Q66 / 110
A cardiac surgery patient has a lactate level of 6 mmol/L and a lactate-to-pyruvate (L/P) ratio of 12 (normal is roughly 10:1). What is the most likely mechanism?
Correct answer: C — Accelerated aerobic metabolism
A normal L/P ratio (here, 12, near the normal ~10:1) favors increased lactate generation from accelerated aerobic metabolism rather than impaired oxygen delivery. The L/P ratio reflects the cytoplasmic NADH/NAD⁺ redox state and rises when oxidative phosphorylation is impaired (tissue hypoxia). In cardiac surgical patients, a normal ratio with elevated lactate commonly reflects stress states and catecholamine exposure driving aerobic glycolysis. In contrast, hypoxic mechanisms increase the ratio — published thresholds for "elevated" vary by source and context, ranging from >18 (Suistomaa et al., general ICU admissions) to >20 (commonly cited for systemic blood) to >25 (used in the congenital lactic acidosis literature), so the specific cutoff should be interpreted alongside the clinical context rather than as a single universal number. The ratio therefore helps distinguish mechanism, not just severity.
Board pearl: A normal lactate-to-pyruvate ratio (~10:1) in the setting of elevated lactate suggests non-hypoxic, aerobic lactate production; "elevated" thresholds vary by source (roughly >18–25) and should be interpreted in context.
A normal L/P ratio (here, 12, near the normal ~10:1) favors increased lactate generation from accelerated aerobic metabolism rather than impaired oxygen delivery. The L/P ratio reflects the cytoplasmic NADH/NAD⁺ redox state and rises when oxidative phosphorylation is impaired (tissue hypoxia). In cardiac surgical patients, a normal ratio with elevated lactate commonly reflects stress states and catecholamine exposure driving aerobic glycolysis. In contrast, hypoxic mechanisms increase the ratio — published thresholds for "elevated" vary by source and context, ranging from >18 (Suistomaa et al., general ICU admissions) to >20 (commonly cited for systemic blood) to >25 (used in the congenital lactic acidosis literature), so the specific cutoff should be interpreted alongside the clinical context rather than as a single universal number. The ratio therefore helps distinguish mechanism, not just severity.
Board pearl: A normal lactate-to-pyruvate ratio (~10:1) in the setting of elevated lactate suggests non-hypoxic, aerobic lactate production; "elevated" thresholds vary by source (roughly >18–25) and should be interpreted in context.
Source(s): Kraut JA, Madias NE. Lactic Acidosis. N Engl J Med. 2014;371(24):2309-19. doi:10.1056/NEJMra1309483. | Suistomaa M, Ruokonen E, Kari A, Takala J. Time-Pattern of Lactate and Lactate to Pyruvate Ratio in the First 24 Hours of Intensive Care Emergency Admissions. Shock. 2000;14(1):8-12. doi:10.1097/00024382-200014010-00002. | Debray FG, Mitchell GA, Allard P, et al. Diagnostic Accuracy of Blood Lactate-to-Pyruvate Molar Ratio in the Differential Diagnosis of Congenital Lactic Acidosis. Clin Chem. 2007;53(5):916-21. doi:10.1373/clinchem.2006.081166.
Q67 / 110
Which of the following best distinguishes hypoxic from non-hypoxic hyperlactatemia?
Correct answer: C — Lactate-to-pyruvate ratio
When oxidative phosphorylation is impaired, pyruvate is increasingly converted to lactate and the L/P ratio rises. In non-hypoxic hyperlactatemia, lactate may be elevated while the ratio remains relatively normal. This makes the ratio more mechanistically informative than lactate alone, helping separate impaired oxygen utilization from stress-mediated aerobic lactate production. Rimachi et al. confirmed this prognostic relevance in circulatory and septic shock: the L/P ratio at shock onset was significantly higher in non-survivors than survivors (24 vs 15), and the authors concluded that hyperlactatemia is frequently, but not solely, due to hypoxia — reinforcing that the ratio, not the absolute lactate level, is what identifies the hypoxic component.
Board pearl: An elevated lactate-to-pyruvate ratio suggests hypoxic metabolism; in shock, a higher L/P ratio at onset (e.g., ~24 vs ~15) has been associated with higher mortality.
When oxidative phosphorylation is impaired, pyruvate is increasingly converted to lactate and the L/P ratio rises. In non-hypoxic hyperlactatemia, lactate may be elevated while the ratio remains relatively normal. This makes the ratio more mechanistically informative than lactate alone, helping separate impaired oxygen utilization from stress-mediated aerobic lactate production. Rimachi et al. confirmed this prognostic relevance in circulatory and septic shock: the L/P ratio at shock onset was significantly higher in non-survivors than survivors (24 vs 15), and the authors concluded that hyperlactatemia is frequently, but not solely, due to hypoxia — reinforcing that the ratio, not the absolute lactate level, is what identifies the hypoxic component.
Board pearl: An elevated lactate-to-pyruvate ratio suggests hypoxic metabolism; in shock, a higher L/P ratio at onset (e.g., ~24 vs ~15) has been associated with higher mortality.
Source(s): Rimachi R, Bruzzi de Carvahlo F, Orellano-Jimenez C, et al. Lactate/Pyruvate Ratio as a Marker of Tissue Hypoxia in Circulatory and Septic Shock. Anaesth Intensive Care. 2012;40(3):427-32. doi:10.1177/0310057X1204000307.
