Why are heart sounds audible in a 43‑year‑old man with pulseless electrical activity (PEA) after prolonged cardiopulmonary resuscitation—does residual organized electrical activity generate mechanical vibrations without producing a palpable pulse?

Why Heart Sounds Are Audible in Pulseless Electrical Activity

Audible heart sounds during PEA occur because organized electrical activity on the cardiac monitor generates mechanical vibrations of the heart valves and myocardium, but this activity is insufficient to produce a palpable pulse or measurable arterial pressure. 1

The Physiological Mechanism

PEA represents electromechanical dissociation where electrical depolarization occurs without effective myocardial fiber shortening and cardiac output. 1, 2 The key distinction is:

• Organized electrical activity persists on the ECG monitor, showing coordinated depolarization waves 3, 1
• Mechanical vibrations are generated by valve movements and minimal myocardial wall motion, creating audible sounds 1
• However, the stroke volume and systemic vascular resistance product is inadequate to generate a clinically detectable pulse 4

Critical Clinical Implications

The presence of heart sounds does NOT indicate return of spontaneous circulation (ROSC) and should never be used to infer adequate perfusion. 1 This is a common and dangerous pitfall:

• Only a palpable carotid or femoral pulse, or an arterial waveform, confirms ROSC 1
• Pulse checks must not exceed 10 seconds—if no pulse is felt, immediately resume chest compressions 1
• The absence of a palpable pulse remains the defining feature of cardiac arrest, regardless of audible heart sounds or electrical activity 1

The Spectrum of PEA States

Bedside cardiac ultrasound should be performed immediately (≤10 seconds interruption) to differentiate true PEA from pseudo-PEA. 1 This distinction is crucial:

• Pseudo-PEA shows visible cardiac wall motion on ultrasound but still no palpable pulse—indicating some mechanical activity 5
• True PEA shows minimal to no effective ventricular contraction despite electrical activity 5
• Both states require continued CPR, as neither produces adequate cardiac output 1

Why the Dissociation Occurs

PEA typically represents a late phase in the clinical dying process, resulting from tissue hypoxia and metabolic substrate depletion. 5 The mechanism involves:

• Diffuse myocardial ischemia prevents coordinated fiber shortening despite electrical depolarization 2
• Impaired cardiac filling (from hypovolemia, tamponade, tension pneumothorax, or massive PE) limits stroke volume 4
• Severe vasodilatory shock reduces systemic vascular resistance to the point where minimal cardiac output cannot generate a palpable pulse 4

Management Priorities

Continue high-quality chest compressions with minimal interruptions and systematically evaluate reversible causes (H's and T's) during each 2-minute CPR cycle. 1 The presence of electrical activity with heart sounds does not change the fundamental approach:

• Administer epinephrine 1 mg IV/IO every 3-5 minutes 1
• Aggressively search for reversible causes: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis (coronary/pulmonary), and trauma 1
• Do NOT defibrillate—PEA is a non-shockable rhythm 3

Prognostic Context

Survival to hospital discharge for adult patients with PEA is approximately 11%, compared with 36% for shockable rhythms. 1 After prolonged resuscitation (e.g., 45 minutes) following conversion from VF to PEA, the probability of meaningful neurologic recovery is extremely low, though not absolutely zero 1. This underscores why the presence of heart sounds, while mechanically explainable, does not indicate a favorable prognosis without addressing the underlying cause.