TY - JOUR
T1 - Pathogenesis of congestive state in chronic obstructive pulmonary disease
T2 - Studies of body water and sodium, renal function, hemodynamics, and plasma hormones during edema and after recovery
AU - Anand, Inder
AU - Chandrashekhar, Y S
AU - Ferrari, R.
AU - Sarma, R.
AU - Guleria, R.
AU - Jindal, S. K.
AU - Wahi, P. L.
AU - Poole-Wilson, P. A.
AU - Harris, P.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1992
Y1 - 1992
N2 - Background. The pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved. Methods and Results. Hemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8±0.26 l/min · m2) was normal, but right atrial (11±1 mm Hg) and mean pulmonary arterial (41±3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11±1 mm Hg) was normal. Pulmonary vascular resistance (8.6±1.3 mm Hg · min · m2/l) was increased, but systemic vascular resistance (19.3±1.3 mm Hg · min · m2/l) and mean arterial pressure (83±4 mm Hg) were low. All patients were hypoxemic (PaO2, 40±2 mm Hg) and hypercapnic (PaCO2, 60±2 mm Hg). There was a significant increase in total body water (+21%), extracellular volume (+45%), plasma volume (+45%), blood volume (+88%), and exchangeable sodium (+38.2%). Renal plasma flow was severely reduced (-63.2%), but glomerular filtration rate was only mildly decreased (-32%). Significant increases were seen in plasma norepinephrine (3.5-fold normal), renin activity (7.6-fold normal), vasopressin (twice normal), atrial natriuretic peptide (9.4-fold normal), growth hormone (10.7-fold normal), and cortisol (1.9-fold normal). After recovery, the PaO2 increased (50±3 mm Hg) and PaCO2 fell (45±4 mm Hg), and the patients became free from edema. All the body compartments returned toward normal, although they did not entirely reach normal values. Renal plasma flow increased significantly, and glomerular filtration became normal. Right atrial and pulmonary arterial pressures and pulmonary vascular resistance decreased (p<0.01). Cardiac output decreased but not significantly. Blood pressure increased but not significantly. However, systemic vascular resistance increased significantly to a normal value. Conclusions. We conclude that patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edema due to myocardial disease. However, unlike the latter, in chronic obstructive pulmonary disease cardiac output is normal, and systemic vascular resistance and arterial blood pressure are low. This probably is due to the vasodilator properties of hypercapnia. The consequent low arterial blood pressure may be the stimulus for the neurohormonal activation and retention of salt and water.
AB - Background. The pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved. Methods and Results. Hemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8±0.26 l/min · m2) was normal, but right atrial (11±1 mm Hg) and mean pulmonary arterial (41±3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11±1 mm Hg) was normal. Pulmonary vascular resistance (8.6±1.3 mm Hg · min · m2/l) was increased, but systemic vascular resistance (19.3±1.3 mm Hg · min · m2/l) and mean arterial pressure (83±4 mm Hg) were low. All patients were hypoxemic (PaO2, 40±2 mm Hg) and hypercapnic (PaCO2, 60±2 mm Hg). There was a significant increase in total body water (+21%), extracellular volume (+45%), plasma volume (+45%), blood volume (+88%), and exchangeable sodium (+38.2%). Renal plasma flow was severely reduced (-63.2%), but glomerular filtration rate was only mildly decreased (-32%). Significant increases were seen in plasma norepinephrine (3.5-fold normal), renin activity (7.6-fold normal), vasopressin (twice normal), atrial natriuretic peptide (9.4-fold normal), growth hormone (10.7-fold normal), and cortisol (1.9-fold normal). After recovery, the PaO2 increased (50±3 mm Hg) and PaCO2 fell (45±4 mm Hg), and the patients became free from edema. All the body compartments returned toward normal, although they did not entirely reach normal values. Renal plasma flow increased significantly, and glomerular filtration became normal. Right atrial and pulmonary arterial pressures and pulmonary vascular resistance decreased (p<0.01). Cardiac output decreased but not significantly. Blood pressure increased but not significantly. However, systemic vascular resistance increased significantly to a normal value. Conclusions. We conclude that patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edema due to myocardial disease. However, unlike the latter, in chronic obstructive pulmonary disease cardiac output is normal, and systemic vascular resistance and arterial blood pressure are low. This probably is due to the vasodilator properties of hypercapnia. The consequent low arterial blood pressure may be the stimulus for the neurohormonal activation and retention of salt and water.
KW - chronic obstructive pulmonary disease
KW - congestive heart failure
KW - cor pulmonale
KW - edema
KW - extracellular volume
KW - hormones, plasma
KW - renal blood flow
KW - sodium
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U2 - 10.1161/01.CIR.86.1.12
DO - 10.1161/01.CIR.86.1.12
M3 - Article
C2 - 1617764
AN - SCOPUS:0026696733
SN - 0009-7322
VL - 86
SP - 12
EP - 21
JO - Circulation
JF - Circulation
IS - 1
ER -