Richard F. Davis

Acute oliguria after cardiopulmonary bypass: renal functional improvement with low-dose dopamine infusion

Hemodynamic and renal function response to low-dose (100 and 200 μg/min) dopamine infusion was studied in 15 adult cardiac surgical patients who manifested combined oliguria and left ventricular dysfunction postoperatively. Patients were studied an average of 6.6 h after ICU admission, at normothermia and after 2 consecutive hourly urine output determinations of less than 0.5 ml/kg h in the presence of a left atrial or pulmonary artery occlusion pressure over 12 mm Hg. Dopamine infusion at 100 μg/min produced improvement in creatinine, osmolar and free water clearances (70 ± 10 to 115 ± 13, 37 ± 4 to 93 ± 16 and –15 ± 2 to –37 ± 10 ml/min, respectively), and urinary sodium concentration (15 ± 5 to 29 ± 10 mEq/L). Urine flow improved overall from 22 ± 2 to 54 ± 9 ml/h; however, in 9 of 15 patients, flow was less than 0.5 ml/kg h (33 ± 5 to 50 ± 6 ml/h). In each of these 9 patients, dopamine infusion at 200 μg/min further improved urine flow as well as measured renal function. Plasma renin activity measured in 9 of the 15 patients before and during the 100 μg/min dopamine infusion was decreased from 1.95 ± 0.57 to 0.73 ± 0.39 mg/ml h. The hemodynamic effect of both dopamine doses was increased cardiac output coupled with decreased systemic (SVRI) and pulmonary vascular resistance index (PVRI). In these 15 patients, low-dose dopamine infusion produced significant improvement in renal function, with resolution of oliguria in every case, and with no deleterious hemodynamic effect.

The Effect of Halothane Anesthesia on Myocardial Necrosis,Hemodynamic Performance, and Regional Myocardial Blood Flow in Dogs Following Coronary Artery Occlusion

: The effect of halothane anesthesia on myocardial necrosis resulting from coronary artery ligation was examined in 28 anesthetized mongrel dogs. In 18 dogs, the left anterior descending coronary artery (LAD) was ligated immediately proximal to the first apical diagonal branch, and 1 h later the dogs were assigned randomly either to receive halothane, 0.5-1.0% inspired in room air for 12 h (n = 10) or to awaken without further intervention (control, n = 8). Infarct size was measured by staining the myocardium with triphenyl tetrazolium chloride 24 h after LAD ligation. Infarct size in halothane-treated dogs was 17.8 +/- 2.0% of the left ventricle, compared with 27.3 +/- 3.3% in control dogs (P less than 0.05). Myocardial salvage was present transmurally but was greatest in epicardial regions. In 10 additional dogs, hemodynamic variables (heart rate, arterial pressure, left ventricular end-diastolic pressure, peak left ventricular dP/dt, tension-time index, and rate-pressure product) were measured or calculated, and radionuclide-labeled microspheres were injected for measurement of cardiac output and regional myocardial blood flow (RMBF). Thirty minutes after LAD ligation and after initial hemodynamic measurements and microsphere injection, these dogs were assigned randomly to receive either halothane, 1.0%, inspired in room air (n = 5) or no intervention (control, n = 5). After 15 min of halothane inhalation (45 min after LAD ligation in control dogs), measurements were repeated. Halothane inhalation reduced heart rate, arterial pressure, and indexes of left ventricular contractile and pump performance. During halothane treatment, RMBF declined in normal myocardium but not in ischemic regions, while neither normal nor ischemic zone RMBF changed in control dogs. Systemic vascular resistance was unchanged in either group. Thus, halothane was associated with a 35% smaller myocardial infarct, transmural myocardial salvage, reduced heart rate, reduced left ventricular contractile and pump performance, reduced RMBF to nonischemic regions, and unchanged RMBF in the ischemic myocardium.

Regional myocardial lidocaine concentration determines the antidysrhythmic effect in dogs after coronary artery occlusion.

