Acute smoking increases ST depression in humans during general anesthesia.

We tested the hypothesis that acute smoking is associated with ST segment depression during general anesthesia in patients without ischemic heart disease. The carbon monoxide (CO) concentration in expired gas and hemodynamic data was measured during general anesthesia for noncardiac or nonperipheral vascular surgery in patients without symptoms or evidence of ischemic heart disease. Increased expired CO concentrations are indicators of recent smoking. Logistic regression analysis identified significant predictors of ST segment depression > or = 1 mm. Both rate pressure product (odds ratio 1.20 for each increase of 1000, 95% confidence interval = 1.04-1.41, P = 0.007) and expired CO concentration (odds ratio 1.05 for each part per million increase, 95% confidence interval = 1.03-1.08, P = 0.001) were significant predictors of ST segment depression when considered simultaneously. Males demonstrated a lower probability of having an episode of ST depression (odds ratio = 0.16, P = 0.01), but this did not change the relationship between rate pressure product and CO as predictors of ST depression. Approximately 25% of chronically smoking patients smoked on the morning of surgery despite instructions not to smoke. IMPLICATIONS: Patients under age 65 without symptoms of ischemic heart disease who smoked shortly before surgery had more episodes of rate pressure product-related ST segment depression than nonsmokers, prior smokers, or chronic smokers who did not smoke before surgery. Females were at greater risk of ST depression than males.     

ST segment depression during labor and delivery.

ECG changes suggestive of myocardial ischemia are common during cesarean delivery under regional anesthesia. To determine the time course, duration, and significance of these ECG changes, we monitored 111 parturients with continuous ambulatory ECG (Holter) during and after cesarean delivery. Twenty-two parturients undergoing vaginal delivery were similarly monitored. ST segment depression was present in 25% of patients undergoing cesarean delivery but was not found in those patients delivering vaginally. ST segment elevation was not detected in either group. The incidence of ST segment depression during cesarean delivery was similar with epidural (29%), spinal (17%), and general (18%) anesthesia, occurring most commonly in the 30 min following delivery (P less than 0.001). Transthoracic echocardiographic imaging was performed in 23 patients undergoing cesarean section. Five of the 23 patients had seven episodes of intraoperative ST segment depression. Regional wall motion abnormalities were not present in any patient. A decrease in ejection fraction area greater than 15% from baseline or from previous interval ejection fraction area was present during four episodes of ST change. Three episodes of ST depression were not associated with significant decreases in ejection fraction area. Precordial Doppler monitoring for detection of venous air embolism in 25 patients revealed no association between the occurrence of venous air embolism and ST segment depression. We conclude that although significant myocardial impairment during cesarean delivery does not occur, episodes of ST depression may not all be merely an artifact of parturition.     

Dobutamine stress echocardiography and the resting but not exercise electrocardiograph predict severe coronary artery disease in renal transplant candidates.

BACKGROUND: After renal transplantation half of all deaths are cardiac, so prior detection and treatment of severe coronary artery disease (CAD) is advocated. The aim of this study was to identify non-invasive predictors of severe CAD in a group of renal transplant candidates. METHODS: One hundred and twenty-five renal transplant candidates (mean age 52+/-12 years, 80 male, mean creatinine 608+/-272 micromol/l) were studied. All had coronary angiography, dobutamine stress echocardiography, and resting and exercise electrocardiograph (ECG). Severe CAD was defined as luminal stenosis >70% by visual estimation in at least one epicardial artery. The resting ECG was recorded as abnormal if there was evidence of pathological Q waves, left ventricular hypertrophy, ST depression or elevation > or=1 mm, T wave inversion or bundle branch block. Total exercise time, maximal ST segment change, maximal heart rate and systolic blood pressure, limiting symptoms and Duke score were calculated during the exercise ECG test. RESULTS: Of the patients, 36 (29%) had severe CAD, 55% were on dialysis and 39% were diabetic. Patients with severe CAD were significantly older (P<0.001), had higher total cholesterol (P = 0.05), higher CRP level (P = 0.05), larger left ventricular (LV), end systolic and end diastolic diameter (P = 0.007 for each), and lower LV ejection fraction (P = 0.01). A significantly higher percentage were diabetic (P = 0.05), had previous graft failure (P = 0.05), mitral annular calcification (P = 0.04), an abnormal resting ECG (P = 0.001) and positive stress echo result (P<0.001). Cardiac symptoms and exercise ECG parameters were not significantly different in the two groups. Stepwise logistic regression identified an abnormal resting ECG (OR 7, 95% CI 2, 34, P = 0.013) and positive stress echo result (OR 23, 95% CI 6, 88, P<0.001) as independent predictors of severe CAD. CONCLUSIONS: In selecting which potential renal transplant candidates should undergo coronary angiography, resting ECG and dobutamine stress echocardiography are the best predictors of severe CAD.     

