Hemodynamic effects of sodium bicarbonate
Post on 10-Jul-2016
Intensive Care Med (1994) 20:306-310
Intensive Care Medicine 9 Springer-Verlag 1994
Hemodynamie effects of sodium bicarbonate
In an uncontrolled study in critically ill neonates Fanconi et al. [11 concluded that "Sodium bicarbonate in neonates with metabolic acido- sis induces an increase in contractility". This conclusion cannot be justi- fied by their data and is not supported by other recent data  not cited in the Fanconi paper, nor in the accompanying editorial .
In a recent controlled study in critically ill adults with lactic acidosis Cooper et al.  reported that transiently increased cardiac output dur- ing bicarbonate infusion was due to increased preload associated with the intravenous infusion of a hypertonic solution. Increased cardiac output did not relate to changes in pH and occurred equally during a control infusion of equimolar sodium chloride,
Fanconi etal . reported that bicarbonate infusion increased cardiac output (maximal at 1 min). Increased cardiac output was not due to de- creased afterload (blood pressure increased at that time) or to increased heart rate (no change). Increased cardiac output must therefore have been due either to increased left ventricular (LV) preload, increased LV contractility or increased LV diastolic compliance. LV preload must in- crease during infusion of a hypertonic solution which expands in- travascular volume, but in this study left ventricular preload was not ac- curately measured. Central venous pressure was reported but is a highly insensitive index of left ventricular preload (especially when low) and furthermore a small increase in preload will cause a large increase in cardiac output when starting from a point low on the cardiac function curve. LV contractility was not measured in the study of Fanconi etal., but other recent studies report that sodium bicarbonate infusion does not increase LV contractility either in animals [4, 5] or in adult patients . Therefore it seems unlikely that bicarbonate would increase LV con- tractility in neonates. LV diastolic compliance may have increased in the study of Fanconi et al. if pulmonary artery pressures had decreased fol- lowing improvement in acidemic pulmonary hypertension. However, pulmonary artery pressures were not measured in this study (and pa- tients with clinical signs of pulmonary hypertension were specifically excluded) so this possibility is purely speculative.
In summary, Fanconi eta l .  reported that sodium bicarbonate transiently increased cardiac output when infused intravenously in neo- nates with metabolic acidosis. This study did not identify the cause of increased cardiac output, not did it identify any change in myocardial contractility. Uncontrolled, unblinded studies whether in neonates or in adults should be interpreted with caution.
1. Fanconi S, Burger R, Ghelfi D, Uehlinger J, Arbenz U (1993) Hemodynamic effects of sodium bicarbonate in critically ill neo- nates. Intensive Care Med 19:65-69
2. Cooper DJ, Walley KR, Rnssel JA (t990) Bicarbonate does not im- prove hemodynamics in human lactic acidosis: a prospective, con- trolled study. Ann Intern Med 112:492-498
3. Tibballs J (1993) Bicarbonate and haemodynamics in neonates. In- tensive Care Med 19:63-64
4. Cooper DJ, Walley KR (1993) Bicarbonate does not improve de- creased left ventricular contractility during lactic acid infusion in pigs. Am Rev Respir Dis (in press)
5. Walley KR, Cooper DJ (1992) Neither hypertonic saline nor bicar- bonate improve left ventricular contractility during hypovolemic shock in pigs. J Crit Care 7:14-21
Dr. D.J. Cooper, Intensive Care Department, Alfred Hospital, Com- mercial Rd, Prahran, 3181, Melbourne, VIC, Australia
Hemodynamic effects of sodium bicarbonate - authors reply
I completely agree that unblinded studies should be interpreted with caution and I accept the criticism of Dr. Cooper that in our study, at least theoretically, a rise in left ventricular preload can not be excluded and that we had no direct measurement of contractility.
From a scientific point of view double blind randomized studies with the exact measurement of all interesting variables are the only true answer to clinical questions. Unfortunately, especially in human neo- nates, this is difficult. Talking sodium bicarbonate, what is the correct control substance? Is it equimolar sodium chloride, normal saline, or rather another alkalizing agent like dichloroacetate, tromethamine, or cabicarb? A crossover study in which each patient sequentially receives sodium chloride and sodium bicarbonate like Cooper et al. performed is questionable in neonates due to their tendency to develop hyper- natremia and its possible association with intraventricular hemorrhage . Besides, equimolar sodium solutions certainly allow to demonstrate if the effects of sodium bicarbonate are related to the volume load or to the osmolality of the solution. This is physiologically interesting, but from a clinical point of view this is not the question; we give sodium bicarbonate to our patients because we want to correct the metabolic ac- idosis and primarily not because we want to improve cardiac output. In other words, hyperosmolar solutions are not a true alternative to sodi- um bicarbonate because they do not improve the pH.
In spite of the fact that we had no direct measurement of contractili- ty, which would be difficult in neonates (available echocardiographic data also depend on the loading conditions of the heart), and that we had no measurement of left ventricular preload, we still feel that the rise in cardiac output and aortic blood flow velocity just when blood pres- sure increased and in the absence of an increase in central venous pres- sure suggest that bicarbonate had a positive effect on contractility. Ad- ditionally, the results in five control patients that were not included in the paper, who received a comparable amount of normal saline (there was a not significant and transient increase in cardiac output of 4.6~ one minute after the infusion), also suggest that an increase in preload may not be that important. NudeI et al.  also found indications that sodium bicarbonate, in contrast to normal saline restored contractility in newborn swine with hypoxic lactic acidosis. In their study pH after correction reached a low normal mean value (7.30) similar to the one in our patients (7.30) which is significantly lower than the one achieved in the study of Cooper and coworkers (7.45). This "overcorrection"of the metabolic acidosis and/or the age of the animals may in fact explain the absence of an increase in contractility possibly through an addition-