BCCCP Study Guide: Mastering ACLS, Vasopressors, and Mechanical Ventilation for the Critical Care Pharmacy Board Exam

BCCCP Study Guide: Mastering ACLS, Vasopressors, and Mechanical Ventilation for the Critical Care Pharmacy Board Exam

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Preparing for the Board Certified Critical Care Pharmacist (BCCCP) exam is about thinking like the pharmacist at the bedside. You must know what to do in the first five minutes of a code, which vasopressor to hang for each shock state, and how to make the ventilator your ally. This guide focuses on three high-yield areas: ACLS, vasopressors and inotropes, and mechanical ventilation. You’ll get the “why” behind each move, so you can reason through tricky questions and real cases.

What BCCCP Expects on These Topics

  • ACLS: Correct drug, dose, route, and sequence. Know when NOT to give a drug.
  • Vasopressors: Match receptor profile to shock type. Titrate safely. Manage adverse effects and line issues.
  • Ventilation: Pick initial settings, adjust for gas exchange, and prevent harm. Tie sedation and NMB decisions to vent goals.

The exam favors cases over recall alone. Expect questions that force you to weigh trade-offs. For example, choose a pressor in a patient with sepsis and atrial fibrillation, or adjust a vent in ARDS with rising plateau pressures.

ACLS Essentials for Pharmacists

Cardiac arrest (VF/pulseless VT):

  • Defibrillate fast. Early shock restores organized rhythm and perfusion.
  • Epinephrine: 1 mg IV/IO every 3–5 minutes. It raises aortic diastolic pressure, which improves coronary perfusion during CPR.
  • Antiarrhythmics if refractory after shocks:
    • Amiodarone: 300 mg IV push, then 150 mg once. Then 1 mg/min for 6 hours, 0.5 mg/min thereafter. It stabilizes myocardium and reduces recurrence.
    • Lidocaine (alternative): 1–1.5 mg/kg IV, then 0.5–0.75 mg/kg; max 3 mg/kg.
    • Magnesium: 1–2 g IV for torsades de pointes. It treats triggered activity from prolonged repolarization.
  • Sodium bicarbonate: Not routine. Consider for severe hyperkalemia, TCA overdose, or prolonged arrest with severe acidosis. It can worsen intracellular acidosis if used indiscriminately.
  • Calcium: For hyperkalemia or calcium channel blocker overdose. It stabilizes the cardiac membrane.

Bradycardia with poor perfusion:

  • Atropine: 1 mg IV every 3–5 minutes, max 3 mg. Blocks vagal tone to increase SA/AV node activity.
  • If atropine fails, use transcutaneous pacing and start an infusion:
    • Epinephrine: 2–10 mcg/min IV titrated to response, or
    • Dopamine: 5–20 mcg/kg/min.

Tachycardia with a pulse:

  • Stable narrow-complex SVT: Vagal maneuvers, then adenosine 6 mg rapid IV push; if no response, 12 mg. It transiently blocks AV node conduction.
  • Stable monomorphic wide-complex VT: Amiodarone 150 mg in 100 mL D5W over 10 minutes; repeat as needed. Avoid adenosine in irregular WCT.
  • AF with RVR: If decompensated HF or hypotension, avoid diltiazem. Consider amiodarone or cautious beta-blockade.
  • Unstable tachycardia: Synchronized cardioversion. Drugs do not fix hypotension fast enough.

Push-dose pressors (peri-arrest):

  • Phenylephrine: 50–200 mcg every 1–2 min (from 100 mcg/mL dilution). Raises MAP without tachycardia.
  • Epinephrine: 5–20 mcg every 1–2 min (10 mcg/mL dilution). Useful when there is profound vasodilation plus low output.
  • Use only with clear orders, correct dilution, and continuous monitoring. They can overshoot MAP and cause ischemia if mis-dosed.

