Efficacy of noninvasive transcutaneous cardiac pacing patients undergoing cardiac surgery.

Noninvasive transcutaneous cardiac pacing (NTP) is a rapid, safe, and easily utilized form of emergency cardiac pacing, with hemodynamics similar to right ventricular endocardial pacing. Although the technique has proven effective for hemodynamically significant bradycardias and early use during cardiopulmonary resuscitation, NTP under anesthetic conditions has been poorly characterized. In particular, it is unknown to what degree the multiple physiologic perturbations of cardiac surgery and cardiopulmonary bypass (CPB) affect myocardial thresholds and the efficacy of the unit itself. Patients undergoing procedures utilizing CPB (n = 23) were studied in an effort to address these issues. All patients were able to be paced at all points throughout the 24-h study interval, although four patients developed hemodynamic instability during this period causing their exclusion from additional investigation. Only one patient requested discontinuation from the study due to discomfort. A statistically significant increase in mean current requirements for capture was demonstrated over time (P less than 0.0001), with baseline thresholds being significantly less than other study points (P less than or equal to 0.05). Thresholds following chest wall closure were significantly greater than all other study points (P less than or equal to 0.05), possibly due to accumulation of pericardial and mediastinal air. Multiple measured variables changed significantly during the study, but only increases in cardiac output and core temperature were related to statistically significant increases in current thresholds (P less than or equal to 0.05). Increasing age and pump time were of borderline importance. NTP represents an effective pacing alternative in cardiac surgical patients.

Alfentanil plasma concentration v. effect relationships in cardiac surgical patients.

Effects of alfentanil, preceded by lorazepam, on suppression of haemodynamic and somatic responses to noxious stimuli was studied in patients undergoing CABG. Plasma concentration of alfentanil, somatic and haemodynamic responses were measured at loss of consciousness, tracheal intubation, sternotomy and during multiple application of electrocoagulation. Additional alfentanil was administered i.v. to control unwanted responses. Study 1 (six patients): lorazepam 0.08 mg kg-1 by mouth 1-2 h before operation, alfentanil priming infusion (60 micrograms kg-1 min-1 for 10 min) followed by maintenance infusion (4.5 micrograms kg-1 min-1). With mean plasma alfentanil 1178 (SEM 54) ng ml-1, two patients required supplementary alfentanil to suppress somatic motor responses; one patients required nitroglycerin to control an increase in arterial pressure which was unresponsive to additional alfentanil following sternotomy. Study 2 (13 patients): lorazepam 0.04 mg kg-1 by mouth as premedication; one of three maintenance infusion rates of alfentanil: 5.4 (n = 4), 6.6 (n = 5), or 7.8 (n = 4) micrograms kg-1 min-1, each preceded by a proportional priming infusion. With plasma alfentanil 2181 (62) ng ml-1, somatic motor responses requiring additional alfentanil occurred in nine patients; haemodynamic responses in four of seven patients tested could not be controlled by alfentanil. The highest plasma concentration of alfentanil to prevent response to a stimulus other than tracheal intubation was different between the two studies (P less than 0.05). We conclude that alfentanil alone is insufficient to suppress haemodynamic and somatic motor responses to noxious stimulation during CABG and that the role of premedication is significant.

Rapid administration of a narcotic and neuromuscular blocker: a hemodynamic comparison of fentanyl, sufentanil, pancuronium, and vecuronium.

High-dose narcotic anesthetic inductions usually avoid circulatory depression better than do other techniques; however, the selection of a narcotic and neuromuscular blocker influences subsequent hemodynamic responses. One hundred-one patients having aortocoronary bypass graft (CABG) surgery were investigated using four combinations of a narcotic and neuromuscular blocker: group FP (fentanyl 50 micrograms/kg, pancuronium 100 micrograms/kg); group FV (fentanyl 50 micrograms/kg, vecuronium 80 micrograms/kg); group SP (sufentanil 10 micrograms/kg, pancuronium 100 micrograms/kg); and group SV (sufentanil 10 micrograms/kg, vecuronium 80 micrograms/kg), each combination being administered over 2 minutes. Hemodynamic functions were then monitored for 10 minutes before tracheal intubation. Significant changes included increases in heart rate in the groups receiving pancuronium and decreases in those receiving vecuronium. In all groups mean arterial pressure initially decreased; systemic vascular resistance index decreased significantly in all groups except SV. Cardiac index decreased significantly only in group SV. Circulatory depression requiring treatment with vasopressor or anticholinergic drugs was more common in patients given vecuronium. Cardiac arrhythmia occurred most often in group SP; only in group FP were there no arrhythmias, ischemic changes, or hemodynamic disturbances requiring intervention. Time to onset of neuromuscular blockade did not differ among the four groups, but transient chest wall rigidity occurred significantly more often with sufentanil than with fentanyl. Overall, the fentanyl/pancuronium combination afforded the greatest hemodynamic stability, whereas the sufentanil/vecuronium combination proved least satisfactory because of bradycardia and hypotension, requiring treatment in 35% of group SV patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management.

