Changes In CVP Research Articles

Comparaison de la nicardipine et de l’isradipine dans l’hypertension artérielle observée après pontage aorto-coronarien

Objective: Compare the efficacy of isradipine to that of nicardipine for the control of arterial hypertension following coronary artery bypass graft (CABG). Study design: Clinical prospective, randomised study. Material and methods: 40 patients ASA II or III, mean age 66 ± 8 years, scheduled for elective CABG were included. If the mean arterial pressure (MAP) was ≥ 100 mmHg within the first six post operative hours, the patients were included and randomly attributed to either one of the 2 groups : Gr I (n=20) received nicardipine, Gr II (n=20) received isradipine in bolus then in continuous perfusion. HR, MAP, MPAP, CVP, PCWP, CI, SVRI, PVRI and SVI were recorded at : T0 before administration of drugs, T1 = 2 min after the first bolus. T2 when MAP reached 85±5 mmHg. T 3, T 4, T 5, T 6, T 7 and T 8 at 5, 10, 30, 60, 90 and 120 min after the continuous perfusion. T 9 before stopping the perfusion. Results: No significant changes in HR, CVP, PCWP, MPAP or PVRI at any time in both groups. Significant increase in CI at T2 in both groups. Reduction of MAP at T2 was more important (-27 %) in Gr I compared to that in Gr II (-22 %). This was mainly due to a significant decrease in SVRI. Conclusion: Isradipine is effective in the treatment of arterial hypertension following CABG. However there is not any significant beneficial effect of isradipine over nicardipine.

Effect of lymphatic outflow pressure on lymphatic albumin transport in humans.

The effects of posture on the lymphatic outflow pressure and lymphatic return of albumin were examined in 10 volunteers. Lymph flow was stimulated with a bolus infusion of isotonic saline (0.9%, 12.6 ml/kg body wt) under four separate conditions: upright rest (Up), upright rest with lower body positive pressure (LBPP), supine rest (Sup), and supine rest with lower body negative pressure (LBNP). The increase in plasma albumin content (Delta Alb) during the 2 h after bolus saline infusion was greater in Up than in LBPP: 82.9 +/- 18.5 vs. -28.4 mg/kg body wt. Delta Alb was greater in LBNP than in Sup: 92.6 vs. -22.5 +/- 18.9 mg/kg body wt (P < 0.05). The greater Delta Alb in Up and Sup with LBNP were associated with a lower estimated lymphatic outflow pressure on the basis of the difference in central venous pressure (Delta CVP). During LBPP, CVP was increased compared with Up: 3.8 +/- 1.4 vs. -1.2 +/- 1.2 mmHg. During LBNP, CVP was reduced compared with Sup: -3.0 +/- 2.2 vs. 1.7 +/- 1.0 mmHg. The translocation of protein into the vascular space after bolus saline infusion reflects lymph return of protein and is higher in Up than in Sup. Modulation of CVP with LBPP or LBNP in Up and Sup, respectively, reversed the impact of posture on lymphatic outflow pressure. Thus posture-dependent changes in lymphatic protein transport are modulated by changes in CVP through its mechanical impact on lymphatic outflow pressure.

Diminished baroreflex control of forearm vascular resistance following training

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR units in mm Hg.min.100 ml.ml-1) were studied in 14 volunteers before and after 10 wk of endurance training. We assessed the relationship between reflex stimulus (changes in central venous pressure, CVP) and response (FVR) during unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP, 0 to -20 mm Hg). Changes in CVP during LBNP were estimated from pressure changes in a large peripheral vein in the dependent arm of the subject in the right lateral decubitus position. Maximal oxygen uptake (VO2max) and total blood volume increased with endurance training from 37.8 +/- 1.4 ml.min-1.kg-1 and 63.6 +/- 2.1 ml.kg-1 to 45.3 +/- 1.4 ml.min-1.kg-1 and 69.3 +/- 2.8 ml.kg-1, respectively (P less than 0.05). Reflex forearm vasoconstriction occurred in response to a reduction in estimated CVP, and the absolute change in FVR per unit of CVP was reduced from -5.96 +/- 0.79 to -4.06 +/- 0.52 units.mm Hg-1 (P less than 0.05) following exercise training but was unchanged from -6.10 to 0.57 to -6.22 +/- 0.94 units.mm Hg-1 for the time control group (N = 7). Resting values for FVR were similar before and after exercise training; however, resting estimated CVP was elevated from 9.5 +/- 0.5 mm Hg before training to 11.3 +/- 0.6 mm Hg after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Contribution of peripheral blood pooling to central hemodynamic disturbances during endotoxin insult in intact dogs

