Cardiology · Resuscitation and Arrhythmias
The facts most likely to be tested
Defibrillation is the definitive treatment for pulseless ventricular tachycardia and ventricular fibrillation.
High-quality CPR requires a chest compression rate of 100–120 compressions per minute with a depth of 2–2.4 inches and full chest recoil.
Epinephrine (1 mg every 3–5 minutes) is indicated for all rhythms in cardiac arrest, prioritizing non-shockable rhythms like asystole and pulseless electrical activity (PEA).
Amiodarone (300 mg first dose) or lidocaine is the antiarrhythmic of choice for refractory ventricular fibrillation or pulseless ventricular tachycardia after the third shock.
End-tidal CO2 (ETCO2) monitoring is the most reliable indicator of CPR quality and a sudden increase in values is a primary sign of return of spontaneous circulation (ROSC).
Reversible causes of cardiac arrest, known as the H's and T's, include hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade (cardiac), toxins, and thrombosis (coronary or pulmonary).
Synchronized cardioversion is the mandatory intervention for unstable supraventricular tachycardia, atrial fibrillation, or atrial flutter with a pulse.
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A 65-year-old male is brought to the emergency department after collapsing at home. Upon arrival, the patient is unresponsive, and the monitor displays ventricular fibrillation. The team initiates high-quality CPR and delivers a defibrillation shock. Despite two additional shocks and two doses of epinephrine, the patient remains in ventricular fibrillation.
What is the most appropriate next pharmacological intervention?
Amiodarone
This tests the ACLS algorithm for refractory ventricular fibrillation, where an antiarrhythmic agent like amiodarone is indicated after the third shock.
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Etiology / Epidemiology
Primary cause is ventricular fibrillation secondary to coronary artery disease. Sudden cessation of cardiac output requires immediate CPR and defibrillation.
Clinical Manifestations
Patient is unresponsive, pulseless, and apneic. Loss of consciousness occurs within seconds of arrest.
Diagnosis
Diagnosis is clinical: absence of carotid pulse and unresponsiveness. ECG confirms rhythm (shockable vs. non-shockable).
Treatment
High-quality CPR is the foundation. Epinephrine is the first-line vasopressor; amiodarone is the first-line antiarrhythmic for shock-refractory VF/pVT.
Prognosis
Survival depends on time to defibrillation. Neurological injury is the primary long-term morbidity.
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Epidemiology & Etiology
Most cases are due to ischemic heart disease and sudden cardiac death. Other causes include H's and T's: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade, toxins, and thrombosis (coronary or pulmonary).
Pertinent Anatomy
The left ventricle is the most common site of origin for lethal arrhythmias. The conduction system (SA node to Purkinje fibers) is the primary target of electrical instability.
Pathophysiology
Cardiac arrest results in immediate cessation of systemic perfusion, leading to global cerebral ischemia. Anaerobic metabolism ensues, causing rapid lactic acidosis. If not reversed, myocardial stunning and irreversible cellular death occur within minutes.
Clinical Manifestations
The patient presents with sudden collapse, agonal breathing, and absent pulses. Fixed and dilated pupils are late signs of cerebral hypoperfusion. Always assess for pulseless electrical activity (PEA) where the monitor shows a rhythm but the patient has no pulse.
Diagnosis
Diagnosis is made by clinical assessment of pulse and respiration. ECG is the gold standard for rhythm classification. Capnography (ETCO2 > 10-20 mmHg) is used to monitor CPR quality and confirm return of spontaneous circulation (ROSC).
Treatment
Initiate high-quality CPR (100-120 compressions/min) immediately. For VF/pulseless VT, perform defibrillation (200J biphasic). Administer epinephrine 1mg every 3-5 minutes. Do not delay compressions for rhythm checks or pulse checks.
Prognosis
Outcomes are poor without early bystander CPR. Post-cardiac arrest syndrome includes multi-organ failure and anoxic brain injury. Targeted temperature management is often utilized to improve neurological outcomes.
Differential Diagnosis
Vasovagal syncope: transient, pulse returns spontaneously
Seizure: rhythmic muscle activity, pulse present
Cardiac tamponade: Beck's triad, muffled heart sounds
Tension pneumothorax: tracheal deviation, absent breath sounds
Pulmonary embolism: S1Q3T3 pattern, obstructive shock