Increases in P-wave dispersion predict postoperative atrial fibrillation after coronary artery bypass graft surgery

Atrial fibrillation (AF) is a common complication after coronary artery bypass graft (CABG) surgery. In this study we examined the effect of surgery on atrial electrophysiology as measured by P-wave characteristics and to determine the potential predictive value of P-wave characteristics on the incidences of postoperative AF in patients undergoing CABG surgery. Patients undergoing elective CABG surgery were monitored by continuous electrocardiogram (ECG) telemetry during the in-hospital period until discharge for the occurrence of postoperative AF. Differences in P-wave characteristics (P-wave duration, amplitude, axis, dispersion, PR interval, segment depression, and dispersion) were compared between the pre- and postoperative 12-lead ECG measurements, and also between patients with and without postoperative AF. The association of postoperative AF and potential clinical predictors and P-wave characteristics were determined by multivariate logistic regression. Postoperative AF occurred in 81 (27%) of 300 patients. Univariate analysis showed that patients who subsequently developed postoperative AF compared with those without AF were significantly older (mean age 68 +/- 8 versus 63 +/- 10 yr, P < 0.0001), had a larger body surface area (BSA) (2.03 +/- 0.24 versus 1.92 +/- 0.22 m(2), P = 0.0002), were more likely to have a history of AF (8 of 81 versus 1 of 219, P = 0.003), used preoperative antiarrhythmic medications more frequently (7 of 81 versus 4 of 219, P = 0.01), and had a more frequent rate of return to the operating room for postoperative complications (9 of 81 versus 9 of 219, P = 0.029). Furthermore, the postoperative P-wave duration decreased to a larger extent (mean change -11.3 +/- 0.1 ms versus -8.4 +/- 0.1 ms, P < 0.0001), and the P-wave dispersion increased postoperatively to a larger extent (3.1 +/- 15.5 ms versus -1.6 +/- 14.6 ms, P = 0.028) in those who subsequently developed AF compared with those without AF. Multivariate logistic regression showed age (odds ratio [OR] = 1.1, 95% confidence interval [CI]: 1.06-1.15, P < 0.0001), BSA (OR = 38.1, 95% CI: 8.2-176, P < 0.0001), and an increase in postoperative P-wave dispersion (OR = 1.03, 95% CI: 1.01-1.05, P = 0.01) to be independent predictors of postoperative AF. No surgical factor was identified to be responsible for this postoperative change in atrial electrophysiology. IMPLICATIONS: In addition to clinical factors, such as advanced age and body surface area, we demonstrated that electrophysiologic changes involving an increase in P-wave dispersion postoperatively independently predict atrial fibrillation after coronary artery bypass graft surgery.     

Effect of autonomic nervous system dysfunction on sudden death in ischemic patients with anginal syndrome died during electrocardiographic monitoring in Intensive Care Unit

AIM: The aim of this study was to investigate the role of sympathovagal imbalance in patients with 'ischemic' sudden death (arrhythmic death preceded by ST segment shift). Although heart rate variability is a powerful tool for risk stratification after myocardial infarction, the mechanism precipitating sudden death is poorly known. METHODS: We analyzed the records of 10 patients who had ischemic sudden death during ECG Holter monitoring. Thirty patients with angina and transient myocardial ischemia during Holter monitoring served as control subjects. Arrhythmias, ST segment changes and heart rate variability were analyzed by a computed interactive Holter system. RESULTS: In 8 patients the sudden death was induced by ventricular fibrillation; in 2 by atrioventricular block followed by sinus arrest. All 10 patients showed ST segment shift. ST depression (maximal change 0.54+/-0.16 mV) occurred in 6 patients and ST elevation (maximal change 0.65+/-0.24 mV) in 4. The standard deviation of normal RR intervals (SDNN) was 92+/-30 ms during total Holter monitoring period vs 70+/-10 ms and 46+/-8 ms in epoch 1 and epoch 2 respectively. The SDNN was lower before the occurrence of ischemic sudden death: 54+/-12 ms (P< 0.005) in epoch 3 and 26+/-5 (P<0.005) in epoch 4 (i.e. 5 min before the onset of fatal ST segment shift). In controls the SDNN was 108+/-30 ms during total Holter monitoring period, whereas is measured 58+/-28 ms 5 min before the most significant episode of ST shift vs 26+/-5 in the group with sudden death (P<0.001). CONCLUSION: Sympathovagal imbalance, as detected by a marked decrease in heart rate variability, is present in the period (5 min) immediately preceding the onset of the ST shift precipitating ischemic sudden death. These findings suggest that transient autonomic dysfunction may facilitate, during acute myocardial ischemia, fatal arrhythmias precipitating in sudden death.     

