When a person collapses from sudden cardiac arrest, the heart’s electrical activity fails, and blood flow immediately stops. Cardiopulmonary Resuscitation (CPR) provides artificial circulation and ventilation to keep oxygenated blood moving to the brain and other vital organs. The ultimate goal of these efforts is to achieve Return of Spontaneous Circulation (ROSC), which is when the heart begins to beat effectively enough to restore its own sustained, perfusing activity. Recognizing this shift requires a rapid and accurate assessment, as the continuation of life support efforts must change immediately to prevent further harm.
Recognizing Return of Spontaneous Circulation
The first and most direct sign of ROSC is the sudden appearance of a sustained, palpable pulse that is not caused by the chest compressions themselves. Rescuers must check for a central pulse (carotid or femoral artery) during a brief pause in compressions. An effective pulse indicates the heart is generating enough pressure to circulate blood independently.
The return of responsiveness, which can include spontaneous movement, coughing, or even normal breathing, also suggests blood flow to the brain has been restored. While these visible changes are helpful, healthcare providers use an objective measure called End-Tidal Carbon Dioxide (EtCO2) monitoring.
EtCO2 measures the carbon dioxide level in the patient’s exhaled breath, which is directly related to blood flow to the lungs and heart function. During effective CPR, the EtCO2 level is typically low, but a sudden and sustained increase, often rising above 40 mmHg, strongly suggests that ROSC has occurred. This spike in exhaled carbon dioxide is one of the most accurate indicators of restored circulation. The confirmation of ROSC triggers an immediate change in patient management, moving the focus from chest compressions to stabilization.
Halting Chest Compressions and Ventilation
Once ROSC is confirmed by a palpable pulse, measurable blood pressure, or a sudden rise in EtCO2, chest compressions and ventilation must cease immediately. The rationale for stopping CPR is that continued compressions on a heart that is already beating are not only unnecessary but actively damaging. The mechanical force of chest compressions can cause direct injury to the heart muscle, a condition known as myocardial contusion, and may disrupt the newly established, fragile rhythm.
Continuing to push on the chest when the heart is contracting spontaneously can reduce the heart’s own output and lower the patient’s blood pressure, which reverses the goal of resuscitation. Compressions can also increase the risk of internal injuries, such as rib fractures, lung punctures, and liver or spleen lacerations, that are no longer justified. The immediate cessation of CPR marks the transition to the stabilization phase of care.
Priorities After Stopping CPR
With the heart beating again, the immediate priorities shift entirely toward managing the patient’s overall physiology and preventing a second cardiac arrest. This post-resuscitation period is unstable, and the patient must be rapidly stabilized to ensure oxygen and nutrients continue to reach the brain and other organs. The initial focus is on Airway and Breathing Management; the patient’s airway is secured, typically with an advanced device, and ventilation is strictly controlled.
Caregivers must avoid hyperventilation (too much breathing) and hyperoxia (too much oxygen), as both can worsen brain injury. Oxygen saturation is carefully maintained within a target range, often between 94% and 98%, and the EtCO2 is regulated to a normal level, typically between 35 and 45 mmHg. This precise control helps prevent secondary injury to the already fragile brain tissue.
Simultaneously, the focus turns to Circulation Management, ensuring that blood pressure is adequate to perfuse the vital organs. Hypotension, or low blood pressure, is common and is treated aggressively with intravenous fluids and sometimes with vasopressor medications to maintain a target systolic blood pressure above 90 mmHg or a Mean Arterial Pressure (MAP) greater than 65 mmHg. This pressure control is necessary to protect the brain and heart from further ischemic damage.
The final priority is Addressing the Cause of the arrest, which involves rapidly identifying and treating the underlying problem that led to the heart stopping in the first place. A quick 12-lead electrocardiogram (ECG) is obtained to check for signs of an acute heart attack, which would necessitate immediate intervention like cardiac catheterization. Many patients who remain unconscious receive Targeted Temperature Management (TTM), where the body temperature is maintained between 32°C and 36°C for at least 24 hours to help protect the brain from injury.