Your FREE CCT Flashcards 2026 – 100+ Cards

Clean and dry the skin, remove hair where it blocks an electrode, wipe off oils, and lightly abrade so the gel makes firm contact.

Confirm identity with at least two identifiers (full name + date of birth) against the order and wristband — never the room number.

Explaining the procedure, its purpose, and any risks so the patient understands and agrees before the test begins.

Checking the patient's medications before a study because drugs (e.g., beta-blockers, digoxin) can alter heart rate and rhythm.

Checking for an allergic reaction to electrode adhesive before applying long-term (Holter) monitoring electrodes.

The CCT acquires and recognizes cardiographic tracings but does not diagnose or treat; recognizing and escalating a dangerous rhythm is in scope.

The Health Insurance Portability and Accountability Act — federal law protecting patients' protected health information (PHI).

Treat every patient's blood and body fluids as potentially infectious: hand hygiene, gloves, and cleaning equipment between patients.

An electrode is a sensor on the skin; a lead is a calculated electrical view of the heart. A 12-lead ECG uses only 10 electrodes.

The standard resting ECG: 10 electrodes (4 limb + 6 precordial) produce 12 views of the heart's electrical activity.

The six chest leads V1–V6 that view the heart in the horizontal plane.

4th intercostal space at the right sternal border.

4th intercostal space at the left sternal border.

5th intercostal space at the left midclavicular line. V3 sits midway between V2 and V4.

Left midaxillary line, level with V4 and V5.

The imaginary inverted triangle formed by the right-arm, left-arm, and left-leg electrodes that defines limb leads I, II, and III.

White = right arm, black = left arm, green = right leg (ground), red = left leg. 'White on right; smoke over fire.'

A reference electrode that reduces interference; it does not form one of the recorded leads.

Calibrating the ECG so a 1-mV signal deflects exactly 10 mm and the paper runs at 25 mm/s, making tracings comparable.

25 mm/s — so 1 small box = 0.04 s and 1 large box = 0.20 s.

1 small box = 0.04 s; 1 large box (5 small boxes) = 0.20 s at 25 mm/s.

A slow up-and-down drift of the tracing from movement, breathing, or loose/dried electrodes. Fix: re-prep skin, replace electrodes.

Fuzzy, erratic spikes from shivering, tension, or a Parkinsonian tremor. Fix: warm and relax the patient, reposition the limbs.

Uniform thick fuzz over the trace from nearby electrical equipment or crossed/frayed lead wires. Fix: unplug devices, uncross leads, check grounding.

A drop in heart rate and blood pressure (pallor, sweating, faintness); lay the patient flat and elevate the legs, monitor vitals.

Small QRS complexes in all leads (gain too low, obesity, effusion, or COPD); first verify standardization and increase the gain.

Setting the gain to 5 mm/mV (instead of 10 mm/mV) when complexes are too tall to fit the paper.

Swapped arm electrodes that produce an inverted P-QRS-T in lead I — recheck placement before re-recording.

The rectangular standardization pulse printed on the strip confirming 1 mV = 10 mm of deflection.

V4 mirrored to the RIGHT 5th intercostal space, midclavicular line — used to detect right-ventricular infarction in inferior MI.

Leads placed around the left posterior chest (posterior axillary, midscapular, paraspinal), level with V6, to detect posterior MI.

A standard 12-lead plus extra leads (commonly V4R, V8, V9) to better see the right ventricle and posterior wall.

The first deflection — atrial depolarization (the atria contracting). Upright in lead II in normal sinus rhythm.

Ventricular depolarization; tall and narrow, normally < 0.12 s. A wide QRS suggests a ventricular origin or bundle branch block.

Ventricular repolarization (the ventricles recovering). Atrial repolarization is hidden inside the QRS.

Start of the P wave to start of the QRS; normal 0.12–0.20 s. Reflects AV conduction time.

Start of the QRS to end of the T wave; rate-dependent. A prolonged QT raises the risk of torsades de pointes.

The flat line between the QRS and the T wave. Elevation suggests injury/MI; depression suggests ischemia.

Less than 0.12 s (under 3 small boxes). Widening points to a ventricular origin or a bundle branch block.

The net/average direction of the heart's depolarization in the frontal plane, estimated mainly from leads I and aVF.

For a regular rhythm: rate = 300 ÷ number of large boxes between two R waves (300, 150, 100, 75, 60, 50).

For a regular rhythm (most precise): rate = 1500 ÷ number of small boxes between two R waves.

For an irregular rhythm: count the QRS complexes in a 6-second strip and multiply by 10.

Elevation ≥ 1 mm in two contiguous leads (without Q waves) suggests acute myocardial infarction (STEMI) — escalate.

A broad, dome-shaped ST elevation merging with the T wave — a marker of acute, extensive STEMI.

A slurred upstroke of the QRS with a short PR interval — the hallmark of Wolff-Parkinson-White (WPW) pre-excitation.

A widened, M-shaped P wave (P mitrale) that suggests left atrial enlargement.

A small deflection after the T wave; prominent U waves suggest hypokalemia, and an inverted U wave can indicate ischemia.

Tall, tented, symmetric T waves — a classic early ECG sign of hyperkalemia.

A wide QRS (≥ 0.12 s) from delayed conduction down a bundle branch; RBBB shows 'rabbit ears' (rSR') in V1.

Pre-excitation via an accessory pathway: a short PR interval and a delta wave on the QRS upstroke.

Tall, peaked T waves first, then a widening QRS, a flattening P wave, and eventually a sine-wave pattern.