Ischemic ventricular dysrhythmias were produced in 40 of 47 anesthetized mongrel dogs by high ligation of the left anterior descending coronary artery. Dysrhythmias were treated with a single iv bolus of 20, 40, 80, or 120 mg of lidocaine (L) in order to determine the dose at which approximately 50% of animals had an antidysrhythmic response. Cardiac output and regional myocardial blood flow (RMBF) were measured by using radionuclide labeled microspheres. Lidocaine concentration ([L]) was measured from samples of arterial and venous blood and normal and ischemic myocardium. All dogs treated with 40, 80, or 120 mg of L had an antidysrhythmic effect. However, with 20 mg of L the dysrhythmia persisted in 12 and resolved in 14. With 20 mg of L, ischemic myocardial [L] was greater in dogs with an antidysrhythmic effect than in those with persistent dysrhythmias (1.14 ± 0.12 vs. 0.76 ± 0.04 μg · g−1), but no difference was seen for arterial, venous, and normal myocardial [L]. Ischemic RMBF was higher in the dogs that had an antidysrhythmic effect than in those that did not, 9.8 ± 1.5 versus, 6.9 ± 1.3% of normal. With 20 mg of L, [L] in ischemic myocardium correlated well with ischemic RMBF. The antidysrhythmic response to L had a threshold at a tissue concentration of greater than or equal to 1.0 μg · g−1 (chisquare = 8.55, P < 0.005). For this model, the [L] in ischemic myocardium during acute ischemia correlates with the antidysrhythmic response to L, while the concentration in normal myocardium or blood does not.

Brain tissue pressure measurement during sodium nitroprusside infusion.

The effect of an acute 25% decrease in mean arterial pressure (MAP) produced by sodium nitroprusside (SNP) infusion on mean intracerebral and cerebral perfusion pressures was examined in 7 swine with intracranial hypertension. All animals were anesthetized (a-chloralose), paralyzed (pancuronium bromide), orotracheally intubated and mechanically ventilated to maintain normocapnia. An epidural balloon was incrementally inflated to produce the desired brain tissue pressure (BTP) which was measured by an intracerebral microtransducer implanted contralat-eral to the balloon. MAP was measured from the carotid artery; cerebral perfusion pressure (CPP) was calculated as: MAP - BTP. During mildly (14 ± 1 (se) mm Hg) or moderately (37 ± 3 mm Hg) increased BTP, SNP infusion further increased BTP (17 ± 1 and 44 ± 3 mm Hg, respectively) (p < 0.05). During severely increased BTP (70 ± 4 mm Hg), SNP decreased BTP (53 ± 4 mm Hg, p < 0.05). Despite this variable BTP, CCP consistently decreased during SNP infusion. BTP and supratentorial subarachnoid cerebrospinal fluid pressure correlated closely; however, the supratentorial subarachnoid pressure consistently underestimated BTP. These findings suggest that estimation of BTP obtained from subarachnoid screw-type devices may not accurately record the pressure within cerebral tissue and the SNP should not be administered to patients with known or suspected intracranial hypertension unless an intracranial (either BTP or subarachnoid) pressure is being monitored.

The Effect of Halothane Anesthesia on Myocardial Necrosis, Hemodynamic Performance, and Regional Myocardial Blood Flow in Dogs Following Coronary Artery Occlusion

The effect of halothane anesthesia on myocardial necrosis resulting from coronary artery ligation was examined in 28 anesthetized mongrel dogs. In 18 dogs, the left anterior descending coronary artery (LAD) was ligated immediately proximal to the first apical diagonal branch, and 1 h later the dogs were assigned randomly either to receive halothane, 0.5–1.0% inspired in room air for 12 h (n = 10) or to awaken without further intervention (control, n = 8). Infarct size was measured by staining the myocardium with triphenyl tetrazolium chloride 24 h after LAD ligation. Infarct size in halothane-treated dogs was 17.8 ± 2.0% of the left ventricle, compared with 27.3 ± 3.3% in control dogs (P ≤ 0.05). Myocardial salvage was present transmurally but was greatest in epicardial regions. In 10 additional dogs, hemodynamic variables (heart rate, arterial pressure, left ventricular end-diastolic pressure, peak left ventricular dP/dt, tension-time index, and rate-pressure product) were measured or calculated, and radionuclide-labeled microspheres were injected for measurement of cardiac output and regional myocardial blood flow (RMBF). Thirty minutes after LAD ligation and after initial hemodynamic measurements and microsphere injection, these dogs were assigned randomly to receive either halothane, 1.0%, inspired in room air (n = 5) or no intervention (control, n = 5). After 15 min of halothane inhalation (45 min after LAD ligation in control dogs), measurements were repeated. Halothane inhalation