Benefit of glyceryl trinitrate on arterial stiffness is directly due to effects on peripheral arteries.

OBJECTIVE: To determine how the vasodilator glyceryl trinitrate (GTN) alters arterial stiffness and improves left ventricular afterload. METHODS: Ascending aortic pressure waves were measured with fluid filled catheters of high fidelity in 50 patients undergoing cardiac surgery, before cardiopulmonary bypass, both before and after intravenous infusion of GTN. In all 50 patients, wave reflection was identifiable as a secondary boost to late systolic pressure, permitting the pressure wave to be separated into a primary component, attributable to left ventricular ejection and properties of the proximal aorta, and a secondary component, attributable to reflection of the primary wave from the peripheral vasculature. RESULTS: GTN infusion caused no change in amplitude of the primary wave (mean (SD) 0.0 (1.4) mm Hg, not significant) but substantial reduction (14.6 (9.6) mm Hg, p < 0.0001) in amplitude of the secondary reflected wave. Fall in mean pressure was attributable to a mix of arteriolar and venous dilatation, with relative contributions unable to be separated. CONCLUSION: Favourable effects of GTN on arterial stiffness can be attributed to effects on peripheral muscular arteries, causing reduction in wave reflection. Results conform with previous invasive studies on vasodilator agents and their known effects on calibre and compliance of muscular arteries.

The second peak of the radial artery pressure wave represents aortic systolic pressure in hypertensive and elderly patients.

BACKGROUND: Simultaneous measurement of ascending aorta and radial artery pressure shows that mean and diastolic pressures (DP) are in close agreement in normotensive adults, while systolic pressures (SP) are not. However, in the aortic pressure wave, a second systolic peak appears with increasing age and increases to represent the SP by age 32 yr, while in the radial artery, a second systolic deflection appears by age 40 yr. We suggest that the second radial systolic wave, sometimes seen during radial arterial pressure monitoring in older hypertensives, represents the aortic SP. We set out to evaluate whether the aortic and radial second systolic peaks agree, and since doubts exist about the agreement between aortic and radial DP in elderly hypertensive patients, we also assessed that relationship. METHODS: We compared simultaneously recorded radial and aortic pressures from 21 anaesthetized adult patients using identical fluid-filled pressure measuring systems. CONCLUSIONS: The second radial pressure peak agreed with that in the aorta within a mean of 0.6 (SD 1.5) mm Hg. The difference between DP in the aorta and radial artery was -1.4 (2) mm Hg. The radial-aortic SP and pulse pressure differences were 5.9 (7.6) and 7.3 (7.6) mm Hg, respectively. These results confirm that when the radial artery pressure wave shows a first and second, or only a second systolic shoulder/peak (on the right side of the pressure wave), the second represents the maximal ascending aortic SP, and that the radial and aortic DP are equivalent, even in older hypertensive patients.

Prospective evaluation of a method for estimating ascending aortic pressure from the radial artery pressure waveform.

Pressure wave reflection in the upper limb causes amplification of the arterial pulse so that radial systolic and pulse pressures are greater than in the ascending aorta. Wave transmission properties in the upper limbs (in contrast to the descending aorta and lower limbs) change little with age, disease, and drug therapy in adult humans. Such consistency has led to use of a generalized transfer function to synthesize the ascending aortic pressure pulse from the radial pulse. Validity of this approach was tested for estimation of aortic systolic, diastolic, pulse, and mean pressures from the radial pressure waveform. Ascending aortic and radial pressure waveforms were recorded simultaneously at cardiac surgery, before initiation of cardiopulmonary bypass, with matched, fluid-filled manometer systems in 62 patients under control conditions and during nitroglycerin infusion. Aortic pressure pulse waves, generated from the radial pulse, showed agreement with the measured aortic pulse waves with respect to systolic, diastolic, pulse, and mean pressures, with mean differences <1 mm Hg. Control differences in Bland-Altman plots for mean+/-SD in mm Hg were systolic, 0.0+/-4.4; diastolic, 0.6+/-1.7; pulse, -0.7+/-4.2; and mean pressure, -0.5+/-2.0. For nitroglycerin infusion, differences respectively were systolic, -0.2+/-4.3; diastolic, 0.6+/-1.7; pulse, -0.8+/-4.1; and mean pressure, -0.4+/-1.8. Differences were within specified limits of the Association for the Advancement of Medical Instrumentation SP10 criteria. In contrast, differences between recorded radial and aortic systolic and pulse pressures were well outside the criteria (respectively, 15.7+/-8.4 and 16.3+/-8.5 for control and 14.5+/-7.3 and 15.1+/-7.3 mm Hg for nitroglycerin). Use of a generalized transfer function to synthesize radial artery pressure waveforms can provide substantially equivalent values of aortic systolic, pulse, mean, and diastolic pressures.