Post-ROSC care:

  • Oxygenation: Target SpO2 92–98%. Hyperoxia increases oxidative injury.
  • Perfusion: MAP ≥65 mmHg with fluids and pressors as needed. Lactate should trend down over time.
  • Temperature: For comatose adults, target 32–36°C. Avoid fever. Sedation and analgesia reduce shivering and ventilator dyssynchrony.
  • Glucose: 140–180 mg/dL. Hypo- and hyperglycemia worsen neurologic outcomes.
  • Seizures: Treat if present. Avoid routine prophylaxis.

Vasopressors and Inotropes—Mechanisms, Selection, Dosing

Why pressors work: Shock is a mismatch of oxygen delivery and demand. Pressors lift MAP to restore perfusion pressure. Inotropes improve cardiac output. Choose by receptor profile and the patient’s physiology.

Core agents and dosing (infusion ranges):

  • Norepinephrine: 0.01–1 mcg/kg/min. Strong α1, some β1. First-line in septic shock because it increases MAP with less tachycardia than dopamine.
  • Epinephrine: 0.02–0.5 mcg/kg/min. Potent β1/β2 and α1. Good for anaphylaxis and refractory vasodilatory shock, but watch for lactate rise and tachyarrhythmias.
  • Phenylephrine: 0.5–3 mcg/kg/min. Pure α1. Useful if tachyarrhythmias limit β-agonists. May reduce stroke volume in poor LV function.
  • Vasopressin: 0.03 units/min fixed in sepsis. Restores V1-mediated tone and lowers norepi needs. Avoid higher doses due to ischemic risk.
  • Dopamine: 5–20 mcg/kg/min. Not first-line; more arrhythmias. Consider only in bradycardic shock when you need rate.
  • Dobutamine: 2–20 mcg/kg/min. β1 inotrope with some β2 vasodilation. For low-output states with adequate MAP or alongside norepi in cardiogenic shock.
  • Milrinone: 0.125–0.75 mcg/kg/min. PDE-3 inhibitor; inodilator. Useful if on beta-blockers or with pulmonary hypertension. Hypotension risk; renal dose adjust.
  • Angiotensin II: Start 20 ng/kg/min for refractory vasodilatory shock. Restores tone via RAAS. Thrombosis risk; use with anticoagulation protocols.

Matching pressors to shock:

  • Septic shock: Norepi first-line. Add vasopressin at 0.03 units/min if norepi dose is rising. Add epinephrine for refractory cases. Why: mixed α/β support raises MAP with fewer arrhythmias; vasopressin addresses vasoplegia.
  • Cardiogenic shock: Norepi to secure MAP. Add dobutamine (or milrinone) for inotropy if low cardiac output. Why: pure vasoconstriction alone worsens afterload.
  • Obstructive shock (PE, tamponade): Norepi as bridge. Fix the obstruction (thrombolysis, pericardiocentesis). Pressors do not cure the cause.
  • Anaphylactic shock: IM epinephrine 0.3–0.5 mg first. If IV infusion is needed, use epinephrine. Add antihistamines and steroids adjunctively.
  • Right ventricular failure/PHTN: Norepi for pressure, add dobutamine or milrinone to improve RV output; consider inhaled pulmonary vasodilators. Avoid high PEEP that impairs RV preload.

Safety and line management:

  • Central line preferred. If peripheral, use large forearm vein, frequent checks, and limit duration. Pressors can cause tissue necrosis if extravasated.
  • Extravasation treatment: Stop infusion; aspirate drug. Infiltrate phentolamine 5–10 mg in 10 mL NS around the site, or use subcutaneous terbutaline. Apply warm compresses. Topical nitroglycerin is an option.
  • Compatibility: Avoid Y-siting with sodium bicarbonate or lipids. Verify compatibility when running multiple infusions.
  • Targets and trends: MAP ≥65 mmHg, urine output ≥0.5 mL/kg/h, down-trending lactate. Why: these reflect organ perfusion, not just pressure.

Fluids still matter: In sepsis, give ~30 mL/kg of balanced crystalloid early unless contraindicated. Why balanced fluids: less hyperchloremic acidosis and renal stress than normal saline in many patients.

