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OBJECTIVES: cross-clamping of the infrarenal aorta is associated with complex haemodynamic disturbances. Several experimental models of aortic cross-clamping (AXC) have been described with heterogeneous results. The main purpose of this study was to establish an animal model in which infrarenal AXC could reproduce similar systemic and renal haemodynamic changes to those observed in humans. METHODS: eleven anaesthetised pigs underwent AXC just below the renal arteries. Renal blood flow was measured using clearance of (131)I hippuran. Systemic and renal parameters were collected at 3 consecutive 30-min periods. RESULTS: AXC did not alter the extraction fraction of (131)I hippuran but was accompanied by significant (13%) decrease in cardiac index (p = 0.005) and a 23% increase in mean arterial pressure (p = 0.005). AXC induced significant 135% increase in renal vascular resistance (p = 0.012) and a 35% decrease in renal blood flow (p = 0.016). This worsened after removal of the aortic clamp, whereas systemic variables returned to baseline levels. CONCLUSIONS: this AXC animal model reproduces the changes observed in humans. It provides a reliable animal model which allows to investigate the underlying mechanisms of renal vasoconstriction and the effect of new drugs.

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BACKGROUND: Renin-angiotensin system antagonists, either angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor (AT(1)) antagonists, may interfere with regulation of arterial pressure during anaesthesia. This study aimed to compare the haemodynamic profile of anaesthetized pigs, which were subjected to haemorrhage in the presence of the ACE inhibitor enalaprilat or the AT(1) antagonist valsartan. METHODS: Thirty-six pigs were assigned randomly to placebo, enalaprilat or valsartan groups. After a 30-min period of stabilization following anaesthesia and injection of the study drug, the animals were bled in two equal steps of 20% of their estimated blood volume (20% BV and 40% BV). RESULTS: After bleeding of 20% BV, the mean arterial pressure (MAP) decreased significantly but similarly in each group (20-25%) but the placebo and the enalaprilat groups had a significant decrease in cardiac index (CI, 22% and 16%, respectively) without significant change in systemic vascular resistance (SVR). Conversely, in the valsartan group, SVR decreased significantly (23%, P<0.02 vs other groups) without significant change in CI (-4%). After bleeding of 40% BV, the CI decreased significantly compared with 20% BV in the three groups (19% in the placebo and enalaprilat groups, 14% in the valsartan group) but the MAP decreased significantly in the enalaprilat group only (23%). The SVR increased significantly in the placebo group (P<0.01 vs each of the other groups), but there were no differences in the change in SVR between the other groups. CONCLUSION: Blockade of the renin-angiotensin system by either enalaprilat or valsartan leads to a similar decrease in arterial pressure during anaesthesia and haemorrhage but the haemodynamic profiles are quite different.

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Renal dysfunction occurring after open heart surgery is multifactorial in origin but activation of the renin-angiotensin system may have a prominent role. Fourteen patients with ischaemic heart dysfunction scheduled for elective coronary artery bypass graft (CABG) surgery were allocated to a treatment group [enalaprilat for 2 days; ACEI (angiotensin-converting enzyme inhibitor) group, n=7] or a control group (n=7). The cardiac index was significantly higher in ACEI-treated patients than in the controls before and after cardiopulmonary bypass (CPB) (P<0.05) and on postoperative day 2 (P<0.05). The systemic vascular resistance was significantly lower in the ACEI-treated patients than in the controls before and after CPB (P<0.05). Renal plasma flow, measured as [131I]orthoiodohippuran clearance (ClH), was higher in the ACEI group than in the control group before CPB, as was endogenous creatinine clearance after CPB (P<0.05). On post-operative day 7, ClH was significantly higher in the ACEI group than in the control group (P<0.05). Plasma renin activity and vasopressin concentration increased in both groups during CPB (P<0.05). The study demonstrates that administration of an i.v. ACEI, enalaprilat, improves cardiac output during CABG surgery in patients with ischaemic heart dysfunction. Moreover, renal perfusion was better maintained during surgery, and this effect was sustained up to post-operative day 7.

