Chest
Volume 125, Issue 2, February 2004, Pages 669-682
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The Pulmonary Manifestations of Left Heart Failure

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Determining whether a patient's symptoms are the result of heart or lung disease requires an understanding of the influence of pulmonary venous hypertension on lung function. Herein, we describe the effects of acute and chronic elevations of pulmonary venous pressure on the mechanical and gas-exchanging properties of the lung. The mechanisms responsible for various symptoms of congestive heart failure are described, and the significance of sleep-disordered breathing in patients with heart disease is considered. While the initial clinical evaluation of patients with dyspnea is imprecise, measurement of B-type natriuretic peptide levels may prove useful in this setting.

Section snippets

The Pathophysiology of Pulmonary Congestion

Clinicians who are experienced in the care of patients with chronic CHF are familiar with the body's remarkable ability to adapt to a chronically elevated pulmonary capillary wedge pressure. How is it that a previously healthy individual develops pulmonary edema when the pulmonary capillary wedge pressure reaches 25 mm Hg, whereas a patient with longstanding CHF is ambulatory at a filling pressure of 40 mm Hg (Fig 1)? The answer lies in a variety of adaptations that occur in an individual who

Pulmonary Function in Heart Disease

Diuresis of healthy subjects results in increased lung volumes and flows, suggesting that, even in health, pulmonary function is influenced by the water content of the lung.28 Abnormalities in the mechanical and gas-exchanging properties of the lung have been described in patients with both acute pulmonary edema and chronic CHF, although the findings differ somewhat (Table 2 includes these abnormalities).

Sleep Disorders in CHF

Evidence is accumulating of an important association between sleep-disordered breathing and CHF. Either obstructive sleep apnea (OSA) or, more commonly, Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) has been detected in as many as 50% of patients with chronic CHF.59606162 Each disorder is considered separately below.

The risk factors for OSA in a population of 450 men and women with CHF who had been referred to a sleep laboratory for evaluation differed according to gender. Body

Wheezing

Although airflow obstruction in the setting of pulmonary edema has long been familiar to clinicians,85 the mechanisms responsible for this observation remain obscure. The elevation of pulmonary or bronchial vascular pressure likely results in reflex bronchoconstriction.86 Other potential causes of airway narrowing include a geometric decrease in airway size from reduced lung volume, obstruction from intraluminal edema fluid, and bronchial mucosal swelling.86 Some investigators,8788 but not all,

Unusual Pulmonary Manifestations of Heart Disease

Underdeveloped regions of the world have produced large numbers of patients with rheumatic heart disease. Much of the literature describing unusual pulmonary manifestations of heart disease consists of descriptive studies of such patients, particularly those with mitral stenosis. Hemosiderosis from microvascular hemorrhage may be visible radiographically as small nodules, 1 to 5 mm in size, that generally, but not exclusively, are in the lower lobes.105106 Ossific nodules consist of lamellated

Diagnostic Difficulties in Left Heart Failure

A comprehensive discussion of all of the diagnostic tools used to evaluate cardiopulmonary disease is beyond the scope of this review. Herein we highlight selected difficulties encountered in the routine evaluation of patients with pulmonary edema.

Clinicians often are required to differentiate heart disease from lung disease in a patient with breathlessness. Unfortunately, the initial clinical evaluation of dyspnea is imprecise, with one review suggesting an overall accuracy of approximately

Summary

The pulmonary manifestations of heart disease are diverse (Table 2). Pulmonary function is frequently abnormal, with a fall in vital capacity shown to precede the clinical recognition of CHF.134 While a restrictive defect may be seen in patients with both chronic CHF and acute pulmonary edema, significant airflow obstruction is more likely to occur in the latter. The Dlco is often mildly reduced and does not normalize following heart transplantation. Reduced lung compliance, increased dead

ACKNOWLEDGMENT

We are grateful to Dr. Elizabeth Sengupta for providing us with electron micrographs of the lung. We affirm that there are no other individuals who contributed significantly to this work.

References (135)

  • JD Hosenpud et al.

    Abnormal pulmonary function specifically related to congestive heart failure: comparison of patients before and after cardiac transplantation

    Am J Med

    (1990)
  • P Assayag et al.

    Alteration of the alveolar-capillary membrane diffusing capacity in chronic left heart disease

    Am J Cardiol

    (1998)
  • SW Davies et al.

    Reduced pulmonary microvascular permeability in severe chronic left heart failure

    Am Heart J

    (1992)
  • F Lofaso et al.