Mechanical Ventilation Basics You Must Know

Common modes:

  • Volume assist-control (VAC): Set tidal volume (Vt) and rate. Good for ARDS to control Vt. Peak and plateau pressures guide safety.
  • Pressure control (PC): Set inspiratory pressure and rate. Helpful for poor compliance; Vt varies with lung mechanics.
  • Pressure support (PS): Spontaneous breaths supported by a set pressure. Use during weaning and SBTs.

Initial settings (general adult):

  • Vt: 6–8 mL/kg ideal body weight. Lower (4–6) for ARDS. Why: prevents volutrauma.
  • Rate: 14–20 breaths/min. Adjust for PaCO2.
  • FiO2: Start 1.0, then titrate quickly to SpO2 92–96%.
  • PEEP: 5 cm H2O initially; higher in ARDS as needed. Why: recruits alveoli and improves oxygenation.

ARDS strategy (lung-protective):

  • Vt 4–6 mL/kg IBW. Keep plateau pressure <30 cm H2O. Lower driving pressure (plateau − PEEP) if possible.
  • PEEP/FiO2 ladder: Use higher PEEP with refractory hypoxemia. Why: reduces shunt by recruiting alveoli.
  • Permissive hypercapnia: Accept pH 7.15–7.25 if needed to avoid high Vt. Buffer only for severe acidemia.
  • Prone positioning: For PaO2/FiO2 <150. It improves V/Q matching and survival in severe ARDS.
  • Neuromuscular blockade: Consider short course for severe dyssynchrony. Ensure deep sedation first.

ABG-driven adjustments (why each change works):

  • Low PaO2/SpO2: Increase FiO2 or PEEP. PEEP recruits alveoli; FiO2 raises oxygen gradient. Avoid prolonged FiO2 of 1.0 to limit toxicity.
  • High PaCO2/respiratory acidosis: Increase minute ventilation. Raise rate first in ARDS to keep Vt low.
  • Low PaCO2/respiratory alkalosis: Lower rate if patient is over-ventilated. Check for pain/anxiety.

Dyssynchrony and sedation:

  • Analgesia first: Fentanyl infusion 25–200 mcg/h. Pain drives tachypnea and dyssynchrony.
  • Light sedation goal: RASS −1 to 0 for most. Propofol 5–50 mcg/kg/min helps synchrony; watch for hypotension, hypertriglyceridemia, and PRIS. Dexmedetomidine 0.2–1.5 mcg/kg/h for agitation with minimal respiratory depression; watch for bradycardia. Midazolam 1–5 mg/h if deep sedation needed; risk accumulation and delirium. Ketamine 0.1–0.5 mg/kg/h helps in bronchospasm and hypotension.
  • Daily SAT/SBT: Reduces ventilator days and delirium. Resume sedation only if needed.

Neuromuscular blockade (when and how):

  • Use for severe ARDS or life-threatening ventilator dyssynchrony.
  • Cisatracurium: Load 0.1–0.2 mg/kg, then 1–3 mcg/kg/min infusion. Organ-independent metabolism is helpful in multi-organ failure.
  • Ensure deep sedation and analgesia. Provide eye lubrication and DVT prophylaxis. Avoid prolonged use to reduce weakness risk.

Weaning and extubation readiness:

  • Consider SBT when FiO2 ≤0.4–0.5, PEEP ≤5–8, hemodynamically stable on low pressors, and mental status is adequate.
  • RSBI (f/VT) <105 predicts readiness. Not perfect—use clinical judgment.
  • Dexmedetomidine can facilitate extubation in agitated hypoxic patients because it spares respiration.

Vent alarms—think fast and targeted:

  • High pressure: Secretions, bronchospasm, biting, kinks. Suction, bronchodilator, bite block, check tubing.
  • Low exhaled volume: Leak or disconnection. Reconnect, check cuff.
  • High rate: Pain, anxiety, hypoxia, or acidosis. Treat the cause, not just the number.