Effect of cardiopulmonary bypass on hand and forearm blood flow.

We have assessed the relationship between the aorto-radial pressure difference at the conclusion of cardiopulmonary bypass and blood flow to the hand. Hand blood flow was estimated from the difference between forearm blood flow measured without and with exclusion of the hand circulation. On the same hand, the skin temperature on the palm and on the middle finger was recorded, with the amplitude of the finger pulse oximeter trace. The aorto-radial pressure difference, after cardiopulmonary bypass, correlated with hand blood flow (r = 0.59, P = 0.002). There was a significant (P < 0.0001) palm-finger temperature gradient before and after cardiopulmonary bypass. In conclusion, while the mean aorto-radial pressure difference after bypass results from increased hand blood flow, the finger is not a reliable site to assess the state of the systemic circulation, before or after cardiopulmonary bypass.

Cardiopulmonary bypass and forearm blood flow.

STUDY OBJECTIVE: To assess the effect of cardiopulmonary bypass (CPB) on muscle blood flow (MBF) when measured in the forearm by venous occlusion plethysmography. DESIGN: This was a prospective study. SETTING: Operating room area of a tertiary care university medical center. PARTICIPANTS: Twenty-seven patients (25 men and 2 women), aged 62 +/- 1.5 years, undergoing elective coronary bypass grafting. INTERVENTIONS: Measurements were made during the surgical procedure: before, during cold and warm, and after discontinuation of CPB. MEASUREMENTS AND RESULTS: Changes in forearm blood flow (FBF), derived forearm vascular resistance (FVR), mean arterial pressure (MAP), and cardiac output (CO) were evaluated by repeated measures analysis of variance. The control FBF (measured before CPB) was found to be approximately 50 percent lower than that previously reported for awake volunteers and patients. The FVR was similarly higher. From these low values, the FBF increased significantly (p < 0.001) during normothermic bypass and after CPB. Forearm vascular resistance decreased significantly (p < 0.001) throughout the cold, warm, and postbypass periods. Only during the warm and the postbypass periods did FBF and FVR reach normal values. Mean arterial pressure decreased significantly (p < 0.01) throughout. There was no statistically significant association between any of the variables and FBF or FVR. After correcting for patient and surgical phase variability, only MAP had a statistically significant effect (p = 0.042) on FVR; blood temperature, skin temperature, hematocrit level, PaCO2, serum potassium, and systemic vascular resistance (SVR) had no effect on either FBF or FVR when tested singly or in combination. When correction for multiple comparisons was applied, the lowest probability value became greater than 0.25. There was no correlation between combinations of covariates and FBF or FVR after adjustments for the surgical phase of the study either. CONCLUSION: These findings indicate that the increase in MBF seen during warm and the post-CPB periods is only a recovery toward normal blood flow. The role of this change in the low SVR that usually accompanies CPB is equivocal.

Reliability of the radial arterial pressure during anesthesia. Is wrist compression a possible diagnostic test?