Q68 / 110
Which of the following is a common cause of non-hypoxic hyperlactatemia after cardiac surgery?
Correct answer: B — Epinephrine infusion
Beta-2-adrenoceptor–mediated stimulation increases glycolysis and lactate production even when global oxygen delivery is adequate, and epinephrine is a classic example of this phenomenon after cardiac surgery. In contrast, severe anemia, cardiogenic shock, and mesenteric ischemia are more concerning for hypoxic lactate generation. This distinction is important because treatment differs — epinephrine-associated hyperlactatemia does not, by itself, mandate escalation of hemodynamic support. The mechanism is not purely "aerobic" in every setting, however: in healthy volunteers, epinephrine-induced hyperlactatemia appears predominantly aerobic, with increased mitochondrial respiration and no change in oxygen uptake. But in endotoxin/septic shock models, epinephrine has been shown to increase both systemic and regional (particularly splanchnic) L/P ratios, suggesting it can also contribute a regional hypoperfusion component in critically ill patients — so the mechanism in a given post-cardiac-surgery patient may be mixed rather than purely aerobic.
Board pearl: Epinephrine commonly causes aerobic hyperlactatemia via beta-2-mediated glycolysis, but in critically ill or shock states it can also worsen regional (e.g., splanchnic) hypoperfusion — the mechanism may be mixed rather than purely aerobic.
Beta-2-adrenoceptor–mediated stimulation increases glycolysis and lactate production even when global oxygen delivery is adequate, and epinephrine is a classic example of this phenomenon after cardiac surgery. In contrast, severe anemia, cardiogenic shock, and mesenteric ischemia are more concerning for hypoxic lactate generation. This distinction is important because treatment differs — epinephrine-associated hyperlactatemia does not, by itself, mandate escalation of hemodynamic support. The mechanism is not purely "aerobic" in every setting, however: in healthy volunteers, epinephrine-induced hyperlactatemia appears predominantly aerobic, with increased mitochondrial respiration and no change in oxygen uptake. But in endotoxin/septic shock models, epinephrine has been shown to increase both systemic and regional (particularly splanchnic) L/P ratios, suggesting it can also contribute a regional hypoperfusion component in critically ill patients — so the mechanism in a given post-cardiac-surgery patient may be mixed rather than purely aerobic.
Board pearl: Epinephrine commonly causes aerobic hyperlactatemia via beta-2-mediated glycolysis, but in critically ill or shock states it can also worsen regional (e.g., splanchnic) hypoperfusion — the mechanism may be mixed rather than purely aerobic.
Source(s): Garcia-Alvarez M, Marik P, Bellomo R. Stress Hyperlactataemia: Present Understanding and Controversy. Lancet Diabetes Endocrinol. 2014;2(4):339-347. doi:10.1016/S2213-8587(13)70154-2. | Martikainen TJ, Tenhunen JJ, Giovannini I, Uusaro A, Ruokonen E. Epinephrine Induces Tissue Perfusion Deficit in Porcine Endotoxin Shock. Am J Physiol Gastrointest Liver Physiol. 2005;288(3):G586-92. doi:10.1152/ajpgi.00378.2004. | Grip J, Jakobsson T, Hebert C, et al. Lactate Kinetics and Mitochondrial Respiration in Skeletal Muscle of Healthy Humans Under Influence of Adrenaline. Clin Sci. 2015;129(4):375-84. doi:10.1042/CS20140448.
Q69 / 110
Which of the following best explains renal dysfunction in isolated right ventricular failure?
Correct answer: B — Increased renal venous pressure
In right ventricular failure, elevated central venous pressure is transmitted to the renal veins and lowers the transrenal perfusion gradient. This can impair kidney function even when systemic output is not profoundly reduced. The mechanism is therefore not just low forward flow but also venous congestion. Recognizing this changes management priorities toward decongestion and RV support.
Board pearl: Venous congestion is a major driver of kidney injury in right ventricular failure.
In right ventricular failure, elevated central venous pressure is transmitted to the renal veins and lowers the transrenal perfusion gradient. This can impair kidney function even when systemic output is not profoundly reduced. The mechanism is therefore not just low forward flow but also venous congestion. Recognizing this changes management priorities toward decongestion and RV support.
Board pearl: Venous congestion is a major driver of kidney injury in right ventricular failure.
Q70 / 110
Which hemodynamic profile is most characteristic of isolated right ventricular failure?
Correct answer: B — High central venous pressure with low left ventricular filling
When the right ventricle fails, blood backs up into the systemic venous system, increasing central venous pressure. At the same time, forward flow into the pulmonary circulation and then to the left ventricle falls, reducing LV preload. This combination is highly suggestive of isolated or predominant RV failure. It also helps distinguish RV from isolated LV pathology.
Board pearl: Isolated RV failure causes venous congestion and reduced left-sided filling.
When the right ventricle fails, blood backs up into the systemic venous system, increasing central venous pressure. At the same time, forward flow into the pulmonary circulation and then to the left ventricle falls, reducing LV preload. This combination is highly suggestive of isolated or predominant RV failure. It also helps distinguish RV from isolated LV pathology.
Board pearl: Isolated RV failure causes venous congestion and reduced left-sided filling.