Effect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

doi:10.1378/chest.107.3.780

Chest

Volume 107, Issue 3, March 1995, Pages 780-786

https://doi.org/10.1378/chest.107.3.780 Get rights and content

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 ± 5 mm Hg) and at control periods, before (36 ± 4 mm Hg) and after (42 ± 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.

Section snippets

Patients

The study involved seven male patients with COPD with acute respiratory failure, 64 ± 2 years old, and referred to the Critical Care Unit for ventilatory support. The diagnosis of COPD was established from a history of chronic bronchitis and the evidence of airflow limitations on pulmonary function tests, ie, forced expiratory volume in 1 s (FEV₁) less than 40% predicted¹³ and a ratio of FEV₁ to forced vital capacity (FEV₁/FVC) less than 60%. At the time of hospital admission, all patients had

Results

Results are shown in Tables 2 (cardiorespiratory data) and 3 (hormonal data).

Discussion

This study showed no variation of plasma hormones involved in the circulatory and body fluid homeostasis, during an isolated acute hypercapnia, in patients with COPD sedated under mechanical ventilation. It should be emphasized that hypercapnia was really the sole variable parameter in the study: P0₂ was maintained above 100 mm Hg and cardiac filling pressures did not change during the whole study. In the absence of variation in VE and airway pressure, since these patients were sedated and

ACKNOWLEDGMENT

The authors thank S. Maire and M.F. Mathis for typing the manuscript.

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Cited by (22)

Neurohumoral activation as a link to systemic manifestations of chronic lung disease
2005, Chest
Citation Excerpt :
Autonomic dysfunction evaluated by heart rate variability may be linked to sodium and water retention in COPD.23 Hypercapnia has not been shown to play an important role in modulation of the renin-angiotensin system.24 There is therefore consistent evidence of augmented sympathic nerve traffic, elevated catecholamines, as well as an activated renin-angiotensin system in COPD patients.
COPD is a major cause of death and disability worldwide. Treatment of COPD improves lung function but is unlikely to slow the steady downhill course of the disease or reduce mortality. In COPD, numerous abnormalities can be found outside the lung. These include systemic inflammation, cachexia, and skeletal muscle dysfunction. Thus, COPD has been called a systemic disease. Convincing data demonstrate that COPD causes neurohumoral activation. By precedents derived from chronic heart failure and other diseases characterized by neurohumoral activation, we propose that the negative consequences of neurohumoral activation, namely inflammation, cachexia, effects on ventilation, and skeletal muscle dysfunction, give rise to a self-perpetuating cycle that contributes to the pathogenesis of COPD, and which may involve respiratory muscle dysfunction as well as systemic inflammation. This concept may further help explain the increased cardiovascular morbidity and mortality in COPD patients. Currently, little is known about the effect of treatments directed at neurohumoral activation and COPD. As this aspect of COPD becomes better understood, new insights may direct novel therapeutic approaches.
Disorders of water imbalance
2005, Emergency Medicine Clinics of North America
Systemic diseases associated with disorders of water homeostasis
2002, Endocrinology and Metabolism Clinics of North America
Opioid peptides attenuate blood pressure increase in acute respiratory failure
2001, Peptides
Plasma opioid peptides, norepinephrine, atrial natriuretic factor (ANF) and blood pressure (BP) were assessed in 24 chronic obstructive pulmonary disease patients with acute respiratory failure. Hypoxemic-hypercapnic patients had high BP, β-endorphin, Met-enkephalin and dynorphin B, whereas hypoxemic-normocapnic and hypoxemic-hypocapnic patients showed normal BP, high β-endorphin, and normal Met-enkephalin and dynorphin B. Norepinephrine and ANF were high in all patients, particularly in hypoxemic-hypercapnic patients. Infusion with the opioid antagonist naloxone hydrochloride significantly increased systolic blood pressure (SBP) in hypoxemic-hypercapnic (182.0 ± 3.2 versus 205.1 ± 3.0 mmHg; P < 0.01), hypoxemic-normocapnic (149.3 ± 1.8 versus 169.1 ± 2.2 mmHg; P < 0.01) and hypoxemic-hypocapnic (147.3 ± 1.3 versus 166.8 ± 2.2 mmHg; P < 0.01) patients, norepinephrine in hypoxemic-hypercapnic patients (3583.2 ± 371.8 versus 5371.3 ± 260.0 fmol/ml; P < 0.01), and reduced ANF in hypoxemic-normocapnic (18.3 ± 0.8 versus 11.9 ± 1.0 fmol/ml; P < 0.05) and hypoxemic-hypocapnic (18.1 ± 1.2 versus 12.1 ± 2.1 fmol/ml; P < 0.05) patients. These results indicate that the endogenous opioid system attenuates SBP responses in acute respiratory failure by affecting norepinephrine or ANF release.
Mechanisms of hypertension in patients with chronic obstructive pulmonary disease and acute respiratory failure
2000, American Journal of Medicine
Citation Excerpt :
The pressor effects of hypercapnia were also seen in patients who were breathing supplemental low-flow oxygen, which corrected the hypoxemia. Our results are consistent with experiments in animals (7), healthy subjects (8,9), and patients with chronic obstructive pulmonary disease (5) showing that when carbon dioxide was added to the inspired mixture, there was an increase in blood pressure associated with an increase in plasma catecholamine levels (8). Carbon dioxide induces norepinephrine hypersecretion by stimulating the sympathetic nervous system through a direct central action (20,21), as well as through activation of the baroreceptor reflex after vasodilation (22).
PURPOSE: To investigate the effects of hypoxemia, hypercapnia, and cardiovascular hormones (norepinephrine, endothelin-1, and atrial natriuretic factor) on blood pressure during acute respiratory failure.
PATIENTS AND METHODS: Patients with chronic obstructive pulmonary disease and acute respiratory failure were divided into four groups of 10 patients each: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, and normoxemia-hypercapnia. Plasma norepinephrine levels were determined by high-performance liquid chromatography with electrochemical detection. Plasma endothelin-1 and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction.
RESULTS: Systolic blood pressure and cardiovascular hormone levels were greater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (± SD) systolic blood pressure was 183 ± 31 mm Hg and the mean norepinephrine level was 494 ± 107 pg/mL, as compared with 150 ± 6 mm Hg and 243 ± 58 pg/mL in those with normocapnia and hypoxemia (both P <0.05). Similar results were seen for endothelin-1 and atrial natriuretic factor levels, and for the comparisons of hypoxemic patients who were hypercapnic with those who were normocapnic.
CONCLUSIONS: These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respiratory failure, perhaps as a result of enhanced sympatho-adrenergic activity.
Neurohormonal responses during positive pressure mechanical ventilation
1999, Heart and Lung: Journal of Acute and Critical Care
Positive pressure mechanical ventilation is used daily in critical care units to support ventilation and improve oxygenation in critically ill patients. One adverse response to positive pressure mechanical ventilation is a reduction in urinary output and sodium and water retention. This consequence is attributed to complex neurohormonal responses intended to maintain hemodynamic homeostasis. This article reviews the physiologic nature of these responses and research findings related to these responses and provides clinicians with information about the importance of these responses, particularly in patients with underlying cardiac dysfunction. (Heart Lung® 1999;28:149-65)