STUDY OBJECTIVE: To evaluate wrist compression as a test to identify low radial from low systemic pressure and to see if the gradient found after cardiopulmonary bypass is also present whenever hand vascular resistance may decrease. DESIGN: This was a prospective study. SETTING: Operating room area of a university medical center. PARTICIPANTS: (1) Forty patients undergoing coronary bypass grafting studied at discontinuation of cardiopulmonary bypass. (2) Twenty-six patients received isoflurane anesthesia before major noncardiac operations. (3) Hydraulic model: a fluid container with a tube 66-cm long, 6- to 1.8-mm internal diameter, connected at its base. INTERVENTIONS: Before induction of anesthesia, the radial artery was cannulated and, in the first group, the aorta or femoral arteries as well. The radial pressure was compared consecutively with and without wrist compression. In the model, the pressure was recorded simultaneously at three sites along the tube while different flows ran through its distal end. MEASUREMENTS AND RESULTS: Overall, wrist compression increased radial (p < 0.001) systolic, diastolic, and mean arterial pressures. In the first group, compression reduced the femoral/aortic-radial mean pressure difference by 50 percent and never produced higher radial than central mean pressure. Plot of the pressure difference produced by wrist compression against the average of the (compared) radial pressures and considering increases > or = 4 mm Hg as real, showed that, in the first group, systolic arterial pressure (SAP) increased 13 +/- 1.4 mm Hg in 22 of 40 patients; diastolic arterial pressure (DAP) increased 7.8 +/- 1.1 mm Hg in 4; and mean arterial pressure (MAP) increased 7.7 +/- 1.6 mm Hg in 9 patients. In the second group, SAP increased 16.0 +/- 1.7 mm Hg in 24 of 26 patients, DAP increased 6.0 +/- 1.4 mm Hg in 5, and MAP increased 7.0 +/- 0.7 mm Hg in 18 of 26 patients. In the model, base pressure at 94 mm Hg, the pressures were 1.2 to 28.1 mm Hg lower for flows ranging from 10 to 122 ml/min at the 54-cm distance (wrist equivalent). CONCLUSION: The systemic-radial artery pressure gradient seen at the end of cardiopulmonary bypass seems to be a phenomenon common to patients with decreased hand vascular resistance. Wrist compression decreases or abolishes the gradient in most cases. It does not produce false positives, so an increase indicates a greater aortic than radial pressure. The difference is likely to be only temporary.

Does radial artery pressure accurately reflect aortic pressure?

STUDY OBJECTIVE: Our objective was to determine whether the systolic, diastolic, and mean arterial pressures measured in the radial artery accurately reflect corresponding pressures in the ascending aorta in narcotic-anesthetized patients with known obstructive coronary artery disease, before being subjected to cardiopulmonary bypass (CPB). DESIGN: This was a prospective study. SETTING: The cardiac operating room of a large, tertiary-care university medical center. PARTICIPANTS: Fifty-one patients (45 men and six women; age range, 48 to 77 years) with documented atherosclerotic coronary artery disease were studied. All patients underwent elective coronary artery bypass grafting after the study. INTERVENTIONS: Patients were premedicated with lorazepam and morphine 60 min before administration of Fentanyl-pancuronium anesthesia. The radial artery was cannulated before induction of anesthesia and the aorta approximately 45 min later. Comparisons of radial and aortic pressures were then performed. MEASUREMENTS AND RESULTS: Radial and aortic pressures were recorded through standard, fluid-filled, high-pressure, 91-cm (36-in) long tubing and disposable transducers, meticulously cleared of air bubbles. Additional measurements included cardiac output, central venous pressure, core temperature, blood gas levels, and hematocrit reading. Radial-aortic pressure differences were as follows: systolic arterial pressure (SAP), 12 +/- 1 mm Hg; mean arterial pressure (MAP), -0.8 +/- 0.3 mm Hg; and diastolic arterial pressure (DAP), -1.0 +/- 0.3 mm Hg. All were significant (p < 0.001), but the SAP difference was more than ten times that of either the MAP or the DAP values. The coefficients of determination (r2) indicated that the radial-aortic dependence was 0.44 for the SAP, 0.90 for the DAP, and 0.98 for the MAP relationship. Plotting the respective differences against the arithmetic mean of simultaneously measured pressures indicated that the radial SAP was 4 to 35 mm Hg higher than the aortic in 42 patients (82 percent) and was 10 to 35 mm Hg higher in 26 patients (51 percent); radial-aortic MAP differences clustered within 3 mm Hg in 47 patients (92 percent); radial DAP was +/- 3 mm Hg different from the aortic in 46 patients (90 percent). The largest MAP difference was -6 mm Hg in one patient. The largest DAP difference was +/- 5 mm Hg in three patients. CONCLUSIONS: In this group of patients, who were studied before undergoing CPB, the radial SAP gave a poor estimate of that present in the ascending aorta, since in more than 50 percent of the cases, the radial SAP was 10 to 35 mm Hg higher than that in the aorta. The radial MAP and DAP are reliable, since in 90 percent and 92 percent of the patients, respectively, the pressure differences were within +/- 3 mm Hg of those in the aorta.