    Prevalence of sleep-disordered breathing in patients on a heart transplant waiting list

    Chest

    (1994)
  • J Chan et al.

    Prevalence of sleep-disordered breathing in diastolic heart failure

    Chest

    (1997)
  • P Buckle et al.

    The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure

    Chest

    (1992)
  • PQ Eichacker et al.

    Methacholine bronchial reactivity testing in patients with chronic congestive heart failure

    Chest

    (1988)
  • K Wasserman

    Diagnosing cardiovascular and lung pathophysiology from exercise gas exchange

    Chest

    (1997)
  • National Heart, Lung, and Blood Institute

    National Institutes of Health. Congestive heart failure in the United States: a new epidemic

  • MR Flick et al.

    Pulmonary edema and acute lung injury

  • JMB Hughes

    Pulmonary complications of heart disease

  • J Bhattacharya

    Physiological basis of pulmonary edema

  • JB West et al.

    Distribution of blood flow in isolated lung: relation to vascular and alveolar pressures

    J Appl Physiol

    (1963)
  • JB Glazier et al.

    Measurements of capillary dimensions and blood volume in rapidly frozen lungs

    J Appl Physiol

    (1969)
  • JF Murray

    The lungs and heart failure

    Hosp Pract

    (1985)
  • NC Staub

    Pathophysiology of pulmonary edema

  • NC Staub

    Pulmonary edema

    Physiol Rev

    (1974)
  • AB Malik et al.

    Pulmonary circulation and regulation of fluid balance

  • NC Staub et al.

    Pulmonary edema in dogs, especially the sequence of fluid accumulation in lungs

    J Appl Physiol

    (1967)
  • VC Broaddus et al.

    Clearance of lung edema into the pleural space of volume-loaded anesthetized sheep

    J Appl Physiol

    (1990)
  • HN Uhley et al.

    Role of pulmonary lymphatics in chronic pulmonary edema

    Circ Res

    (1962)
  • MA Matthay et al.

    Salt and water transport across alveolar and distal airway epithelia in the adult lung

    Am J Physiol

    (1996)
  • K Tsukimoto et al.

    Ultrastructural appearances of pulmonary capillaries at high transmural pressures

    J Appl Physiol

    (1991)
  • ML Costello et al.

    Stress failure of alveolar epithelial cells studied by scanning electron microscopy

    Am Rev Respir Dis

    (1992)
  • JB West et al.

    Vulnerability of pulmonary capillaries in heart disease

    Circulation

    (1995)
  • Parker F Jr, Weiss S. The nature and significance of the structural changes in the lungs in mitral stenosis. Am J...
  • SG Haworth et al.

    Peripheral pulmonary vascular and airway abnormalities in adolescents with rheumatic mitral stenosis

    Int J Cardiol

    (1998)
  • JM Kay et al.

    Ultrastructure of the alveolar-capillary wall in mitral stenosis

    J Pathol

    (1973)
  • SC Jordan et al.

    Pathology of the lungs in mitral stenosis in relation to respiratory function and pulmonary haemodynamics

    Br Heart J

    (1966)
  • CP Aber et al.

    Significance of changes in the pulmonary diffusing capacity in mitral stenosis

    Thorax

    (1965)
  • BE Heard et al.

    Oedema and fibrosis of the lungs in left ventricular failure

    Br J Radiol

    (1968)
  • DL Moraes et al.

    Secondary pulmonary hypertension in chronic heart failure: the role of the endothelium in pathophysiology and management

    Circulation

    (2000)
  • JK Kirklin et al.

    Pulmonary vascular resistance and the risk of heart transplantation

    J Heart Transplant

    (1988)
  • S Javaheri et al.

    Effects of hypohydration on lung functions in humans

    Am Rev Respir Dis

    (1987)
  • AL Muir et al.

    Cardiorespiratory effects of rapid saline infusion in normal man

    J Appl Physiol

    (1975)
  • S Puri et al.

    Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction

    Circulation

    (1999)
  • JT Sharp et al.

    Ventilatory mechanics in pulmonary edema in man

    J Clin Invest

    (1958)
  • RS Cosby et al.

    Pulmonary function in left ventricular failure, including cardiac asthma

    Circulation

    (1957)
  • RW Light et al.

    Serial pulmonary function in patients with acute heart failure

    Arch Intern Med

    (1983)
  • WH Noble et al.

    Lung mechanics in hypervolemic pulmonary edema

    J Appl Physiol

    (1975)
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