10 free Paramedic practice questions: Dysrhythmia Recognition and Management

The radial count ran over too short an interval to be valid: The pulse was counted for a full minute, which is exactly what an irregular rhythm requires. A shorter count would be unreliable, and that is not what happened here.

The monitor is counting artifact along with the true complexes: Artifact makes a tracing look messy and usually appears as spikes that do not fit the rhythm. An irregularly irregular rhythm with a clean complex count is not an artifact problem.

The patient converted between the two measurements: Conversion would change the rhythm rather than create two different rates for the same rhythm at the same moment.

Second degree atrioventricular block type I: Second degree type I, or Wenckebach, is the block that dropped beats should point to, since the PR interval lengthens with each conducted beat until one P wave fails to conduct. This strip shows no warning: the PR interval stays fixed on every conducted beat before the drop, pointing to a block below the AV node.

First degree atrioventricular block: First degree block only prolongs the PR interval past 0.20 seconds while every P wave still conducts a QRS, nothing ever drops. This strip has P waves that are not followed by a QRS complex, so conduction is failing outright, not just slowing at the node.

Third degree atrioventricular block: Third degree block means complete AV dissociation, with the atria and ventricles each pacing independently and no fixed relationship between P waves and QRS complexes. This strip keeps a constant PR interval on every conducted beat, proving some P waves are still capturing the ventricle.

Adenosine 12 mg as the first dose, since a wide rhythm needs the larger dose: Adenosine is reasonable for a wide complex tachycardia that is regular and monomorphic, so the drug is not the error. The dose is. The first dose is 6 mg no matter how wide the QRS is, and 12 mg comes only if 6 mg fails. Adenosine is never for an irregular or polymorphic wide complex rhythm.

Verapamil, since the young age makes a supraventricular origin likely: Age is not a differential. Young patients have ventricular tachycardia, and a calcium channel blocker given on that assumption can drop the pressure out from under the rhythm.

Synchronized cardioversion, since any wide complex rhythm is unstable: Cardioversion is the answer when the patient is unstable. Alert, warm, dry, and 118 systolic is not unstable, and sedating and shocking a stable patient skips a step a drug can handle.

Albuterol by nebulizer at a high dose: Albuterol does move potassium into the cells, and it takes time to do it. Time is what this rhythm does not have while the QRS keeps widening.

Sodium bicarbonate by intravenous push: Sodium bicarbonate shifts potassium as well, and like the other shifting agents it is an adjunct rather than the opening move once the membrane is already destabilized.

Atropine by intravenous push: Atropine is the reflex for a rate of 52, and it treats vagal tone, which is not what is slowing this heart. Potassium has stalled the conduction system, and atropine does nothing for that membrane; calcium does, and the rate follows it.

QRS width, PR interval, P waves, regularity, rate: All five components are present, but the sequence is inverted. It opens with the most granular measurement and ends with the one you can see from across the room. There is one setting where width does come first, the crashing tachycardic patient where wide versus narrow drives the treatment path, but that is a treatment shortcut, not the systematic strip analysis this question is asking about.

P waves, rate, QRS width, regularity, PR interval: Again all five components, scrambled. The tell is P waves in the lead position with regularity buried at fourth. Studying P-wave morphology before you know the rate means examining a detail without the context that tells you what the detail means.

Regularity, rate, PR interval, P waves, QRS width: This is the closest wrong answer and the one worth learning from: it swaps only the first two steps and moves the PR interval ahead of the P waves. Both errors matter. Rate is step one, and measuring a PR interval before confirming that P waves exist is measuring from a landmark you have not established yet.

A regular rhythm with a sawtooth baseline pattern: A sawtooth baseline with a regular ventricular response is atrial flutter, one organized reentrant circuit looping the atrium at a fixed rate and conducting in a set ratio like 2:1 or 3:1. Both rhythms are atrial and both can run fast; the split is organized versus chaotic. Flutter has a repeating pattern you can measure, fibrillation has none.

An irregular rhythm with P waves of changing shape before each QRS complex: An irregular rhythm with P waves that change shape from beat to beat describes a wandering atrial pacemaker: the pacemaker site drifts among different atrial foci, so each P wave looks different, but a P wave still precedes each QRS. That is the discriminator: atrial fibrillation has no P waves to find, so the presence of discrete P waves of any shape excludes it.

A narrow, regular rhythm at 180 with no visible P waves: This is the trap worth naming, because no visible P waves matches. A narrow, regular rhythm at 180 is supraventricular tachycardia (SVT), where the P waves are buried in or behind the QRS at that speed. The clinching differentiator is not the P waves at all, it is regularity: SVT is metronome-regular, atrial fibrillation never is.

Vagal maneuvers followed by reassessment before any further intervention: Vagal maneuvers work by stimulating the vagus nerve to slow conduction through the AV node, and they're the correct first move in a stable, narrow-complex SVT. The BP of 74/42 with confusion shows this patient can't tolerate that delay. Vagal maneuvers belong to the stable pathway, not this unstable one.

