CRAS cheat sheet

The SA node sits at the junction of the superior vena cava and right atrium and normally fires at 60-100 bpm, making it the dominant pacemaker.

Normal intrinsic rates: SA node 60-100 bpm, AV junction 40-60 bpm, ventricular Purkinje system 20-40 bpm.

Coronary perfusion of the left ventricle occurs mainly during diastole; tachycardia shortens diastole and can precipitate ischemia.

Cardiac output = heart rate x stroke volume; stroke volume depends on preload, afterload, and contractility.

The right coronary artery supplies the SA node in roughly 60% of people and the AV node in roughly 90%.

The AV node conducts slowly (about 0.05 m/s) creating a physiologic delay that allows ventricular filling before contraction.

The Purkinje system conducts fastest (about 2-4 m/s), enabling rapid, synchronized ventricular depolarization.

The left ventricle has the thickest wall and generates systemic pressures; the right ventricle pumps against low pulmonary resistance.

Phase 4 depolarization slope determines automaticity; increased slope raises firing rate, as with catecholamines or digoxin toxicity.

The fast-response action potential has phases 0-4; phase 0 upstroke is mediated by rapid sodium channels in atrial and ventricular myocytes.

The slow-response AV and SA nodal action potential depends on calcium current for phase 0 and has no true phase 1.

Reentry requires an anatomic or functional circuit, unidirectional block, and slowed conduction; it is the mechanism of most paroxysmal SVT and flutter.

Triggered activity arises from early afterdepolarizations (bradycardia/long QT) or delayed afterdepolarizations (calcium overload, digoxin).

Enhanced automaticity originates from cells firing faster than the SA node, producing a gradual warm-up rather than abrupt onset.

Refractoriness is set by action potential duration; drugs prolonging repolarization (class III) lengthen the effective refractory period.

The vulnerable period for inducing ventricular fibrillation corresponds to the peak of the T wave (relative refractory period).

Standard paper speed is 25 mm/s; one small box = 0.04 s, one large box = 0.20 s, and 300 divided by large boxes between R waves estimates rate.

Normal PR interval is 0.12-0.20 s; QRS duration under 0.12 s is narrow; QTc is prolonged above 0.44 s in men and 0.46 s in women.

Sinus rhythm requires a P wave before every QRS, upright P in lead II, constant PR, and rate 60-100 bpm.

Atrial fibrillation shows irregularly irregular RR intervals with absent discrete P waves and fibrillatory baseline.

Atrial flutter typically shows sawtooth flutter waves at about 250-350 bpm with a fixed or variable AV conduction ratio.

Ventricular tachycardia is a wide-complex tachycardia (QRS >0.12 s) at rate >100 bpm; AV dissociation and capture beats support the diagnosis.

First-degree AV block is PR >0.20 s with every P conducted; second-degree type I shows progressive PR lengthening before a dropped beat.

Second-degree type II shows constant PR with sudden dropped QRS complexes; third-degree shows complete AV dissociation with an escape rhythm.

A 12-lead ECG is the first-line test for rhythm; a 24-48 hour Holter monitor suits symptoms occurring at least daily.

Event recorders or 14-30 day patch monitors are used when symptoms occur weekly to monthly; implantable loop recorders cover up to 2-3 years.

Treadmill exercise testing helps provoke exercise-induced arrhythmias and assess rate response and chronotropic competence.

Echocardiography assesses structural disease, ejection fraction, and chamber size, which guide device and ablation decisions.

Tilt-table testing is used for suspected vasovagal syncope when history and ECG are nondiagnostic.

Electrolytes (potassium, magnesium, calcium) and thyroid function are core labs in arrhythmia evaluation; TSH screens for thyrotoxic atrial fibrillation.

Ambulatory monitoring yield depends on symptom frequency; the recording duration should match the symptom interval.

Cardiac catheterization or stress imaging is used when ischemia is suspected as an arrhythmia trigger.

Vaughan-Williams classes: I sodium-channel blockers, II beta-blockers, III potassium-channel blockers, IV calcium-channel blockers.

Class I drugs slow phase 0 depolarization and are subdivided: IA (quinidine, procainamide), IB (lidocaine, mexiletine), IC (flecainide, propafenone).

