Free CRAT Exam Flashcards

The SA node at the SVC-right atrium junction is the heart's primary pacemaker with an intrinsic rate of 60-100 bpm. It normally suppresses slower secondary pacemakers (AV junction 40-60, Purkinje 20-40) by firing first, a mechanism called overdrive suppression.

When the SA node fails or is blocked, the AV junction (AV node and proximal His) takes over at 40-60 bpm as a junctional escape rhythm. The slower rate and loss of atrial kick often cause symptoms, so CRAT escalation is warranted.

The AV node introduces roughly 0.10 seconds of physiologic delay (most of the PR interval) so the atria finish contracting before ventricular systole begins. This atrial kick adds about 20-30% of ventricular filling and lets the AV node filter rapid atrial rhythms before they reach the ventricles.

The absolute refractory period (phase 0 through early phase 3) blocks any stimulus, protecting against re-entrant arrhythmias. The relative refractory period (late phase 3) allows a strong premature stimulus to fire abnormally, which is why a PVC landing on the T-wave upslope (R-on-T) can trigger torsades or VFib.

Sympathetic norepinephrine on beta-1 receptors raises SA rate and speeds AV conduction (positive chronotropy and dromotropy). Parasympathetic acetylcholine via the vagus nerve slows SA firing and AV nodal conduction, which is the basis of vagal maneuvers (Valsalva, carotid sinus massage) for SVT termination.

At the standard paper speed of 25 mm/s, one 1-mm small box equals 0.04 seconds (40 ms), and five small boxes form one 5-mm large box equal to 0.20 seconds. These two values anchor every interval, rate, and duration measurement on a rhythm strip.

Standard calibration is 10 mm per millivolt, so a 10-mm calibration pulse equals 1 mV. Verifying the calibration box before interpretation prevents misreading a low-voltage QRS as small or exaggerating voltage as LVH; half-standard (5 mm/mV) is used when QRS is too tall to fit the strip.

Count QRS complexes in a 6-second strip (30 large boxes at 25 mm/s) and multiply by 10 to estimate ventricular rate per minute. It is the preferred method for irregular rhythms such as atrial fibrillation, because beat-to-beat methods give unreliable results when R-R intervals vary.

For a regular rhythm, divide 300 by the number of large boxes between two consecutive R waves: one large box = 300 bpm, two = 150, three = 100, four = 75, five = 60. Fast and accurate for regular rhythms, but unreliable whenever R-R intervals are irregular.

The three bipolar limb leads I (RA to LA), II (RA to LL), and III (LA to LL) form Einthoven's triangle in the frontal plane. Lead II runs along the heart's normal depolarization axis, which is why it shows the largest upright P waves and is the default continuous monitoring lead.

Lead II is most parallel to the heart's normal axis of depolarization, so it shows tall upright P waves, a clear PR interval, and a distinct QRS, ideal for rhythm analysis. Most bedside monitors default to lead II for these reasons; an inverted P in aVR (positive P in II) also confirms correct limb-lead placement.

On a 12-lead, V1 sits at the fourth intercostal space just right of the sternum, V2 mirrors it on the left, V4 at the fifth ICS midclavicular, V5 anterior axillary, V6 midaxillary. On 5-lead telemetry the mnemonic 'White on Right' places white at the right upper chest (RA), black left upper (LA), red left lower (LL), green right lower (RL), brown at V1.

NSR requires a rate of 60-100 bpm, a regular R-R interval (variation typically <0.12 s), an upright P wave before every QRS in lead II, a constant PR interval of 0.12-0.20 s, and a 1:1 P-to-QRS ratio. Missing any one of these means the rhythm is not NSR.

A sinus rhythm (upright P, normal PR, 1:1 ratio) with a rate below 60 bpm. Common in athletes and during sleep, but symptomatic bradycardia with hypotension, dizziness, or ischemia is unstable per ACLS and requires immediate RN notification; treatment (atropine, pacing) is outside CRAT scope.

A sinus rhythm at a rate above 100 bpm with upright P waves preceding each QRS. It is typically a response to a trigger (pain, fever, hypovolemia, anxiety, PE, sepsis, drugs), so CRAT escalation centers on verifying the rhythm is genuine and notifying the RN so the underlying cause can be addressed.

Heart rate speeds up on inspiration and slows on expiration, with constant P-wave morphology and PR interval. It is a normal vagal-tone variation most common in young, healthy individuals, distinct from wandering atrial pacemaker, which shows at least three different P morphologies.

In sinus arrest the SA node fails to fire at all, producing a pause that is NOT a multiple of the prior P-P interval. In sinus exit block the SA node fires but the impulse does not exit into atrial tissue, so the pause IS approximately a multiple of the underlying P-P interval. Pauses of 3 seconds or longer in awake patients warrant clinical notification.

An early beat from an ectopic atrial focus producing an abnormally shaped P wave followed by a narrow QRS (because conduction below the AV node is normal). The pause after a PAC is usually noncompensatory because the PAC resets the SA node, unlike a PVC, which leaves the SA node undisturbed and produces a full compensatory pause.

