Free CCT Exam Flashcards

Rate 60-100 bpm, regular rhythm, an upright P wave before every QRS in lead II, a constant PR interval (0.12-0.20 s), and a narrow QRS (<0.12 s). The impulse originates in the SA node.

SA node fires 60-100 bpm (primary pacemaker). The AV junction escapes at 40-60 bpm, and the ventricular/Purkinje system escapes at 20-40 bpm. Lower sites take over only when higher pacemakers fail.

A sinus rhythm with all normal features except a rate below 60 bpm. Can be normal in athletes or during sleep; pathologic causes include increased vagal tone, beta-blockers, and inferior MI.

A sinus rhythm with a rate above 100 bpm (typically 100-150). P waves precede each QRS but may blend into the preceding T wave. Usually a response to fever, pain, exertion, hypovolemia, or anxiety - not a primary arrhythmia.

Divide 300 by the number of large (5 mm) boxes between two consecutive R waves. Memorize the sequence 300-150-100-75-60-50. Best for regular rhythms.

1500 method: divide 1500 by the number of small (1 mm) boxes between R waves - precise for regular rhythms. 6-second method: count QRS complexes in a 6-second strip and multiply by 10 - best for irregular rhythms.

Measured from the start of the P wave to the start of the QRS; normal is 0.12-0.20 s (3-5 small boxes). It represents atrial depolarization plus the AV node delay. A PR >0.20 s indicates first-degree AV block.

Irregularly irregular rhythm with no discernible P waves - only chaotic fibrillatory (f) waves. Atrial rate is 350-600 with a variable ventricular response. Main risk: atrial thrombus formation leading to embolic stroke.

Regular sawtooth flutter (F) waves at an atrial rate of 250-350 bpm (classically ~300). The AV node conducts in ratios (often 2:1), so a 300 atrial rate commonly gives a ventricular rate near 150.

An early beat from an ectopic atrial focus with an abnormally shaped P wave and a normal, narrow QRS. It is usually followed by a non-compensatory (incomplete) pause because it resets the SA node.

An early, wide (>0.12 s), bizarre QRS with no preceding P wave and a T wave in the opposite direction. It is typically followed by a full compensatory pause. Three or more in a row is ventricular tachycardia.

A regular narrow-complex tachycardia at 150-250 bpm with sudden onset and termination. P waves are often buried in the preceding T wave or not visible because the rate is so fast.

Originates in the AV junction at 40-60 bpm. P waves are inverted (retrograde) and may appear just before, during (hidden), or after the narrow QRS. Accelerated junctional is 60-100; junctional tachycardia is >100.

Every atrial impulse conducts, but the PR interval is prolonged beyond 0.20 s and stays constant beat to beat. No QRS complexes are dropped. It is generally benign.

The PR interval lengthens progressively over successive beats until one P wave fails to conduct and a QRS is dropped, producing grouped beating. The cycle then repeats. Usually a benign AV-nodal block.

The PR interval stays constant, then a P wave suddenly fails to conduct and a QRS is dropped without any PR change. More dangerous than Mobitz I because it can progress to complete heart block; often needs a pacemaker.

Complete AV dissociation: atria and ventricles beat independently, so P waves and QRS complexes have no relationship and the atrial rate exceeds the ventricular rate. A junctional (40-60) or ventricular (20-40) escape rhythm sustains output.

Three or more consecutive PVCs; a regular wide-complex (>0.12 s) tachycardia at 100-250 bpm with no normal P waves. May be pulseless. Sustained VT is a medical emergency that can deteriorate into ventricular fibrillation.

Chaotic, disorganized electrical activity with no identifiable P waves, QRS complexes, or T waves and no effective cardiac output. It is a lethal rhythm requiring immediate defibrillation and CPR.

Absence of all ventricular electrical activity - a flat line. Confirm in two or more leads to rule out fine VF or a disconnected lead. Asystole is NOT shockable; treatment is high-quality CPR and epinephrine.

Use the net QRS in leads I and aVF. Both positive = normal axis. Lead I positive, aVF negative = possible left axis deviation (check lead II). Lead I negative, aVF positive = right axis deviation. Both negative = extreme (northwest) axis.

A mean QRS axis between -30 and -90 degrees. Lead I is positive and lead II is negative. Common causes: left anterior fascicular block, left ventricular hypertrophy, inferior MI, and some conduction abnormalities.

A mean QRS axis between +90 and +180 degrees. Lead I is negative and aVF is positive. Common causes: right ventricular hypertrophy, left posterior fascicular block, acute pulmonary embolism, and lateral MI.

Ischemia = ST-segment depression and/or T-wave inversion (reversible). Injury = ST-segment elevation (acute, ongoing). Infarction/necrosis = pathologic Q waves (established tissue death). They can appear together as an MI evolves.

LVH is suggested when the S wave in V1 plus the R wave in V5 or V6 is 35 mm (3.5 mV) or greater. An R wave in aVL of 11 mm or more is another supportive sign. Often accompanied by ST-T strain.

QRS 0.12 s or wider with an rSR' ('rabbit ears') pattern in V1-V2 and a wide, slurred S wave in leads I and V6. The right ventricle depolarizes late.

