Chronic Lung Disease, Polycythemia and Congestive Heart Failure

Lewis, Ceylon S.; Samuels, Arthur J.; Daines, Merrill C.; Hecht, Hans H.

doi:10.1161/01.cir.6.6.874

Cited by 37 publications

(6 citation statements)

References 25 publications

(6 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…or FF. Both groups, however, had a low GFR and a high FF, a pattern found in cardiac failure but not in chronic lung disease without evident cardiac involvement [4], Thus, the high efferent arteriolar resistance and FF in cor pulmonale may be related both to the accompanying cardiac decompensation and to the polycythaemia. This may explain why we did not see a uniform reduction in FF or rise in RPF following ex change transfusion since this does not produce consistent changes in resting cardiac output in patients with cor pul monale [I].…”

Section: Discussionmentioning

confidence: 84%

“…Patients with cor pulmonale have a markedly increased renal vascular resistance and filtration fraction even in the absence of polycythaemia [3,4], These results were taken to imply that the site of increased resistance was pre dominantly post-glomerular. There were no significant differences between those with or without polycythaemia with respect to GFR.…”

Section: Discussionmentioning

confidence: 99%

“…In some patients hypoxaemia produces poly cythaemia and a rise in haematocrit (Hct) [I], A steep rise in the apparent viscosity of the blood occurs as the Hct rises above the normal range and this contributes to the increased pulmonary vascular resistance [1,2], Fishman et al [3] and Lewis et al [4] observed that in patients with cor pulmonale the renal vascular resistance was also in creased. They found that the effective renal plasma flow rate (RPF) was reduced whilst the glomerular filtration rate (GFR) was preserved (except with the development of overt cardiac failure when the GFR fell also); conse quently, there was an increase in filtration fraction (FF), defined as the ratio of GFR to RPF.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Renal Function in Patients with Chronic Hypoxaemia and Cor Pulmonale Following Reversal of Polycythaemia

Wilcox¹,

Payne²,

Harrison³

1982

Nephron

View full text Add to dashboard Cite

The renal function of 7 patients with cor pulmonale and secondary polycythaemia was studied by clearance methods. Their haematocrit (Hct) was initially 62 ± 6% (mean ± SD). Their effective renal plasma flow rates (RPF) were reduced and filtration fractions (FF) increased. They were restudied 5–7 days after Hct reduction to 49 ± 5%. There were no significant changes in glomerular filtration rate (GFR), RPF, FF, effective renal blood flow (RBF) or body weight. However, 5 of 7 patients had a reduction in FF and a fall in body weight. Serial measurements in one patient demonstrated that immediately following the reduction in Hct there was an increase in RPF and a fall in FF, but these reverted to previous levels within 1 week. Overall, a positive correlation was obtained between changes in body weight and FF (r = 0.85, n = 7, p < 0.015). Polycythaemia is only one factor contributing to a low RPF and high FF in patients with cor pulmonale; reduction of the Hct reduces the FF in some patients and leads to a diuresis which may be beneficial in those with fluid retention.

show abstract

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Renal Function in Patients with Chronic Hypoxaemia and Cor Pulmonale Following Reversal of Polycythaemia

Wilcox¹,

Payne²,

Harrison³

1982

Nephron

View full text Add to dashboard Cite

show abstract

“…Polyglobulie pflegt im allgemeinen beim Emphysem niedriger zu sein als die erwarteten Werte, die durch den Vergleich mit ge sunden, in großen Höhen lebenden Personen erzielt werden (6,7,16 …”

Section: Diskussionunclassified

Anoxie und ihre Kompensationsmechanismen bei Cor pulmonale bei TBC

Widimský¹,

Valach²,

Vyslouzil³

et al. 1960

Cardiology

View full text Add to dashboard Cite

“…This concept of emphysema heart fits several observed facts, as for example the sharp decline in renal blood flow in the face of a normal output. 35,48 Cyanosis. is dependent on an absolute amount of reduced hemoglobin present in the capillary bed,49 ( fig.…”

Section: Emphysema Heartmentioning

confidence: 99%

Heart Failure and Lung Disease

Hecht

1956

Circulation

Self Cite

View full text Add to dashboard Cite

The confusing and complex interplay of factors leading to "cor pulmonale" may be somewhat clarified if the effects of excessive pulmonary hypertension causing right heart overloading ("pulmonary hypertensive heart disease") are separated from the ventilatory defects that result in arterial desaturation, erythrocytosis, and moderate pulmonary hypertension ("emphysema heart"). In the former group, heart failure dominates the clinical picture; in the latter, it is assumed that heart failure occurs on the basis of a "myocardial factor"—presumably arteriosclerotic heart disease—whose manifestations are colored and modified by the coexisting and contributing respiratory dysfunction. Overlapping of these two distinct forms occurs frequently, and pulmonary hypertension may be severe enough to be the chief precipitating cause of failure in emphysema, particularly in young subjects and in patients with kyphoscoliosis. Respiratory disturbances, fibrosis, and loss of pulmonary elasticity may accompany heart failure secondary to right ventricular overloading which may ultimately lead to significant arterial desaturation at rest and the development of polycythemia, even in this group. It is typical, however, that the disturbances leading to cor pulmonale rarely, if ever, involve the actual pulmonary function of alveolar-capillary gas exchange; they are confined to the abnormalities of the precapillary pulmonary vasculature and to the mechanical apparatus of the chest cage and of the pulmonary parenchyma concerned with breathing mechanisms. Pulmonary hypertensive heart disease, whatever its cause, has a monotonous symptomatology that is dominated by the signs of heart failure. In cor pulmonale due to emphysema and its allied types, the clinical picture is varied, and oxygen deficiency with arterial desaturation is of central significance. It raises pulmonary artery pressure by a mechanism not fully understood, and it stimulates erythropoiesis. When erythrocytosis has occurred, heart failure from cor pulmonale will soon make its appearance. Unless the arterial oxygen content falls sharply on exercise, resting oxygen saturation values in excess of 80 per cent do not cause this type of polycythemia; nor does polycythemia as such, as in erythremia ("vera"), result in significant arterial desaturation, pulmonary hypertension, or heart failure. However, little is known concerning the hemodynamic load imposed by an increase in blood viscosity. The management of cor pulmonale must recognize the multiplicity of factors that are concerned and should weigh their relative significance in any given subject. The kaleidoscopic appearance of cor pulmonale requires flexibility of therapy based on a grasp of the individual pathophysiologic interrelations, which may differ from patient to patient.

show abstract

Chronic Lung Disease, Polycythemia and Congestive Heart Failure

Cited by 37 publications

References 25 publications

Renal Function in Patients with Chronic Hypoxaemia and Cor Pulmonale Following Reversal of Polycythaemia

Renal Function in Patients with Chronic Hypoxaemia and Cor Pulmonale Following Reversal of Polycythaemia

Anoxie und ihre Kompensationsmechanismen bei Cor pulmonale bei TBC

Heart Failure and Lung Disease

Contact Info

Product

Resources

About