Rory S. Jaffe

Cardiovascular function during induced hypotension by fenoldopam or sodium nitroprusside in anesthetized dogs

Fenoldopam, a selective dopamine1 receptor agonist, has been recommended for induced hypotension because it effectively lowers arterial blood pressure and improves renal perfusion. We examined cardiovascular functions during hypotension induced by fenoldopam or sodium nitroprusside. In eight halothane-anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers for the assessment of LV contractility using the analysis of the pressure-diameter relationship. Blood flow distribution was measured by radioactive microspheres. Doses of fenoldopam and nitroprusside were titrated to reduce mean arterial blood pressure to 60 mm Hg. After 40 min of hypotension, fenoldopam and nitroprusside caused similar increases in heart rate (17% ± 4% vs 19% ± 10%, respectively) and decreases in systemic vascular resistance (−24% ± 5% vs-27% ± 4%). Hypotension induced by fenoldopam was associated with higher LV end-diastolic pressure (4.4 ± 0.6 vs 2.5 ± 1.1 mm Hg) and end-systolic meridional wall stress (33.0 ± 4.3 vs 17.8 ± 2.1 g/cm2) when compared with nitroprusside. There were no significant changes in cardiac output and cardiac contractility as expressed by the slope (Ees) of the LV end-systolic pressure-diameter relationship, velocity of shortening of the diameter, and percentage of wall thickening of the LV. In contrast to nitroprusside, which decreased renal blood flow from 197 ± 19 to 163 ± 15 mL/min, renal blood flow increased during fenoldopam-induced hypotension from 187 ± 20 to 239 ± 18 mL/min. The increase in renal perfusion was similar in upper, middle, and lower regions of the kidney; however, it was more in the medulla compared with the cortex (37% ± 17% vs 25% ± 7%). Both fenoldopam and nitroprusside decreased splenic blood flow, but neither altered flow to the brain, skin, or myocardium. Muscle and hepatic arterial blood flow were significantly less with fenoldopam than with nitroprusside. Fenoldopam was associated with significantly larger increases in plasma renin activity compared with nitroprusside. The results of this study show an increase in renal blood flow during fenoldopam infusion that may be of advantage particularly when renal hypoperfusion should be avoided.

Optimal frequency ranges for extracting information on autonomic activity from the heart rate spectrogram.

Heart rate variability spectrum analysis provides useful quantitative indices of neural control of the SA node. This method is attractive both for its simplicity and the lack of invasive instrumentation, particularly for human investigation. The differing spectral characteristics of parasympathetic and sympathetic control of heart rate allows separate measurement. However, there are widely varying opinions as to the appropriate frequency bands to represent these two inputs. We compared the heart rate variability spectra of 16 humans in supine and upright positions. Adequate measures of parasympathetic or sympathetic activity change should correlate respectively inversely or directly with heart rate change. Frequently used spectral measures of sympathetic activation did not correlate with heart rate changes. With optimization of frequency bands, we found that restricting the sympathetic band to frequencies below 0.1 Hz and above 0.05 Hz (0.055 to either 0.086-0.098 Hz), and dividing by total spectral amplitude 0.004-0.5 Hz (to account for parasympathetic fluctuations within the sympathetic band) produced the best results. The parasympathetic band was best from 0.1 Hz to a frequency greater than that of the respiratory sinus arrhythmia. The optimization method detailed here is easily applied to circumstances other than active orthostasis, and should provide a means of empirically determining useful frequency limits.

Nalbuphine antagonism of fentanyl-induced ventilatory depression: a randomized trial.

The authors anesthetized 18 patients with good pulmonary and ventricular function for coronary artery bypass grafting with high doses of fentanyl. When the patients were arousable and their vital signs stable in the intensive care unit, the authors administered nalbuphine or placebo (randomly and double-blinded) until extubation criteria were met, and subsequently gave nalbuphine for analgesia. In one of ten placebo patients, tracheal extubation was accomplished without nalbuphine. This patient then retained CO2 and required nalbuphine; the other nine placebo patients could not be extubated after placebo trials and were given nalbuphine. In all other patients in both groups, tracheal extubation was successful following nalbuphine (median dose 60 micrograms/kg, range 30-180 micrograms/kg). One patient became renarcotized 4 h after tracheal extubation without an increase in plasma fentanyl concentration; he received an additional dose of nalbuphine and recovered without further incident. Nine patients required treatment with vasoactive agents or beta-blockers for hypertension or tachycardia associated with the administration of nalbuphine. Eight of 18 patients were not satisfied with nalbuphine analgesia, and required morphine for relief of their pain. Recurrent elevations of fentanyl concentrations in plasma were observed and appeared to be related to increasing motor activity. Nalbuphine is an effective opioid antagonist after fentanyl anesthesia, but its use is associated with side effects, and analgesia for the post-sternotomy patient may be unsatisfactory unless the dose is carefully titrated to the minimum required to antagonize respiratory depression.

Altering Capitation to Reduce the Incentive to Undertreat Patients Inappropriately

Capitation, the payment of a fixed monthly fee for covered people, is being used by insurers to eliminate the financial incentive for over-provision of services that is present in fee-for-service plans. Physicians typically respond by forming groups to manage the financial risk associated with capitation. These groups institute methods of sharing the “cap” dollar among the involved primary care practitioners and specialists. To reduce utilization groups commonly “subcap” each specialty, giving them fixed payments per month regardless of the mount of care they provide to the covered members. Thus, individual physicians are rewarded with a payment per unit of work that rises towards infinity as work declines towards zero. This inappropriate incentive is counterbalanced by the internalized norms we assume all physicians gain as part of their professional education and experience. Unfortunately, it appears that this financial incentive can overwhelm these internalized norms in a number of physicians to the point of not only reducing care below levels associated with what an individual patient would regard as appropriate, but also below levels associated with maximal societal gain. In this paper I present a compensation method that can be adjusted to provide a financial incentive to reduce services when they seem to be excessive, while reducing or eliminating the incentive to reduce services when utilization is already low. It uses a payoff function to adjust fee-for-service payments based on utilization. The function allows maximal incentive (measured as the derivatives ofthe functio fee [utilization]) to be placed where it judged most appropriate, with little additional incentive at already-low untilization levels.