CET NHA Certified EKG Technician - Set 5 - Part 3

Correct Answer: Hyperkalemia from kidney failure

Hyperkalemia progresses on the EKG from tall peaked T waves to prolonged PR, then wide QRS, and eventually a sine wave or asystole. A patient with kidney failure who missed dialysis is at high risk for this pattern. Option a is incorrect because hypokalemia produces flat T waves, prominent U waves, and ST depression rather than tall peaked T waves with wide QRS. The two potassium abnormalities cause opposite EKG patterns. Option b is incorrect because hypercalcemia shortens the QT interval rather than prolonging PR and widening QRS. The calcium effects target QT primarily, not the AV conduction and ventricular widening described here. Option c is incorrect because hypocalcemia prolongs the QT interval primarily through the ST segment rather than producing tall peaked T waves. The hypocalcemia pattern does not match the findings in the scenario.

Correct Answer: Hypokalemia from diuretic loss

Hypokalemia produces flattened or inverted T waves, prominent U waves, ST depression, and increased risk of torsades de pointes. Thiazide diuretics commonly cause potassium loss and produce this classic EKG pattern. Option b is incorrect because hyperkalemia produces tall peaked T waves, prolonged PR, and wide QRS rather than prominent U waves. The two potassium abnormalities produce opposite EKG patterns. Option c is incorrect because hyponatremia primarily affects mental status and seizure risk rather than producing specific EKG patterns. Sodium imbalances do not produce the U-wave pattern described in the scenario. Option d is incorrect because hypercalcemia shortens the QT interval rather than producing U waves with ST depression. Calcium abnormalities target the QT interval, not the T-U wave morphology.

Correct Answer: Hypercalcemia produces shortened QT

Hypercalcemia produces a shortened QT interval as the principal EKG change, and severe cases may show an Osborn or J wave. The shortening reflects calcium's effect on ventricular repolarization in the action potential. Option a is incorrect because hypercalcemia shortens, not prolongs, the QT interval. The directional language is reversed in this option, since the patient's elevated calcium would shorten the interval. Option b is incorrect because hyperkalemia produces peaked T waves, prolonged PR, and wide QRS rather than a shortened QT. The two electrolyte effects target different parts of the cardiac cycle. Option d is incorrect because hyponatremia does not specifically shorten the QT interval. Sodium imbalances affect neurologic status more than they produce specific QT changes.

Correct Answer: Rate control and anticoagulation assessment

Stable atrial fibrillation with rapid ventricular response is typically managed with rate control using beta-blockers or calcium channel blockers, plus anticoagulation assessment based on stroke risk scoring. Cardioversion is reserved for selected cases under clinician decision. Option a is incorrect because immediate synchronized cardioversion is reserved for unstable patients with hemodynamic compromise. A stable patient with adequate blood pressure does not warrant emergency cardioversion as the default. Option b is incorrect because defibrillation is for pulseless ventricular rhythms, not for atrial fibrillation. Defibrillation in stable AFib would be both inappropriate and ineffective for the underlying atrial mechanism. Option c is incorrect because watchful neglect of a rapid AFib leaves the patient at increased risk for stroke and heart failure decompensation. Stable does not mean untreated; it means treatment can be measured rather than emergent.

Correct Answer: Synchronized cardioversion under clinician direction

Unstable atrial fibrillation with rapid ventricular response and signs of poor perfusion is treated with synchronized cardioversion under clinician direction. Synchronization with the R wave avoids the vulnerable T-wave period when shocking the patient. Option a is incorrect because watchful waiting with rate control alone is inadequate for an unstable patient with hypotension and altered mental status. Hemodynamic instability requires more aggressive intervention than rate control offers. Option c is incorrect because defibrillation is unsynchronized and is reserved for pulseless ventricular fibrillation or pulseless VT. Using unsynchronized shocks for AFib could trigger ventricular arrhythmias from the vulnerable period. Option d is incorrect because the asystole protocol applies to flatline arrest, not to atrial fibrillation with a pulse. The two clinical scenarios require very different treatment approaches.

