What causes metabolic acidosis in an ICU patient after a stroke from an air embolism post-mitral valve repair?

Metabolic Acidosis After Stroke from Air Embolism Post-Mitral Valve Repair

Metabolic acidosis in this clinical scenario develops primarily from tissue hypoperfusion and ischemia caused by the air embolism-induced stroke, leading to lactic acidosis from inadequate oxygen delivery to tissues, compounded by potential mesenteric ischemia if emboli affect splanchnic circulation. 1

Primary Pathophysiological Mechanisms

Tissue Hypoperfusion and Lactic Acidosis

• Air embolism during mitral valve repair causes cerebral and potentially systemic tissue ischemia, resulting in anaerobic metabolism and lactate accumulation as the primary driver of metabolic acidosis. 1
• Lactic acidosis results from inadequate oxygen delivery to tissues, with lactate levels >2 mmol/L indicating tissue hypoxia and correlating with mortality in shock states. 1
• The metabolic acidosis is characterized by decreased blood pH (<7.35), reduced serum bicarbonate (<22 mmol/L), elevated blood lactate levels, and increased base deficit. 1

Air Embolism-Specific Mechanisms

• Air embolization during transcatheter mitral valve procedures occurs from blood stasis in combination with missing atrial contraction, creating a thrombogenic status that predisposes to thrombus formation at the puncture site, on the mitral annulus, or on the device itself. 2
• The prothrombotic state of each patient determines the risk of thrombosis, especially in patients with very low cardiac output, which further compromises tissue perfusion. 2
• Gaseous emboli can occur because of inarticulate de-airing techniques during the procedure, directly causing tissue ischemia in multiple vascular beds. 2

Mesenteric Ischemia Contribution

• If air emboli reach the mesenteric circulation, acute mesenteric ischemia can develop, causing severe metabolic acidosis and hyperkalemia due to bowel infarction and reperfusion injury. 2
• Right-sided abdominal pain associated with passage of maroon or bright red blood in the stool is highly suggestive of non-occlusive mesenteric ischemia (NOMI) in post-cardiac surgery patients. 2
• Gastrointestinal perfusion is often impaired early in situations of critical illness and major surgery, characterized by increased demands on circulation to maintain tissue oxygen delivery. 2
• Any negative changes in patient physiology, including new onset of organ failure and increased vasoactive support, should raise suspicion of mesenteric ischemia in ICU patients. 2

Secondary Contributing Factors

Cardiovascular Compromise

• Fast or rapid pacing techniques during transcatheter valve deployment can result in cerebral hypoperfusion and create watershed infarcts, further compromising tissue perfusion. 2
• Drop in blood pressure from blood volume shifts, changes in drug dosing, or balloon inflation during the procedure contributes to global hypoperfusion. 2
• Decreased cardiac output from the stroke itself or post-operative cardiac dysfunction reduces systemic oxygen delivery. 1

Renal Dysfunction

• Acute kidney injury superimposed on the critical illness impairs the kidney's ability to excrete hydrogen ions and maintain bicarbonate homeostasis. 3
• The kidneys normally maintain acid-base homeostasis through elimination of protons and reabsorption/generation of bicarbonate, but these mechanisms become overwhelmed in critical illness. 4

Iatrogenic Factors

• Hyperchloremic acidosis can develop from aggressive crystalloid resuscitation with normal saline, though this is typically less severe than lactic acidosis. 5
• Vasopressor use, while necessary to maintain blood pressure, can worsen mesenteric hypoperfusion and contribute to ongoing lactic acidosis. 2

Diagnostic Approach

Initial Assessment

• Measure arterial blood gases to determine pH, PaCO2, and calculate base deficit, along with serum lactate and bicarbonate levels. 1
• Calculate the anion gap [(Na+ + K+) - (Cl- + HCO3-)] to determine if this is an elevated anion gap acidosis (expected with lactic acidosis) or normal anion gap acidosis. 6, 5
• Serial measurements of lactate, base deficit, and pH provide valuable information about shock severity and response to treatment. 1

Identifying Specific Causes

• Evaluate for mesenteric ischemia if the patient develops new abdominal pain, distension, bloody stools, or unexplained worsening of acidosis despite treatment. 2
• Base deficit is an independent predictor of mortality in shock states, reflecting global tissue acidosis due to impaired perfusion. 1
• Monitor for signs of multiple organ dysfunction, as septic shock can exhibit complex metabolic acidosis with contributions from lactic acidosis, hyperchloremic acidosis, and increased strong ion gap. 1

Management Strategy

Addressing the Underlying Cause

• The primary treatment is restoring tissue perfusion through hemodynamic optimization, not bicarbonate administration, as treating the underlying cause is essential. 7, 8
• Fluid resuscitation with crystalloid and blood products is essential, with early hemodynamic monitoring to guide effective resuscitation. 2
• Vasopressors should be used with caution and only to avoid fluid overload; dobutamine, low-dose dopamine, and milrinone have less impact on mesenteric blood flow than other vasopressors. 2

Bicarbonate Therapy Considerations

• Bicarbonate therapy is controversial in acute metabolic acidosis and should only be considered when pH falls below 7.2, as it lacks definitive benefit and carries potential complications. 9, 8
• In cardiac arrest scenarios, rapid intravenous doses of 44.6 to 100 mEq may be given initially, but caution is required as bicarbonate solutions are hypertonic and may produce undesirable rises in plasma sodium. 9
• For less urgent metabolic acidosis, 2 to 5 mEq/kg body weight over 4 to 8 hours may be administered, with therapy monitored by measuring blood gases, plasma osmolarity, arterial blood lactate, and hemodynamics. 9
• It is unwise to attempt full correction of low bicarbonate during the first 24 hours, as this may be accompanied by unrecognized alkalosis due to delayed readjustment of ventilation. 9

Supportive Care

• Maintain oxygen saturation >94% to optimize tissue oxygen delivery. 2
• Correct electrolyte abnormalities, particularly hyperkalemia, which may be present due to underlying tissue infarction and reperfusion. 2
• Broad-spectrum antibiotics should be administered immediately given the high risk of infection from bacterial translocation if bowel ischemia is present. 2

Critical Pitfalls to Avoid

• Do not assume elevated lactate always signifies cell ischemia; other causes include medications, seizures, and liver dysfunction, though in this post-operative stroke scenario, tissue hypoperfusion is most likely. 5
• Avoid aggressive bicarbonate administration without addressing the underlying perfusion deficit, as this can worsen intracellular acidosis and cause rebound alkalosis. 8
• Do not overlook mesenteric ischemia in post-cardiac surgery patients with unexplained acidosis, as prompt laparotomy may be life-saving if bowel infarction has occurred. 2
• Prevent complications during resuscitation including hypothermia, hypocalcemia, and worsening acidosis, as these can exacerbate coagulopathy and shock. 1
• Monitor for respiratory compensation impairment in severe shock, as this can lead to combined metabolic and respiratory acidosis. 1