Heart and Circulation – Key Vocabulary

A comprehensive set of vocabulary flashcards covering cardiac physiology, electrophysiology, pathology, and pharmacology from the lecture notes.

Nodal / Conducting Cells

Specialized myocardial cells with few myofibrils that spontaneously generate and rapidly conduct action potentials; include SA node, AV node, Bundle of His, and Purkinje fibers.

Sinoatrial (SA) Node

Pacemaker of the heart located in the upper posterior wall of the right atrium; first area to spontaneously depolarize each beat.

Atrioventricular (AV) Node

Node that electrically connects atria and ventricles; slows impulse conduction, allowing atrial contraction before ventricular excitation.

Bundle of His

Conducting fibers that carry impulses from the AV node down the interventricular septum toward the ventricles.

Purkinje Fibers

Rapid‐conducting fibers that distribute action potentials throughout ventricular myocardium for coordinated contraction.

Chronotropic Effect

Change in heart rate produced by altering SA-node firing; positive increases HR, negative decreases HR.

Dromotropic Effect

Change in conduction velocity, primarily at the AV node; positive shortens PR interval, negative lengthens it.

Inotropic Effect

Change in force of cardiac contraction; positive strengthens, negative weakens contractility.

Sympathetic Cardiac Effects

β1-receptor stimulation causing positive chronotropic, dromotropic, and inotropic effects plus coronary vasodilation.

Parasympathetic Cardiac Effects

Vagal (ACh) input causing negative chronotropic, dromotropic, and slight negative inotropic effects with coronary vasoconstriction.

Arrhythmia

Abnormal rhythm due to disturbed impulse formation or conduction.

Sinus Tachycardia

Resting sinus rate > 100 bpm with regular rhythm (e.g., exercise, fever).

Sinus Bradycardia

Resting sinus rate < 50–60 bpm with regular rhythm.

Extrasystole (ES)

Premature heartbeat arising from ectopic focus in atria, AV node, or ventricles.

Supraventricular Arrhythmia

Rhythm disturbance originating above ventricles, typically from atrial or nodal extrasystoles; QRS complex usually normal.

Ventricular Premature Complex (VPC)

Ectopic ventricular beat originating distal to His-Purkinje system; deformed QRS complex.

Automaticity (in VPCs)

Development of spontaneous depolarization site in non-nodal tissue, often from ischemia or electrolyte imbalance.

Reentry Circuit

Arrhythmia mechanism where impulse circles between slow- and fast-conducting tissue, common post-MI.

Ventricular Tachycardia (VT)

Rapid sequence of ectopic ventricular impulses (120–250 bpm) that may lead to fibrillation.

Atrial Tachycardia

Regular rapid atrial rhythm (100–250 bpm) arising in atria.

Atrial Fibrillation

Completely irregular rapid atrial activity with irregular ventricular response; risk of atrial clot formation.

Atrial Flutter

Fast but regular atrial rhythm in which atria beat faster than ventricles.

First-Degree AV Block

PR interval > 0.20 s; conduction delayed but all atrial impulses reach ventricles.

Second-Degree AV Block

Some atrial impulses fail to conduct; P waves without following QRS complexes.

Third-Degree (Complete) AV Block

No atrial impulses reach ventricles; ventricular bradycardia results.

Contractile Cells

Cardiac muscle cells with single nucleus, abundant mitochondria, and intercalated discs that perform pumping work.

Intercalated Disc

Special junction containing tight and gap junctions linking cardiac cells for electrical continuity.

Excitation-Contraction Coupling

Process where AP triggers Ca²⁺ entry, Ca²⁺-induced Ca²⁺ release from SR, troponin binding, filament sliding, and contraction.

Contractility (Inotropism)

Intrinsic ability of myocardium to develop force at given length; estimated by ejection fraction.

Positive Inotropic Agent

Factor that increases contractility (e.g., sympathetic stimulation, digitalis).

Negative Inotropic Agent

Factor that decreases contractility (e.g., parasympathetic ACh).

Preload

End-diastolic volume that stretches ventricular fibers before contraction.

Afterload

Pressure ventricles must overcome during ejection; aortic pressure for LV, pulmonary artery pressure for RV.

Frank-Starling Relationship

Stroke volume and CO increase with greater venous return/end-diastolic volume due to length-tension properties.

Stroke Volume (SV)

Volume ejected per beat = EDV – ESV.

Cardiac Output (CO)

Blood volume pumped per minute = SV × HR; about 5 L/min at rest.

Ejection Fraction (EF)

SV / EDV; normal ≈ 55 %; indicator of contractility.

Pressure-Volume Loop

Graph showing ventricular pressure vs. volume during cardiac cycle; width reflects stroke volume.

Isovolumetric Contraction

Early systole phase with rising pressure but constant volume; all valves closed.

Ventricular Ejection Period

Phase when aortic/pulmonary valves open; blood leaves ventricles and volume falls.

Isovolumetric Relaxation

Early diastole phase with falling pressure, constant volume; all valves closed.

Ventricular Filling

Late diastole phase when AV valves open and ventricles fill to EDV.

First Heart Sound (S1)

Vibration created by closure of AV valves at start of systole; low pitch, long duration.

Second Heart Sound (S2)

Vibration from closure of aortic and pulmonary valves at end of systole; higher pitch, shorter.

Third Heart Sound (S3)

Mid-diastolic rumble due to rapid ventricular filling; often normal in youth but faint.

Fick Principle

Method for measuring CO: CO = O₂ consumption / (arterial O₂ – venous O₂).

Class I Antiarrhythmics

Na⁺ channel blockers (e.g., lidocaine, phenytoin) that alter cardiac AP conduction.

Class II Antiarrhythmics

β-blockers (e.g., atenolol, propranolol) reducing sympathetic effects and AV conduction.

Class III Antiarrhythmics

K⁺ channel blockers (e.g., sotalol) prolonging repolarization without slowing conduction.

Class IV Antiarrhythmics

Ca²⁺ channel blockers (e.g., verapamil, diltiazem) slowing AV conduction and reducing contractility.

Digitalis (Cardiac Glycoside)

Positive inotropic drug that increases intracellular Ca²⁺ by inhibiting Na⁺/K⁺-ATPase.

Atherosclerosis

Inflammatory disease with lipid-rich plaques in medium/large arteries leading to vessel narrowing.

Endothelial Dysfunction

Impaired endothelium that reduces nitric oxide, promotes adhesion molecules, and initiates vascular inflammation.

Dyslipidemia

Abnormal plasma lipids predisposing to atherosclerosis; elevated LDL/VLDL or low HDL.

Heart Murmur

Sound caused by turbulent blood flow; may be benign or due to valve pathology.

Valvular Stenosis

Narrowing of a heart valve opening causing turbulent flow during forward passage.

Valve Regurgitation (Insufficiency)

Incompetent valve allowing backflow when closed, creating abnormal murmur.