The aim of the present study was to determine possible effects of Escherichia coli endotoxin on peripheral vascular compliance and relate them to concomitant central hemodynamic disturbances. Endotoxin was infused at 0.25 micrograms/kg.min during 2 h in six anesthetized dogs, while six additional animals served as controls. Vascular compliance of the systemic circulation was calculated in intact animals from the changes in CVP after known changes in systemic blood volume. In control dogs, vascular compliance averaged 2.3 ml/mm Hg.kg body weight. During slow endotoxin infusion, cardiovascular effects were measurable only after a certain period of time had elapsed from the start of endotoxin insult and consisted of hypotension associated with systemic vasodilation. Systemic BP decreased gradually from 124 to 68 mm Hg while vascular compliance was finally increased by 100%, when compared to control values. This latter rise was responsible for a reduction in the cardiac preloads. Pulmonary wedge pressure and CVP were decreased from 7.1 to 3.4 and from 4.5 to 2.6 mm Hg, respectively. However, parallel to the decrease in left ventricular preload, endotoxin induced a progressive decrease in left ventricular afterload. Because of the balance in ventricular loading, cardiac output remained almost unchanged. After volume loading (dextran 30 ml/kg), cardiac output was remarkably increased from 3.28 to 6.24 L/min.m2 while peripheral vasodilation was not affected by this maneuver. It is concluded that low dose endotoxin infusion induces in dogs a hemodynamic pattern similar to human sepsis. The left ventricular loading changes are related to an enhanced systemic vascular compliance from 2.3 to 4.5 ml/mm Hg.kg. High flow shock state is encountered provided peripheral blood pooling is compensated by adequate volume replacement.

Cardiac transplantation: A prospective comparison of ketamine and sufentanil for anesthetic induction

The hemodynamic effects of ketamine, 1.5 mg/kg, or sufentanil, 3.4 +/- 0.3 micrograms/kg, were studied prospectively for the anesthetic induction of 20 patients with cardiomyopathies undergoing cardiac transplantation. Plasma epinephrine (EPI), norepinephrine (NE), and sufentanil levels were also obtained. Measurements were taken at various times before induction and following intubation. Following ketamine, progressive increases (P less than 0.05) in mean arterial pressure (28%, MAP), mean pulmonary artery pressure (56%, PAP), central venous pressure (109%, CVP), and pulmonary capillary wedge pressure (84%, PCWP) occurred over time, whereas the cardiac index (CI), stroke volume index (SVI), and stroke work index (SWI) remained unchanged or decreased. The use of sufentanil was associated with no significant changes in MAP, PAP, CVP, PCWP, CI, SVI, or SWI. The heart rate (HR) did not significantly change in either group. Plasma NE significantly increased (31%) in the ketamine group, peaking at 10 minutes; whereas EPI levels did not significantly change in either group. Plasma sufentanil did not reflect the microgram/kg or microgram/BSA administered dose, suggesting individualized distribution kinetics. Since perioperative morbidity and mortality did not differ between groups, both ketamine and sufentanil are acceptable drugs for the anesthetic induction for cardiac transplantation. However, the dissimilar hemodynamic effects caused by ketamine and sufentanil suggest that this conclusion may not be applicable to the patient with a cardiomyopathy undergoing noncardiac surgery.

Cardiovascular and endocrine responses to head-up tilt and vasopressin infusion in humans.

The effects of passive tilt on arterial and central venous pressures (MAP and CVP), heart rate (HR), arterial concentrations of vasopressin (AVP) and aldosterone (ALDO), osmolality, and hematocrit were studied in eight healthy young men. Tilting was performed at 30 degrees/min to 20 or 40 degrees and maintained for 45 min. The 20 degrees tilt did not change MAP while CVP fell by 5.9 mmHg (P less than 0.01) and HR increased by 5 beats/min (51-56 beats/min, P less than 0.05). AVP and ALDO concentrations were unchanged. At 40 degrees, MAP increased by 5.7 mmHg (86.0-91.7 mmHg, P less than 0.01), CVP decreased by 7.4 mmHg (P less than 0.01), HR rose by 8 beats/min (55-63 beats/min, P less than 0.01), and pulse pressure fell by 6 mmHg (P less than 0.05). ALDO increased fivefold (P less than 0.05), but AVP did not change. Infusions of AVP at 0.25 or 1.0 ng X min-1 X kg body wt-1 elevated plasma AVP to 11 +/- 1 and 52 +/- 8 pg/ml. Only the larger dose caused a small increase in MAP while CVP and HR remained unchanged; however, washout of a subcutaneous depot of Xe was reduced greater than 60% even by the lower dose. It is concluded that small-angle nonhypotensive passive tilt does not affect AVP measurably despite substantial reductions of CVP and a marked increase in ALDO. Elevations of AVP elicit marked subcutaneous vasoconstriction also in the absence of changes in CVP, HR, and MAP.

CVP Changes in Hemodynamics with Vasoactive Drugs

CVP Changes in Hemodynamics with Vasoactive Drugs

Immediate hemodynamic effects of high-dose furosemide in normovolemic and hypovolemic dogs.

