METABOLIC ACIDOSIS

th
18 Annual Update in Cardiopulmonary Bypass
Albert T. Cheung, M.D.
Anesthesiology and Critical Care

University of Pennsylvania, Philadelphia, PA

Metabolic Acidosis in Cardiac Surgical Patients

Metabolic acidosis is a common finding in the perioperative period among

cardiac surgical patients. Although mild metabolic acidosis is common,
severe or persistent metabolic acidosis is a nonspecific sign of tissue
ischemia or hypoperfusion and associated with an unfavorable prognosis (1-
3). In the absence of pre-existing acid-base disorders, acquired metabolic
acidosis during cardiac surgery is almost always caused by excessive acid
production that overwhelms the buffering capacity of the body and exceeds
the ability of the kidneys and lung to eliminate the excess acid. The
detection of metabolic acidosis should prompt a search for sites of tissue
ischemia and initiation of medical interventions to improve tissue perfusion.
Despite the frequency of this problem, considerable controversy exists
regarding the physiologic consequences of acute metabolic acidosis and the
role of sodium bicarbonate for the treatment of this problem.
The Physiologic Consequences of Metabolic Acidosis

Several of the physiologic consequences of metabolic acidosis are well

established. Metabolic acidosis causes a decrease in the pH within the
central nervous system that increases respiratory drive to increase minute
ventilation and decrease arterial Pa CO2. The normal respiratory response to
-
metabolic acidosis is an arterial P aCO 2 (mm Hg) = 1.5 [HCO3 ]2, but the
effects of metabolic acidosis on respiratory drive may be masked by general
anesthesia, controlled mechanical ventilation, or cardiopulmonary bypass.
Metabolic acidosis also causes a right shift of the oxygen-hemoglobin
dissociation curve to favor the unloading of oxygen to tissues.
The precise cardiovascular consequences of metabolic acidosis in the clinical
setting are more difficult to establish because it is not possible to separate
the independent cardiovascular actions of acidosis from the cardiovascular
effects of the underlying conditions that produce acidosis. Laboratory
investigations suggest that severe metabolic acidosis with pH values less
than 7.2 cause the release of endogenous catecholamines, direct myocardial
depression, a decreased responsiveness of the myocardium to
catecholamines, arterial vasodilation, and even bradycardia at extremely low
pH values (4). Based on these laboratory findings, a pH value of 7.2 is
commonly considered the clinical threshold for treatment with alkalinizing
agents such as sodium bicarbonate. Because the cardiovascular actions of
metabolic acidosis depend upon many factors, the precise cardiovascular
responses in among individual patients may vary
over time depending upon pre-existing conditions, ongoing drug
therapy, and endogenous sympathoadrenal function.
Metabolic Acidosis and the Cardiopulmonary Bypass (CPB) Pump
Prime

The rapid expansion of plasma volume with crystalloid solution upon the
initiation of CPB produces may contribute to metabolic acidosis (5-9). The
metabolic acidosis caused by the CPB prime is associated with a decrease in
-
the pH, a decrease in [HCO3 ], a decrease in the base excess, an increase in
- + - -
[Cl ], and a decreased or normal anion gap ([Na ]-[Cl ]-[HCO 3 ]).
Explanations for the acute non-anion gap acidosis caused by CPB include
dilution of the plasma bicarbonate pool, hyperchloremia caused by the
administration of a chloride solution at supra-physiologic concentrations
(normal saline), hemodilution-induced decrease in plasma protein
concentration (that act as weak acids), or the addition of unmeasured anions
in the CPB prime solution (lactate, gluconate, or acetate). Acute non-anion
gap metabolic acidosis caused by acute hemodilution has also been reported
in response to rapid volume expansion with normal saline and acute
normovolemic hemodilution with 5% albumin or 6% hydroxyethyl starch (10-
11). The metabolic acidosis caused by acute plasma dilution accompanying
the onset of CPB can be attenuated by priming the CPB circuit with solutions
containing physiologic concentrations of bicarbonate or with solutions
containing lactate to balance the concentration of chloride. The use of
balanced crystalloid solutions containing lactate can increase plasma lactate
concentrations during CPB.
Lactic Acidosis

