What are the expected changes in pH and pO2 (partial pressure of oxygen) levels during a cardiac arrest, before cardiac function is restored?

Expected Blood Gas Changes During Cardiac Arrest

During cardiac arrest, before cardiac function is restored, a technician would expect to see decreased pH and pO2 (option D).

Pathophysiological Changes During Cardiac Arrest

During cardiac arrest, circulation ceases, leading to profound physiological derangements that can be observed in arterial blood gases:

Acid-Base Status

• When cardiac arrest occurs, tissue perfusion stops, resulting in anaerobic metabolism and lactic acid production 1
• Metabolic acidosis rapidly develops due to accumulation of lactic acid from anaerobic metabolism
• Respiratory acidosis simultaneously develops as carbon dioxide (CO2) cannot be eliminated through the lungs due to cessation of pulmonary blood flow
• These combined effects lead to a significant decrease in pH (acidemia)

Oxygen Status

• Without circulation, oxygen delivery to tissues ceases
• Oxygen in the blood is rapidly consumed by tissues
• Without pulmonary circulation, oxygen cannot be replenished in the blood
• This results in a progressive decrease in partial pressure of oxygen (pO2) 1

Carbon Dioxide Status

• CO2 continues to be produced by tissues but cannot be eliminated through the lungs
• This leads to a dramatic increase in pCO2 levels
• Studies have shown that intramyocardial pCO2 can increase from normal levels (around 54 mmHg) to as high as 346 mmHg during cardiac arrest 2

Evidence from Research

• Animal studies have demonstrated that during cardiac arrest, pH decreases from approximately 7.20 to 6.38, while pCO2 increases dramatically 2
• In human studies, patients still receiving CPR on arrival to the emergency department had significantly lower pH (7.18 ± 0.20) compared to those with return of spontaneous circulation (7.40 ± 0.13) 3
• Patients with ongoing cardiac arrest show significantly higher pCO2 (101 ± 33 mmHg) and lower pO2 (41 ± 69 mmHg) compared to patients with restored circulation 3

Clinical Implications

• The degree of acidosis and hypoxemia correlates with the duration of cardiac arrest and can predict outcomes
• Survivors of cardiac arrest typically have higher coronary artery perfusion pressures, higher pCO2, and lower pH values than non-survivors 4
• The adequacy of ventilation during CPR is a principal determinant of the severity of acidosis 3
• After successful resuscitation, these abnormalities begin to normalize, with myocardial pCO2 returning almost completely to pre-arrest levels within 30 minutes 2

Post-Resuscitation Care Considerations

• Once spontaneous circulation is restored, the American Heart Association recommends titrating oxygen to achieve arterial oxygen saturation of 94-98% to avoid both hypoxia and hyperoxia 5
• Normocapnia should be maintained by targeting paCO2 of 35-45 mmHg to optimize cerebral blood flow 1
• Hyperventilation should be avoided as it may cause cerebral vasoconstriction and worsen cerebral ischemic injury 1

In summary, the physiological hallmarks of cardiac arrest include decreased pH due to combined metabolic and respiratory acidosis, and decreased pO2 due to cessation of pulmonary gas exchange, making option D the correct answer.