Twenty-eight adult patients anesthetized with fentanyl, then subjected to hypothermic cardiopulmonary bypass (CPB), were studied to determine the effect of phenylephrine-induced changes in mean arterial pressure (MAP) on cerebral blood flow (CBF). During CPB patients managed at 28 degrees C with either alpha-stat (temperature-uncorrected PaCO2 = 41 +/- 4 mmHg) or pH-stat (temperature-uncorrected PaCO2 = 54 +/- 8 mmHg) PaCO2 for blood gas maintenance received phenylephrine to increase MAP greater than or equal to 25% (group A, n = 10; group B, n = 6). To correct for a spontaneous, time-related decline in CBF observed during CPB, two additional groups of patients undergoing CPB were either managed with the alpha-stat or pH-stat approach, but neither group received phenylephrine and MAP remained unchanged in both groups (group C, n = 6; group D, n = 6). For all patients controlled variables (nasopharyngeal temperature, PaCO2, pump flow, and hematocrit) remained unchanged between measurements. Phenylephrine data were corrected based on the data from groups C and D for the effect of diminishing CBF over time during CPB. In patients in group A CBF was unchanged as MAP rose from 56 +/- 7 to 84 +/- 8 mmHg. In patients in group B CBF increased 41% as MAP rose from 53 +/- 8 to 77 +/- 9 mmHg (P less than 0.001). During hypothermic CPB normocarbia maintained via the alpha-stat approach at a temperature-uncorrected PaCO2 of approximately equal to 40 mmHg preserves cerebral autoregulation; pH-stat management (PaCO2 approximately equal to 57 mmHg uncorrected for temperature, or 40 mmHg when corrected to 28 degrees C) causes cerebrovascular changes (i.e., impaired autoregulation) similar to those changes produced by hypercarbia in awake, normothermic patients.

Cerebral blood flow does not change following sodium nitroprusside infusion during hypothermic cardiopulmonary bypass.

Changes in cerebral blood flow (CBF) associated with decreases in mean arterial pressure (MAP) produced by sodium nitroprusside (SNP) infusion were measured by intra-aortic injection of 133Xe in 17 patients during hypothermic cardiopulmonary bypass (CPB). In each patient, CBF was determined at baseline and then again following SNP-induced reduction of MAP. Two groups were studied. In Group I (n = 9), PaCO2 was maintained near 42 mm Hg uncorrected for nasopharyngeal temperature (NPT). In Group II (n = 8), PaCO2 was maintained near 60 mm Hg, uncorrected for NPT. Nasopharyngeal temperature, MAP, pump oxygenator flow, PaO2, and hematocrit were maintained within a narrow range in each patient during both studies. Since the baseline CBF determinations were conducted at the higher MAP in all subjects, we corrected post-SNP CBF data for the spontaneous decline that occurs over time during CPB. In Group I, a reduction in MAP from 76 +/- 9 mm Hg (mean +/- SD) to 50 +/- 6 mm Hg was associated with a reduction in CBF from 17 +/- 5 to 13 +/- 3 ml.100 g.min-1 (P less than 0.01), a decrease that became statistically insignificant once the time correction factor had been applied (16 +/- 4 ml.100 g-1.min-1). In Group II, MAP declined from 75 +/- 5 mm Hg to 54 +/- 5 mm Hg, and CBF declined from 25 +/- 10 to 17 +/- 7 ml.100 g.min-1 (P less than 0.01), but, again, after time correction, the CBF decline was statistically insignificant (22 +/- 8 ml.100 g-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)