Effect of pethidine premedication and halothane anaesthesia on upper limb blood flow.

Forearm blood flow (FBF), hand blood flow (HBF) and arterial pressure were measured in 12 patients, before and after premedication with pethidine and during halothane anaesthesia. After pethidine there was a significant (P less than 0.01) increase in HBF (180%) and decreased hand vascular resistance; heart rate also increased significantly (P less than 0.05), whilst mean arterial pressure (MAP) did not change. The large increase in HBF without hypotension suggests a local effect. With halothane, there was a significant (P less than 0.05) decrease in MAP, increase in HBF and decrease in hand vascular resistance compared with either control or effects produced by pethidine; there was a significant decrease in FBF and reversal of the action of pethidine on forearm vascular resistance.

Systolic pressure measurement in the ascending aorta: augmentation at the aortic cannula sideport.

To assess whether arterial blood pressure measured at the sideport of the aortic cannula mirrors that measured within the ascending aorta, the two pressures were compared in 10 consecutive patients undergoing cardiopulmonary bypass. The mean arterial pressures (MAP) were equal both before and after bypass, but the sideport systolic arterial pressure (SAP) was 6.0 +/- 0.8 mm Hg higher than the aortic SAP before bypass and 9.1 +/- 0.5 mm Hg higher than the aortic SAP after bypass (P less than 0.001). Hematocrit, blood temperature, cardiac output, and heart rate did not correlate with the differences in SAP, suggesting that the higher SAP seen at the sideport was generated within the tube connecting the oxygenator to the aorta. This theory was investigated by decreasing the tube length distal to the sideport in three patients in this group who had sideport SAPs higher than their aortic SAPs, a measure that decreased the SAP difference between the two sites. At the end of cardiopulmonary bypass in 20 other consecutive patients, the effect of shortening the aorta-oxygenator tube from 1.8 to 0.25 m was tested. The SAP in the sideport decreased by 4 to 12 mm Hg in 12 of the 20 patients, while the MAP was unaffected by this maneuver. It is concluded that the MAP measured at the sideport of the aortic cannula closely reflects the MAP in the ascending aorta, whereas the SAP measured at the sideport does not reflect the aortic SAP. Thus, when aortic pressure is measured at the sideport to confirm an artificially low radial arterial pressure, systolic amplification at the sideport might simulate or exaggerate radial artery hypotension.

Radial artery-to-aorta pressure difference after discontinuation of cardiopulmonary bypass.

