The accuracy of the central venous blood gas for acid-base monitoring.

BACKGROUND: Routine use of central venous blood gases (VBGs) may reduce complications from prolonged arterial cannulation. We investigated the reliability of the VBG as a substitute for arterial blood gas (ABG) in multiple care settings. METHODS: We developed a VBG adjustment rule of ABG pH = VBG pH + 0.05, ABG CO(2) = VBG PCO(2) -5 mm Hg from prior studies and validated this relationship with simultaneous venous and arterial blood obtained from 187 medical/surgical intensive care, cardiac catheterization laboratory, and coronary care unit patients with central venous access. RESULTS: The overall accuracy of a normal adjusted VBG (aVBG) to predict a normal ABG was 90%. After adjustment, the mean systematic difference (bias) between ABG and VBG pH decreased from 0.035 +/- 0.02 to -0.015 +/- 0.02 and PCO(2) bias decreased from -4.5 +/- 3.5 to 0.5 +/- 3.5. Intraclass correlation coefficients for agreement improved after applying the adjustment rule to venous pH (from 0.84 to 0.93, P < .001) and PCO(2) (from 0.66 to 0.84, P < .001). Overall diagnostic accuracy of VBG improved from 45% to 74% after adjustment. Multiple logistic regression demonstrated that the factor independently associated with discrepancy between VBG and ABG diagnoses was an abnormal aVBG (OR 6.8, 95% CI 2.8-16.5). CONCLUSIONS: Because of the high agreement between a normal aVBG with a normal ABG and the small bias between these tests, we recommend use of the adjusted central VBG.

Alcoholic and cocaine-associated cardiomyopathies.

Alcohol and cocaine use are associated with significant cardiovascular complications, including cardiomyopathy. The pathophysiologic mechanisms underlying the development of these toxic cardiomyopathies vary depending on the inciting agent but include direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. The typical patient with alcoholic cardiomyopathy is a long-term excessive alcohol consumer who is otherwise indistinguishable from other patients with nonischemic cardiomyopathy. The typical patient with cocaine cardiomyopathy is a young male smoker who presents with signs of adrenergic excess. Management of these patients is similar to that of patients with other forms of dilated cardiomyopathy, although beta-blockers should be avoided in patients with cocaine-associated heart failure and benzodiazepines should be given in this setting to blunt adrenergic excess. Left ventricular function may improve dramatically with abstinence from alcohol or cocaine. Unfortunately, the rate of recidivism is high and left ventricular dysfunction and symptomatic heart failure often recurs.

Managing the post-myocardial infarction patient with asymptomatic left ventricular dysfunction.

The percentage of post-myocardial infarction (MI) patients with asymptomatic left ventricular dysfunction (ALVD) is now estimated at 10%, and that number is expected to grow as reperfusion procedures increasingly become routine. Since average all-cause mortality risk in these patients is high (up to 27%), definitive diagnostics are recommended to screen all post-MI patients for ALVD, defined as left ventricular systolic dysfunction in the absence of heart failure symptoms. Post-MI management strategies for patients with ALVD target the two routes of progression to heart failure: (1) cardiac remodeling mediated by neurohormonal activation, and (2) continued and recurrent myocardial ischemic events. Clinical trials of neurohormonal antagonists in post-MI ALVD patients have shown that angiotensin-converting enzyme inhibitors attenuate left ventircular remodeling and that beta-blocker therapy reverses remodeling for patients already on angiotensin-converting enzyme inhibitor therapy. Neurohormonal antagonist therapy is also associated with significant reductions in sudden death in post-MI ALVD patients.