Disorders of Cardiac Rhythm, Pericardial Disorders & Circulatory Shock

Vocabulary flashcards covering cardiac conduction, arrhythmias, pharmacology, pericardial disorders, and stages/types of circulatory shock.

Sinoatrial (SA) Node

Primary cardiac pacemaker located in the right atrium; fires 60–100 bpm and initiates each heartbeat.

Atrioventricular (AV) Node

Backup pacemaker (40–50 bpm) that delays impulses from atria to ventricles to allow ventricular filling.

Purkinje Fibers

Specialized conduction fibers that rapidly transmit impulses through ventricular myocardium (15–40 bpm if pacemaker).

Phase 0 (Depolarization)

Rapid Na⁺ influx causing the upstroke of the cardiac action potential; target of sodium-channel blockers.

Phase 1 (Early Repolarization)

Brief initial repolarization immediately after depolarization; few drug targets.

Phase 2 (Plateau)

Ca²⁺ influx balances K⁺ efflux, sustaining contraction; slowed by calcium-channel and β-blockers.

Phase 3 (Final Repolarization)

Rapid K⁺ efflux restores resting potential; prolonged by potassium-channel blockers.

Phase 4 (Resting Potential)

Diastolic period preparing for next impulse; affected by β-blockers and calcium-channel blockers.

Absolute Refractory Period

Time during phases 0–2 (early 3) when no stimulus can trigger another action potential; prevents extra beats.

Relative Refractory Period

Late phase 3 period when a stronger-than-normal stimulus can generate an impulse.

Supernormal Excitatory Period

End of phase 3 to early phase 4 when a very weak stimulus can cause an arrhythmia.

P Wave

ECG representation of atrial depolarization.

QRS Complex

ECG tracing of ventricular depolarization (and hidden atrial repolarization).

T Wave

Represents ventricular repolarization on an ECG.

U Wave

Small wave sometimes seen after T wave; prominent in hypokalemia.

Sinus Bradycardia

SA node rhythm < 60 bpm with otherwise normal conduction.

Sinus Tachycardia

SA node rhythm > 100 bpm with normal conduction pathway.

Sinus Arrest

Transient failure of SA node resulting in pause with no backup pacemaker impulse.

Supraventricular Tachycardia (SVT)

Rapid rhythm originating above ventricles (atria or AV junction).

Atrial Flutter

Atrial rate 250–350 bpm causing saw-tooth P waves; ventricular rate may be regular or variable.

Atrial Fibrillation

Chaotic atrial activity with no distinct P waves; major risk for embolic stroke.

Premature Atrial Contraction (PAC)

Early ectopic atrial impulse producing premature P wave and compensatory pause.

Junctional Tachycardia

Rapid rhythm originating in AV junctional tissue.

Long QT Syndrome

Prolonged QT interval predisposing to ventricular arrhythmias such as torsades de pointes.

Premature Ventricular Contraction (PVC)

Early ventricular beat with wide, bizarre QRS and full compensatory pause.

Ventricular Tachycardia (V-tach)

≥3 consecutive PVCs at > 100 bpm; can be life-threatening due to poor perfusion.

Ventricular Fibrillation (V-fib)

Chaotic ventricular quivering with no cardiac output; requires immediate defibrillation.

Torsades de Pointes

Polymorphic VT associated with prolonged QT and often hypomagnesemia.

First-Degree AV Block

Prolonged PR interval (> 0.20 s) with all impulses conducted to ventricles.

Second-Degree AV Block

Intermittent failure of conduction from atria to ventricles (Mobitz I or II).

Third-Degree AV Block

Complete dissociation of atrial and ventricular activity; requires pacing.

Ectopic Beat

Impulse originating outside normal pacemaker pathway causing premature contraction.

Pulsus Paradoxus

Drop ≥ 10 mm Hg in systolic BP during inspiration; classic sign of cardiac tamponade.

Pericardial Effusion

Accumulation of serous, purulent, or sanguineous fluid in pericardial cavity.

