Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Puri, Sundeep; Dutka, David P.; Baker, B. L.; Hughes, J. M. B.; Cleland, J. G. F.

doi:10.1161/01.cir.99.9.1190

Cited by 78 publications

(54 citation statements)

References 46 publications

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“…25 Conversely, infusion of 10 ml/kg of saline into 10 patients with a left ventricular ejection fraction (LVEF) <40% resulted in a fall in forced expiratory volume in 1 s (FEV1), forced expiratory ratio (FER) and diffusing capacity for carbon monoxide (DLCO). 26 The same study also demonstrated lower baseline FEV1, FVC and DLCO in these subjects compared with a control group. Studies of patients undergoing acute hospitalisation for HF demonstrated increased pulmonary resistance and reduced compliance 27 as well as reductions in FEV1, FVC and TLC but no change to DLCO compared to follow up testing.…”

Section: Effects Of Hf On Respiratory Function Testingmentioning

confidence: 68%

Heart Failure and the Lung

Kee

Naughton

2010

Circ J

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Heart failure (HF) is a highly prevalent disease that leads to significant morbidity and mortality. There is increasing evidence that the symptoms of HF are exacerbated by its deleterious effects on lung function. HF appears to cause airway obstruction acutely and leads to impaired gas diffusing capacity and pulmonary hypertension in the longer term. It is postulated that this is the result of recurrent episodes of elevated pulmonary capillary pressure leading to pulmonary oedema and pulmonary capillary stress fracture, which produces lung fibrosis. It is likely that impaired lung function impairs the functional status of HF patients and makes them more prone to central sleep apnoea. (Circ J 2010; 74: 2507 - 2516

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Section: Effects Of Hf On Respiratory Function Testingmentioning

confidence: 68%

Heart Failure and the Lung

Kee

Naughton

2010

Circ J

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“…In fact, it has been shown that acute infusion of 1-2 l saline can increase pulmonary capillary blood volume by 120 % and decrease haemoglobin concentration by 17 % (Farney et al 1977), all of which leaves unchanged (Puri et al 1999) or improves lung diffusion capacity in healthy subjects (Farney et al 1977). …”

Section: Figurementioning

confidence: 99%

Acute Hypervolaemia Improves Arterial Oxygen Pressure in Athletes with Exercise‐Induced Hypoxaemia

Zavorsky¹,

Walley²,

Hunte³

et al. 2003

Experimental Physiology

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The aim of this study was to determine the effect of acute plasma volume expansion on arterial blood-gas status during 6.5 min strenuous cycling exercise comparing six athletes with and six athletes without exerciseinduced arterial hypoxaemia (EIAH). We hypothesized that plasma volume expansion could improve arterial oxygen pressure in a homogeneous sample of athletes -those with EIAH. In this paper we have extended the analysis and results of our recently published surprising findings that lengthening cardiopulmonary transit time did not improve arterial blood-gas status in a heterogeneous sample of endurance cyclists. One 500 ml bag of 10 % Pentastarch (infusion condition) or 60 ml 0.9 % saline (placebo) was infused prior to exercise in a randomized, double-blind fashion on two different days. Power output, cardiac output, oxygen consumption and arterial blood gases were measured during strenuous exercise. Cardiac output and oxygen consumption were not affected by acute hypervolaemia. There were group w condition interaction effects for arterial oxygen pressure and alveolar-arterial oxygen pressure difference, suggesting that those with hypoxaemia experienced improved arterial oxygen pressure (+4 mmHg) and lower alveolar-arterial oxygen pressure difference (_2 mmHg) with infusion. In conclusion, acute hypervolaemia improves blood-gas status in athletes with EIAH. The impairment of gas exchange occurs within the first minute of exercise, and is not impaired further throughout the remaining duration of exercise. This suggests that arterial oxygen pressure is only minimally mediated by cardiac output. Experimental Physiology (2003) 88.4, 555-564.

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“…According to the basic experimental evidence that pulmonary interstitial fluid accumulation is secondary to a dysregulation of Na+ handling, changes in Dm following saline infusion have been investigated in patients with chronic HF of varying severity. In a study performed in post-MI patients with normal LV systolic function, an infusion of ~800 mL of saline reduced Dm by 13% 49 . In patients with mild to severe HF, a 150 ml infusion of saline produced a significant Dm reduction equivalent to 750 ml saline, whereas a 750 mL infusion of isotonic glucose solution did not decrease DLco and Dm 50 .…”

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confidence: 98%

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Guazzi¹,

Phillips²,

Arena³

et al. 2015

Progress in Cardiovascular Diseases

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Cardiac dysfunction of both systolic and diastolic origin leads to increased left atrial pressure, lung capillary injury and increased resistance to gas transfer. Acutely, pressure-induced trauma disrupts the endothelial and alveolar anatomical configuration and definitively causes an impairment of cellular pathways involved in fluid-flux regulation and gas exchange efficiency, a process well identified as stress failure of the alveolarcapillary membrane. In chronic heart failure (HF), additional stimuli other than pressure may trigger the true remodeling process of capillaries and small arteries characterized by endothelial dysfunction, proliferation of myofibroblasts, fibrosis and extracellular matrix deposition. In parallel there is a loss of alveolar gas diffusion properties due to the increased path from air to blood (thickening of extracellular matrix) and loss of fine molecular mechanism involved in fluid reabsorption and clearance. Deleterious changes in gas transfer not only reflect the underlying lung tissue damage but also portend independent prognostic information and may play a role in the pathogenesis of exercise limitations and ventilatory abnormalities observed in these patients. Few currently approved treatments for chronic HF have the potential to positively affect structural remodeling of the lung capillary network; angiotensin-converting enzyme inhibitors are one of the few currently established options. Recently, more attention has been paid to novel therapies specifically targeting the nitric oxide pathway as a suitable target to improve endothelial function and permeability as well as alveolar gas exchange properties.

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Acute Saline Infusion Reduces Alveolar-Capillary Membrane Conductance and Increases Airflow Obstruction in Patients With Left Ventricular Dysfunction

Cited by 78 publications

References 46 publications

Heart Failure and the Lung

Heart Failure and the Lung

Acute Hypervolaemia Improves Arterial Oxygen Pressure in Athletes with Exercise‐Induced Hypoxaemia

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

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