Abstract

Introduction: Elevated lactic acid (LA) levels carry a poor prognosis in patients admitted with shock. Data is lacking on the association of LA level with the severity of decompensated heart failure (HF). This study assesses the relationship between LA levels, invasive hemodynamics and clinical outcomes. Methods: Patients presenting to the cardiac care unit with decompensated HF between 2015-18 were prospectively enrolled into an invasive hemodynamics study. LA (normal 0.7-2.1 mmol/L) levels were obtained within 12 hours prior to right heart catheterization (RHC). No significant changes in therapy were made in the time between LA level collection & RHC. Patients were divided into 4 groups: 1) normal pulmonary capillary wedge pressure (PCWP) (< 18 mmHg)/ normal Fick cardiac index (CI) (≥ 2.2 L/min/m 2 ), 2) normal PCWP/ low CI (< 2.2 L/min/m 2 ) 3) elevated PCWP (≥ 18 mmHg )/ normal CI, 4) elevated PCWP / low CI. Results: 80 patients were enrolled. Mean age 58±14 years; 78% male, left ventricular ejection fraction was 24±4%. Prior to RHC, 55% patients were on vasoactives and/or inotropes. Mean (SD) PCWP was 26 ± 8.8 mmHg and mean CI was 2.06 ± 0.61 L/min/m 2 . Overall 48 (60%) of the patients had high PCWP and low CI (group 4). 81% had normal LA (≤2.1 mmol/L) prior to RHC. There was no correlation between LA level and PCWP (R=0.12; p=0.30); there was a moderate inverse correlation between LA level and CI (R=-0.40; p<0.01). Only 25% of patients with the highest risk hemodynamic profile (elevated PCWP/low CI) had an elevated LA level (Figure A). 90- day all cause mortality was 33% When LA was stratified by tertile, there was no significant difference in mortality between the tertiles (Figure B). Conclusion: In patients with decompensated HF, normal LA levels do not exclude the presence of cardiogenic shock with profoundly impaired cardiac output. Invasive assessment of hemodynamics should not be delayed based on LA level alone.

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