To test whether the radial artery-to-aorta pressure gradient seen in some patients after cardiopulmonary bypass (CPB) is due to reduction in hand vascular resistance, the authors compared pressures in the ascending aorta with pressures in the radial artery before and after CPB in 12 patients. They increased hand vascular resistance by briefly occluding the radial and ulnar arteries at the wrist and recorded that effect on the radial artery-to-aorta pressure relationship. They also recorded the effect of wrist compression on radial artery pressures before and after CPB in 38 patients not having aortic pressure measurements. Before CPB in the first 12 patients, the radial systolic arterial pressure (SAP) was significantly higher (P less than 0.05) than the ascending aortic SAP, and wrist compression did not significantly affect that difference (P greater than 0.05). After CPB, the radial artery and aortic SAPs were not statistically different (P greater than 0.05), but wrist compression restored the higher radial artery SAP. The mean arterial pressure (MAP) was equal in four patients and 1-3 mmHg higher or lower in eight patients before CPB, and wrist compression did not alter those relationships. After CPB, MAP was equal in four patients; radial MAP was 1-3 mmHg higher or lower in six patients, and 7 and 10 mmHg lower in the last two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of radial, brachial, and aortic pressures after cardiopulmonary bypass.

Previous investigations have identified falsely low radial artery pressures after cardiopulmonary bypass (CPB). The present study investigates the relationship among radial, brachial, and aortic arterial pressures in 33 cardiac surgical patients following CPB. Two minutes after separation from CPB, clinically important (greater than or equal to 10 mmHg) underestimation of systolic aortic pressures occurred in 17 of 33 (52%) radial artery catheters, while occurring in seven of 33 (21%) brachial artery catheters. Radial artery mean pressure underestimated aortic mean pressure by greater than or equal to 5 mmHg in 21 of 33 (61%) patients two minutes after CPB, while an equivalent aortic-to-brachial artery mean arterial pressure difference occurred in nine of 33 (27%) patients. The incidence of aortic-to-radial mean arterial pressure differences greater than or equal to 5 mmHg decreased to 40% (four of ten patients) by ten minutes after CPB, although interpretation is complicated by decreased availability of aortic pressure measurements. Multivariate analysis failed to identify factors predisposed to central-to-peripheral pressure gradients. Radial and brachial arterial pressures were compared both before and after CPB in all 33 patients. Brachial artery systolic and mean pressures were higher than corresponding radial artery measurements two minutes after CPB (P less than 0.05), followed by gradual resumption of a normal brachial-to-radial pressure relationship over 60 minutes. Either vasospasm in the brachial and radial arteries or profound arteriolar vasodilation in the upper extremity might cause the observed central-to-peripheral arterial pressure differences. The progressive central-to-peripheral decrease in mean arterial pressure favors the latter mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Upper limb blood flow during hexamethonium-induced hypotension. Studies in patients anaesthetized with halothane.

We report the effect of hypotensive anaesthesia on blood flow in the upper limbs of 17 patients before the start of surgery. Under light halothane-oxygen anaesthesia, patients (n = 17) were given hexamethonium 0.5-1.0 mg kg-1. Forearm blood flow (FBF), hand blood flow (HBF) and systemic arterial pressure (AP) were measured before, and 9 and 18 min after the administration of hexamethonium. During the control period of halothane anaesthesia, HBF was AP-dependent, but FBF was not. Hexamethonium produced a statistically significant (P less than 0.001) decrease in systolic AP by 9 and 18 min, but significant reductions in FBF and HBF were seen only at 9 min. During the hypotensive period neither HBF nor FBF correlated with the systolic AP, which had decreased from an average of 98 mm Hg to an average of 65 mm Hg (range 95-50 mm Hg), but the changes in HBF and FBF did correlate with the changes in systolic AP. As a secondary factor, the control FBF correlated inversely with the reduction in FBF after hexamethonium. We concluded that hypotension induced by hexamethonium during halothane anaesthesia produced a transient reduction in limb blood flow that was dependent on the change in AP. A range of systolic AP from 95 to 50 mm Hg did not correlate with either FBF or HBF during the hypotensive period.

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)

Predicting the pharmacodynamics of heparin: a clinical evaluation of the Hepcon System 4.

