Oxygen and Effective Vascular Compliance in Acute Heart Failure

1975 ◽  
Vol 53 (3) ◽  
pp. 504-507
Author(s):  
P. Larochelle ◽  
R. I. Ogilvie
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Compensatory Mechanism ◽  
Venous Bypass ◽  
Vascular Compliance ◽  
Anesthetized Dogs ◽  
Cardiac Filling ◽  
Effective Vascular Compliance

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.

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
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Time Course ◽  
Ethacrynic Acid ◽  
Circulatory Arrest ◽  
Aortic Constriction ◽  
Venous Bypass ◽  
Vascular Compliance ◽  
Effective Vascular Compliance ◽  
Sustained Increase

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.

Total vascular pressure-volume relationship in conscious rats with chronic heart failure

1986 ◽  
Vol 251 (3) ◽  
pp. H483-H489 ◽  
Author(s):  
R. Gay ◽  
S. Wool ◽  
M. Paquin ◽  
S. Goldman
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Blood Volume ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Venous Capacitance ◽  
Vascular Volume ◽  
Conscious Rats ◽  
Vascular Compliance ◽  
Effective Vascular Compliance

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)

Resting Arterial Oxygen Tension Influences Pulmonary Vascular Resistance in Heart Failure

2006 ◽  
Vol 12 (6) ◽  
pp. S11
Author(s):  
Thomas P. Olson ◽  
Robert P. Frantz ◽  
Kathy A. O'Malley ◽  
Bruce D. Johnson
Keyword(s):  
Heart Failure ◽  
Pulmonary Vascular Resistance ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen

Distinct roles for renal particulate and soluble guanylyl cyclases in preserving renal function in experimental acute heart failure

2007 ◽  
Vol 293 (4) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Fernando L. Martin ◽  
Thanom Supaporn ◽  
Horng H. Chen ◽  
Sharon M. Sandberg ◽  
Yuzuru Matsuda ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Acute Heart Failure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Therapeutic Implications ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Poor Outcomes

Worsening renal function in the setting of human acute heart failure (AHF) predicts poor outcomes, such as rehospitalization and increased mortality. Understanding potential renoprotective mechanisms is warranted. The guanylate cyclase (GC) enzymes and their second messenger cGMP are the target of two important circulating neurohumoral systems with renoprotective properties. Specifically, natriuretic peptides (NP) released from the heart with AHF target particulate GC in the kidney, while the nitric oxide (NO) system is an activator of renal soluble GC. We hypothesized that both systems are essential to preserve renal excretory and hemodynamic function in AHF but with distinct roles. We investigated these roles in three groups of anesthetized dogs (6 each) with AHF induced by rapid ventricular pacing. After a baseline AHF clearance, each group received intrarenal vehicle (control), NG-monomethyl-l-arginine (l-NMMA), a competitive NO inhibitor (50 μg·kg−1·min−1) or a specific NP receptor antagonist, HS-142-1 (0.5 mg/kg). We observed that intrarenal l-NMMA decreased renal blood flow (RBF) without significant decreases in glomerular filtration rate (GFR), urinary sodium excretion (UNaV), or urinary cGMP. In contrast, HS-142-1 resulted in a decrease in UNaV and cGMP excretion together with a reduction in GFR and an increase in distal fractional tubular sodium reabsorption. We conclude that in AHF, the NP system plays a role in maintaining sodium excretion and GFR, while the function of NO is in the maintenance of RBF. These studies have both physiological and therapeutic implications warranting further research into cardiorenal interactions in this syndrome of AHF.

scholarly journals Assessment of early treatment response by rapid cardiothoracic ultrasound in acute heart failure: Cardiac filling pressures, pulmonary congestion and mortality