Treatment of intraoperative refractory hypotension with terlipressin in patients chronically treated with an antagonist of the renin-angiotensin system.

The goal of the present study was to determine whether terlipressin, an agonist of the vasopressin system, could counteract perioperative hypotension refractory to common vasopressor therapy and to analyze its circulatory effects. We enrolled 51 consecutive vascular surgical patients chronically treated with angiotensin-converting enzyme inhibitors or antagonists of the receptor of angiotensin II, who received a standardized opioid-propofol anesthetic. Of these 51 patients, 32 had at least one episode of hypotension, which responded to epinephrine or phenylephrine. In 10 other patients, systolic arterial pressure (SAP) did not remain above 100 mm Hg for 1 min, despite three bolus doses of ephedrine or phenylephrine. In these patients, we injected a bolus of 1 mg of terlipressin, repeated twice if necessary. Hemodynamic and echocardiographic variables were recorded every 30 s over 6 min. In eight patients, arterial pressure was restored with one injection of terlipressin; in two other patients, three injections were necessary. One minute after the last injection of terlipressin, the SAP increased from 88+/-3 to 100+/-4 mm Hg and reached 117+/-5 mm Hg (P = 0.001) 3 min after the injection and remained stable around this value. This increase in SAP was associated with significant changes in left ventricular end-diastolic area (17.9+/-2 vs 20.2+/-2.2 cm2; P = 0.003), end-systolic area (8.1+/-1.3 vs 9.6+/-1.5 cm2; P = 0.004), end-systolic wall stress (45+/-8 vs 66+/-12; P = 0.001), and heart rate (60+/-4 vs 55+/-3 bpm; P = 0.001). Fractional area change and velocity of fiber shortening did not change significantly. No additional injection of vasopressor was required during the perioperative period. No change in ST segment was observed after the injection. IMPLICATIONS: Terlipressin is effective to rapidly correct refractory hypotension in patients chronically treated with antagonists of the renin-angiotensin system without impairing left ventricular function.     

Haemodynamic and catecholamine responses to calcitonin gene-related peptide during volatile anaesthesia

PURPOSE: Calcitonin gene-related peptide (CGRP) produces vasodilatation, hypotension, and tachycardia. Tachycardia induced by CGRP may be due to sympathetic activation. Volatile anaesthetics attenuate activation of arterial baroreflexes. We examined the haemodynamic and endocrine effects of CGRP infusion (4 micrograms.kg-1) during anaesthesia with either enflurane or isoflurane in dogs. METHODS: Measurements of haemodynamic variables and hormone assays for plasma catecholamines were made before, during, and after CGRP infusion. Anaesthesia consisted of induction with 25 mg.kg-1 pentobarbital, followed by either enflurane (n = 7) or isoflurane (n = 7) to achieve a 1.0 end-tidal minimum alveolar concentration in oxygen 100%. RESULTS: Mean arterial pressure and systemic vascular resistance decreased (P < 0.01) and the reductions in both variables were similar during CGRP infusion in both groups. Cardiac index (CI) was increased (P < 0.01) in the enflurane group throughout the study while CI increased (P < 0.01) only during infusion in the isoflurane group. Heart rate (HR) remained unchanged (from 135 +/- 6 bpm to 134 +/- 7 bpm) in the enflurane group but tended to increase (from 162 +/- 9 bpm to 171 +/- 9 bpm) in the isoflurane group during infusion. Intergroup differences in HR were found (P < 0.05). Plasma epinephrine concentrations increased (from 42.4 +/- 12.7 pg.ml-1 to 115.3 +/- 41.8 pg.ml-1, P < 0.01) during infusion in the isoflurane group. However, these increases were suppressed (from 46.6 +/- 23.2 pg.ml-1 to 64.7 +/- 32.4 pg.ml-1) to a greater extent in the enflurane group. CONCLUSION: The haemodynamic responses, except for HR, of CGRP infusion are similar during enflurane and isoflurane anaesthesia. Suppression of tachycardia induced by CGRP is greater with enflurane than with isoflurane. The differences in HR may be due to the roles of catecholamine responses resulting from the anaesthetic-induced sympathetic suppression.     

