Are beta-blockers useful to protect high-risk patients scheduled for open cholecystectomy?
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Biomedical subjects
Publications and source records attributed to Pierre Albaladejo.
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OBJECTIVE: This prospective, observational study evaluated the safety and efficacy of cryopreserved arterial allograft reconstruction in the management of major peripheral arterial graft infections. METHODS: From April 1996 to May 2003, data from patients with major peripheral arterial graft infection who underwent graft excision and cryopreserved arterial allograft reconstruction were prospectively collected. Arterial allografts were harvested from multiple organ donors and cryopreserved at -80 degrees C. The patients were observed for survival, limb salvage, persistence or recurrence of infection, and allograft patency. The results were calculated with the Kaplan-Meier method. RESULTS: During the 7-year study period, 17 patients (14 men, 3 women; mean age, 68 years) with major peripheral graft infection underwent graft excision and cryopreserved arterial allograft reconstruction. Eight patients (47%) had systemic sepsis, 5 (29%) had acute ischemia at the time of the allograft reconstruction, and 9 (53%) had experienced anastomotic rupture. Allograft reconstruction was performed as an emergency procedure in 7 patients (41%). There were no perioperative deaths or early amputations. Two patients had allograft ruptures in the groin during the early postoperative period. The mean follow-up period was 34 months (range, 8 to 80 months). There was no persistent or recurrent infection, and none of the patients received long-term (>3 months) antibiotic therapy. Reoperation for allograft revision, excision, or replacement was performed in 2 patients. The 18-month primary and secondary allograft patency rates were 68% and 86%; the overall limb salvage rate was 82% at 2 years. CONCLUSION: Our experience with cryopreserved arterial allograft in the management of major peripheral bypass graft infection suggests that this technique seems to be a useful option for treating one of the most dreaded vascular complications.
BACKGROUND: At dosages above 0.1 mg/kg, droperidol induces a dose-dependent QTc interval prolongation. Although subject to controversy, low-dose droperidol has recently been suspected to induce cardiac arrhythmias. Hence, 5-hydroxytryptamine type 3 antagonists have become the first-line drug for management of postoperative nausea and vomiting. These drugs are also known to prolong the QTc interval at high dosages. This study describes QTc interval changes associated with postoperative nausea and vomiting treatment by droperidol or ondansetron at low doses. METHODS: Eighty-five patients with postoperative nausea and vomiting were included in this prospective, single-blind study. Patients received either 0.75 mg intravenous droperidol (n = 43) or 4 mg intravenous ondansetron (n = 42). Electrocardiographic recordings were obtained before administration of antiemetic drug and then 1, 2, 3, 5, 10, and 15 min after. Electrocardiographic monitoring was maintained for 3 h in eight patients in each group. RESULTS: The QTc interval was prolonged (> 450 ms in men, > 470 ms in women) in 21% of the patients before antiemetic drug administration. This was significantly correlated with lower body temperature and longer duration of anesthesia. Compared with predrug QTc measurement, both antiemetics were associated with a significant QTc interval prolongation (P < 0.0001). The mean maximal QTc interval prolongation was 17 +/- 9 ms after droperidol occurring at the second minute and 20 +/- 13 ms after ondansetron at the third minute (both P < 0.0001). Compared with predrug measurement, the QTc interval was significantly lower after the 90th minute in both groups. CONCLUSIONS: Droperidol and ondansetron induced similar clinically relevant QTc interval prolongations. When used in treatment of postoperative nausea and vomiting, a situation where prolongation of the QTc interval seems to occur, the safety of 5-hydroxytryptamine type 3 antagonists may not be superior to that of low-dose droperidol.
OBJECTIVE: Prevention of secondary insults, such as hyperthermia, is a major goal after traumatic brain injury. The aim of our study was to identify risk factors for early hyperthermia in severe head-injured patients. DESIGN: Retrospective cohort study. SETTING: A 17-bed multidisciplinary ICU of a 700-bed teaching hospital. PATIENTS: A total of 101 adult patients admitted from January 1999 to December 2001 requiring continuous monitoring of intracranial pressure according to international guidelines. MEASUREMENT AND RESULTS: Forty-four patients experienced early hyperthermia (at least one episode of body temperature >38.5 degrees C within the first 2 days). On univariate analysis five variables were associated with early hyperthermia: sex; body temperature; white blood cell count on admission; prophylactic use of acetaminophen; and diabetes insipidus within 2 days. On multivariate analysis, white blood cell count >14.5 x 10(9)/l on admission (odds ratio, 7.1; 95% confidence interval, 2.4-20.5; p=0.001) and a body temperature on admission >36 degrees C (odds ratio, 6.7; 95% confidence interval, 2.3-20.1) were strong risk factors of early hyperthermia. Prophylactic use of acetaminophen was negatively associated with early hyperthermia (odds ratio, 0.1; 95% confidence interval, 0.02-0.4). Patients who experienced early hyperthermia were less prone to have good recovery (GOS=5; p=0.03). More patients with severe or moderate disability (GOS=3 or 4) experienced early hyperthermia ( p=0.01). CONCLUSION: We identified a subgroup of patients at high risk of early hyperthermia, which is common in severe head-injured patients. These results could have clinical implications for prevention of hyperthermia after traumatic brain injury in adults.
