Henti Jantung

01Pathophysiology

Cardiac arrest represents the complete cessation of effective cardiac mechanical activity, resulting in the absence of systemic circulation. It is not a single disease but rather a final common pathway of many etiologies.

The most frequent underlying mechanism in adults is acute myocardial ischemia or infarction. When a coronary artery occludes, the resulting ischemia destabilizes the electrical conduction system of the ventricle. Ischemic myocytes develop abnormal automaticity and create re-entrant circuits, which degenerate into ventricular fibrillation, the most common initial rhythm in witnessed out-of-hospital cardiac arrest. VF produces chaotic, disorganized electrical activity with no coordinated contraction, meaning the ventricles quiver rather than pump. Without defibrillation, VF deteriorates into asystole within minutes.

Pulseless ventricular tachycardia functions similarly: a re-entrant loop fires so rapidly (usually > 180 bpm) that the ventricles cannot fill adequately and produce no effective cardiac output. Because VF and pVT both involve aberrant ventricular electrical activity that can be terminated by depolarizing the entire myocardium at once, they are classified as shockable rhythms.

Pulseless electrical activity (PEA) is fundamentally different. The monitor shows organized electrical complexes, but there is no corresponding mechanical contraction or pulse. This dissociation between electrical and mechanical function is almost always caused by a reversible extrinsic insult to the heart: massive hypovolemia reduces preload to zero, cardiac tamponade prevents ventricular filling, tension pneumothorax compresses the great vessels, pulmonary embolism obstructs right ventricular outflow, or severe hyperkalemia poisons the conduction system. This is why PEA mandates an aggressive search for reversible causes rather than defibrillation; the electrical system is technically working, but something is preventing the heart from pumping.

Asystole represents the complete absence of electrical and mechanical cardiac activity. It generally indicates prolonged ischemia and diffuse myocardial damage. Asystole carries the worst prognosis of all arrest rhythms because it reflects a heart that has essentially exhausted its electrical reserves.

Within seconds of arrest, cerebral perfusion ceases. Neurons begin to suffer irreversible injury after approximately 4 to 6 minutes of anoxia, which is why the time to initiation of CPR and defibrillation is the single strongest predictor of survival. CPR functions as a temporary bridge, generating roughly 25 to 33% of normal cardiac output through direct cardiac compression and the thoracic pump mechanism, just enough to maintain marginal cerebral and coronary perfusion until definitive therapy (defibrillation, reversal of the underlying cause) can restore spontaneous circulation.

02Classification and Clinical Manifestation

Arrest Rhythm Classification

Reversible Causes (H's and T's)

This table is among the most tested frameworks in emergency medicine. Every time a vignette presents PEA or asystole, the question is almost always asking you to identify which of these reversible causes is present and how to correct it.

03Diagnostic Workup

The "diagnostic workup" in cardiac arrest is unique because treatment begins before diagnosis is confirmed. You do not pause resuscitation to order tests. The best initial diagnostic tool is the cardiac monitor or defibrillator, which categorizes the arrest into shockable versus non-shockable. This single determination dictates the entire management algorithm.

During resuscitation, the priority is to identify reversible causes. Point-of-care labs (potassium, glucose, blood gas) are drawn during CPR without interrupting compressions. A stat potassium of 7.2 mEq/L, for example, immediately changes your management (calcium, insulin, glucose, bicarbonate).

Point-of-care ultrasound has become a central diagnostic tool during arrest. It must be performed during the rhythm/pulse check window (under 10 seconds) to avoid interrupting compressions. Findings that change management include pericardial effusion with tamponade physiology (immediate pericardiocentesis), severely dilated RV suggesting pulmonary embolism (consider thrombolytics), absent cardiac motion suggesting true asystole with poor prognosis, and an empty hyperdynamic LV suggesting hypovolemia (aggressive fluid resuscitation).

After achieving ROSC, the workup transitions to identifying the cause of arrest and assessing end-organ damage. The 12-lead ECG is the most important immediate post-ROSC test. If it shows ST elevation, the patient goes directly to the catheterization lab for percutaneous coronary intervention (PCI). Current guidelines also recommend considering emergent angiography even without obvious STEMI if there is a high clinical suspicion that the arrest was caused by an acute coronary event.

04Management and Treatment

Step 1: Recognition and Activation. The moment a patient is found unresponsive with no pulse and no effective breathing, activate the emergency response system and call for a defibrillator. Begin CPR immediately. Every minute without CPR reduces survival by approximately 7 to 10%.

Step 2: High-Quality CPR. This is the single most important intervention and the foundation upon which everything else rests. Compress the chest at a rate of 100 to 120 compressions per minute to a depth of at least 5 cm but no more than 6 cm. Allow complete chest recoil between compressions. Minimize interruptions: chest compression fraction (the percentage of time spent actively compressing) should exceed 80%. Switch compressor roles every 2 minutes to prevent fatigue-related decline in quality. Without an advanced airway, deliver ventilations at a 30:2 ratio. Once an advanced airway is placed, provide continuous compressions with one breath every 6 seconds (10 breaths per minute), and do not pause compressions for ventilations.

