Effect of Drugs on Effective Vascular Compliance in Acute Heart Failure

1975 ◽  
Vol 53 (5) ◽  
pp. 850-858 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Effective vascular compliance determined by the ΔV/ΔP relationship was measured repeatedly in anesthetized open-chest dogs without circulatory arrest utilizing a closed circuit venous bypass system with a constant cardiac output. Production of acute heart failure by gradual aortic constriction was associated with a significant decrease in total effective vascular compliance. The effect of loading and 20-min maintenance doses of different drugs on vascular compliance of animals in acute heart failure was studied. Phenoxybenzamine (total dose 2 mg/kg) produced a rapid and sustained increase in effective vascular compliance and theophylline (12 mg/kg) produced an increase which was more gradual in development than with phenoxybenzamine. Morphine (1 mg/kg) produced a rapid but transient increase in compliance. In contrast, ethacrynic acid (100 mg) or nitroglycerin (0.6 or 1.2 mg) did not alter vascular compliance significantly. These agents differ markedly in the magnitude and time-course of effect on effective vascular compliance.


1975 ◽  
Vol 53 (3) ◽  
pp. 504-507
Author(s):  
P. Larochelle ◽  
R. I. Ogilvie

The effect of hypoxemia on total vascular compliance was studied in anesthetized dogs using a venous bypass technique. Cardiac output was kept constant with an extracorporeal pump and respiration controlled to maintain normocapnia. When nitrogen was added to the respired gas to produce an arterial [Formula: see text], total vascular compliance was rapidly and significantly reduced to 0.93 ml (mm Hg)−1 kg−1 with incomplete recovery to baseline values of 1.30 ± 0.06 ml (mm Hg)−1 kg−1 during subsequent ventilation with 100% oxygen. Acute heart failure was induced by gradual aortic constriction. Ventilation with 100% oxygen failed to prevent a gradual reduction in total vascular compliance to 0.86 ml (mm Hg)−1 kg−1 from a baseline value of 1.23 ± 0.06 ml (mm Hg)−1 kg−1. Ventilation with 100% oxygen following the reduction in vascular compliance during acute heart failure also failed to significantly alter this parameter. Thus, improvement of arterial oxygen tension in patients with acute heart failure would be beneficial in providing greater oxygen delivery to the tissues without abolishing a compensatory mechanism of reduced vascular compliance which attempts to maintain a cardiac filling gradient of pressure.



2009 ◽  
Vol 15 (8) ◽  
pp. 639-644 ◽  
Author(s):  
Guillermo Torre-Amione ◽  
Olga Milo-Cotter ◽  
Edo Kaluski ◽  
Loic Perchenet ◽  
Isaac Kobrin ◽  
...  


2020 ◽  
Vol 59 (22) ◽  
pp. 2839-2847
Author(s):  
Shota Yokoyama ◽  
Ryo Kawakami ◽  
Atsushi Tobiume ◽  
Keisuke Onishi ◽  
Takuro Fujita ◽  
...  


1986 ◽  
Vol 251 (3) ◽  
pp. H483-H489 ◽  
Author(s):  
R. Gay ◽  
S. Wool ◽  
M. Paquin ◽  
S. Goldman

To define the changes in the venous circulation in chronic left ventricular (LV) failure, we measured the mean circulatory filling pressure (MCFP), blood volume, and effective vascular compliance in conscious rats with heart failure, 3 wk after coronary ligation. Rats with myocardial infarction and LV end-diastolic pressure (EDP) greater than 15 mmHg were considered to have chronic heart failure. Rats with chronic heart failure (n = 11) showed an increase (P less than 0.001) in LV EDP to 24 +/- 2 mmHg compared with 6 +/- 1 mmHg in sham-operated (n = 9) and 7 +/- 1 mmHg in normal (n = 6) rats. In the rats with chronic heart failure the MCFP was increased to 9.9 +/- 0.2 mmHg (P less than 0.001) compared with 7.6 +/- 0.2 mmHg in the sham-operated and 7.7 +/- 0.2 mmHg in the normal rats. Effective vascular compliance was determined from MCFP-blood volume curves. In rats with chronic heart failure, the effective vascular compliance was decreased to 2.40 +/- 0.08 ml X mmHg-1 X kg-1 from 3.34 +/- 0.16 in sham-operated rats and 3.35 +/- 0.22 ml X mmHg-1 X kg-1 in normal rats. The blood volume and the unstressed vascular volume of the rats with chronic heart failure were not statistically different from the sham-operated rats. These results suggest that venous capacitance is decreased in chronic heart failure, due to a decrease in effective vascular compliance with no significant change in unstressed vascular volume. Hexamethonium chloride did not alter the effective vascular compliance of the rats with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)