Monitoring cardiovascular changes during hemodialysis in children

Hemodialysis (HD) causes rapid volume shifts and circulatory changes. In chronic renal failure (CRF) Na+/K+ATP-ase is depressed, whereas endogenous digoxin-like factor (EDLF) is elevated. Our aim was to characterize HD-induced cardiovascular adaptation and its possible links to Na+/K+ATP-ase and EDLF. Eleven children with CRF on HD (aged 14.7 +/- 3.7 years) and 11 healthy children were investigated for basic circulatory parameters. Thoracic impedance (Zo) and circulatory parameters were monitored by impedance cardiography (ICG) during HD. Erythrocyte Na+/K+ATP-ase and EDLF were measured before and after HD. Up to the loss of 6% of total body weight, Zo rose linearly with fluid removal, above this no further increase occurred. Heart rate and mean arterial pressure (MAP) were inversely related (r = -0.97); MAP rose in the first and decreased in the second part of HD. Systemic vascular resistance paralleled MAP, whereas stroke volume rapidly decreased, but stabilized in the second part of HD. The ratio of preejection period/ventricular ejection time (PEP/VET) correlated positively with HD duration (r = 0.92), suggesting diminished cardiac filling. Cardiac index (CI) remained stable. EDLF was high in uremia accompanied by depressed Na+/K+ATP-ase (P < 0.05 and P < 0.01, respectively). Following HD Na+/K+ATP-ase normalized. Correlation between Na+/K+ATP-ase activity and MAP was linear (r = 0.85). In conclusion, ICG during HD provides detailed information concerning circulatory adaptation resulting in stable CI, suggesting that the dialysis-induced hypovolemia is compensated by the centralization of the blood volume. Changes of Na+/K+ATP-ase indicate that dialyzable blood pressure-regulating substance(s) inhibit(s) the pump. However, lack of further correlation between Na+/K+ATP-ase, EDLF, and cardiovascular parameters indicates the complexity of the regulatory processes.     

Risk factors for failure to extend labor epidural analgesia to epidural anesthesia for Cesarean section

AIM: To identify parturients at risk of inability to extend labor epidural analgesia in whom alternative methods of anesthesia should be considered for Cesarean section (CS). METHODS: For 6 months, we prospectively studied women undergoing CS with a functioning epidural catheter in place from the delivery ward. All parturients received the same epidural protocol: bolus of bupivacaine 0.1% and fentanyl, followed by bupivacaine 0.1% and fentanyl (2 microg/ml) 10-15 ml/h and an additional 5 ml of bupivacaine 0.125% as top-up according to patient request. Sixteen milliliters of lidocaine 2%, 1 ml of bicarbonate and 100 microg of fentanyl were given for CS. Failed epidural analgesia was defined as the need to convert to general anesthesia. RESULTS: Of the 101 parturients studied, 20 (19.8%) required conversion to general anesthesia. In univariate analysis, the likelihood of failed epidural anesthesia was inversely correlated with parturient age (P = 0.014) and directly correlated with pre-pregnancy weight (P = 0.019), weight at the end of pregnancy (P = 0.003), body mass index at the end of pregnancy (P = 0.0004), gestational week (P = 0.008), number of top-ups (P = 0.0004) and visual analog scale (VAS) score 2 h before CS (P = 0.03). In multivariate analysis, the number of top-ups in the delivery ward was the best predictor of epidural anesthesia failure (odds ratio, 4.39; P = 0.005). CONCLUSION: Younger, more obese parturients at a higher gestational week, requiring more top-ups during labor and having a higher VAS score in the 2 h before CS are at risk for inability to extend labor epidural analgesia to epidural anesthesia for CS.     

Risk factors for failure to extend labor epidural analgesia to epidural anesthesia for Cesarean section

OBJECTIVE: To identify parturients at risk of inability to extend labor epidural analgesia in whom alternative methods of anesthesia should be considered for Cesarean section (CS). METHODS: For 6 months, we prospectively studied women undergoing a CS with a functioning epidural catheter in place from the delivery ward. All parturients received the same epidural protocol: bolus of bupivacaine 0.1% and fentanyl, then bupivacaine 0.1% and fentanyl (2 microg/ml) 10-15 ml/h and an additional 5 ml of bupivacaine 0.125% top-ups according to patient request. Sixteen millilitres of lidocaine 2%, 1 ml of bicarbonate, and 100 microg of fentanyl were given for CS. Failed epidural analgesia was defined as the need to convert to general anesthesia. RESULTS: Of the 101 parturients studied, 20 (19.8%) required conversion to general anesthesia. In univariate analysis, the likelihood of failed epidural anesthesia was inversely correlated with parturient's age (P = 0.014) and directly correlated with pre-pregnancy weight (P = 0.019), weight at the end of pregnancy (P = 0.003), body mass index (BMI) at the end of pregnancy (P = 0.0004), gestational week (P = 0.008), number of top-ups (P = 0.0004) and visual analog scale (VAS) 2 h before CS (P = 0.03). In multivariate analysis, the number of top-ups in the delivery ward was the best predictor of epidural anesthesia failure (odds ratio 4.39, P = 0.005). CONCLUSION: Younger, more obese parturients at a higher gestational week, requiring more top-ups during labor, having a higher VAS in the 2 h before CS are at risk of inability to extend labor epidural analgesia to epidural anesthesia for CS.     