2017 ◽  
Vol 7 (4) ◽  
pp. 311-320 ◽  
Author(s):  
Jonas Öhman ◽  
Veli-Pekka Harjola ◽  
Pasi Karjalainen ◽  
Johan Lassus
Keyword(s):  
Heart Failure ◽  
Treatment Response ◽  
Acute Heart Failure ◽  
Early Treatment ◽  
Vena Cava ◽  
Composite Endpoint ◽  
Pulmonary Congestion ◽  
Early Treatment Response ◽  
All Cause Mortality ◽  
Cardiac Filling

Background: It is unclear how to optimally monitor acute heart failure (AHF) patients. We evaluated the timely interplay of cardiac filling pressures, brain natriuretic peptides (BNPs), lung ultrasound (LUS) and symptoms during AHF treatment. Methods: We enrolled 60 patients who had been hospitalised for AHF. Patients were examined with a rapid cardiothoracic ultrasound (CaTUS) protocol, combining LUS and focused echocardiographic evaluation of cardiac filling pressures (i.e. medial E/e’ and inferior vena cava index [IVCi]). CaTUS was done at 0, 12, 24 and 48 hours (±3 hours) and on the day of discharge, alongside clinical evaluation and laboratory samples. Patients free of congestion (B lines or pleural fluid) on LUS at discharge were categorised as responders, whereas the rest were categorised as non-responders. Improvement in congestion parameters was evaluated separately in these groups. The effect of congestion parameters on prognosis was also analysed. Results: Responders experienced a significantly larger decline in E/e’ (2.58 vs. 0.38, p = 0.037) and dyspnoea visual analogue scale (1–10) score (7.68 vs. 3.57, p = 0.007) during the first 12 hours of treatment, while IVCi and BNPs declined later without no such rapid initial decline. Among patients experiencing a >3 U decline in E/e’ during the first 12 hours of treatment, 18/21 were to become responders ( p < 0.001). LUS response was the only congestion parameter independently predicting both 6-month survival regarding all-cause mortality and the composite endpoint of all-cause mortality or rehospitalisation for AHF. Conclusion: E/e’ seemed like the most useful congestion parameter for monitoring early treatment response, predicting prognostically beneficial resolution of pulmonary congestion.

Equimolar doses of atrial and brain natriuretic peptides and urodilatin have differential renal actions in overt experimental heart failure

2005 ◽  
Vol 288 (5) ◽  
pp. R1093-R1097 ◽  
Author(s):  
Horng H. Chen ◽  
Alessandro Cataliotti ◽  
John A. Schirger ◽  
Fernando L. Martin ◽  
John C. Burnett
Keyword(s):  
Heart Failure ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Rank Order ◽  
Urinary Sodium Excretion ◽  
Ventricular Pacing ◽  
Brain Natriuretic Peptides ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Cardiac Filling

A hallmark of overt congestive heart failure (CHF) is attenuated cGMP production by endogenous atrial natriuretic peptide (ANP) with renal resistance to ANP. ANP and brain natriuretic peptides (BNP) are of myocardial origin, whereas urodilatin (Uro) is thought to be derived from kidney. All three peptides are agonists to the natriuretic peptide-A receptor. Our objective was to compare the cardiorenal and humoral actions of ANP, BNP, and Uro in experimental overt CHF. We determined cardiorenal and humoral actions of 90 min of intravenous equimolar infusion of ANP, BNP, and Uro (2 and 10 pmol·kg−1·min−1) in three separate groups of anesthetized dogs with rapid ventricular pacing-induced overt CHF (240 beats/min for 10 days). BNP resulted in increases in urinary sodium excretion (UNaV) (2.2 ± 0.7 to 164 ± 76 μeq/min, P < 0.05) and glomerular filtration rate (GFR) (27 ± 4 to 52 ± 11 ml/min, P < 0.05) that were greater than those with Uro ( P < 0.05), whereas ANP did not result in increases in UNaV or GFR. Increases in plasma cGMP (25 ± 2 to 38 ± 2 pmol/ml, P < 0.05) and urinary cGMP excretion with BNP (1,618 ± 151 to 6,124 ± 995 pmol/min, P < 0.05) were similar to those with Uro; however, there was no change with ANP. Cardiac filling pressures were reduced in all three groups. These studies also support the conclusion that in experimental overt CHF, renal resistance to natriuretic peptides in increasing rank order is BNP < Uro < ANP.