2009 ◽  
Vol 66 (9) ◽  
pp. 639-642 ◽  
Author(s):  
Thenral Socrates ◽  
Alexandre Mebazaa

Dyspnea is the most common presenting symptom of patients with acute heart failure (AHF). Although dyspnea is an important target for treatment in clinical practice and clinical trials, there remains a lack of consensus on how to assess it. We describe and recommend to use absolute scales such the Likert 5-point or the Visual Analogue Scale rather than any comparator scale such as the Likert 7-point scale. We further recommend starting dyspnea measurements in sitting position and perform, if possible, similar measurements in lying position. The same set of measurements may be repeated as needed during the time course of disease and the treatment.



1975 ◽  
Vol 53 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Effective vascular compliance was measured repeatedly in dogs without circulatory arrest utilizing a closed-circuit venous bypass system and constant cardiac output. Compliance, determined by the ΔV/ΔP relationship at the end of a 1-min infusion of 5% of the circulating volume into the inferior vena cava, was independent of the initial venous pressure, total circulating volume and systemic arterial pressure. It remained constant over a 3 h experimental period at 1.55 ± 0.05 ml (mm Hg)−1 kg−1 body weight. Elevation of mean left atrial pressure and mean pulmonary arterial pressure by gradual aortic constriction was associated with a large and significant reduction in vascular compliance to a value of 1.14 ± 0.06 ml (mm Hg)−1 kg−1 after 2 h. This reduction was independent of the initial venous pressure and total circulating volume but was associated with the changes in left atrial and pulmonary artery pressures and an increase in plasma catecholamine concentrations. The mechanism responsible for the reduction in effective compliance is not clear from the present experiments. Increased circulating catecholamines and sympathetic nerve traffic resulting from baro- and volume receptor stimulation in the vascular tree may be the causative mechanism.



PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0187410 ◽  
Author(s):  
Takeshi Yagyu ◽  
Masahiro Kumada ◽  
Tsutomu Nakagawa


1976 ◽  
Vol 54 (2) ◽  
pp. 154-159 ◽  
Author(s):  
Pierre Larochelle ◽  
Richard I. Ogilvie

Total effective vascular compliance was measured repeatedly in open-chest dogs without circulatory arrest, utilizing a closed-circuit venous bypass system with a constant cardiac output. Mutual inductance coils were used to measure the diameter of the inferior vena cava above the diaphragm at the position where the pressure change was recorded during a volume load (ΔV). In all experiments, there was a relationship which tended to be curvilinear between the diameter of the inferior vena cava and the venous pressure before ΔV. No relationship was demonstrated between the initial diameter or pressure and the calculated effective vascular compliance. During aortic constriction or infusion of noradrenaline, the effective compliance was reduced in value at any given initial venous diameter and pressure. An unaltered venous diameter and plasma volume excluded the possibility of a large change in initial venous volume as a cause of the observed changes in compliance during aortic constriction or during infusion of noradrenaline. A relationship was observed between compliance and calculated venous wall tension so that as the wall tension, developed during a fixed volume load, increased, there was an associated reduction in compliance. These results demonstrate that the measurement of effective compliance provides an assessment of combined active and passive venous wall tension and venous tone.



2021 ◽  
Vol 8 (12) ◽  
pp. 184
Author(s):  
Ioannis Ventoulis ◽  
Angelos Arfaras-Melainis ◽  
John Parissis ◽  
Eftihia Polyzogopoulou

Cognitive impairment (CI) represents a common but often veiled comorbidity in patients with acute heart failure (AHF) that deserves more clinical attention. In the AHF setting, it manifests as varying degrees of deficits in one or more cognitive domains across a wide spectrum ranging from mild CI to severe global neurocognitive disorder. On the basis of the significant negative implications of CI on quality of life and its overwhelming association with poor outcomes, there is a compelling need for establishment of detailed consensus guidelines on cognitive screening methods to be systematically implemented in the population of patients with heart failure (HF). Since limited attention has been drawn exclusively on the field of CI in AHF thus far, the present narrative review aims to shed further light on the topic. The underlying pathophysiological mechanisms of CI in AHF remain poorly understood and seem to be multifactorial. Different pathophysiological pathways may come into play, depending on the clinical phenotype of AHF. There is some evidence that cognitive decline closely follows the perturbations incurred across the long-term disease trajectory of HF, both along the time course of stable chronic HF as well as during episodes of HF exacerbation. CI in AHF remains a rather under recognized scientific field that poses many challenges, since there are still many unresolved issues regarding cognitive changes in patients hospitalized with AHF that need to be thoroughly addressed.



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