PURPOSE: To report a case of severe and fatal cardiac complication following pericardiotomy to relieve a malignant tamponade. Right ventricular (RV) failure was responsible for major hypoxemia and for a persistent shunt through a patent foramen ovale. In the absence of pulmonary embolism and coronary occlusion, possible pathophysiologic mechanisms are discussed. CLINICAL FEATURES: This 53-yr-old patient presented with oropharyngeal carcinoma previously treated by chemotherapy. One month later, he showed clinical and echocardiographic signs of cardiac tamponade. He had a circumferential pericardial effusion with complete end-diastolic collapse of the right cavities. After an emergent pericardiotomy, he rapidly presented severe hypoxemia. Transesophageal echocardiography showed an akinetic and dilated right ventricle, paradoxical septal wall motion and a normal left ventricular function. A contrast study revealed a right-to-left shunt. No residual pericardial effusion was detectable. Pulmonary angiography excluded a pulmonary embolism and the coronary angiogram was normal. Troponin Ic was elevated postoperatively and peaked on day two (3.78 micro g x L(-1)). The patient died of refractory shock with persistent intracardiac shunt and RV akinesia on day nine. CONCLUSION: Although pulmonary embolism or thrombus of a coronary vessel are the most common causes of prolonged RV failure after pericardiotomy, other mechanisms may be invoked. The possibility is raised that a rapid increase in RV tension may induce the development of muscular injury and impair coronary blood flow, despite a normal coronary angiogram. These could result in a stunned myocardium and opening of a patent foramen ovale. We hypothesize that gradual decompression of a chronic pericardial effusion might be beneficial in patients at risk.
BACKGROUND: Although oxytocin, a uterotonic agent, may cause short-term vasodilation that results in severe hypotension, it is still routinely given as an intravenous bolus injection during surgical suction curettage. Two reported cases of ventricular tachycardia after oxytocin bolus in patients with long QT interval syndrome led us to assess the effect of oxytocin on QT interval. METHOD: Thirty-eight healthy women scheduled for a surgical suction curettage with general anesthesia were enrolled. General anesthesia was induced by propofol and maintained by either propofol (n = 18) or sevoflurane (n = 20). Electrocardiographic recordings were obtained before and at 1, 2, 3, and 5 minutes after a 10-U intravenous bolus of oxytocin. RESULTS: Intravenous oxytocin induced a pronounced QTc interval prolongation of 41 +/- 21 ms ( P < .0001), which was maximal 1 minute after administration. The QTc interval returned to control values 3 minutes after oxytocin bolus. Oxytocin bolus also induced an increase in heart rate of 19 +/- 10 beats/min and a significant decrease in systolic arterial pressure of 11 +/- 9 mm Hg (both P < .0001). The drug used to maintain anesthesia was not an independent factor of QT interval prolongation in ANOVA analysis. CONCLUSIONS: Oxytocin intravenous bolus induced a large and transient QTc interval prolongation, suggesting that it may lead to proarrhythmia in circumstances favoring QTc interval increase.
BACKGROUND: Early onset pneumonia occurs frequently in head trauma patients, but the potential consequences and the risk factors of this event have been poorly studied. METHODS: This prospective observational study was undertaken in the surgical intensive care unit of a university teaching hospital in Clichy, France. Head trauma patients requiring tracheal intubation for neurologic reasons and ventilation for at least 2 days were studied to assess the risk factors and the consequences of early onset pneumonia. RESULTS: During a 2-yr period, 109 head trauma patients were studied. The authors found an incidence of early onset pneumonia of 41.3%. Staphylococcus aureus was the most common bacteria involved in early onset pneumonia. Patients with early onset pneumonia had a lower worst arterial oxygen tension:fraction of inspired oxygen ratio, more fever, more arterial hypotension, and more intracranial hypertension, factors known to worsen the neurologic prognosis of head trauma patients. Nasal carriage of S. aureus on admission (odds ratio, 5.1; 95% confidence interval, 1.9-14.0), aspiration before intubation (odds ratio, 5.5; 95% confidence interval, 1.9-16.4) and barbiturate use (odds ratio, 3.9; 95% confidence interval, 1.2-12.8) were found to be independent risk factors of early onset pneumonia. CONCLUSIONS: The results suggest that early onset pneumonia leads to secondary injuries in head-injured patients. Nasal carriage of S. aureus, aspiration before intubation, and use of barbiturates are specific independent risk factors for early onset pneumonia and must be assessed to find and evaluate strategies to prevent early onset pneumonia.