Adenosine administration only, with no further escalation planned: Adenosine blocks AV nodal conduction and is the drug of choice for stable, regular narrow-complex SVT. The BP of 74/42 with confusion and diaphoresis makes this patient unstable, where drug therapy alone can't be chosen over cardioversion; it treats the rhythm while the perfusion failure keeps going untreated.

Supportive care, oxygen, and transport with continuous monitoring only: Supportive oxygen and monitoring fits a patient who's tachycardic but still perfusing adequately, tolerating the rate without symptoms. Here the BP of 74/42, confusion, and cool, diaphoretic skin show decompensation already underway, so monitoring alone withholds the cardioversion needed to correct the rhythm causing that hypotension.

Aortic dissection: the answer to sudden tearing or ripping pain, often radiating to the back, with a blood pressure or pulse difference between the arms and sometimes a new murmur or a focal neurologic deficit. It has to be considered in any chest pain, but nothing here supports it, since the pain is sharp and clearly positional, it followed a viral illness rather than starting abruptly at maximum intensity, and the vital signs are unremarkable. The clinching separator is the positional quality, because dissection pain does not care what position the patient sits in, while pain that eases leaning forward points straight at the pericardium.

Anterior myocardial infarction: the right read when ST elevation is confined to the anterior precordial leads with reciprocal depression in the inferior leads, in a patient with pressure-like discomfort and a sympathetic response. Two findings rule it out here: the elevation crosses nearly every lead group, which no single coronary artery supplies, and there are no reciprocal depressions at all. This is the classic pair to separate, and the single clinching discriminator is reciprocal change, because regional injury produces it and diffuse inflammation cannot, since there is no uninvolved opposite wall.

Pulmonary embolism: produces sudden pleuritic pain with difficulty breathing, tachycardia, and hypoxemia, usually with a risk factor such as recent immobility, surgery, or malignancy, and pleuritic pain is a genuine overlap with pericarditis. This patient's lungs are clear, the neck veins are flat, the respiratory rate is 18, and the pain is positional rather than simply pleuritic. The key wins on the tracing, because diffuse elevation with depression of the segment between the P wave and the ventricular complex is an atrial-injury pattern an embolus does not create.

Amiodarone 150 mg over 10 minutes: Amiodarone belongs to a stable wide-complex tachycardia, or to ventricular tachycardia with a pulse, where the origin is below the atrioventricular node and a nodal blocking drug would accomplish nothing. The complexes here are narrow, which places the origin above the ventricles and puts this patient on a different branch of the algorithm entirely. The key also does something amiodarone cannot: it both treats and diagnoses, because interrupting the node either breaks the circuit or unmasks the underlying atrial rhythm within seconds, while amiodarone is a ten-minute infusion aimed at a ventricular origin this patient does not have.

Adenosine 12 mg rapid intravenous push: Twelve milligrams is the correct adenosine dose, just not the first one. It is what follows when a properly pushed 6 mg dose has failed to convert the rhythm, and skipping ahead to it delivers more drug than needed along with a larger burst of the unpleasant effects patients report, chest pressure, flushing, a brief sense of doom, and a several-second pause. This choice and the key are the same drug and the same mechanism, and the key wins purely on sequence, which is the point the item is testing.

Synchronized cardioversion at 100 J: Synchronized cardioversion is the answer for an unstable narrow-complex tachycardia, meaning hypotension, altered mental status, ischemic chest discomfort, or acute heart failure that is being caused by the rate. This patient is alert, with warm dry skin, clear lungs, and a blood pressure of 118/74, and mild lightheadedness at a rate of 186 does not meet the definition of instability. The stability question is what sorts this algorithm into its two branches, and the stable branch earns a trial of a drug before electricity and the sedation that goes with it.

Administer epinephrine 0.01 mg/kg intravenously: Epinephrine 0.01 mg/kg IV is correct for pediatric bradycardia persisting despite oxygenation, ventilation, and compressions, and a heart rate of 44 makes it the immediate reach, but compressions haven't started, and a drug pushed into an uncirculated heart never reaches the coronary arteries in useful concentration. This is a sequence error, not a drug error.

Administer atropine 0.02 mg/kg intravenously: Atropine 0.02 mg/kg treats bradycardia from vagal stimulation, such as during intubation or suctioning, or from organophosphate poisoning; this infant's bradycardia developed over three days of vomiting and poor feeding from hypoxia, not vagal tone, so blocking the vagus does nothing for a starved myocardium.

Initiate transcutaneous pacing at 100: Transcutaneous pacing at 100 fits complete heart block or sick sinus syndrome, where the conduction system fails but the muscle is otherwise healthy; this hypoxic infant's myocardium can't mechanically respond, so pacing would capture electrically on the monitor while producing no real cardiac output.