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OBJECTIVE: In order to determine if routine use of transthoracic echocardiography (TTE) shortly after heart surgery could have a role in postoperative management, we carried out TTE in postoperative patients operated on for CABG or valvular repair. PATIENTS AND METHODS: For a 3 months period, we prospectively enrolled 51 patients for TTE. We performed a TTE using a Hewlett Packard Sonos 1500 and a 2.5 MHz probe. Feasibility, left ventricular kinesis, valve function, intracardiac thrombi, and pericardial effusion were noted for each patient. Patients have been divided into 2 groups: patients with or, without haemodynamic disturbance (HD, mean arterial blood pressure < or = 80 mmHg). RESULTS: Nine TTE were impossible for bad acoustic images. Feasibility was about 82% (42 TTE/51 patients). Two ETT views were easily obtained: the apical 4-chambers (75%) and the subcostal (30%) views. TTE examination induced treatment change in 12 patients for hypovolaemia (ten patients), left ventricular dysfunction (one patient), and systolic anterior motion of mitral valve (one patient). In patients without HD (41 patients) only hypovolaemia was found (three patients) and TTE returned to normal with fluid challenge. In patients with HD (ten patients), one patient returned to the operating room for valvular replacement, one patient was treated with dobutamine for left ventricular dysfunction, seven patients with hypovolaemia recovered with fluid challenge. CONCLUSION: TTE can guide postoperative management of patients operated on for heart surgery especially in patients with haemodynamic disturbance. Because of its safety and easiness, TTE may be the first-line examination in these patients before any invasive evaluation.

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BACKGROUND: Favourable outcome of phaeochromocytoma surgery requires that paroxysmal hypertension and arrhythmia be controlled, and that hypotension be prevented. Is nicardipine, a calcium channel blocking drug, always adequate? METHODS: Nineteen consecutive patients underwent surgery for phaeochromocytoma. Management was standardised with regards to anaesthesia and antihypertensive treatment. Nicardipine was used as a vasodilator and was given in order to maintain systemic vascular resistance lower than 1600 dyn.s.cm-5. RESULTS: Hypertension did not occur at any time during surgery in 6/19 patients. Blood pressure rose acutely in 3/19 patients at the time of tracheal intubation or surgical approach to the tumour, and was controlled by increased depth of anaesthesia. Hypertensive episodes occurred in 11/19 patients during tumour manipulation. Nicardipine always succeeded in maintaining low systemic vascular resistance but its dosage varied widely between patients (0.5 to 70 mg), a fact that may be accounted for by the striking intersubject variability of haemodynamic behaviour during surgery. In 7/11 patients, despite nicardipine treatment, sustained increase in blood pressure persisted with increased cardiac index, but low systemic vascular resistance. Following tumour removal, transient serious hypotension (MAP < 60 mmHg) occurred in 4 patients, and was corrected by fluid volume expansion. Perioperative incidence of hypertension or hypotension was not related to preoperative clinical status. CONCLUSION: Adequate management of patients operated upon for phaeochromocytoma requires invasive monitoring, since the mechanisms underlying hypertensive crises are heterogeneous with regards to systemic vascular resistance and not predictable from preoperative data. Nicardipine provides a good control of vasoconstriction during phaeochromocytoma surgery with limited risk of serious hypotension after tumour removal.

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OBJECTIVE: The aim of the study was to assess the value of dobutamine echocardiography (DE) for detecting coronary artery disease (CAD) in patients scheduled for abdominal aortic surgery. STUDY DESIGN: Preliminary prospective open study. PATIENTS: Thirty-three consecutive patients due to undergo effective abdominal aortic surgery, assessed by preoperative DE. METHODS: Previous myocardial infarction and atherosclerotic risk factors (RF) were noted. Incremental doses of dobutamine were administered in order to reach 85% of age-predicted maximal heart rate. The occurrence of regional wall motion abnormalities was considered as a positive test. In this case a coronary angiography was performed. RESULTS: Four patients had a history of angina pectoris. DE was not interpretable in five patients. Among the patients without symptoms, 12 had three RF or more, 12 had less than three RF. In eight patients with a positive test, coronary angiography showed one or more significant main coronary artery stenoses. All patients with angina pectoris had a positive test. None of patients without symptoms and less than three RF had a positive test, one third of patients with no symptomatology but with three RF or more had a positive test (P < 0.05). CONCLUSION: DE has the ability to identify patients with asymptomatic CAD. DE is recommended in patients with high probability of CAD, i.e. with three RF or more.