Class IC agents are contraindicated in structural heart disease or reduced ejection fraction because of proarrhythmia risk.

Amiodarone is a class III agent with thyroid, pulmonary, hepatic, corneal, and neurologic toxicity requiring periodic monitoring.

Adenosine transiently blocks the AV node and terminates AV nodal reentrant tachycardia; its half-life is under 10 seconds.

Beta-blockers reduce automaticity and AV conduction and are first-line for rate control in atrial fibrillation and for catecholaminergic arrhythmias.

Digoxin slows AV conduction and increases vagal tone; toxicity is aggravated by hypokalemia and renal impairment.

Sotalol and dofetilide prolong QT and require monitoring for torsades de pointes; correct potassium and magnesium before initiation.

The five-position NBG pacemaker code describes chamber paced, chamber sensed, response to sensing, rate modulation, and multisite pacing.

VVI paces and senses the ventricle and inhibits on sensed events; DDD paces and senses both chambers with dual inhibition and tracking.

Pacemaker spikes followed by capture confirm pacing; failure to capture shows a spike without a subsequent P or QRS.

Undersensing appears as paced spikes occurring despite intrinsic beats; oversensing appears as inappropriate inhibition from noncardiac signals.

ICDs terminate ventricular tachycardia or fibrillation by antitachycardia pacing or defibrillation; pacing also provides bradycardia support.

Secondary prevention ICD indications include survivors of cardiac arrest or sustained VT; primary prevention uses reduced ejection fraction criteria.

Pacemaker syndrome from VVI pacing is corrected by upgrading to a dual-chamber or physiologic pacing mode.

Magnet application generally converts pacemakers to asynchronous pacing and suspends ICD tachytherapy.

The electrophysiology study uses multipolar catheters in the high right atrium, His bundle, coronary sinus, and right ventricle to map activation.

Radiofrequency ablation creates thermal lesions; cryoablation offers reversible lesion testing and is used near the AV node.

AV nodal reentrant tachycardia is treated by slow-pathway modification; accessory pathways are ablated at the earliest ventricular or atrial activation.

Typical atrial flutter is ablated at the cavotricuspid isthmus with a bidirectional conduction block endpoint.

Atrial fibrillation ablation targets pulmonary vein isolation; success is assessed by freedom from atrial arrhythmia on monitoring.

Complications of ablation include vascular injury, cardiac perforation and tamponade, thromboembolism, and AV block requiring pacing.

Anticoagulation is typically continued or bridged around left-sided ablation to reduce thromboembolic risk.

Sedation or general anesthesia may be used; post-procedure monitoring includes access-site checks and rhythm surveillance.

Teach patients to monitor pulse rate and rhythm and to report palpitations, syncope, or sustained rates outside prescribed parameters.

Patients with ICDs need education that shocks may occur and that a shock with symptoms warrants emergency evaluation.

Anticoagulated atrial fibrillation patients need education on bleeding signs, adherence, and drug or diet interactions.

Activity and driving restrictions after device implantation or ablation follow institutional and physician guidance for a defined period.

Device follow-up involves scheduled interrogation, battery assessment, lead impedance, sensing, and capture threshold checks.

Pulse generators are typically replaced when elective replacement indicator is reached, not at end of battery life.

Medication adherence education includes refill timing, side-effect recognition, and avoiding missed antiarrhythmic doses.

Patients should avoid strong magnetic fields and carry device identification; MRI requires device-specific clearance.

Universal precautions and sterile technique reduce bloodstream infection risk during device implantation and invasive procedures.

Defibrillation safety includes clearing all personnel, removing oxygen sources, and ensuring dry skin and correct pad placement.

Radiation safety uses time, distance, and shielding; dosimeters track cumulative occupational exposure.

Chain-of-command and rapid response activation are used when a patient deteriorates; early escalation improves outcomes.

Fall and syncope precautions include bed in low position, call light within reach, and assistance with ambulation.

Scope of practice defines which tasks the monitor technician or nurse may perform; interpretation of arrhythmias requires training and competency validation.

Incident reporting systems capture near misses and adverse events to support quality improvement without blame.

Handoff communication using structured formats (SBAR) reduces omission of critical rhythm and device information.