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Correspondence

Cardiac Contractility during Severe Ketoacidosis

N Engl J Med 1999; 341:1938December 16, 1999

Article

To the Editor:

Experimental studies suggest that metabolic acidosis impairs the contractile function of the heart, but whether this occurs in humans is uncertain.1,2 During a six-month period, we measured fractional shortening of the left ventricle during systole in 10 consecutive patients (6 women and 4 men; mean [±SD] age, 42±18 years), 7 of whom were admitted for treatment of diabetic ketoacidosis and 3 of whom were admitted for alcoholic ketoacidosis. We focused on these conditions because the ketoacidosis associated with them, although frequently severe, is usually rapidly reversible.

Treatment included intravenous rehydration (mean volume of fluid infused, 3.1±1.6 liters), insulin administration in the patients with diabetes, and antibiotic therapy as needed (in two patients). No alkali therapy was administered. Fractional shortening of the left ventricle was measured by transthoracic echocardiography (with a 2.5- or 3.5-MHz probe, Sonos 100, Hewlett–Packard, Orsay, France) before treatment and 24 to 36 hours later, after correction of the ketoacidosis. No patient had a systolic blood pressure of less than 90 mm Hg on admission or during follow-up, and none received plasma expanders or vasopressors. Echocardiography revealed no regional wall-motion abnormalities, and the fractional shortening of the left ventricle was normal at both times in all patients (Table 1Table 1Mean Arterial Blood pH, Plasma Bicarbonate Concentrations, and Fractional Shortening of the Left Ventricle during Systole in 10 Patients before and after Correction of Ketoacidosis.), including three patients who had extremely severe acidosis (pH, 6.90, 6.76, and 6.75).

Although cardiac contractility is a multifactorial function, we think that it can be reliably evaluated by measurements of left ventricular fractional shortening. For this reason, it seems unlikely that ketoacidosis had a clinically important effect in our patients. Our findings do not support the notion that short-lived metabolic acidosis, even when severe, has a detrimental effect on cardiac contractility.

Eric Maury, M.D.
Thierry Vassal, M.D.
Georges Offenstadt, M.D.
Hôpital Saint-Antoine, 75571 Paris CEDEX 12, France

2 References
  1. 1

    Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. N Engl J Med 1998;338:26-34
    Full Text | Web of Science | Medline

  2. 2

    Shapiro JI. Pathogenesis of cardiac dysfunction during metabolic acidosis: therapeutic implications. Kidney Int Suppl 1997;61:S47-S51
    Medline

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    J. M. Handy, N. Soni. (2008) Physiological effects of hyperchloraemia and acidosis. British Journal of Anaesthesia 101:2, 141-150
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    Georges Offenstadt, Philippe Amstutz. (2008) Acid-base balance. Critical Care Medicine 36:5, 1690-1691
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    Daniel L. Levin. (2008) Cerebral edema in diabetic ketoacidosis. Pediatric Critical Care Medicine 9:3, 320-329
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    Viktor Rosival. (2005) Diabetic Ketoacidosis. Pediatric Emergency Care 21:1, 76
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    Jacques Levraut, Dominique Grimaud. (2003) Treatment of metabolic acidosis. Current Opinion in Critical Care 9:4, 260-265
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