Lactic Alkalosis: an Unusual and Confusing Presentation of Pulmonary Embolism

1UMDNJ‐Cooper University Hospital, Camden, NJ
2Hospital of University of Pennsylvania, Philadelphia, PA
3UMDNJ‐Cooper University Hospital, Camden, NJ

Meeting: Hospital Medicine 2008, April 3-5, San Diego, Calif.

Abstract number: 156

Case Presentation:

A 63‐year‐old woman with a history of obesity and breast cancer metastatic to the spine presented with 3 days of fatigue, decreasing exercise tolerance, and dyspnea. She had gemcitabine and carboplatin 4 days prior. Home medications included venalafaxine, irbesartan, and amlodipine. On physical examination, blood pressure was 100/65, heart rate 110, temperature 96.5, respiratory rate 24, and pulse oximetry 98% on room air. She had 2+ bilateral lower extremity edema, but her exam was otherwise normal. Admission labs were Na 127, K 4.0, Cl 86, HCO3 28, BUN 44, creatinine 1.1, glucose 270, WBC 15, Hgb 12.8, PLT 194, and lactic acid 6.5. Infection was considered, and a workup including a chest x‐ray, urinalysis, and cultures was unremarkable. The next day lactate was 5.4; consultants recommended an ABG, which was 7.53/27/78. Because of respiratory alkalosis and concern for pulmonary embolism (PE), a CT chest was done and revealed a right‐sided PE. The patient was started on anticoagulation and was discharged a few days later without complications.


Respiratory alkalosis has been documented to cause a rise in serum lactic acid level in both in vitro and in vivo studies. The underlying proposed mechanisms are stimulation of anaerobic glycolysis at high pH values, microcirculatory vasoconstriction with local underperfusion, and reduced urinary lactic acid clearance. Pulmonary embolism is a common disease with high mortality if not recognized. Although our patient had risk factors for PE (neoplasia and obesity) and presented with dyspnea, tachypnea, and tachycardia, the elevated serum lactate did not fit with the classical description. Because of the elevated serum lactate, the clinician may algorithmically start searching for an anion gap metabolic acidosis such as sepsis. This approach may be too restrictive and lead to anchoring bias and delay or missed diagnosis. In this case the diagnosis of PE was not considered until 24 hours later.


Our case illustrates an unusual presentation of lactic acidosis in the setting of respiratory alkalosis and PE. It highlights the importance of evaluating arterial blood gas in any acid‐base disturbance. The concept of respiratory alkalosis leading to lactic acidosis is underappreciated and underresearched and thus may not be readily considered. Anchoring bias and dependence solely on algorithms can lead to missed or delayed diagnosis; therefore, a broad differential should be maintained until final conclusions are made.

Author Disclosure:

E. Kupersmith, Ortho‐McNeal, speakers bureau; J. Rachoin, none; E. Cerceo, none.

To cite this abstract:

Kupersmith E, Cerceo E, Rachoin J. Lactic Alkalosis: an Unusual and Confusing Presentation of Pulmonary Embolism. Abstract published at Hospital Medicine 2008, April 3-5, San Diego, Calif. Abstract 156. Accessed December 10, 2018.

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