BACKGROUND: The heart rate (HR) reduction obtained by ivabradine is associated in rats with a decrease in diastolic blood pressure (DBP) and mean blood pressure (MBP), and with an increased pulsatile carotid arterial diameter. OBJECTIVE: To determine, in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, whether acute reductions of the HR in response to ivabradine induced changes in the carotid visco-elastic behavior, as assessed by echo-tracking techniques. METHODS: The hysteresis of the carotid diameter/pressure curve was used to determine the dissipated energy per cardiac cycle, a classical index of arterial viscosity. Four doses of 1 mg/kg intravenous ivabradine were repeated in anesthetized rats to obtain subsequent HR reductions. RESULTS: In WKY, repeated administration of ivabradine produced reduction of MBP, DBP and HR, without change of systolic blood pressure (SBP). In SHR, ivabradine produced a higher reduction in DBP, SBP and HR than in WKY rats, but the increase in pulse pressure was similar in both strains. In SHR and WKY rats, ivabradine did not modify the incremental elastic modulus-stress curves, and shifted the distensibility-pressure curves through changes in blood pressure, indicating no modification in isobaric carotid stiffness. In both strains, ivabradine produced an identical increase of the energy dissipated per cardiac cycle. CONCLUSION: In WKY rats and SHR, acute ivabradine reduces MBP and DBP and increases pulse pressure, but without change in arterial stiffness. In both strains, the HR reduction due to ivabradine induces an identical increase of the energy dissipation of the arterial wall.
BACKGROUND: Left ventricular ejection time (LVET) measured in central arteries is modified during hypovolemia. We compared modifications of the pulse wave in a central artery (carotid) and in a peripheral artery (digital) during central hypovolemia induced by lower body negative pressure (LBNP) in conscious volunteers. METHODS: Hypovolemia was simulated with progressive LBNP (baseline, -10, -20, and -30 mm Hg) in nine young healthy volunteers. The carotid arterial pressure waveform was recorded using a Millar tonometric method. The digital pulse wave was measured with a volume-clamp method (Finapres) and the stroke volume with a thoracic impedance method (Biomed). RESULTS: Mean arterial pressure did not change during LBNP. Compared with baseline values, heart rate increased significantly at the -30 mm Hg level (68 +/- 13 beats/min vs. 59 +/- 11 beats/min), and stroke volume decreased as soon as -10 mm Hg was achieved (113 +/- 41 mL vs. 127 +/- 35 mL). Both carotid and digital LVET decreased significantly at the -10 mm Hg level (337 +/- 26 and 339 +/- 24 ms vs. 360 +/- 35 and 361 +/- 24 ms, respectively). CONCLUSION: Peripheral LVET could reflect variation of central LVET during LBNP and be a reliable noninvasive parameter for monitoring hypovolemia.
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Aspirin is used mainly to prevent arterial events in patients with arteriopathy. Myocardial infarction and cerebrovascular events have been described after recent aspirin withdrawal. Experimental data suggest rebound platelet activity after aspirin discontinuation. Among a retrospective cohort of 181 patients admitted for acute lower limb ischemia for 4 yr, we studied 11 patients who had recently stopped taking aspirin. Aspirin was administered for vascular event prevention. The median duration of aspirin treatment without vascular events was 12 mo (range, 6-60 mo). The median time between aspirin withdrawal and lower limb ischemia was 23 days (range, 7-60 days). Four of the 11 patients stopped aspirin before a surgical procedure, without any substitution. In five patients, a recent diagnosis of neoplasia was observed. This study should alert clinicians to the risk of discontinuing chronic aspirin therapy in patients with severe peripheral vascular disease.
BACKGROUND: Although mean blood pressure (MBP) remains unmodified along the arterial tree, pulse pressure (PP) increases physiologically from the central to the peripheral arteries. Amplification of PP is known to be influenced by heart rate (HR), but the impact of this alteration has never been tested in patients with hypertension. METHODS: A total of 712 hypertensive subjects, either treated or untreated, were divided into three classes of HR level. Carotid and brachial systolic blood pressure (SBP), carotid augmentation index, a marker of wave reflections, and carotid-brachial PP amplification were measured using applanation tonometry. RESULTS: Independent of age, sex, and antihypertensive drugs, subjects with HR >80 beats/min were characterized, in comparison with those with lower HR, by reduced carotid SBP, PP, and augmentation index, resulting in a significant increase in PP amplification. In men but not in women, this pattern was associated with higher values of brachial SBP and DBP and by higher incidences of elevated glycemia and atherosclerotic alterations. In the male population, PP amplifications was, independent of HR, associated with the presence of beta blocking agents (negative association) and elevated plasma glucose. CONCLUSIONS: Hypertensive men and women with high HR have significant PP amplifications, principally because of reduced central SBP and disturbed wave reflections. beta-blocking agents and plasma glucose independently alter PP amplification in men but not in women. Whether these opposite patterns influence the gender difference in cardiovascular risk should be prospectively studied.