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Anesthesia may induce hemodynamic instability in patients treated with angiotensin-converting enzyme inhibitors (ACEIs). To assess the hemodynamic effects of anesthesia in patients treated (n = 9) or not treated (n = 9) with ACEIs for ischemic left ventricle dysfunction after myocardial infarction, we studied 18 patients scheduled for elective coronary artery bypass graft surgery. Induction of anesthesia with fentanyl (5 micrograms/kg), flunitrazepam (30 micrograms/kg), and pancuronium (100 micrograms/kg) was followed by a significant decrease in mean arterial blood pressure in both groups (-18.6% +/- 8.1% in controls and -25.7% +/- 7.8% in ACEI-treated patients, P = 0.01). In controls, cardiac index and systemic vascular resistance were not significantly altered (-11.2% +/- 9.4% and -16.2% +/- 4.6%, respectively, not significant [NS]). In ACEI-treated patients, cardiac index decreased significantly (-27.3% +/- 11.6%, P = 0.01 from baseline and P = 0.03 when compared with controls), and systemic vascular resistance was unchanged (1.0% +/- 18.7%, NS from baseline and P = 0.04 when compared with controls). Two patients from each group experienced a transient severe hypotensive episode. ACEI treatment in patients with infarction-induced myocardial dysfunction does not increase the incidence of severe hypotension after induction of anesthesia.

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Voltage-gated Na+ currents (INaS) are usually not found in arterial smooth muscle. We enzymatically isolated myocytes from the media of left coronary arteries of heart transplant patients with ischemic cardiopathy. Using the whole-cell voltage-clamp technique (20 degrees C to 22 degrees C), we detected no INa in any of the freshly isolated myocytes. In contrast, when the cells were grown in culture, we could record a large INa. This INa was characterized by a biexponential decay comprising a fast inactivating and sustained components that could not be separated by their electrophysiological and pharmacological properties. INa activated at depolarizations positive to -50 mV, was maximal at 0 mV, and was available from relatively low resting membrane potentials (half-inactivation at -46 mV). INa was modulated by several ligands known to bind selectively at different sites of Na+ channels. It was blocked with high affinity by tetrodotoxin (IC50, approximately 10 nmol/L) and local anesthetics (bupivacaine and lidocaine; IC50, approximately 100 nmol/L) and by Cd2+ (IC50, approximately 300 mumol/L). INa was modulated by Na+ channel agonists such as toxin AsV from Anemonia sulcata and veratridine, which slowed current kinetics dramatically. In conclusion, human coronary myocytes in culture can express an atypical tetrodotoxin-sensitive INa with a large sustained component, which is expected to contribute to massive Na+ influx into these cells. Phenotypic modulation of the expression of this INa may be related to cell dedifferentiation and proliferation.

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The combination of surgery and heart disease is common. The incidence of both heart disease and surgery increase with the age of patients. However, the surgical risk in the cardiac patient and particularly in the coronary or heart failure patient is considerably aggravated. Surgery is a major factor in cardiac decompensation, which can accelerate the progress of the disease. Pre-anesthetic cardiological consultation is therefore an important part of the evaluation and preparation of the patient before surgery. This is carried out at the request of the anesthetist and can provide a diagnosis or adapt a treatment and above all define the cardiovascular competence of the patient. Diagnostic and therapeutic means available to the cardiologist are essential in defining and if possible reducing the cardiac handicap of patients before the hemodynamic challenge represented by the combination of anesthesia and surgery.

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