2.2 Advanced Life Support (ALS): Emergency Pharmacopeia, Reversals & Defibrillation

Advanced Life Support (ALS): Emergency Pharmacopeia, Reversals & Defibrillation

Core Knowledge: Advanced Life Support (ALS) builds upon uninterrupted, high-quality BLS. ALS encompasses the systematic identification of arrest rhythms, establishment of vascular or intraosseous access, administration of emergency vasopressors and reversal agents, and prompt electrical defibrillation. High-performance resuscitation teams execute ALS interventions seamlessly without interrupting 2-minute BLS compression cycles.

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1. Rhythm Diagnosis: Shockable vs. Non-Shockable Pathways

At the conclusion of each 2-minute BLS cycle, compressions pause for no more than 3 to 5 seconds to evaluate the electrocardiographic (ECG) rhythm.

                    [2-Minute BLS Cycle Ends]
                               │
                  < 5s Rhythm & Pulse Check
                               │
        ┌──────────────────────┴──────────────────────┐
   [SHOCKABLE]                                  [NON-SHOCKABLE]
   • Ventricular Fibrillation (VF)              • Asystole
   • Pulseless Vent. Tachycardia (pVT)          • Pulseless Elec. Activity (PEA)
        │                                             │
   1. Clear & Deliver Shock (2-4 J/kg biphasic)  1. Low-Dose Epinephrine (0.01 mg/kg)
   2. RESUME COMPRESSIONS IMMEDIATELY                 or Vasopressin (0.8 U/kg)
   3. Complete full 2-min cycle                  2. Atropine (0.04 mg/kg) if high vagal
   4. Antiarrhythmics if refractory              3. Administer Reversals if indicated

Rhythm Definitions

1. Ventricular Fibrillation (VF): Chaotic, disorganized baseline without recognizable P-QRS-T complexes, representing uncoordinated, ineffective myocardial fibrillatory activity.
2. Pulseless Ventricular Tachycardia (pVT): Rapid, wide, and bizarre QRS complexes at rates typically >200 bpm with absent peripheral pulses and no cardiac output.
3. Asystole (Flatline): Complete absence of electrical and mechanical ventricular activity (ventricular standstill). Always verify lead attachment, gain settings, and switch leads before confirming.
4. Pulseless Electrical Activity (PEA): Presence of organized, near-normal or wide electrical waveforms on ECG in the complete absence of myocardial contraction and palpable pulses.

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2. Emergency Vasopressors & Inotropes

Vasopressors induce peripheral arterial vasoconstriction, preventing peripheral vascular collapse and shunting available blood volume to the central circulation, thereby boosting Coronary Perfusion Pressure (CPP) and Cerebral Perfusion Pressure.

Epinephrine (Adrenaline)

• Mechanism: Potent endogenous catecholamine stimulating $\alpha_1$, $\beta_1$, and $\beta_2$ adrenergic receptors. The therapeutic benefit during CPR is driven almost exclusively by $\alpha_1$-mediated peripheral arterial vasoconstriction.
• Low-Dose Epinephrine Protocol (Standard of Care):
  • Dose: 0.01 mg/kg IV or IO (equivalent to 0.01 mL/kg of 1:1,000 [1 mg/mL] solution, or 0.1 mL/kg of 1:10,000 [0.1 mg/mL] solution).
  • Frequency: Administered every other 2-minute cycle (every 3 to 5 minutes) in non-shockable rhythms (asystole and PEA).
• High-Dose Epinephrine (0.1 mg/kg): RECOVER guidelines specifically remove high-dose epinephrine from routine resuscitation algorithms. Clinical trials demonstrate that while high-dose epinephrine may transiently increase initial ROSC rates, it causes profound post-resuscitation myocardial dysfunction, severe cerebral ischemia, malignant arrhythmias, and significantly worsens survival to hospital discharge. It is reserved only for prolonged, refractory CPR (>10–15 minutes) at clinician discretion.

Vasopressin (Antidiuretic Hormone)

• Mechanism: Stimulates vascular $V_1$ receptors on vascular smooth muscle, causing profound peripheral vasoconstriction through non-adrenergic pathways.
• Dose: 0.8 U/kg IV or IO.
• Key Clinical Advantage: Unlike catecholamines (epinephrine), vasopressin remains fully active in severe acidemia and hypoxemia, where adrenergic receptors are desensitized. It does not stimulate cardiac $\beta_1$ receptors, avoiding increases in myocardial oxygen consumption. Can be used in place of, or alternated with, low-dose epinephrine.

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3. Parasympatholytics: Atropine

• Mechanism: Competitive muscarinic acetylcholine receptor antagonist that blocks parasympathetic vagal input to the sinoatrial (SA) and atrioventricular (AV) nodes.
• Dose: 0.04 mg/kg IV or IO.
• Clinical Indications: Indicated in CPA driven by high vagal tone (e.g., gastrointestinal disease, respiratory tract obstruction, ocular surgery, neurological disease, or severe sinus bradycardia degenerating into asystole/PEA). RECOVER recommends administration during the first cycle of asystole/PEA.

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4. Antidotes & Anesthetic Reversal Agents

If the patient arrested following the administration of sedatives, opioids, or anesthetics, specific competitive antagonists must be administered immediately during ALS:

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5. Electrical Defibrillation Mechanics & Safety

Defibrillation is the definitive and sole curative therapy for shockable rhythms (VF and pulseless VT). The electrical current depolarizes a critical mass of chaotic myocardium simultaneously, rendering the cells refractory so that the primary pacemaker (SA node) can resume coordinated pacing.

Energy Dosing Guidelines

• Biphasic Defibrillator (Preferred): Delivers current bidirectionally, requiring lower energy and causing less myocardial damage.
  • Initial Shock Dose: 2 to 4 J/kg (start at 2 J/kg; escalate to 4 J/kg if VF persists on subsequent cycles).
• Monophasic Defibrillator: Delivers current in a single direction.
  • Initial Shock Dose: 4 to 6 J/kg.

The Strict Post-Shock Rule

$\text{Deliver Shock} \longrightarrow \text{IMMEDIATELY RESUME COMPRESSIONS (2 min)} \longrightarrow \text{Check ECG at Cycle End}$

VTS Critical Concept: Never check the ECG or palpate pulses immediately after delivering a shock! Defibrillation rarely results in an immediate organized, perfusing rhythm; instead, the stunned myocardium requires several minutes of continuous perfusion generated by BLS compressions to restore intracellular ATP and coordinated mechanical contraction. Halting compressions to view the monitor post-shock induces severe myocardial ischemia.

Antiarrhythmic Therapy for Refractory VF / Pulseless VT

When VF or pulseless VT persists despite $\ge 2$ electrical shocks:

1. Amiodarone: Class III antiarrhythmic (prolongs action potential and refractory period). Dose: 5 mg/kg slow IV/IO. First-line antiarrhythmic for refractory VF in dogs and cats.
2. Lidocaine: Class IB antiarrhythmic. Dose: 2 to 8 mg/kg IV/IO (Dogs only; caution/avoid in cats). Second-line agent when amiodarone is unavailable.

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6. Routes of Emergency Drug Administration