QRS 0.12 s or wider with a broad, notched (monophasic) R wave in leads I, aVL, V5-V6, a deep S in V1, and absent septal Q waves. New LBBB with ischemic symptoms is treated as a possible acute MI.

ST elevation in leads II, III, and aVF indicates an inferior-wall MI, most often from occlusion of the right coronary artery (RCA). Watch for accompanying bradycardia and heart block.

Septal changes appear in V1-V2 and anterior changes in V3-V4; together V1-V4 point to an anteroseptal MI from the left anterior descending (LAD) artery. Large anterior MIs carry a high risk of heart failure.

ST changes in leads I, aVL, V5, and V6 indicate a lateral-wall MI, usually from the left circumflex (LCx) artery. V5-V6 are the low-lateral leads; I and aVL are the high-lateral leads.

There are no standard posterior leads, so look for reciprocal changes in V1-V2: tall broad R waves with ST-segment depression (a mirror image of elevation). Confirm with posterior leads V7-V9 showing ST elevation; usually RCA or LCx.

V1: 4th ICS right sternal border. V2: 4th ICS left sternal border. V3: midway between V2 and V4. V4: 5th ICS midclavicular line. V5: 5th ICS anterior axillary line (level with V4). V6: 5th ICS midaxillary line.

Place electrodes on the four limbs: RA = white, LA = black, LL = red, RL = green (ground). Mnemonics: 'white on right,' 'smoke (black) over fire (red)' on the left, 'snow over grass' on the right.

Standard speed is 25 mm/s. One small (1 mm) box = 0.04 s and one large (5 mm) box = 0.20 s horizontally. Standard calibration is 10 mm = 1 mV, verified by a rectangular standardization mark before recording.

The QRS represents ventricular depolarization and is normally under 0.12 s (typically 0.06-0.10 s). A QRS of 0.12 s or wider suggests a bundle branch block, a ventricular rhythm, or an aberrantly conducted beat.

The QT spans ventricular depolarization and repolarization and shortens as heart rate rises, so it is rate-corrected (QTc, e.g., Bazett). A prolonged QTc (>0.44 s in men, >0.46 s in women) raises the risk of torsades de pointes.

For a suspected posterior MI, add posterior leads V7-V9 across the back. For suspected right-ventricular involvement (often with inferior MI), add right-sided leads, especially V4R, by mirroring V4 to the right chest.

Wandering baseline = slow drift from movement, respiration, or loose/dried electrodes. Somatic (muscle) tremor = fuzzy, irregular baseline from muscle activity or shivering. AC (60-Hz) interference = uniform fine spikes from nearby electrical equipment or poor grounding.

Before any ECG, confirm the patient's identity with two identifiers (such as full name and date of birth), verify the physician's order, and enter demographics accurately so the tracing is matched to the correct record.

Clean the skin, let it dry, and lightly abrade the outer layer to lower impedance. Clip (do not shave) excess hair, and remove lotion, oils, or sweat. Poor prep is a leading cause of artifact and loose leads.

The angle of Louis is the ridge where the manubrium meets the sternal body, level with the 2nd costal cartilage/2nd rib. Find the 2nd intercostal space there, then count down to the 4th ICS to place V1 and V2 accurately.

Before acquisition, confirm the machine is set to 25 mm/s and 10 mm/mV, verify the standardization mark, and check that all lead wires are securely attached. This prevents distorted amplitudes and missing leads.

Switching the right- and left-arm electrodes inverts lead I (negative P wave and QRS in I) and swaps aVR/aVL, which can mimic dextrocardia. Recognizing this lets the technician correct placement rather than misreport pathology.

The diagnostic target is 85% of the age-predicted maximum: Target HR = 0.85 x (220 - age). For a 50-year-old, max HR = 170 and target = ~145 bpm. Reaching 85% indicates an adequate diagnostic stress.

The standard Bruce treadmill protocol uses 3-minute stages that increase BOTH speed and grade at each stage (Stage 1: 1.7 mph / 10%). It is the most common exercise stress protocol for reasonably fit patients.

Modified Bruce adds two easier warm-up stages (1.7 mph at 0%, then 5%) before standard Bruce. The Naughton protocol keeps a low constant speed and raises the grade in small steps (~1 MET each) - both suit deconditioned or cardiac patients.

Stop the test for ST elevation >1 mm in leads without Q waves, a drop in systolic BP of 10 mmHg or more with ischemia, moderate-to-severe angina, sustained ventricular tachycardia, CNS symptoms (dizziness, near-syncope), or the patient's request.

For patients who cannot exercise, dobutamine raises myocardial oxygen demand (like exercise), while vasodilators - adenosine, regadenoson, or dipyridamole - dilate coronary arteries to reveal perfusion differences during nuclear imaging.

A Holter records the ECG continuously for 24-48 hours (extended devices last up to ~14 days). The patient keeps a symptom diary so recorded events can be correlated with activity and symptoms.

A post-event recorder is activated by the patient when symptoms occur. A loop recorder continuously overwrites a memory loop and, when triggered, saves the ECG from just before and after the event - capturing brief, infrequent arrhythmias a Holter may miss.