Effect of erythropoietin on ischemia tolerance in anemic hemodialysis patients with confirmed coronary artery disease.

From a total of 81 patients on maintenance hemodialysis who underwent coronary angiography, 8 patients fulfilled the criteria: significant coronary artery disease, hematocrit less than 27%, reproducible (ECG) positive treadmill test, no disturbance of repolarization in ECG at rest. Exercise stress testing was performed at a hematocrit of 25 +/- 2% and following erythropoietin therapy at a hematocrit of 34 +/- 0.5%. Symptom-limited exercise performance increased in all patients (1.10 +/- 0.3 W/kg b.w. vs. 1.44 +/- 0.31 W/kg b.w., p less than 0.01) as well as exercise duration (489 vs. 362 s, p +/- 0.01). ST segment depression during maximal exercise was reduced from a mean of 2.1 to 0.4 mm (p less than 0.01). It is concluded that amelioration of renal anemia by erythropoietin in dialysis patients with significant coronary artery disease reduces exercise-induced myocardial ischemia.     

Aortic and large artery compliance in end-stage renal failure

Pulse wave velocity (PWV) was measured in the aorta, right leg and arm of 90 control subjects (CS) and 92 hemodialysis patients (HD) of the same age and mean arterial pressure (MAP). Blood chemistry, including blood lipids, and echographic dimensions of the aorta, were measured in all subjects. Presence of aortic calcification was evaluated by abdominal X-ray and echography. Whereas femoral and brachial PWV were only slightly increased in HD (P less than 0.05), the aortic PWV was significantly elevated (1113 +/- 319 cm/sec) in comparison with CS (965 +/- 216 cm/sec; P = 0.0016). Aortic diameters were larger in HD, both at the root of aorta (32.7 +/- 4 vs. 28.2 +/- 2.8 mm; P less than 0.0001) and aortic bifurcation (16.9 +/- 3.1 vs. 14.6 +/- 2.2 mm; P less than 0.0001). Although the MAP was similar in HD (109.9 +/- 19.3 mm Hg) and CS (110.2 +/- 17.2 mm Hg), the pulse pressure was significantly increased in HD patients (76.6 +/- 23.7 vs. 63.9 +/- 22 mm Hg; P = 0.007). In the two populations, aortic PWV was found to increase with age (P less than 0.0001) and MAP (P less than 0.0001). The presence of aortic calcification showed only a borderline relationship with the increase in aortic PWV (P = 0.050 in CS and P = 0.069 in HD). As change in PWV is directly related to change in distensibility, and the aortic diameters were increased in HD, these results indicate that aortic wall compliance is decreased in HD, resulting in an increase in the pulsatile component of arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of arteriovenous fistulas on cardiac oxygen supply and demand

BACKGROUND: Arteriovenous (AV) fistulas used for hemodialysis access may affect cardiac load by increasing the preload while decreasing the afterload. In dogs, AV fistulas have also been shown to affect coronary perfusion negatively. We investigated the net effect of AV fistulas on cardiac oxygen supply and demand. METHODS: Aortic pressure waves were reconstructed from finger pressure recordings obtained on the nonfistula arm using a wave-form filter. Changes in systolic, mean, and diastolic aortic pressure were calculated, together with changes in heart rate (HR), stroke volume (SV), cardiac output (CO), and systemic vascular resistance (SVR) during a 60-second compression of AV fistulas in 10 patients. Changes in cardiac supply and demand were estimated by calculating the area under the aortic pressure curve during diastole [diastolic pressure time index (DPTI)] and systole [systolic pressure time index (SPTI)], respectively. RESULTS: During fistula compression, systolic, mean and diastolic pressure increased by 4.2 +/- 4.3, 2.6 +/- 3.0, and 2.8 +/- 2.9 mm Hg (mean +/- SD, all P < 0.05). The HR decreased by 3.8 +/- 2.5 beats per minute (P < 0.01), and SV decreased 3.7 +/- 6.1% (NS). CO decreased 9.4 +/- 8.6%, and SVR increased 14.3 +/- 11.7% (both P < 0.05). The SPTI increased by 1.5 +/- 1.5 mm Hg.sec (P < 0.01), and the DPTI increased by 7.6 +/- 8.1 mm Hg.sec (14.8% increase, P < 0.05) during compression. The ratio of supply and demand (DPTI/SPTI) improved by 13.5 +/- 13.0% (P < 0.01) when the fistula was compressed. CONCLUSION: AV fistulas have a small effect on left ventricular oxygen demand, but decrease cardiac oxygen supply considerably.     