Putting It Together: Case Patterns You’ll See

  • Case 1: Septic shock, AF with RVR, MAP 52 on 2 L/min IV norepi.
    • Add vasopressin 0.03 units/min to reduce norepi needs without more tachycardia. For rate control, avoid diltiazem in shock; consider amiodarone. Why: amiodarone controls rate/rhythm without negative inotropy.
  • Case 2: Cardiogenic shock, cold and clammy, MAP 58, echo shows low EF.
    • Start norepinephrine to get MAP ≥65, then add dobutamine for inotropy. Why: you must support perfusion pressure and forward flow together.
  • Case 3: ARDS with plateau 32 and PaO2 55 on FiO2 0.8 and PEEP 8.
    • Lower Vt toward 4–6 mL/kg, increase PEEP, and consider prone positioning. Why: reduce overdistension and recruit lung units to improve oxygenation.
  • Case 4: VF arrest refractory after two shocks, epi x1 given.
    • Give amiodarone 300 mg IV push. If suspected torsades, give magnesium 2 g IV. Why: stabilize myocardium and correct polymorphic VT trigger.
  • Case 5: Profound hypotension during intubation, peri-arrest.
    • Give push-dose phenylephrine 100 mcg or epinephrine 10 mcg while setting up a norepi infusion. Why: immediate vasoconstriction buys time.

High-Yield Numbers and Targets

  • Epinephrine (arrest): 1 mg IV/IO every 3–5 minutes.
  • Amiodarone (arrest): 300 mg, then 150 mg IV push.
  • Adenosine: 6 mg, then 12 mg rapid IV push for SVT.
  • Atropine: 1 mg IV every 3–5 minutes to 3 mg total.
  • Norepinephrine: 0.01–1 mcg/kg/min; first-line in septic shock.
  • Vasopressin (sepsis): 0.03 units/min fixed.
  • Dobutamine: 2–20 mcg/kg/min for low output.
  • Vent safety: Vt 4–6 mL/kg in ARDS; plateau <30 cm H2O.
  • Perfusion: MAP ≥65, UOP ≥0.5 mL/kg/h, lactate down.
  • SpO2 (post-ROSC): 92–98%; TTM: 32–36°C.
  • SAT/SBT daily: Lighter sedation shortens vent time.

Study Strategy and Test Tactics

  • Learn dose–response logic. Do not memorize doses in isolation. For each drug, know its receptor profile, hemodynamic effect, and top two adverse effects.
  • Use case checklists. In any shock case, run: airway, oxygen, IV access, fluids, pressor choice, source control, and endpoints.
  • Practice “if-then” thinking. If AF with hypotension in sepsis, then norepi + vasopressin, consider amiodarone; avoid diltiazem.
  • Anticipate complications. High PEEP lowers preload. Propofol drops BP. Milrinone causes vasodilation. Integrate these when choosing therapies.
  • Know when not to use a drug. Succinylcholine in hyperkalemia or neuromuscular disease. Diltiazem in decompensated HFrEF. Dopamine in sepsis unless bradycardic.
  • Write quick cards. Have one card for ACLS doses, one for pressor ranges and receptors, one for ARDS vent targets.

Final Checks for Clinical Practice Safety

  • Dilutions and concentrations: Verify push-dose pressor concentrations and double-check syringes with a second clinician.
  • Mixing and compatibility: Separate pressors from bicarbonate and lipids. Use dedicated lumens when possible.
  • Metabolic monitoring: With propofol, check triglycerides and CK if prolonged/high dose. With vasopressors, monitor extremity perfusion.
  • Renal/hepatic function: Adjust sedatives and inotropes; critical illness alters volume of distribution and clearance.
  • Document targets: Write the MAP, SpO2, PaCO2, and sedation goals in the order. It aligns the team and prevents over- or under-titration.

Mastering ACLS, vasopressors, and mechanical ventilation is about pattern recognition plus physiology. Know why each drug and setting works, and you will handle both exam vignettes and real-world chaos with calm. Keep doses at your fingertips, think in algorithms, and always tie therapy back to perfusion and lung protection.

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