RESUS BLOG - Back to the Basics: The Effect of Acidemia on Catecholamine Response
CASE PRESENTATION
A 35-year-old male with unknown medical history was brought into the Emergency Department after an unwitnessed cardiac arrest outside of the hospital. Bystander cardiopulmonary resuscitation (CPR) was ongoing when EMS squad arrived. The patient received 3 doses of epinephrine while in transport to the ED.
On arrival to the ED, chest compressions were ongoing. Patient was in ventricular fibrillation rhythm with initial heart rate in the 140s. Patient received defibrillation and obtained return of spontaneous circulation (ROSC) but was then found to be in ventricular tachycardia. He was given amiodarone and underwent synchronized cardioversion, at which point he went into sinus tachycardia.
The patient was found to have a significant lactic acidosis (lactate= 14, pH=6.87) on initial venous blood gas. He was given bicarbonate for profound metabolic acidemia. He was started on an epinephrine drip for persistent shock.
What is the effect of acidemia on myocardial contractility and vascular tone?
Acidosis is a significant predictor of mortality in critically ill patients, and early blood pH has been shown to be a prognostic factor of neurological outcome after cardiac arrest. As expected, those with higher pH at the onset of advanced life support (ALS) were more likely to achieve ROSC and had higher rates of survival to hospital discharge. Acidemia can lead to perturbations in both myocardial contractility and vasomotor tone
Mechanisms behind the impact of acidemia on cardiac function have been studied in vivo models for decades. A drop in intracellular pH reduces muscle twitch-force and myofilament sensitivity to calcium, thus reducing cardiac contractility and cardiac output. In 2012, in one of the first in-vitro studies, Schotola et al. demonstrated that even a mild metabolic acidosis (pH=7.2) led to decreased twitch-force amplitude in patients with heart failure, when compared with pH=7.4.
Vascular responsiveness to catecholamines is also reduced in an acidemic state. This is thought to be due to vascular smooth muscle relaxation, an overproduction of vasodilatory molecules (nitric oxide [NO] and prostacyclin), a reduced number of adrenoceptors on endothelial cell surfaces, and inactivation of catecholamines by oxidation during states of acidosis.
If acidemia is bad for the heart and the vasculature, should we correct it with Sodium Bicarbonate in patients requiring catecholamines following cardiac arrest?
The use of sodium bicarbonate during CPR remains controversial. A recent prospective double-blind, single center trial aimed to investigate if sodium bicarbonate utilization in patients who failed to achieve ROSC after 10 minutes of CPR in the setting of severe metabolic acidosis (pH<7.1, or bicarb <10mEq/L). Results of the 2018 study demonstrated that routine use of sodium bicarbonate improved acid-base status, but did not increase rate of ROSC or neurological survival at 1 month, and thus did not provide evidence supporting use of bicarb in severely acidotic patients after 10 minutes without ROSC in cardiac arrest.
CASE CONTINUED
After initially uptitrating epinephrine drip to 0.6mg/kg to maintain mean arterial pressure >60mm the patient was stabilized. He remained in sinus tachycardia, but blood pressure steadily increased, and epinephrine drip was weaned to 0.1mg/kg with adequate mean arterial pressures >80mm. An ABG returned with improved acidosis (pH=7.26) and decreased, yet still elevated, lactate to 11.
This patient had a severe acidosis on initial blood gas requiring a significant dose of epinephrine to maintain perfusing blood pressure. However, with improvement in acid-base status, this case demonstrates a significant improvement in blood pressure response to exogenous catecholamines. Bicarbonate was used in this case given the profound metabolic acidemia (pH < 7.0), though its effects on this patients’ outcome is unknown. Sodium bicarbonate can be considered for use in patients with profound metabolic acidemia requiring catecholamines and vasopressors.
POST BY: JILAN SHIMBERG (MS4 - CWRU)
FACULTY EDITING BY: DR. COLIN MCCLOSKEY (EM-INTENSIVIST)
Sources
Ahn S, Kim YJ, Sohn CH, et al. Sodium bicarbonate on severe metabolic acidosis during prolonged cardiopulmonary resuscitation: a double-blind, randomized, placebo-controlled pilot study. J Thorac Dis. 2018;10(4):2295-2302. doi:10.21037/jtd.2018.03.124
Kimmoun A, Novy E, Auchet T, Ducrocq N, Levy B. Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside [published correction appears in Crit Care. 2017 Feb 21;21(1):40]. Crit Care. 2015;19(1):175. Published 2015 Apr 9. doi:10.1186/s13054-015-0896-7
Lin CH, Yu SH, Chen CY, Huang FW, Chen WK, Shih HM. Early blood pH as an independent predictor of neurological outcome in patients with out-of-hospital cardiac arrest: A retrospective observational study. Medicine (Baltimore). 2021;100(17):e25724. doi:10.1097/MD.0000000000025724
Schotola H, Toischer K, Popov AF, et al. Mild metabolic acidosis impairs the β-adrenergic response in isolated human failing myocardium. Crit Care. 2012;16(4):R153. Published 2012 Aug 13. doi:10.1186/cc11468
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