We investigated whether the large dose (7 mg/kg) of iv furosemide often recommended for patients with oliguric acute renal failure impaired hemodynamic function in dogs. Six normovolemic and six hypovolemic animals were anesthetized, intubated, and ventilated. Femoral and pulmonary artery catheters were inserted. After a stable baseline period, the animals received 7 mg/kg of iv furosemide over 30 sec. Mean systemic artery pressure (MAP), mean pulmonary artery pressure (MPAP), CVP, and ECG were continuously monitored. Cardiac output and mean pulmonary arterial occlusion (wedge) pressures (WP) were recorded 2, 6, 12, 18, 24, 30, and 46 min after injection. Neither group demonstrated significant immediate changes in MAP, CVP, MPAP, heart rate (HR), cardiac output, or systemic and pulmonary vascular resistances (SVR and PVR, respectively). Later in the observation period, cardiac output decreased and SVR and PVR increased significantly. The changes were probably associated with decreased plasma volume causing compensatory increases in baroreceptor activity and vascular tone.

1406 INTRAVENOUS NITROGLYCERIN (NTG) IN THE TREATMENT OF PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)

We report the use of intravenous NTG in a 2600 gram, 37-week gestational age newborn with PPHN unresponsive to hyperventilation(HV). The diagnosis of PPHN was made based on unexplained hypoxemia, initial positive response to HV, and evidence of a ductal level right-to-left shunt. After repeated transient responses to HV and pancuronium therapy, the PaO2/FiO2 dropped to 53. An IV continuous infusion of NTG was begun at 5.9 mcg/kg/ min. at 45 hours of age. The infusion was increased in a step-wise manner to 13 mcg/kg/min. After each increase, a transient elevation in PaO2/FiO2 occurred. After the increase to 13 mcg/kg/min., and without any alteration in ventilatory settings, a sustained rise in PaO2/FiO2 to 242 was noted. No significant changes in CVP (5-6 cm H2O) or arterial blood pressure(mean= 54-59 mm Hg) pre- or post-NTG were seen. NTG was stopped by Day 4, pancuronium and HV by Day 5, and assisted ventilation by Day 9. He was discharged home on Day 19. Twelve month follow-up is normal.Intravenous nitroglycerin may be as effective a pulmonary vasodilator in the treatment of neonates with PPHN and may be used with significantly less side effects than seen with tolazoline. Further clinical trials will be necessary to establish its efficacy.

Prostaglandin F2 aifa Infusion and Halothane Anaesthesia

The cardiovascular reaction to infusion of prostaglandin F2 alfa was examined in seven patients during N2O-jalothane anaesthesia. As in the non-anaesthetized individual, no changes in blood pressure, pulse rate, CVP or ECG occurred during anaesthesia, but a great reflux of enteric juice to the ventricle was noticed only 2-3 min after the beginning of the hormone infusion. It is concluded that prostaglandin F2 alfa may be safely given to patients who are going to be anaesthetized, but the patients must be considered as having a full stomach and therefore treated as such.

The significance of central venous pressure and cardiac output measurements in shock.

Summary The central venous pressure changes which occur in shock syndromes vary with the aetiology and other factors. Two methods of measuring CVP have given different results, and their advantages and disadvantages are discussed, together with an appraisal of the diagnostic and therapeutic value of such measurements. The CVP changes produced by transfusion are related to changes in cardiac output and the value of the latter as a guide to treatment is discussed. The relationship of these measurements to clinical signs is emphasized.

CARDIAC ACTION OF VASOACTIVE POLYPEPTIDES IN THE RAT. I. BRADYKININ. II. ANGIOTENSIN.

Intravenous injection of bradykinin in ganglionically blocked rats has a predominantly pressor effect, instead of the depressor effect it is known to have in unblocked rats. Intra-arterial injection of bradykinin (0.01 to 0.02 µg) either before or after blockade produced a decrease of pressure in the hind limb perfused at a constant rate with autogenous blood. The response of the vascular bed was directly proportional to the perfusion pressure, but at a given pressure no difference was seen between blocked and unblocked animals. At the IV infusion rates used (12.5 and 25 µg/kg/min), bradykinin produced a large increase of CO. Because this action remains after autonomic blockade, it seems probable that its mechanism of action is largely independent of the carotid baroreceptor system. Bradykinin caused a slight increase in heart rate and a marked increase in stroke volume, apparently by a direct effect on the heart. In the blocked animal the vasodilator effect of bradykinin is less than its cardiac stimulating action and the resulting effect is an elevation of arterial pressure. Angiotensin in the rat has twofold action: a constrictor effect on the arterioles, and a stimulating effect on the heart. The vasoconstrictor effect is direct, unmodified by denervation or by sympathetic blockade. In the intact rat the cardiac action is masked by the activation of the baroreceptor mechanism which overrides the direct cardiac action and causes a decrease in CO. After autonomic blockade the cardiac action of angiotensin becomes apparent and an increase of CO is seen, while changes in TPR remain similar to those of unblocked animals. Since the CO effect cannot be explained by changes in HR and CVP, it appears that angiotensin has a positive isotropic action. In blocked, reserpinized animals angiotensin infusion causes no significant change in CO. These results suggest that catecholamines account for at least part of the cardiac activity of angiotensin.