Critical care for paediatric patients with heart failure

2015 ◽  
Vol 25 (S2) ◽  
pp. 74-86 ◽  
Author(s):  
John M. Costello ◽  
Mjaye L. Mazwi ◽  
Mary E. McBride ◽  
Katherine E. Gambetta ◽  
Osama Eltayeb ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Critical Care ◽  
Acute Heart Failure ◽  
Clinical Signs ◽  
Administrative Databases ◽  
Response To Treatment ◽  
Arterial Oxygen ◽  
Circulatory Support ◽  
Positive Pressure

AbstractThis review offers a critical-care perspective on the pathophysiology, monitoring, and management of acute heart failure syndromes in children. An in-depth understanding of the cardiovascular physiological disturbances in this population of patients is essential to correctly interpret clinical signs, symptoms and monitoring data, and to implement appropriate therapies. In this regard, the myocardial force–velocity relationship, the Frank–Starling mechanism, and pressure–volume loops are discussed. A variety of monitoring modalities are used to provide insight into the haemodynamic state, clinical trajectory, and response to treatment. Critical-care treatment of acute heart failure is based on the fundamental principles of optimising the delivery of oxygen and minimising metabolic demands. The former may be achieved by optimising systemic arterial oxygen content and the variables that determine cardiac output: heart rate and rhythm, preload, afterload, and contractility. Metabolic demands may be decreased by a number of ways including positive pressure ventilation, temperature control, and sedation. Mechanical circulatory support should be considered for refractory cases. In the near future, monitoring modalities may be improved by the capture and analysis of complex clinical data such as pressure waveforms and heart rate variability. Using predictive modelling and streaming analytics, these data may then be used to develop automated, real-time clinical decision support tools. Given the barriers to conducting multi-centre trials in this population of patients, the thoughtful analysis of data from multi-centre clinical registries and administrative databases will also likely have an impact on clinical practice.

scholarly journals Measuring Peripheral Chemoreflex Hypersensitivity in Heart Failure

2020 ◽  
Vol 11 ◽  
Author(s):  
Daniel A. Keir ◽  
James Duffin ◽  
John S. Floras
Keyword(s):  
Heart Failure ◽  
Carotid Body ◽  
Vascular Function ◽  
Ventilatory Response ◽  
Arterial Oxygen Tension ◽  
Arterial Oxygen ◽  
Patient Specific ◽  
Hypoxic Exposure ◽  
Chemoreflex Sensitivity ◽  
Peripheral Chemoreflex

Heart failure with reduced ejection fraction (HFrEF) induces chronic sympathetic activation. This disturbance is a consequence of both compensatory reflex disinhibition in response to lower cardiac output and patient-specific activation of one or more excitatory stimuli. The result is the net adrenergic output that exceeds homeostatic need, which compromises cardiac, renal, and vascular function and foreshortens lifespan. One such sympatho-excitatory mechanism, evident in ~40–45% of those with HFrEF, is the augmentation of carotid (peripheral) chemoreflex ventilatory and sympathetic responsiveness to reductions in arterial oxygen tension and acidosis. Recognition of the contribution of increased chemoreflex gain to the pathophysiology of HFrEF and to patients’ prognosis has focused attention on targeting the carotid body to attenuate sympathetic drive, alleviate heart failure symptoms, and prolong life. The current challenge is to identify those patients most likely to benefit from such interventions. Two assumptions underlying contemporary test protocols are that the ventilatory response to acute hypoxic exposure quantifies accurately peripheral chemoreflex sensitivity and that the unmeasured sympathetic response mirrors the determined ventilatory response. This Perspective questions both assumptions, illustrates the limitations of conventional transient hypoxic tests for assessing peripheral chemoreflex sensitivity and demonstrates how a modified rebreathing test capable of comprehensively quantifying both the ventilatory and sympathoneural efferent responses to peripheral chemoreflex perturbation, including their sensitivities and recruitment thresholds, can better identify individuals most likely to benefit from carotid body intervention.

