Cardiac Arrest and Post-Resuscitation Care - NREMT: Paramedic Level

At least 2 in (5 cm), not more than 2.4 in (6 cm). This depth balances effective cardiac compression with minimizing risks like rib fractures or internal injuries.

Restart CPR and follow the cardiac arrest algorithm. Prompt algorithm adherence ensures structured resuscitation, addressing recurrent arrest causes efficiently.

ST-segment elevation myocardial infarction (STEMI). STEMI indicates acute coronary occlusion, where timely reperfusion can salvage myocardium and improve outcomes.

SBP ≥ 90 mmHg (or MAP ≥ 65 mmHg). This target ensures adequate organ perfusion while avoiding excessive vasopressor use in hypotensive states.

Titrate oxygen to SpO2 92%–98%. Avoiding hyperoxia reduces oxidative stress and reperfusion injury in post-arrest tissues.

10 breaths/min; titrate to normal PaCO2/ETCO2. This rate maintains normocapnia, preventing hypocapnia-induced vasoconstriction or hypercapnia-related acidosis.

Continuous waveform capnography. Waveform capnography provides real-time, quantitative confirmation of tube position and ventilation efficacy over other methods.

Resume CPR immediately for 2 minutes. Immediate CPR resumption maintains circulation while allowing rhythm analysis and drug effects to manifest.

Persistently < 10 mmHg. Low ETCO2 reflects inadequate pulmonary perfusion, signaling the need to optimize compression technique and depth.

Abrupt sustained increase in ETCO2 (often to ≥ 40 mmHg). Sudden ETCO2 rise indicates restored pulmonary blood flow from effective cardiac output post-resuscitation.

Asystole and pulseless electrical activity (PEA). These rhythms lack organized ventricular activity amenable to defibrillation, requiring focus on reversible causes and medications.

Ventricular fibrillation and pulseless ventricular tachycardia. These disorganized rhythms respond to electrical cardioversion to restore coordinated cardiac activity.

100–120 compressions/min. AHA guidelines specify this rate to ensure adequate cardiac output and perfusion during resuscitation efforts.

No more than 10 seconds. Minimizing interruptions maintains coronary perfusion pressure and improves survival outcomes in cardiac arrest.

30:2. This ratio optimizes circulation while providing sufficient oxygenation without excessive ventilation pauses.

1 breath every 6 seconds (10/min) with continuous compressions. Asynchronous ventilation prevents hyperventilation and allows uninterrupted chest compressions for better hemodynamics.

360 J. Monophasic defibrillators deliver a single-direction current, necessitating higher energy to terminate ventricular arrhythmias effectively.

1 mg IV/IO. Epinephrine acts as a vasopressor to enhance coronary and cerebral perfusion during low-flow states in arrest.

Every 3–5 minutes. Repeated dosing maintains vasopressor effects without accumulation, aligning with pharmacokinetics in arrest scenarios.

300 mg IV/IO bolus, then 150 mg IV/IO once. Amiodarone stabilizes cardiac membranes and prolongs refractory periods to terminate refractory ventricular arrhythmias.

1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg (max 3 mg/kg). Lidocaine suppresses ventricular ectopy by blocking sodium channels, serving as an alternative antiarrhythmic in persistent cases.

Magnesium sulfate 1–2 g IV/IO. Magnesium corrects electrolyte imbalances that prolong QT interval, stabilizing polymorphic ventricular tachycardia.

120–200 J (use manufacturer recommendation). Biphasic waveforms require lower energy for effective defibrillation compared to monophasic, with doses tailored to device specifics.