3.3 Scenario Practice for Cardiology and Resuscitation

The Bradycardia Algorithm

Bradycardia (rate under 60, but clinically a rate too slow for the patient) is only treated when it produces serious signs and symptoms: hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, or acute heart failure. An asymptomatic patient with a rate of 50 needs monitoring, not drugs.

For symptomatic bradycardia, the first-line drug is atropine 1 mg IV, repeated every 3-5 minutes to a maximum total of 3 mg. (Note the dose: the single dose was raised from the older 0.5 mg to 1 mg in the 2020 guidelines and remains 1 mg.) If atropine fails or the patient is severely unstable, escalate to:

• Transcutaneous pacing (TCP) - the definitive temporizing measure; or
• Dopamine infusion 5-20 mcg/kg/min; or
• Epinephrine infusion 2-10 mcg/min, titrated to response.

High-grade blocks bypass atropine

Atropine acts at the AV node, so it is unlikely to help Mobitz II or third-degree (complete) block, where the lesion is infranodal. For these high-grade blocks, prepare for transcutaneous pacing immediately while readying an infusion - do not waste time cycling atropine. Confirm electrical capture (a wide QRS following each pacing spike on the monitor) and mechanical capture (a palpable pulse that matches the set rate); provide analgesia/sedation, because pacing is painful.

Worked scenario

A 72-year-old presents with a rate of 38, BP 78/40, and confusion; the monitor shows third-degree block. Because the patient is unstable and atropine is unlikely to work in complete block, the best action is immediate transcutaneous pacing with sedation, plus a backup epinephrine or dopamine infusion - not repeated atropine.

Why atropine fails in high-grade block

Atropine works by blocking vagal (parasympathetic) tone at the AV node and sinus node, speeding conduction through the node. In Mobitz II and complete heart block, the conduction failure is below the node (in the His-Purkinje system), where atropine has no useful effect and can even paradoxically worsen the situation by speeding the atrial rate without improving ventricular conduction. That is the conceptual hook the exam tests: match the drug to the site of the lesion. Nodal problems (sinus bradycardia, Mobitz I) may respond to atropine; infranodal problems (Mobitz II, third-degree) need pacing or beta-agonist infusions.

Setting up transcutaneous pacing

Pacing is a procedure with concrete steps the exam may probe. Place the pads (often anterior-posterior), turn on the pacer, set a rate (typically 60-80/min), then increase the milliamp output from zero until you see electrical capture - a pacer spike followed by a wide QRS and a broad T wave for each beat. Then confirm mechanical capture by palpating a femoral or right-side pulse that matches the set rate (palpate the right radial or femoral to avoid mistaking muscle twitch for a pulse).

Pacing is uncomfortable, so provide sedation and analgesia in the conscious patient. If capture cannot be achieved or the patient remains unstable, run a dopamine (5-20 mcg/kg/min) or epinephrine (2-10 mcg/min) infusion as a chemical pacing bridge. The most common pacing error tested is calling failure to capture a success - a spike with no following QRS is electrical output without capture and produces no perfusion.

The Tachycardia Algorithm

Again the pivot is stability. A tachycardic patient who is unstable - hypotensive, altered, in shock, or with ischemic chest pain - gets immediate synchronized cardioversion, regardless of the specific tachycardia. Synchronization times the shock to the R wave to avoid the vulnerable T-wave period (the R-on-T phenomenon that can induce VF).

For the stable patient, classify by QRS width and regularity:

• Narrow, regular (likely SVT/AVNRT): attempt vagal maneuvers first; if unsuccessful, adenosine 6 mg rapid IV push with an immediate saline flush, then 12 mg if needed.
• Narrow, irregular (likely AFib/flutter with RVR): rate control per protocol (e.g., diltiazem or beta-blocker); adenosine is not the answer here.
• Wide, regular: presume VT; an antiarrhythmic such as amiodarone may be used, but if there is any instability, cardiovert.

Worked scenario and trap

A 30-year-old with palpitations, rate 190, narrow QRS, regular, BP 118/72, fully alert. This is stable SVT: try vagal maneuvers, then adenosine 6 mg, then 12 mg. The trap is jumping to cardioversion because the rate looks scary - electricity is reserved for the unstable patient. The opposite trap is treating an unstable wide-complex tachycardia with a slow diagnostic drug instead of immediate synchronized cardioversion.

Defibrillation versus cardioversion

Candidates routinely confuse the two electrical therapies, and the distinction is heavily tested. Defibrillation is an unsynchronized, high-energy shock delivered immediately for pulseless VF/pVT; there is no R wave to time to because the rhythm is disorganized or the patient is in arrest. Synchronized cardioversion is timed to the R wave and used for an unstable patient with a pulse in a tachyarrhythmia (unstable SVT, AFib/flutter with serious symptoms, VT with a pulse).

Synchronizing avoids delivering energy during the relative refractory period (the T wave), which could provoke VF. If you try to synchronize on a polymorphic/disorganized rhythm and the machine cannot find a consistent R wave, treat it as VF and defibrillate. Vagal maneuvers - Valsalva (ideally the modified leg-raise version), carotid sinus massage in younger patients without bruits - are the no-cost first move for stable narrow regular tachycardia and may convert AVNRT outright before any drug is given.