The provision and maintenance of good nutrition in patients with acute and chronic illness is a fundamental part of standard medical and surgical care. Recently, there is great interest in using enteral nutritional support to reverse the morbidity and mortality associated with malnutrition. Enteral nutrition is preferred over parenteral nutrition because it is more physiologic, maintains intestinal structure and function, limits bacterial translocation, has less morbidity, has fewer complications, and is less expensive. However, the decision to feed into the stomach or into the small bowel (postpyloric) continues to be a matter of some debate and continued clinical investigation. Although the gastric route of enteral feeding is easier and less expensive, some physicians worry that gastric feeding may predispose to aspiration and pneumonia, especially in critically ill patients who frequently have delayed gastric transit. In these critically ill patients, small bowel function usually remains relatively intact and placement of a postpyloric feeding tube may permit more effective delivery of nutrients. However, it should be noted that placement of postpyloric feeding tubes can be challenging, and this may lead to a delay in initiation of nutritional support.
Background: We investigated changes in myocardial repolarization and associated outcomes in patients undergoing therapeutic hypothermia after cardiac arrest. Methods: Demographic, clinical, and ECG data on 19 consecutive cardiac arrest survivors (6 females, 59+/-15 years old, 3 with diabetes, 3 with cancer, 3 with CKD, 5 with pulmonary disease and 5 with cardiovascular disease) undergoing therapeutic hypothermia were collected. Absolute QT dispersion was calculated. ANOVA, chi-square, Kaplan-Meier and logistic regression analyses were used. The study was approved by the IRB. Results: Hypothermia resulted in significant prolongation of both minimum (baseline 277+/-74 vs. cooled 408+/-129 vs. re=warmed 313+/-82 msec, p<0.001) and maximum QT intervals (392+/-60 vs. 549+/-147 vs. 453+/-90 msec, respectfully, p<0.001, Figure) but no significant changes in QT dispersion. Age, gender, history of cancer, kidney, pulmonary, or cardiovascular disease, use of thiazide or loop diuretics, ACE inhibitors/ARBs, or potassium supplements had no effect on QT dispersion or hospital mortality . Similarly, Na, K, Mg, Cr, Ca, pH, or hematocrit on admission, during cooling or rewarming had no effect on QT dispersion or hospital mortality. In 7 survivors to hospital discharge QT changes at baseline, during hypothermia, or rewarming were not predictive of mortality or AICD discharges during long-term follow-up (27+/-8 months). Conclusion: Therapeutic hypothermia is associated with significantly prolonged QT intervals. However, these QT abnormalities do not translate into increased mortality and/or AICD therapy during short or long-term follow-up.
Purpose : We hypothesized that advanced circulatory compromise, as manifested by acidosis and hyperkalemia should be associated with worsened clinical outcomes in cardiac arrest patients treated with therapeutic hypothermia. Methods: Results of initial admission laboratory studies, medical history, and echocardiogram in 41 consecutive cardiac arrest patients (13 females, 60+/- 32 years old, 6 with diabetes, 7 with chronic kidney disease, and 8 with history of cardiovascular disease) undergoing therapeutic hypothermia were reviewed. Mortality was ascertained through hospital records and Social Security Death Index. ANOVA, chi-square, Kaplan-Meier, and logistic regression analyses were used. The study was approved by the institutional IRB. Results : Age, gender, medication use, history of CAD, degree of systolic dysfunction by echocardiogram, serum pH, creatinine, sodium, glucose, magnesium, calcium, lactate, BUN, and osmolality were not predictive of mortality in our patient population. However, higher hemoglobin (0.336 per 1 mg/dL, 95% CI 0.138-0.818, p=0.016) and pre-resuscitation ventricular tachycardia or fibrillation (VT-VF vs. pulseless electrical activity or asystole, 0.02, 95% CI 0.002-0.312, p=0.004) were associated with decreased hospital mortality in both univariate and multivariate analyses. Median admission potassium level was 4.0 mEq/L. Unexpectedly, correlation between admission serum potassium and pH was poor (R^2= 0.06). Similarly, actual K requirements were poorly correlated with calculated K deficit (R^2=0.007). VT or VF were more prevalent in patients with K less than 4 (p=0.002). There was also a trend towards improved mortality in patients with lower K levels (72% survival in K≤4 vs. 47% in K>4 mEq/L, p=0.129). Conclusions: Hyperkalemia, pulseless electrical activity, and asystole are predictive of increased hospital mortality in survivors of cardiac arrest. In patients with admission hypokalemia, lack of correlation between admission potassium, pH, and potassium requirements are suggestive for acute event etiology in many cardiac arrests patients. An association between low or low-normal potassium, observed VT-VF, and better outcomes is unexpected and may be used for prognostic purposes. More prospective investigations of mortality predictors in these critically ill patients are needed.
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