A macro-reentrant atrial circuit (typically counterclockwise around the tricuspid annulus) generates sawtooth F waves at 250-350/min, classically about 300/min in typical flutter. The ventricular rate depends on AV conduction: 2:1 about 150, 3:1 about 100, 4:1 about 75 bpm.

Chaotic atrial activity with no discrete P waves (replaced by fibrillatory f waves) and an irregularly irregular R-R pattern, because the AV node conducts impulses unpredictably. AFib is the most common sustained arrhythmia and the leading cardiac cause of stroke.

AFib with a ventricular rate under 100 bpm at rest is considered controlled; rates above 100-110 bpm qualify as RVR. Sustained RVR shortens diastolic filling time, raises myocardial demand, and can cause ischemia, hypotension, or decompensated heart failure, so the CRAT escalates promptly.

Both rhythms show at least three distinct P-wave morphologies and varying PR intervals because the atrial pacemaker shifts between sites. The sole distinction is rate: MAT >100 bpm, WAP <100 bpm. MAT is classically associated with severe COPD and hypoxia; WAP is often a benign vagal variation.

Loss of organized atrial contraction lets blood stagnate, especially in the left atrial appendage, where thrombi can form and embolize to the brain. Anticoagulation per CHA2DS2-VASc score (DOACs or warfarin) is the cornerstone of stroke prevention; aspirin alone is no longer first-line for moderate-to-high scores.

A narrow-QRS rhythm at 40-60 bpm with no preceding upright P wave; retrograde atrial activation may produce an inverted P wave immediately before, buried in, or just after the QRS in inferior leads. It appears when the SA node fails or after AV-nodal-blocking drugs, an escape rhythm is a protective backup, not a primary arrhythmia.

Both originate from the AV junction with narrow QRS and absent or inverted P waves. They are separated by rate: accelerated junctional 60-100 bpm, junctional tachycardia above 100 bpm. Junctional tachycardia is frequently associated with digoxin toxicity, ischemia, or the post-cardiac-surgery setting.

A regular junctional rhythm above 100 bpm with a narrow QRS and no preceding upright P, arising in a patient on digoxin, is a classic digoxin-toxicity presentation. Other digoxin-toxic rhythms include atrial tachycardia with block and bidirectional VT. The CRAT recognizes the pattern and notifies the RN; drug-level and antidote decisions belong to licensed providers.

An early, wide (>=0.12 s) QRS with no preceding P wave and a T wave discordant with the QRS. Unifocal PVCs share one morphology; multifocal PVCs show multiple shapes, signaling several irritable ventricular sites and higher risk of degenerating into VT/VF. Because the ectopic beat does not reset the SA node, a full compensatory pause follows, distinguishing PVCs from PACs.

A PVC that lands on the preceding T wave (the relative refractory period) can trigger polymorphic VT (torsades) or ventricular fibrillation. Recognizing R-on-T warrants immediate RN notification, because deterioration can be sudden and unpredictable.

Bigeminy: every other beat is a PVC. Trigeminy: every third beat is a PVC. Quadrigeminy: every fourth. Frequent patterns can lower effective cardiac output because PVCs eject less blood than sinus beats, but the immediate danger is highest when R-on-T, multifocal morphology, or runs appear.

Nonsustained VT is three or more consecutive ventricular beats at >100 bpm lasting under 30 seconds with spontaneous termination. Sustained VT lasts 30 seconds or longer, or causes hemodynamic compromise requiring termination. Both require documentation and RN notification; sustained VT is immediately life-threatening.

Monomorphic VT has uniform wide QRS complexes beat to beat from a single reentrant circuit or focus. Polymorphic VT shows changing QRS morphology from beat to beat; when it arises in a long-QT setting and appears to twist around the baseline, it is torsades de pointes, which requires IV magnesium and correction of electrolyte and drug causes.

A polymorphic VT in the setting of prolonged QT (QTc >460 ms women, >450 ms men; >500 ms markedly raises risk), where QRS amplitude appears to twist around the isoelectric baseline. Common triggers include hypokalemia, hypomagnesemia, and QT-prolonging drugs (haloperidol, methadone, fluoroquinolones, ondansetron, sotalol, dofetilide). IV magnesium is first-line acute treatment.

Same wide-QRS, no-P morphology separated by rate: idioventricular 20-40 bpm (a slow escape rhythm), accelerated idioventricular (AIVR) 40-100 bpm (often a reperfusion rhythm after MI thrombolytics or PCI), and VT above 100 bpm. Crossing 100 bpm crosses the clinical threshold from a tolerated escape into sustained VT.

Chaotic, irregular, undulating waves of varying amplitude with no identifiable P, QRS, or T waves, with a patient who is unresponsive. The CRAT must immediately summon the bedside team and activate the code or rapid-response process; defibrillation within minutes determines survival. Never delay escalation to investigate gain or leads when the clinical picture matches VF.