Correct Answer: Idioventricular rhythm consistent with dying heart

An idioventricular rhythm at twenty to forty beats per minute with wide QRS and no P waves represents the ventricular escape pacemaker firing when higher pacemakers fail. In a pulseless patient, this often reflects a dying heart. Option b is incorrect because sinus bradycardia uses the SA node as pacemaker, with upright P waves before every QRS and narrow QRS complexes. The wide QRS and absent P waves rule out sinus origin. Option c is incorrect because junctional rhythm typically produces narrow QRS at forty to sixty beats per minute, not the wide QRS at thirty described. Junctional and ventricular escape rhythms are different in both rate range and QRS width. Option d is incorrect because atrial flutter shows sawtooth atrial waves, which are absent here. The pulseless patient with wide QRS at thirty fits an escape rhythm rather than an atrial arrhythmia.

Correct Answer: Accelerated idioventricular rhythm reperfusion pattern

Accelerated idioventricular rhythm at forty to one hundred beats per minute is a classic post-thrombolysis reperfusion rhythm that is usually transient and well-tolerated. The wide QRS reflects ventricular origin while the rate sits above pure idioventricular escape. Option a is incorrect because sinus tachycardia with bundle block would still show P waves before each QRS. The absence of P waves rules out sinus origin for this rhythm. Option b is incorrect because atrial fibrillation is irregularly irregular without organized P waves. The regular wide-complex rhythm described does not match fibrillation despite the absent P waves. Option d is incorrect because sinus bradycardia uses the SA node with upright P waves before narrow QRS complexes. Wide QRS without P waves rules out sinus origin.

Correct Answer: Normal ventricular pacing with capture

A pacing spike followed by a wide QRS that captures the ventricle represents normal ventricular pacing function. The capture confirms the device fires at the right time and triggers depolarization as intended in the chamber. Option a is incorrect because failure to capture would show a spike without a subsequent depolarization wave. The presence of the wide QRS after the spike confirms successful capture. Option b is incorrect because failure to sense involves the pacemaker firing when it should not, often during the patient's own beats. The scenario describes appropriate timed pacing rather than inappropriate firing. Option c is incorrect because magnet mode activates asynchronous pacing at a fixed rate and is used for device testing. Standard ventricular pacing with capture is the routine function, not the magnet override mode.

Correct Answer: Antiarrhythmic drugs like amiodarone first

Stable ventricular tachycardia with a pulse and adequate perfusion is typically treated first with antiarrhythmic medications such as amiodarone, lidocaine, or procainamide. Expert consultation is often obtained before considering more aggressive interventions like cardioversion. Option b is incorrect because immediate defibrillation is reserved for pulseless VT or VF, not for stable VT with a pulse. Defibrillating a perfusing patient with VT could itself trigger more dangerous rhythms. Option c is incorrect because watchful waiting in sustained VT, even when stable, ignores the risk of deterioration to pulseless VT or VF. Active management is appropriate even when the patient remains conscious. Option d is incorrect because the asystole protocol applies to flatline cardiac arrest rather than to a perfusing rhythm. Applying asystole care to a stable VT patient would be inappropriate and would skip the actual indicated treatment.

Correct Answer: Non-sustained ventricular tachycardia with PVCs

Non-sustained ventricular tachycardia is defined as three or more consecutive PVCs lasting less than thirty seconds. The pattern of multiple PVCs and brief runs of VT in an alert patient matches this definition rather than sustained VT. Option a is incorrect because sustained VT lasts thirty seconds or longer or requires intervention to terminate. Brief runs that self-terminate fall into the non-sustained category instead. Option b is incorrect because atrial fibrillation with aberrancy would be irregularly irregular, while VT runs are typically regular within each run. The scenario describes ventricular ectopy rather than an atrial source. Option d is incorrect because sinus tachycardia with PACs produces atrial ectopic beats and narrow complexes rather than wide ventricular complexes. The scenario clearly describes ventricular ectopy with PVCs.