The magnitude of the anticoagulation response to heparin (heparin responsiveness) varies substantially from patient to patient. Identifying extremes of sensitivity and resistance prior to intravenous administration of heparin would facilitate anticoagulation for cardiopulmonary bypass (CPB). The performance of the Hepcon System 4 (HemoTec, Inc, Englewood, CO), an instrument designed for that purpose, was tested. Using nonheparinized blood samples from 157 patients scheduled for surgery requiring CPB, this device performed activated coagulation times (ACT) with three different concentrations of in vitro heparin. After determining each patient's in vitro heparin response, the heparin dose predicted to produce ACT values of 480 seconds (group 1, N = 77) or 600 seconds (group 2, N = 80) was administered. Five minutes later each patient's ACT was determined with the Hemochron method (International Technidyne, Inc, Edison, NJ). Simultaneously, several other variables that might predict heparin responsiveness were investigated. When compared with the observed ACT, the Hepcon System 4 inadequately predicted the response. There was considerable scatter in this comparison, but most frequently the in vitro method substantially underestimated the in vivo heparin dose requirement. Heparin responsiveness decreased significantly with high platelet counts and advanced age, but was unaffected by the initial hematocrit, ACT, partial thromboplastin time, or preoperative heparin therapy. Previous investigations have not identified a relationship between advanced age and reduced heparin responsiveness. Combining the Hepcon heparin dose-response in vitro method with the other parameters evaluated, stepwise regression could only account for 39% of the observed variability in heparin responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertensive response to thiopental in man during cardiopulmonary bypass.

We report the effect of 250 mg of sodium thiopental on vascular tone at constant blood flow in 26 patients undergoing cardiopulmonary bypass while the ascending aorta was cross-clamped. Light anaesthesia was effected with fentanyl and enflurane, muscle relaxation with pancuronium. After a latent period of 10.5 +/- 0.7 s there was a hypertensive response of 9.8 +/- 0.5 s duration and of 21.4 +/- 1.7 mmHg (2.8 +/- 0.2 kPa) magnitude; this was followed by hypotension of 39.6 +/- 4.2 s duration and of 18.4 +/- 1.9 mmHg (2.4 +/- 0.3 kPa) magnitude. There was a statistically significant inverse correlation between the hypertension and body temperature (P = 0.005); the time to onset of hypertension correlated directly with pump volume (P = 0.001), weight of the patient (P = 0.03), and cross-clamp time before the drug was given (P = 0.002), and correlated inversely with the serum sodium concentration (P = 0.001). The duration of hypertension was inversely related to the plasma bicarbonate (P = 0.01) and body temperature (P = 0.04). The duration of hypotension was significantly longer in women (P = 0.0001) and was directly related to the duration of cross-clamping (P = 0.0007), to pH (P = 0.0016), and to PCO2 (P = 0.04). We speculate that thiopental induced the hypertensive response due to a potentiation of the vasoconstrictive (local) effect of norepinephrine, and induced the hypotensive response by a central nervous system effect. Thiopental had no apparent effect on venous tone.

Effect of pethidine, fentanyl and morphine on post-operative shivering in man.

One hundred consecutive patients who shivered following general or regional anesthesia and a surgical procedure were randomly treated with 25 mg pethidine, 2.5 mg morphine, 25 micrograms fentanyl or sodium chloride 0.9%, given in equal intravenous volumes over a 15-min period. The effects were evaluated every 5 min after the first injection. There was a spontaneous, time-related disappearance of shivering in the sodium chloride-treated patients. In the pethidine-treated group, shivering disappeared more than twice as fast as in the control group. The difference was highly significant at 15 and 20 min (P less than 0.001) and was unrelated to weight, body temperature or duration of anesthesia. Women responded sooner than men, reaching significance at 10 min (P less than 0.05), while men did so only at 20 min. Morphine or fentanyl had no effect. Nausea and vomiting were minimal and of equal incidence in narcotic- and placebo-treated patients.