Association between high ultrafiltration rates and mortality in uraemic patients on regular haemodialysis. A 5-year prospective observational multicentre study.

BACKGROUND: High ultrafiltration rate on haemodialysis (HD) stresses the cardiovascular system and could have a negative effect on survival. METHODS: The effect of ultrafiltration rate (UFR; ml/h/kg BW) on mortality was prospectively evaluated in a cohort of 287 prevalent uraemic patients in regular HD from 1 January 2000 to 31 December 2005. Patients: 165 men and 122 women, age 66 +/- 13 years, on regular HD for at least 6 months, median: 48 months (range 6-372 months). Mean UFR was 12.7 +/- 3.5 ml/h/kg BW, Kt/V: 1.27 +/- 0.13, body weight (BW): 62 +/- 13 kg, PCRn: 1.11 +/- 0.20 g/kg/day, duration of dialysis: median 240 min (range 180-300 min), mean arterial blood pressure (MAP) 99 +/- 9 mm/Hg. One hundred and forty nine patients (52%) died, mainly for cardiovascular reasons (69%). Multivariate Cox regression analysis was utilized to evaluate the effect on mortality of UFR, age, sex, dialytic vintage, cardiovascular disease (CVD), diabetes, dialysis modality, duration of HD, BW, interdialytic weight gain (IWG), body mass index (BMI), MAP, pulse pressure (PP), Kt/V, PCRn. RESULTS: Age (HR 1.06; CI 1.04-1.08; P < 0.0001), PCRn (HR 0.17, CI 0.07-0.43; P < 0.0001), diabetes (HR 1.81, CI 1.24-2.47; P = 0.007), CVD (HR 1.86; CI 1.32-2.62; P = 0.007) and UFR (HR 1.22; CI 1.16-1.28; P < 0.0001) were identified as factors independently correlated to survival. We estimated the discrimination potential of UFR, evaluated at baseline, in predicting death at 5 years, calculating the relative receiver operating characteristic (ROC) curves and the cut-off that minimizes the absolute difference between sensitivity and specificity. CONCLUSIONS: High UFRs are independently associated with increased mortality risk in HD patients. Better survival was observed with UFR < 12.37 ml/h/kg BW. For patients with higher UFRs, longer or more frequent dialysis sessions should be considered in order to prevent the deleterious consequences of excessive UFR.     

Acute arterio-venous fistula occlusion decreases sympathetic activity and improves baroreflex control in kidney transplanted patients.

BACKGROUND: The acute bradycardia induced by the occlusion of an arteriovenous fistula (AVF), known as the Nicoladoni-Branham sign, is considerably larger than that which occurs during carotid sinus massage. This suggests increased arterial baroreflex sensitivity during acute AVF occlusion. Moreover, the influence of acute AVF occlusion on muscle sympathetic nerve traffic (MSNA, by microneurography) is unknown. We therefore assessed the effects of acute AVF occlusion on baroreflex sensitivity and on MSNA in patients with stable functional kidney grafts and patent AVF. METHODS: We measured blood pressure (BP), MSNA (n = 11), heart rate (HR), cardiac output (CO) and arterial baroreflex sensitivity (n = 18) at baseline and during acute, 30-s pneumatic AVF occlusions in 23 renal transplanted recipients. RESULTS: During the first 5 s of the AVF occlusion, mean BP increased from 98+/-4 to 112+/-4 mmHg (P<0.0001) while MSNA decreased to 28+/-5% of baseline values (P<0.0001) and HR decreased from 71+/-3 to 61+/-3 b.p.m. (P<0.0001). The largest increases in BP were accompanied by the most marked decreases in MSNA (r = -0.79, P = 0.003) and HR (r = -0.49; P = 0.01) during the first 5 s of the AVF occlusion. During AVF occlusion baseline CO of 6.9+/-0.3 decreased to 5.6+/-0.3 l/min (P<0.0001) while baroreflex sensitivity increased from 10+/-1 to 17+/-2 ms/mm Hg (P<0.001). CONCLUSIONS: Arterial baroreceptor activation and increased arterial baroreflex sensitivity decrease heart rate during AVF occlusion. In addition, our study is the first to demonstrate that arterial baroreflex activation decreases sympathetic nerve traffic during the Nicoladoni-Branham sign.     