Lactate is a metabolic product of glycolysis and accumulates when the body

must generate ATP in the absence of oxygen. Lactate is buffered by
bicarbonate and is mostly oxidized in the liver, but can also be cleared to a
lesser extent by renal excretion or gluconeogenesis. Normal arterial
concentrations of lactate are less than 1.5 mM per liter. Plasma
concentrations of lactate in the range of 4-5 mM per liter or greater will
produce lactic acidosis with an accompanying decrease in serum bicarbonate
associated with an increased anion gap. The most common cause of lactic
acidosis (type A) is overproduction as a consequence of hypoperfusion,
hypoxemia, circulatory failure, malperfusion, severe anemia, hypotension,
sepsis, or carbon monoxide poisoning (12). The reperfusion of ischemic
tissue or a period of circulatory arrest during CPB will reliably produce lactic
acidosis in cardiac surgical patients. Lactic acidosis can also occur in the
absence of hypoperfusion or hypoxia (type B) as a consequence of liver
disease, diabetes mellitus, hypoglycemia, renal failure, malignancies, certain
drugs, thiamine deficiency, metabolic toxins, and hereditary defects.
Epinephrine increases glycolysis and inhibits the oxidation of pyruvate and
can contribute to increased blood lactate levels. Metformin has been
implicated in lactic acidosis through its action on inhibiting oxidative
metabolism, gluconeogenesis, and the gastrointestinal absorption of glucose
(13). Lactic acidosis is also a nonspecific sign of nitroprusside toxicity in
cardiac surgical patients. The administration of buffered electrolyte solutions
that contain lactate such as Lactated Ringers solution or Hartmanns
solution will also increase arterial lactate concentrations. As a consequence,
lactic acidosis is a relatively common finding among cardiac surgical patients
with
multiple potential etiologies and typically generates a common
diagnostic and treatment dilemma in the perioperative management of
patients undergoing cardiac operations.
The Treatment of Lactic Acidosis

The definitive treatment of lactic acidosis caused by tissue ischemia,

hypoperfusion, shock, or reperfusion should be the identification of the
source of lactic acidosis and therapeutic interventions to improve perfusion
and oxygen delivery to ischemic tissue. Restoration of tissue perfusion will
decrease the rate of lactic acid production and restoration of hepatic and
renal function will increase the rate of lactic acid oxidation and excretion.
Despite appropriate medical and surgical therapy, the source of lactic
acidosis cannot always be identified, normal hepatic and renal function may
be impaired, and patients may develop severe metabolic acidosis that may
compromise cardiovascular function. For this reason, immediate therapy to
attenuate the deleterious effects of severe acidosis is often justified during
the course of treatment. The administration of sodium bicarbonate is
commonly prescribed as a supportive measure. Although sodium bicarbonate
is commonly administered in the clinical setting for this purpose and is
effective at increasing arterial pH and plasma bicarbonate concentration,
considerable controversy exists regarding its efficacy in the setting of lactic
acidosis (14-15). The administration of sodium bicarbonate is associated with
2+
an increase arterial CO2, decrease plasma ionized Ca , and hypernatremia.
Alkalinization of the plasma may also decrease intracellular pH, increase
lactic acid production, and produce a leftward shift in the oxygen-hemoglobin
dissociation curve that may decrease unloading of oxygen to tissues. Sodium
bicarbonate solutions are very hypertonic compared to serum and the
accumulation of solute will lead to hypernatremia or volume overload.
Clinical studies have yet to demonstrate that sodium bicarbonate
administration for severe metabolic acidosis improves survival (16-17). As an
alternative to sodium bicarbonate, hemodialysis or ultrafiltration has also
been reported as an effective means of clearing plasma lactate and may
even mask lactic acidosis in critically ill patients (18).
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