P1648Prevalence of increased filling pressure assessed by echocardiography in acute dyspnoea cohort

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Cerlinskaite ◽  
D Gabartaite ◽  
J Bugaite ◽  
D Verikas ◽  
A Krivickiene ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Coronary Syndrome ◽  
Acute Heart Failure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Cardiac Filling Pressure ◽  
Heart Failure Patients ◽  
Coronary Syndrome ◽  
Acute Dyspnoea ◽  
Cardiac Filling

Abstract Introduction Acute heart failure (AHF) is frequently associated with congestion leading to elevation of cardiac filling pressure. The present study investigates echocardiographic parameters of diastolic function in patients with AHF or non-AHF aetiology of acute dyspnoea. Purpose To determine the patterns of diastolic dysfunction in different profiles of acute dyspnoea. Methods Prospective multicentre observational study included 1455 acutely dyspnoeic patients in emergency departments from 2015 to 2017. Echocardiography was performed during the first 48 hours in 452 (31%) patients assessing left ventricular (LV) parameters. They were compared in four patient profiles based on dyspnoea cause and history of chronic HF (CHF): 1) AHF; 2) acute coronary syndrome without adjudicated AHF (Non-AHF+ACS); 3) non-AHF with CHF (Non-AHF+CHF); 4) other non-AHF patients (Non-AHF+other). Data were analysed using R statistical package. Results Significant differences in LV morphology and function were observed in the groups (Table 1). Increased LV filling pressure (E/E' >13) was found in most of AHF and Non-AHF+ACS patients, and in around 1/4 of Non-AHF+CHF group. Furthermore, more pronounced left-sided remodelling was observed in the first two groups. 1/3 of AHF patients had restrictive pattern of LV filling. Normal filling pressure dominated in Non-AHF+CHF and Non-AHF+other subgroups. LV parameters in acute dyspnoea profiles Parameter AHF (n=291) Non-AHF + ACS (n=43) Non-AHF + CHF (n=44) Non-AHF + other (n=74) p value Age, years 71 [62–78] 72 [64–78] 71 [65–80] 68 [56–74] 0.045 LVEF, % 38 [25–55] 47 [32–55] 55 [45–55] 55 [50–55] <0.001 LV MMI, g/m2 126 [104.6–150.4] 99.1 [82.9–124] 94.4 [78.3–108.6] 79.6 [70.7–99.4] <0.001 LAVi, cm3 61.7 [50.9–81.1] 40.4 [35.5–46.8] 43.2 [39.8–58.9] 37.2 [32.6–43.8] <0.001 E/E' >13, % 57.7% 57.1% 23.1% 2.9% <0.001 E/E' <10, % 23.4% 38.1% 76.9% 70.6% <0.001 E/A >2, % 34.4% 14.8% 12.5% 3.9% <0.001 E/A <1, % 30.3% 59.3% 66.7% 74.5% <0.001 LVEF, left ventricular ejection fraction; LVdd, left ventricular diastolic diameter; LV MMI, left ventricular myocardial mass index; LAVi, left atrial volume index; AHF, acute heart failure; ACS, acute coronary syndrome; CHF, chronic heart failure. Conclusions Our data confirm the predominance of an increased cardiac filling pressure in acute heart failure patients, differently from chronic heart failure patients admitted due to other causes of dyspnoea. Patients with dyspnoea due to acute coronary syndrome frequently demonstrate elevated left-sided filling pressure. Acknowledgement/Funding The work was supported by the Research Council of Lithuania, grant Nr. MIP-049/2015 and approved by Lithuanian Bioethics Committee, Nr. L-15-01.

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