Key result
Respiratory alkalosis conceals severe hyperlactatemia of ~11 mmol/L in normotensive acute heart failure.
Why the study?
In acute heart failure complicated by acute hypoxemic respiratory failure, when severe hyperlactatemia coexists with a primary respiratory alkalosis, a near-normal pH may conceal the true metabolic severity.
Case Report (n=1)
No
In acute heart failure complicated by acute hypoxemic respiratory failure, severe hyperlactatemia coexisting with primary respiratory alkalosis can result in a near-normal pH that masks profound metabolic severity and high clinical risk even when blood pressure is preserved.
Answers are grounded in this paper and cite their sources.
pH near normal may conceal high-risk hyperlactatemia in acute heart failure; hypothesis-generating for lactate monitoring, needs prospective validation.
Introduction: Acute heart failure (AHF) presenting as acute pulmonary edema is a leading cause of acute hypoxemic respiratory failure (AHRF). Elevated lactate identifies organ injury and a worse prognosis in AHF even without overt hypoperfusion, and lactate combined with acidemia strongly modifies mortality in cardiogenic shock; when severe hyperlactatemia coexists with a primary respiratory alkalosis, a near-normal pH may conceal the true metabolic severity.1–3 Case illustration: A 48-year-old man with a previous ST-elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI) and a prior episode of AHF presented with dyspnea since the previous night, respiratory rate 41 breaths/min, SpO2 78% on room air (87% on a non-rebreathing mask), blood pressure 148/103 mmHg, heart rate 120 beats/min, warm extremities and bilateral crackles with wheezing. Arterial blood gas (reported FiO2 0.81) showed pH 7.35, PaCO2 21 mmHg, PaO2 52 mmHg, HCO3− 11.8 mmol/L, base excess −14 mmol/L and lactate 11.20 mmol/L; PaCO2 below the Winter's range (23.7–27.7 mmHg) indicated a concurrent primary respiratory alkalosis. High-sensitivity troponin I was 65.2 pg/mL (≈1.7 × upper reference limit), creatinine 1.84 mg/dL, potassium 2.8 mmol/L and glucose 300 mg/dL. Despite nitroglycerin, furosemide and mask oxygen he required intubation, after which high respiratory drive (total rate 43 breaths/min; tidal volume ≈10.6 mL/kg predicted body weight), severe hypoxemia (SpO2 93% on FiO2 0.85) and a fall in blood pressure to 101/55 mmHg were documented.4–6 Discussion: The ≈13% reduction in arterial oxygen content could not by itself explain a lactate of 11.2 mmol/L, implying superimposed normotensive low-output hypoperfusion, catecholamine-driven aerobic glycolysis—mirrored by hypokalemia and hyperglycemia—alkalosis-enhanced glycolysis, increased work of breathing and reduced clearance. The near-normal pH concealed a profound base deficit, a metabolic–hemodynamic discordance poorly captured by blood pressure-based staging, while vigorous post-intubation effort carried a risk of patient self-inflicted lung injury.7–10 Conclusion: In AHF complicated by AHRF, severe hyperlactatemia with a mixed acid–base disorder is a high-risk phenotype even when blood pressure is preserved. Systematic acid–base analysis, serial lactate, early echocardiography and lung ultrasound, timely evaluation for acute coronary syndrome, potassium repletion before or with insulin and diuretics, and lung-protective ventilation that controls respiratory drive are essential.11,12
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Anugrah et al. (2026) conducted a case report in Acute heart failure complicated by acute hypoxemic respiratory failure, severe hyperlactatemia, and mixed acid-base disorder (n=1). Severe hyperlactatemia (11.20 mmol/L) with mixed metabolic acidosis and primary respiratory alkalosis was evaluated. Severe hyperlactatemia (11.20 mmol/L) and base excess (-14 mmol/L) were concealed by primary respiratory alkalosis (PaCO2 21 mmHg, pH 7.35) in a normotensive acute heart failure patient.
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