Acid-base changes during resuscitation from out-of-hospital cardiac arrest

Cardiac arrest, the ultimate medical emergency, is cessation of blood flow to all tissues due to sudden failure of the heart to contract (pump) effectively, evident as absence of a palpable carotid pulse. A major consequential symptom is ineffective or absent breathing and therefore no pulmonary gas exchange. 

Reduced perfusion of tissues and absent pulmonary gas exchange together cause: tissue hypoxia; accumulation of lactate and hydrogen ions; accumulation of carbon dioxide (hypercapnia); and reduction in blood oxygen tension (hypoxemia). Given these consequences of cardiac arrest it is easy to appreciate that the condition is associated with abnormality in all measured and calculated blood gas parameters (pH, pCO_2, pO₂, bicarbonate, base excess) and lactate. 

This prospective clinical study reveals just how profound and severe are the changes in blood gas parameters during cardiac arrest. But more than this, it provides evidence to suggest that one parameter in particular, pCO₂, might be useful in predicting which patients are most likely to be resuscitated from cardiac arrest. 

The study population comprised 136 individuals who had suffered out-of-hospital cardiac arrest, before urgent ambulance transfer to hospital emergency room (ER). During transfer, basic prehospital cardiopulmonary resuscitation (CPR) was initiated, but all study patients remained in a non-resuscitated state on arrival at ER. 

Immediately (within 4 minutes) on arrival at ER, as CPR was continued, arterial blood was sampled from each study patient for blood gas analysis; in addition to measurement of standard blood gas parameters, the blood gas analyzer used allowed measurement of four other parameters: lactate, electrolytes (Na⁺ and K⁺) and glucose. 

The outcome measure for this study was sustained return of spontaneous circulation (ROSC) or death. Sustained ROSC, which is of course the immediate objective of CPR, was defined for this study as a palpable pulse for >20 minutes. Of the 136 patients, 67 (49.3 %) achieved sustained ROSC and 69 (50.75 %) did not. 

Admission blood gas results for the 136 patients included the following: median pH 6.89 (Inter-quartile range, IQR 6.80-7.02); median pCO₂ 78.0 mmHg [10.4 kPa] (IQR 63.0-98.0 mmHg [8.4-13.0kPa]); median pO₂ 17.5 mmHg [2.3kPa](IQR 9.0-45.8 mmHg [1.2-6.0 kPa]); and median base excess -15.6 mmol/L (IQR –18.6 to –11.5 mmol/L). 

These extreme blood gas results confirm that cardiac arrest is associated with the most severe metabolic (lactic) acidosis, severe hypercapnia and associated respiratory acidosis, and severe hypoxemia. In the case of 47 patients, the acidosis was so severe that pH was below the blood gas analyzer’s lower limit of measurement, 6.80. The lactate concentration of 40 patients exceeded the upper limit of lactate measurement of the instrument (15.0 mmol/L).

The 67 patients who subsequently achieved sustained ROSC tended to have less severe metabolic acidosis and hypercapnia at ER admission than those 69 who died without being resuscitated. Thus the median pH was significantly higher, and lactate and pCO₂ significantly lower in the ROSC group compared with the non-ROSC group. 

This difference was particularly strong for pCO₂, and in multivariate logistic regression analysis, pCO₂ was found to be an independent predictor of sustained ROSC. In further statistical analysis the authors determined that if pCO₂ is <75 mmHg [9.8 kPa] at admission, then out-of-hospital cardiac arrest victims are 3.3 times more likely to achieve sustained ROSC then those whose admission pCO₂ is >75 mmHg [9.8 kPa].

Read more about acid-base:

• On the relationship between potassium and acid-base balance
• Acid-base disturbance in COPD
• Acid-base and electrolyte disorders in CKD – a review article
• Acid-base disturbance in diabetes