Effects of the Arteriovenous Fistula on Pulmonary Artery Pressure and Cardiac Output in Patients with Chronic Renal Failure

2009 ◽  
Vol 10 (3) ◽  
pp. 160-166 ◽  
Author(s):  
Ali Akbar Beigi ◽  
Amir Mir Mohammad Sadeghi ◽  
Ali Reza Khosravi ◽  
Mehdi Karami ◽  
Hassan Masoudpour
Keyword(s):  
Renal Failure ◽  
Cardiac Output ◽  
Chronic Renal Failure ◽  
Pulmonary Artery ◽  
Arteriovenous Fistula ◽  
Pulmonary Artery Pressure ◽  
Vascular System ◽  
Diabetic Patients ◽  
Artery Pressure ◽  
The Relationship

Introduction Access to the vascular system is necessary in patients with chronic renal failure planned to undergo dialysis. One of the complications of end-stage renal disease patients is pulmonary hypertension (PHT). Temporary arterio-venous access closure and successful kidney transplantation causes a significant fall in cardiac output and pulmonary artery pressure (PAP), indicating the possibility that excessive pulmonary blood flow is involved in the pathogenesis of the disease. We attempted to study the relationship of PHT with arteriovenous fistula (AVF) creation, as well as to assess the relationship between AVF flow and fistula characteristics. Methods Fifty patients were included in the study. Echocardiography was used to evaluate systolic PAP, cardiac output (CO), and ejection fraction (EF) before creating the AVF. After a follow-up interval of at least 6 months, a second echocardiographic assessment and a Doppler sonographic assessment of their fistula flow were carried out. Complete data were available for 34 patients. Results Study data were collected from 34 patients, 28 males and 6 females with a mean age of 52 yrs ranging from 15–78 yrs. The data showed a statistically significant positive correlation between fistula flow and PAP2 and PAP changes (p<0.05). Mean fistula flow was 1322 ml/min in patients without PHt and 2750 ml/min in patients with PHT. this difference (1428 ml/ min) was statistically significant (p=0.03). We found a significant negative correlation between PAP1 and EF1 and PAP2 and EF2 (p<0.05). In addition, the mean EF2 in patients without PHT was 57% in contrast to 46% in patients with PHT. Mean fistula flow in radial fistulae (mean=422 ml/min, range: 370–474 ml/min) was significantly less than brachial fistulae (mean=1463 ml, range: 270–3300 ml/min) (p=0.03). Mean systolic PAP2 of 14.8 mmHg in transplanted patients was 5.9 mmHg less than those who were not transplanted (20.7 mmHg). Diabetes was the most common cause of renal failure and diabetics had a significant reduction in their EF (15.5%) compared with non-diabetic patients (1% reduction) (p=0.016). Conclusion Fistula flow, PAP and EF of all patients should be checked at least 6 months after fistula creation. Patients with higher fistula flow rates and patients with diabetes mellitus need to be more closely observed. In addition, elderly patients with significant cardiac and other comorbidities may be more prone to develop symptoms after AVF creation

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

Effects of Acutely Induced Changes in Arterial pH on Pulmonary Vascular Resistance during Normoxia and Hypoxia in Awake Dogs

1972 ◽  
Vol 42 (3) ◽  
pp. 277-287 ◽  
Author(s):  
O. G. Thilenius ◽  
Carol Derenzo
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Main Pulmonary Artery ◽  
Compensatory Mechanisms ◽  
Artery Pressure ◽  
Arterial Ph ◽  
Small Rise