Step 3: Rhythm Check and Defibrillation. Attach the monitor and determine whether the rhythm is shockable or non-shockable.

For VF or pVT: deliver an unsynchronized shock immediately. Resume CPR for 2 full minutes before the next rhythm check. If the rhythm persists after the second shock, administer epinephrine 1 mg IV/IO and continue CPR. After the third shock, administer amiodarone 300 mg IV/IO. If VF/pVT persists after additional cycles, give a second dose of amiodarone at 150 mg IV/IO. Continue epinephrine every 3 to 5 minutes throughout.

For PEA or asystole: do NOT defibrillate. Administer epinephrine 1 mg IV/IO as early as possible and repeat every 3 to 5 minutes. The entire focus must shift to identifying and correcting the underlying cause. Exam vignettes with PEA are almost always testing whether you can identify the reversible cause: a trauma patient with PEA likely has hypovolemia or tension pneumothorax; a dialysis patient with PEA likely has hyperkalemia; a post-operative patient with PEA and acute dyspnea likely has a pulmonary embolism.

Step 4: Reversible Cause Correction. Treat based on the identified cause:

Step 5: Post-Cardiac Arrest Care (After ROSC). Once spontaneous circulation returns, the patient is not "saved" yet. The post-arrest phase carries substantial mortality from reperfusion injury, hemodynamic instability, and anoxic brain injury.

Targeted Temperature Management (TTM): Current guidelines recommend maintaining a core body temperature of 32 to 36 degrees Celsius for at least 24 hours in comatose patients after ROSC. Cooling can be achieved with surface cooling devices, intravascular catheters, or cold IV saline (though large-volume cold saline infusion is no longer recommended as the sole method prehospitally due to risk of pulmonary edema). Avoid fever (above 37.5 degrees Celsius) aggressively for at least 72 hours.

Hemodynamic optimization: Target a mean arterial pressure of at least 65 mmHg using vasopressors (norepinephrine is first-line) and IV fluids. Obtain an echocardiogram to assess cardiac function.

Neurological prognostication: This is a tested concept. Do NOT make prognostic determinations before 72 hours after the patient has returned to normothermia (not 72 hours after ROSC). Confounders such as sedation, paralytics, and hypothermia make early neurological assessment unreliable. Tools used after 72 hours include bilateral absence of pupillary and corneal reflexes, bilateral absence of N20 cortical responses on somatosensory evoked potentials (SSEP), highly malignant EEG patterns (burst suppression, status epilepticus), diffuse cortical or extensive brainstem injury on MRI, and persistently elevated neuron-specific enolase (NSE > 33 mcg/L at 48-72 hours, though thresholds vary by lab).

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on cardiac arrest questions is confusing shockable and non-shockable rhythms. The foundational rule is simple: defibrillation works for VF and pVT because the goal is to simultaneously depolarize a critical mass of myocardium, terminating the chaotic re-entrant circuits and allowing the SA node to resume normal pacing. Defibrillation does nothing for asystole (there is no electrical activity to reset) and nothing for PEA (the electrical system is already organized; the problem is mechanical). If a vignette shows PEA and offers "defibrillate" as an answer choice, it is a distractor.

The second major trap involves PEA arrest and the failure to look for a cause. When a question stem describes an arrest and the monitor shows an organized rhythm with no pulse, the answer is almost never "continue CPR and epinephrine." The question is almost certainly asking you to identify which reversible cause is present and what intervention corrects it. Read the stem carefully for clues: a dialysis patient suggests hyperkalemia; a postpartum hemorrhage suggests hypovolemia; unilateral absent breath sounds suggest tension pneumothorax; a patient on heparin or with a recent long flight suggests pulmonary embolism; muffled heart sounds and JVD suggest tamponade.

Third, students frequently mistime epinephrine administration. In shockable rhythms, epinephrine is given after the second shock (not immediately). In non-shockable rhythms, epinephrine is given as early as possible once IV/IO access is obtained. Getting this timing wrong is a classic question trap.

Fourth, never prognosticate too early. A vignette describing a comatose patient 24 hours after ROSC who asks "what is the next best step" is testing whether you will inappropriately withdraw care. The correct answer is to continue supportive care and defer prognostication until at least 72 hours after normothermia.

Finally, remember the hypothermia rule. A hypothermic patient in cardiac arrest should not be declared dead until rewarmed to at least 32 degrees Celsius. Hypothermia is neuroprotective, and full neurological recovery has been documented even after prolonged resuscitation in severely hypothermic patients. If the vignette describes a drowning victim pulled from cold water with asystole, the answer is to continue resuscitation and actively rewarm, not to terminate efforts.

The core competency being tested across all cardiac arrest questions is algorithmic thinking under pressure: can you correctly categorize the rhythm, apply the right intervention in the right sequence, and simultaneously hunt for a correctable cause?