Comparison of remifentanil and nitrous oxide in labour analgesia

BACKGROUND: We compared the efficacy and side-effects of remifentanil with those of nitrous oxide during the first stage of labour. METHODS: Twenty parturients participated in a randomized, double-blind, cross-over study. Intravenous remifentanil in 0.4 microg kg(-1) PCA doses with 1-min infusion and lock-out times and intermittent inhaled 50% nitrous oxide were compared during 20-min study periods with a 20-min wash-out sequence after each period. The parturients assessed the intensity of contraction pain (verbal numerical score 0-10), pain relief (score 0-4) and side-effects every 10 min. Noninvasive blood pressure, heart rate (HR), oxyhaemoglobin saturation (SaO2), end-tidal carbon dioxide, fractions of inhaled and exhaled oxygen and nitrous oxide and foetal heart rate (FHR) were recorded. Hypoxaemia and bradycardia were defined as SaO2<90% and HR<50, respectively. RESULTS: Fifteen parturients completed the study. There was no period effect or treatment-period interaction. The median decrease in pain score for remifentanil was 1.5 and that for nitrous oxide 0.5 (P=0.01). The parturients gave better pain relief scores with remifentanil than with nitrous oxide (median 2.5 vs. 0.5, respectively, P<0.001). Sedation was reported more often, and SaO2 was slightly lower during remifentanil administration. No episodes of hypoxaemia occurred. There was no difference in maternal blood pressure and HR or the incidence of abnormal FHR during remifentanil compared to nitrous oxide. Most parturients preferred remifentanil to nitrous oxide (14 vs. 1, P<0.001). CONCLUSIONS: This study suggests that IVPCA remifentanil provides better labour analgesia than intermittently inhaled nitrous oxide.     

Hemodynamic effects of radical left ventricular scar resection in patients with and without congestive heart failure

To evaluate the hemodynamic changes that occur following radical left ventricular scar resection we studied 40 patients (mean age, 59.2 years; 36 males) with complete hemodynamic evaluation preoperatively (preop) and 5 to 12 days postoperatively (postop). Severe congestive heart failure (CHF) was present in 15 patients, ventricular arrhythmias in 19, and angina in 19 patients preop. The operation consisted of extensive scar resection with complete myocardial revascularization (average 2.4 grafts per patient). Ten patients required intraaortic balloon pump assist for up to 8 days postop. Postoperative left ventricular ejection fraction (EF) was estimated with multiple gated acquisition scanning. A significant rise in heart rate was observed in the whole group of patients postop (P = 0.000). In the group of patients with CHF preop the EF was increased from 25.1 +/- 8.4% (mean +/- SD) preop to 30.9 +/- 11.2% postop (P = 0.003), the cardiac index was increased from 2.2 +/- 0.5 liters/min/m2 preop to 2.7 +/- 0.5 liters/min/m2 postop (P = 0.02), and the pulmonary artery wedge pressure was decreased from 22.0 +/- 7.7 mm Hg preop to 15.5 +/- 4.3 mm Hg postop (P = 0.005). In the patients without active CHF preop no improvement in the above hemodynamics was noted. In conclusion, radical left ventricular scar resection significantly increased EF and CI and decreased PAW in patients with preop CHF, whereas in the absence of CHF this procedure resulted in minimal hemodynamic changes.     

Insulin resistance, dyslipidaemia, inflammation and endothelial function in nephrotic syndrome.