Flattened T waves, ST depression, and prominent U waves.

Diffuse (widespread) ST-segment elevation with PR-segment depression across many leads.

A wide/deep initial negative QRS deflection indicating prior (old) myocardial infarction.

A flipped (negative) T wave that can indicate myocardial ischemia or strain.

Leads that view the same region of the heart (e.g., II, III, aVF = inferior); changes in two contiguous leads localize an MI.

Changes in V1–V4 localize an anterior (LAD-territory) myocardial infarction.

Changes in leads II, III, and aVF localize an inferior myocardial infarction.

Bipolar leads from Einthoven's triangle: I = LA−RA, II = LL−RA, III = LL−LA.

Unipolar limb leads viewing the heart from the right shoulder (aVR), left shoulder (aVL), and feet (aVF).

An exercise (or pharmacologic) ECG that records the heart's response to increasing workload to detect ischemia.

The standard treadmill protocol; speed and grade increase every 3 minutes through progressive stages.

A unit of resting oxygen consumption (~3.5 mL O₂/kg/min) used to express exercise workload during a stress test.

Predicted maximum HR = 220 − age; a common exercise endpoint is ~85% of that maximum.

Heart rate × systolic blood pressure — an index of myocardial oxygen demand during exercise.

A fall in systolic BP below baseline during exercise — an abnormal, concerning sign that warrants stopping the test.

Stop now for: ST elevation, a BP drop > 10 mmHg with ischemia, severe angina, sustained VT, poor perfusion, or patient request.

Uses a drug (e.g., adenosine, dobutamine) to stress the heart when a patient cannot exercise adequately.

Emergency equipment (defibrillator, oxygen, medications) that must be available and ready during stress testing.

ST-segment depression that appears with exercise and resolves with rest, suggesting demand ischemia (a positive stress test).

Monitoring after exercise stops; ischemic ST changes and arrhythmias often appear during recovery, so monitoring continues.

A portable ECG worn continuously for 24–48 hours (or longer) to catch intermittent arrhythmias during daily activity.

A monitor worn for weeks to years that records the rhythm around symptomatic events; the patient activates it (or it auto-triggers).

Continuous wireless ECG monitoring of an admitted patient, displayed at a central station for real-time review.

The log the patient keeps of symptoms and activities so events can be correlated with the recorded tracing.

The sinoatrial node — the heart's natural pacemaker in the right atrium; fires 60–100/min and starts each normal beat (the P wave).

The atrioventricular node; delays the impulse ~0.1 s so the atria empty before the ventricles contract. Backup rate 40–60/min.

Conduction fibers carrying the impulse from the AV node into the interventricular septum, where it splits into the bundle branches.

Terminal fibers that spread the impulse rapidly through the ventricular muscle, producing the QRS complex. Backup rate 20–40/min.

Regular, 60–100/min, with one upright P wave before every QRS and normal intervals.

A sinus rhythm at a rate slower than 60/min.

A sinus rhythm at a rate faster than 100/min.

An early beat from an ectopic atrial focus with an abnormal P wave; usually benign.

Organized 'sawtooth' flutter (F) waves at an atrial rate ~250–350/min, often with a regular ventricular response.

An 'irregularly irregular' rhythm with no true P waves — only a chaotic baseline — because the atria quiver instead of contracting.

A fast, narrow-complex supraventricular tachycardia with an abrupt onset and termination.

A rhythm from the AV junction; the P wave is inverted, hidden, or after the QRS, with a narrow QRS at ~40–60/min.

An early, wide, bizarre QRS with no preceding P wave. Frequent or multifocal PVCs are more concerning.

A pattern of grouped beating in which every other beat is a PVC (normal beat–PVC, repeating).

Three or more wide-complex ventricular beats in a row at a fast rate — a life-threatening emergency to escalate at once.

A run of VT lasting < 30 seconds that self-terminates; raises the risk of sustained VT and sudden cardiac death.

A chaotic, quivering baseline with no organized QRS — a shockable, life-threatening rhythm requiring CPR.

A polymorphic VT with QRS complexes that twist around the baseline; associated with a prolonged QT interval.

A flat line with no electrical activity — cardiac standstill. Treated with CPR, not a shock.

A consistently prolonged PR interval (> 0.20 s) with every P wave conducted; usually benign.

The PR interval progressively lengthens until a QRS is dropped, then the cycle repeats.

Intermittent dropped QRS complexes with a constant PR interval; high risk of progressing to complete block.

Complete dissociation — the P waves and QRS complexes march independently with no relationship.

An SVT conducted with a wide QRS that can mimic VT; when in doubt, treat a wide-complex tachycardia as VT.

A normal variant in which the rate speeds up with inspiration and slows with expiration; P waves and intervals are normal.

A slow (20–40/min), wide-complex escape rhythm driven by the ventricles when higher pacemakers fail.

A fast, narrow-complex rhythm originating at or above the AV node (atria or junction).

A PVC that lands on the preceding T wave; it can trigger VT or VF.

Two PVCs in a row (couplet) or three in a row (triplet, a short run of VT).

PVCs of differing shapes arising from more than one ventricular site — more concerning than uniform PVCs.

The fully compensatory pause that follows a PVC, so the next normal beat lands on time.

Defibrillation is an unsynchronized shock for VF/pulseless VT; cardioversion is a synchronized shock for organized rhythms.

Before treating a 'lethal' rhythm, check the patient and look for artifact (movement, loose lead) — a flat line may be a detached electrode.

Bradycardia < 60/min, normal 60–100/min, tachycardia > 100/min.