produces systolic murmur.

Ischemic Heart Failure

Reduced contractility leading to low SV and compensatory rise in EDV; causes congestion.

Beta-Adrenergic Antagonist

Drug (e.g., metoprolol) that decreases HR and contractility by blocking β receptors.

Muscarinic Cholinergic Antagonist

Drug that blocks vagal influence; minimal effect on HR during exercise dominated by SNS.

Calcium Channel Blocker (Cardiac)

Reduces Ca²⁺ influx in nodal and myocardial cells; lowers HR and contractile force.

Hydraulic Principle of Flow

Blood moves from high to low pressure; heart generates pressure, friction drops it along vessels.

Heart as Moving Dipole

During each beat, depolarization wavefront creates a shifting vector detectable by surface leads.

Wide QRS Complex

Indicates slowed ventricular conduction (e.g., bundle-branch block).

Narrow QRS Complex

Indicates rapid, normal ventricular conduction via His-Purkinje system.

Laminar Flow

Smooth, orderly blood movement; occurs in normal vessels when Reynolds number is low.

Turbulent Flow

Disordered movement producing murmurs; increased by high velocity, low viscosity, or stenosis.

Afterload vs. Preload

Afterload = pressure resistance during ejection; preload = ventricular filling stretch before systole.