Cardiac Tamponade

Compression of heart by effusion causing obstructed filling, pulsus paradoxus, and shock.

Acute Pericarditis

Inflammation of pericardium with sharp chest pain, friction rub, and possible effusion.

Cardiomyopathy

Disease of heart muscle affecting structure/function; includes dilated, hypertrophic, restrictive types.

Dilated Cardiomyopathy

Ventricular dilation with systolic dysfunction and reduced ejection fraction.

Hypertrophic Obstructive Cardiomyopathy

Genetic septal thickening causing outflow obstruction and sudden death in athletes.

Restrictive Cardiomyopathy

Rigid ventricular walls resist filling, leading to diastolic dysfunction and venous congestion.

Infective Endocarditis

Infection of endocardial surface (usually valves) forming vegetations; often Staph aureus.

Osler Nodes

Painful red nodules on fingertips/toes seen in infective endocarditis.

Janeway Lesions

Non-tender hemorrhagic lesions on palms/soles in infective endocarditis.

Shock

Life-threatening state of inadequate tissue perfusion to meet cellular oxygen demand.

Hypovolemic Shock

Shock due to loss of 15–30% intravascular volume from hemorrhage or fluid loss.

Cardiogenic Shock

Shock caused by severe pump failure (e.g., large MI) leading to low cardiac output.

Obstructive Shock

Shock from mechanical blockage of circulation (e.g., PE, tamponade, tension pneumothorax).

Distributive Shock

Relative hypovolemia from massive vasodilation (septic, neurogenic, anaphylactic).

Compensatory Stage (Shock)

Early shock phase with SNS activation, tachycardia, vasoconstriction, normal BP.

Progressive Stage (Shock)

Failure of compensation; falling BP, worsening hypoperfusion, organ dysfunction.

Irreversible Stage (Shock)

End-stage shock with severe cellular damage and multiple organ failure.

Multiple Organ Dysfunction Syndrome (MODS)

Failure of ≥2 organs after severe illness/injury; high mortality.

Crystalloids

Isotonic or hypertonic solutions (NS, LR) used for volume replacement in shock.

Colloids

High-molecular-weight solutions (e.g., albumin) that expand plasma volume via oncotic pressure.

Vasoactive Medications

Drugs that adjust vascular tone or cardiac contractility to support BP and perfusion.

Inotropic Agents

Drugs like dobutamine or dopamine that increase myocardial contractility.

Vasopressors

Agents (e.g., norepinephrine, epinephrine) causing vasoconstriction to raise blood pressure.

Vasodilators

Drugs (e.g., nitroglycerin) that decrease preload/afterload by dilating vessels.

Class I Antiarrhythmics

Sodium-channel blockers that slow Phase 0 depolarization (e.g., lidocaine, quinidine).

Class II Antiarrhythmics

β-blockers that slow SA/AV conduction and reduce contractility (e.g., propranolol).

Class III Antiarrhythmics

Potassium-channel blockers that prolong repolarization and QT (e.g., amiodarone).

Class IV Antiarrhythmics

Calcium-channel blockers that depress AV conduction (verapamil, diltiazem).

Class V Antiarrhythmics

Miscellaneous agents affecting conduction (digoxin, adenosine, atropine, magnesium).

Lidocaine

Class IB sodium-channel blocker used IV for acute ventricular arrhythmias; neurologic toxicity possible.

Propranolol

Non-selective β-blocker treating SVT, VT, hypertension, angina; watch for bradycardia and bronchospasm.

Amiodarone

Potent Class III drug for life-threatening VT/VF; risks include pulmonary, thyroid, and liver toxicity.

Adenosine

Ultra-short-acting agent that transiently stops AV conduction to terminate SVT ('resets' SA node).

Atropine

Anticholinergic drug that inhibits vagal tone to treat symptomatic bradycardia.

Magnesium (for Arrhythmia)

IV electrolyte given to treat torsades de pointes and correct hypomagnesemia.

Tension Pneumothorax

Air under pressure in pleural space collapsing lung and obstructing venous return; causes obstructive shock.