CRAT cheat sheet

Rate: count QRS complexes in a 10-second strip and multiply by 6; for regular rhythms use 300 divided by the number of large boxes between R waves.

Regularity: march out R-R intervals with calipers or paper; variation greater than 0.12 s (3 small boxes) between consecutive R-R intervals indicates an irregular rhythm.

P wave axis and morphology: sinus P waves are upright in leads I, II, and aVF and negative in aVR; a negative P in II suggests a low atrial or junctional origin.

PR interval: normal 0.12-0.20 s (3-5 small boxes); shorter suggests pre-excitation or junctional rhythm, longer suggests first-degree AV block.

QRS duration: narrow is less than 0.12 s; wide is 0.12 s or more and implies ventricular origin, aberrancy, or a paced rhythm.

AV block ladder: first-degree = prolonged PR with every P conducted; second-degree type I (Wenckebach) = progressive PR lengthening until a dropped beat; type II = constant PR with sudden dropped QRS; third-degree = no consistent PR relationship and P waves march through independently.

Narrow-complex tachycardia is regular in sinus tachycardia, SVT, and atrial flutter with fixed block; it is irregular in atrial fibrillation, multifocal atrial tachycardia, and flutter with variable block.

Wide-complex tachycardia is ventricular tachycardia until proven otherwise, especially with AV dissociation, fusion beats, capture beats, extreme axis, or a concordant precordial pattern.

Sinus rhythm criteria: rate 60-100 bpm, regular, upright P in lead II before every QRS, PR 0.12-0.20 s, and QRS under 0.12 s.

Standard calibration is 25 mm/s and 10 mm/mV; one small box = 0.04 s and 0.1 mV, one large box = 0.20 s and 0.5 mV.

Lead placement: V1 at the 4th intercostal space right sternal border, V2 at the 4th ICS left sternal border, V4 at the 5th ICS midclavicular line, with V3 midway between V2 and V4; limb leads are RA, LA, LL, and RL as the neutral electrode.

ST elevation is measured at the J point and compared with the TP segment; it is significant when 1 mm or more in two contiguous limb leads or 2 mm or more in two contiguous precordial leads (1.5 mm in women for V2-V3).

Contiguous lead groups: inferior II, III, aVF; lateral I, aVL, V5, V6; anteroseptal V1-V4; anterior V3-V4; extensive anterior V1-V6, I, aVL.

Reciprocal ST depression in inferior leads points to a high lateral or anterior infarction, while reciprocal change in aVL or I points to an inferior infarction.

QTc: Bazett formula QTc = QT divided by the square root of the R-R interval in seconds; normal is under 0.44 s in men and under 0.46 s in women.

Left ventricular hypertrophy by Sokolow-Lyon: S in V1 plus R in V5 or V6 of 35 mm or more; Cornell criteria use R in aVL plus S in V3 with sex-specific thresholds.

Axis: positive QRS in I and aVF is normal; positive I with negative aVF is left axis; negative I with positive aVF is right axis; both negative is extreme axis.

T wave inversion in two or more contiguous leads with a prolonged QT suggests ischemia; hyperacute tall peaked T waves with a widened QRS suggest hyperkalemia.

Conduction pathway: SA node, atria, AV node (delay of about 0.1 s), bundle of His, right and left bundle branches, Purkinje fibers; intrinsic rates are SA 60-100, AV junction 40-60, and ventricles 20-40 bpm.

Coronary supply: the right coronary artery supplies the SA node in about 60 percent of people and the AV node in about 85-90 percent; the left anterior descending supplies the anterior wall and septum.

Cardiac output = heart rate x stroke volume; normal resting output is about 4-8 L/min, and stroke volume is about 60-100 mL.

Frank-Starling relationship: increased preload stretches myocardial fibers and raises stroke volume up to a physiologic limit, after which further stretch reduces contractility.

The left ventricle has a thicker wall than the right because it pumps against systemic pressures of about 120 mmHg versus pulmonary pressures of about 25 mmHg.

The cardiac cycle: atrial systole contributes roughly 20 percent of ventricular filling; the first heart sound is AV valve closure, and the second is semilunar valve closure.

Parasympathetic vagal tone slows the SA node and AV conduction via muscarinic receptors; sympathetic beta-1 stimulation increases rate, contractility, and conduction velocity.

The pericardium and the right ventricle are most vulnerable to increased intrathoracic pressure and rapid volume shifts, which is why positive pressure ventilation can drop venous return and blood pressure.

Continuous monitoring: apply leads to bone or muscle-light areas, avoid placing electrodes over large muscle masses, and confirm a stable baseline before interpreting rhythm changes.

Artifact differentiation: movement, shivering, and loose electrodes produce irregular baseline wander without a true QRS; verify the rhythm at the patient before treating.

Pulse oximetry is unreliable with poor perfusion, motion, nail polish, or severe anemia; correlate SpO2 with the rhythm and the patient's clinical status.

Defibrillation energy for adult ventricular fibrillation or pulseless ventricular tachycardia is biphasic 120-200 J or monophasic 360 J, with compressions resumed immediately after the shock.

Synchronized cardioversion is used for unstable tachycardias with a pulse; the shock is synchronized to the R wave to avoid delivering energy during the T wave.

Adenosine for stable narrow-complex SVT: 6 mg rapid IV push followed by a saline flush, then 12 mg if needed; the half-life is under 10 seconds.

Atropine for symptomatic bradycardia: 1 mg IV every 3-5 minutes to a maximum of 3 mg; transcutaneous pacing is used when atropine fails or is contraindicated.

High-quality CPR: rate 100-120 compressions per minute, depth at least 5 cm (2 inches) but not more than 6 cm, full recoil, and minimal interruptions under 10 seconds.

Documentation must capture the rhythm strip time, the patient's symptoms, vital signs, and every intervention with its response.