A PR interval greater than 0.20 seconds (more than five small boxes) with every P wave conducted to a QRS (1:1 P:QRS ratio) and a constant PR from beat to beat. Generally benign but may signal AV-nodal disease, drug effect (beta-blockers, calcium channel blockers, digoxin), or inferior MI.

Progressive PR-interval lengthening until a QRS is dropped, then the cycle resets. The block is at the AV node, the QRS is usually narrow, and it rarely progresses to complete heart block. Often seen with high vagal tone, inferior MI, or AV-nodal-blocking drugs.

A FIXED PR interval with sudden dropped QRS complexes (no progressive prolongation). The block is usually below the AV node in the His-Purkinje system, so the QRS is often wide. Mobitz II is more dangerous than Mobitz I, can progress to complete heart block, and often requires permanent pacing, so the CRAT must notify the RN immediately.

Atrial P waves and ventricular QRS complexes are completely dissociated: P waves march at one rate, QRS at a slower escape rate, with no fixed relationship. A wide-QRS escape at 20-40 bpm implies a ventricular focus; a narrow-QRS escape at 40-60 implies a junctional focus. Symptomatic complete heart block is unstable and requires emergent transcutaneous pacing.

Symptomatic high-grade AV block with a slow escape rate (e.g., 28 bpm) and hypotension, altered mentation, ischemia, or heart failure is unstable per ACLS. The CRAT recognizes the rhythm and immediately notifies the bedside RN so transcutaneous pacing, atropine, and vasopressor support can be started without delay.

A sharp pacing spike followed by a P wave, then a normal narrow QRS, indicating a single-chamber atrial pacemaker. The QRS stays narrow because the impulse travels through the normal His-Purkinje system once the atrium is captured.

A sharp pacing spike followed by a wide QRS (>=0.12 s) with no preceding P wave, indicating a single-chamber ventricular pacemaker. The wide QRS reflects nonphysiologic activation from a right-ventricular-apex lead; the CRAT documents the paced rhythm and any change in capture or sensing.

Two pacing spikes per cycle: the first elicits a P wave (atrial pacing), the second a wide QRS (ventricular pacing). This sequence restores AV synchrony and is used when the patient has both sinus node dysfunction and AV block. Biventricular (CRT) pacing is a special case used in heart failure with reduced EF and wide LBBB QRS to resynchronize the ventricles.

A pacing spike is delivered but no depolarization follows: no P after an atrial spike, or no QRS after a ventricular spike. Causes include lead dislodgement or fracture, fibrosis at the lead tip, electrolyte disturbance, MI, or battery depletion. The CRAT documents the strip and notifies the RN.

The device does not detect the patient's own intrinsic P or QRS, so it fires inappropriately at its programmed rate; spikes may fall inside or just after an intrinsic complex. This can produce an R-on-T PVC if a ventricular spike lands on a T wave. Distinguish it from failure to capture, where the spike fires but no QRS follows.

New ST elevation at the J point in two or more contiguous leads: >=1 mm in limb leads, and in V2-V3 >=2 mm in men 40 and older, >=2.5 mm in men under 40, and >=1.5 mm in women. Recognition prompts immediate CRAT notification and activation of the door-to-balloon protocol, since time-sensitive reperfusion is the goal.

ST elevation in leads II, III, and aVF localizes injury to the inferior wall, usually supplied by the right coronary artery. Inferior MIs commonly cause bradyarrhythmias and AV blocks and may involve the right ventricle (use right-sided leads, V4R most useful). Reciprocal ST depression in I and aVL supports the diagnosis.

Anterior MI: ST elevation in V1-V4 from LAD occlusion, high risk for cardiogenic shock and life-threatening arrhythmias. Posterior MI does not have direct leads on the standard 12-lead, so it appears as RECIPROCAL ST depression with tall R waves and upright T waves in V1-V3; posterior leads V7-V9 show direct ST elevation.

The CRAT scope is rhythm recognition, strip documentation, and timely communication to the RN, provider, or rapid-response team. It does NOT include medication administration, cardioversion, defibrillation, pacing adjustment, or any bedside procedure. Recognizing this boundary protects patients from delayed escalation and protects the CRAT from practicing outside licensure.

The Joint Commission NPSG on alarm management emphasizes customizing alarm thresholds to each patient's baseline and clinical condition, reducing nuisance alarms while preserving sensitivity for true events. Disabling alarms, using one-size-fits-all factory defaults, or silently ignoring alerts are unsafe and violate safety policy; the correct response is to verify the patient, check lead integrity, and silence per facility policy.

Rhythm strips, monitor displays, and any patient-identifiable ECG data are protected health information under HIPAA. Share them only with members of the care team on a need-to-know basis, avoid discussing rhythms in public areas, store printed strips in the patient record rather than at the monitoring station, and never post or transmit patient monitor data to personal devices or nonsecure channels.