BACKGROUND: Nephrotic syndrome (NS) is associated with an increased risk of cardiovascular disease (CVD). We have shown previously that endothelial function, measured by post-ischaemic flow-mediated dilatation (FMD) of the brachial artery, is impaired in NS. In this study our aim was to assess the potential roles of insulin resistance, plasma non-esterified fatty acids (NEFAs) and inflammation in endothelial dysfunction in NS patients. METHODS: FMD was compared between NS patients (n=19) and controls (CS, n=19). Plasma glucose, insulin and NEFAs were measured. Insulin resistance was calculated using the Homeostasis Model Assessment (HOMA) score. C-reactive protein (CRP), interleukin-6 (IL-6), tumour necrosis factor alpha (TNFalpha) and fibrinogen were measured as markers of inflammation. RESULTS: FMD was significantly lower in the NS group (mean+/-standard error, NS 5.1+/-0.7%, CS 7.3+/-0.7%, P=0.02). Fasting insulin (NS 12.5+/-1.5 mU/l, CS 6.8+/-0.7 mU/l, P<0.01), fasting glucose (NS 5.3+/-0.2, CS 4.8+/-0.1, P=0.02) and the HOMA score (NS 3.0+/-0.4, CS 1.5+/-0.2, P=0.001) were significantly higher in NS. These differences persisted after adjusting for waist circumference. Of the inflammatory markers, only fibrinogen (P<0.01) and IL-6 (P=0.01) were significantly increased in NS. Despite significantly lower plasma NEFAs in NS, the NEFA:albumin ratio showed a non-significant trend to higher levels in NS (NS 10.7+/-0.1 micro mol/g, CS 8.7+/-0.1 micro mol/g, P=0.06). Within the NS group, multivariate backward regression analysis showed that NEFAs (P<0.01) and low-density lipoprotein (LDL) cholesterol (P=0.05) were significant negative independent predictors of FMD. CONCLUSION: Endothelial function in NS is inversely correlated with plasma concentrations of NEFAs and LDL cholesterol. Dyslipoproteinaemia and NEFAs probably contribute to the increased risk of CVD seen in NS. We also postulate that in NS, hypoalbuminaemia increases the delivery of NEFAs to endothelial cells thereby impairing the synthesis and release of nitric oxide.     

Norepinephrine-induced vasoconstriction results in decreased blood volume in dialysis patients.

BACKGROUND: Hypotension during haemodialysis results from an inadequate cardiovascular response to ultrafiltration-induced hypovolaemia. It has been suggested that plasma volume could be increased as a result of systemic vasoconstriction. METHODS: We studied the effect of a norepinephrine (NOR) infusion (30 min), compared with no infusion, on relative blood volume (RBV) in six haemodialysis patients. During infusion we measured RBV, systolic blood pressure (SAP), heart rate (HR), stroke volume index (SI), total peripheral resistance (TPRI), ejection fraction (EF), inferior vena cava diameter (VCD) and core temperature. RESULTS: At the end of the NOR infusion, we observed a significant increase in TPRI (47+/-47% vs 4+/-17%; P<0.01) and SAP (27+/-12% vs 0+/-8%; P<0.01). Norepinephrine-induced vasoconstriction resulted in a significant decrease in RBV (-9+/-3% vs 0+/-1%; P<0.01). No significant changes were seen in SI (-4+/-21% vs 0+/-8%), HR (-5+/-19% vs -4+/-5%), EF (7+/-14% vs -2+/-10%), VCD or temperature. CONCLUSIONS: We conclude that norepinephrine-induced vasoconstriction results in a decrease in RBV. This indicates that improved haemodynamic stability during haemodialysis through vasoconstriction can be accompanied by a decrease in RBV and that part of the variability in blood volume may be due to changes in arterial tone. Such changes must be taken into account if RBV measurements are used to improve the haemodynamic tolerance of dialysis.     

Improvement in ejection fraction by nocturnal haemodialysis in end-stage renal failure patients with coexisting heart failure.

BACKGROUND: Congestive heart failure (CHF) is an independent risk factor for mortality in the end-stage renal disease (ESRD) population. Nocturnal haemodialysis (NHD), a novel mode of renal replacement therapy, may be more effective than conventional haemodialysis in reducing intravascular volume or in removing uraemic toxins with vasoconstrictor or myocardial depressant actions, and may, therefore, improve the left ventricular (LV) systolic function of patients with coexisting cardiac and renal failure. METHODS: To test this hypothesis, we determined, in six patients (mean age+/-SD: 49.5+/-9 years), blood pressure (BP), ejection fraction (EF: radionucleotide angiography), left ventricular mass index (LVMI: echocardiography), LV fractional shortening (FS), and extracellular fluid volume (ECFV: bioelectrical impedance): before and after a mean of 3.2+/-2.1 years following conversion from conventional dialysis (3 days/week x 4 h) to NHD (6 nights/week x 8-10 h). RESULTS: There were significant reductions in systolic and mean arterial BP (138+/-10 to 120+/-9 mmHg, P=0.04; 99+/-6 to 86+/-7 mmHg, P=0.01). There was a significant increase in EF (28+/-12 to 41+/-18%, P=0.01) and a trend to greater LV FS (20+/-10 to 38+/-17%, P=0.06). Post-dialysis ECFV was not affected by dialysis mode (18.5+/-5.1 vs 18.2+/-3.5 l, P=0.76). The number of prescribed cardiovascular medications was reduced (2.2-0.7, P=0.02). CONCLUSIONS: In ESRD patients with systolic dysfunction, NHD leads to a sustained increase of EF and a reduction in the requirement for vasoactive medications in the absence of any reduction in post-dialysis ECFV.