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BACKGROUND: Heart rate and aortic pulse wave velocity (PWV) are both cardiovascular risk factors. The aim of this study was to evaluate the influence of sex on the heart rate-PWV relationship in two populations of normotensive and hypertensive men and women. PATIENTS AND METHODS: In a first study, steady-state data describing the heart rate-PWV relationship were determined in 558 normotensive men, 308 normotensive women, 323 hypertensive men and 93 hypertensive women. In a second study, the changes in blood pressure and PWV under atrial pacing at 60, 80 and 100 beats/min were investigated in 15 men and 15 women who were either normotensive or hypertensive. RESULTS: In women in study 1, 26.8% of PWV variance in normotensive patients and 15.4% of PWV variance in hypertensive patients was explained by a multiple regression including only age and systolic blood pressure as covariates. In men in study 1, 27% of PWV variance in normotensive patients and 28.5% of PWV variance in hypertensive patients was explained by a multiple regression including age, systolic blood pressure, weight, and also heart rate, as covariates. In study 2, atrial pacing in the overall population tended to decrease mean blood pressure (P = 0.05) and increase pulse pressure (P = 0.003), with no substantial change in PWV. However, when heart rate increased, PWV tended to decrease in women and to increase in men (interaction: P = 0.07).CONCLUSION Accelerated heart rate influences PWV in both normotensive and hypertensive men and, through this mechanism, could influence cardiovascular risk. However, heart rate does not influence PWV in women.
UNLABELLED: Pediatric caudal anesthesia is an effective method with an infrequent complication rate. However, little is known about its cardiovascular consequences. Transesophageal Doppler, a noninvasive method, provides the opportunity for a reappraisal of the hemodynamic effects of this technique. After parental informed consent, we studied 10 children aged 2 mo to 5 yr who were scheduled for lower abdominal surgery. General anesthesia was induced using sevoflurane and was followed by the insertion of a transesophageal Doppler probe. Caudal anesthesia was performed using 1 mL/kg of 0.25% bupivacaine with 1/200,000 epinephrine. Hemodynamic variables were collected before and after caudal anesthesia. No complications arose during insertion of the probe. The mean time between the two sets of measurements was 15 min. Heart rate, systolic, diastolic, and mean arterial blood pressures were not modified by caudal anesthesia. Descending aortic blood flow increased significantly from 1.14 to 1.92 L/min. (P = 0.0002). Aortic ejection volume increased from 8.5 to 14.5 mL (P = 0.0002). Aortic vascular resistances decreased from 6279 to 3901 dynes. s(-1) x m(-5) (P = 0.005). Caudal anesthesia did not affect heart rate and mean arterial blood pressure but induced a significant increase in descending aortic blood flow. IMPLICATIONS: Although pediatric caudal anesthesia does not alter heart rate nor arterial blood pressure, significant changes occur in regional blood flow distribution. Descending aortic blood flow increases significantly after caudal anesthesia, whereas lower body vascular resistances decrease.
PURPOSE: To report a case of postoperative bilateral lower limb hypoesthesia occurring after surgery under general anesthesia in the hyperlordotic position for radical prostatectomy. The possible pathophysiologic mechanisms are discussed. CLINICAL FEATURES: This 52-yr-old patient was slightly overweight and was on fenofibrate for hypercholesterolemia. He had no history of cardiovascular disease. Arterial blood pressure was overall well maintained except for a very transient hypotension at surgical incision. Blood loss was moderate and did not require transfusion. Soon after recovery, the patient complained of paresthesia in both legs and neurological examination revealed bilateral lower limb hypoesthesia, compatible with an incomplete medullar syndrome at the level of T12-L1. On postoperative day one, a plain magnetic resonance imaging scan demonstrated a hyperintense signal in the spinal cord from T8 to T9 on T2-weighted images consistent with ischemia of the spinal cord whereas the heterogeneous aspect of the spinal cord was due to an unusually high fat content of the epidural space. Neurological signs improved progressively and one week later the patient had recovered normal sensory functions of both lower limbs. CONCLUSION: Although arterial ischemia is the most common cause of postoperative spinal cord injury, other mechanisms may be invoked. We raise the possibility that a combination of intraoperative risk factors (hypotension, excessive postural changes) with anatomic predispositions (increased epidural venous pressure or fat content, previous bone disease) can produce arterial and/or venous ischemia of the spinal cord.