1. Awake dogs with chronically implanted catheters (pulmonary artery, left atrium, aorta) and electromagnetic flow probe (main pulmonary artery) underwent five types of experiments in succession: (1) slow infusion of 0·4 m-hydrochloric acid; (2) rapid infusion of 1·0 m-sodium bicarbonate; (3) exposure to 30 min of hypoxia (10% O2); (4) exposure to hypoxia after arterial pH had been lowered to 7·30; (5) exposure to hypoxia after pH had been increased to 7·55. Intravascular pressures, pulmonary vascular resistance, cardiac output, arterial gas tension and pH were studied. 2. Acute acidosis (pH 7·21) resulted in a small rise in pulmonary artery pressure, cardiac output and pulmonary vascular resistance, associated with a decrease in Pa,co2. Acute alkalosis (pH 7·61) was accompanied by a small rise in pulmonary artery pressure, marked increase in cardiac output, a fall in pulmonary vascular resistance and mild elevation in Pa,co2. During acidosis hypoxia resulted in a more pronounced rise in pulmonary vascular resistance than during alkalosis (P < 0·01). 3. The study provides evidence that in the intact, awake dog with its compensatory mechanisms acute alkalosis decreases pulmonary vascular resistance by decreasing vascular tone and/or recruitment of pulmonary vascular channels; it diminishes the vasoconstrictive response to hypoxia; conversely, mild acidosis increases the pulmonary vascular resistance slightly and enhances vasoconstriction during hypoxia to a small extent.

Single Injection Thermodilution

1996 ◽  
Vol 85 (3) ◽  
pp. 481-490. ◽  
Author(s):  
Jos R. C. Jansen ◽  
Jan J. Schreuder ◽  
Jos J. Settels ◽  
Lilian Kornet ◽  
Olaf C. K. M. Penn ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Contour Method ◽  
Limits Of Agreement ◽  
Large Variability ◽  
Artery Pressure ◽  
Corrected Equation ◽  
Group A ◽  
Group B

Background Application of the Stewart-Hamilton equation in the thermodilution technique requires flow to be constant. In patients in whom ventilation of the lungs is controlled, flow modulations may occur leading to large errors in the estimation of mean cardiac output. Methods To eliminate these errors, a modified equation was developed. The resulting flow-corrected equation needs an additional measure of the relative changes of blood flow during the period of the dilution curve. Relative flow was computed from the pulmonary artery pressure with use of the pulse contour method. Measurements were obtained in 16 patients undergoing elective coronary artery bypass surgery. In 11 patients (group A), pulmonary artery pressure was measured with a catheter tip transducer, in a partially overlapping group of 11 patients (group B), it was measured with a fluid-filled system. For reference cardiac output we used the proven method of four uncorrected thermodilution estimates equally spread over the ventilatory cycle. Results A total of 208 cardiac output estimates was obtained in group A, and 228 in group B. In group B, 48 estimates could not be corrected because of insufficient pulmonary artery pressure waveform quality from the fluid-filled system. Individual uncorrected Stewart-Hamilton estimates showed a large variability with respect to their mean. In group A, mean cardiac output was 5.01 l/min with a standard deviation of 0.53 l/min, or 10.6%. After flow correction, this scatter decreased to 5.0% (P &lt; 0.0001). With no bias, the corresponding limits of agreement decreased from +/- 1.06 to +/- 0.5 l/min after flow correction. In group B, the scatter decreased similarly and the limits of agreement also became +/- 0.5 l/min after flow correction. Conclusion It was concluded that a single thermodilution cardiac output estimate using the flow-corrected equation is clinically feasible. This is obtained at the cost of a more complex computation and an extra pressure measurement, which often is already available. With this technique it is possible to reduce the fluid load to the patient considerably.

Stability of pulmonary artery pressure during emboli-induced pulmonary edema in dogs

1965 ◽  
Vol 208 (6) ◽  
pp. 1263-1266
Author(s):  
H. Weisberg ◽  
R. T. Jortner ◽  
I. K. Kline ◽  
A. Ellis ◽  
L. N. Katz
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pressure Rise ◽  
Vascular Effects ◽  
Artery Pressure ◽  
Pressure Changes

Changes in some facets of cardiovascular hemodynamics occurring after acute unilateral pulmonary starch embolization were studied in the anesthetized closed-chest dog. While bilateral pulmonary edema and reduced cardiac output occurred in starch-embolized dogs, these phenomena were not seen in control animals. Pulmonary arterial pressure changes were not significant during the present experiments, but the consistent rise in pulmonary vascular resistance after embolization indicates that the latter may be a better index of pulmonary vascular effects of emboli than are pressure changes. The fall in cardiac output was of sufficient magnitude to more completely neutralize the pulmonary artery pressure rise usually expected with increased pulmonary vascular resistance following pulmonary embolization.

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