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Chest

Clinical Investigations in Critical Care: ArticlesEffect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

Section snippets

Patients

Results

Discussion

ACKNOWLEDGMENT

Chest

Chest

Chest

Chest

Oedema in cor pulmonale

Clin Sci

Pathogenesis of congestive state in chronic obstructive pulmonary disease: studies of body water and sodium, renal function, hemodynamics, and plasma hormones during edema and after recovery

Circulation

Atriopeptin: a cardiac hormone intimately involved in fluid, electrolyte, and blood-pressure homeostasis

N Engl J Med

Effects of hypoxia and hypercapnia on atrial natriuretic peptide and plasma renin activity in conscious dogs

Clin Sci

Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs

Am J Physiol

Synergistic effects of acute hypoxemia and hypercapnic acidosis in conscious dogs: renal dysfunction and activation of the renin-angiotensin system

Circ Res

Atrial natriuretic peptide concentrations in hypoxic secondary pulmonary hypertension. Relation to haemodynamic and blood gas variables and response to supplemental oxygen

Thorax

Abnormalities of sodium and H2O handling in chronic obstructive lung disease

Arch Intern Med

Atrial natriuretic peptide concentrations and pulmonary hemodynamics in patients with pulmonary artery hypertension

Am Rev Respir Dis

Plasma levels of atrial natriuretic peptide, renin activity, and aldosterone in patients with chronic obstructive pulmonary disease: response to O2 removal and to hyperoxia

Am Rev Respir Dis

Vagally mediated regulation of renal function in conscious primates

Am J Physiol

Summary equations of reference values

Bull Eur Physiopathol Respir

Immunoassay for LVP: comparison of biological and immunological activity of lysine vasopressin and some of its synthetic analogues

Experentia

Clinical Investigations in Critical Care: Articles
Effect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

Abnormalities of sodium and H₂O handling in chronic obstructive lung disease

Plasma levels of atrial natriuretic peptide, renin activity, and aldosterone in patients with chronic obstructive pulmonary disease: response to O₂ removal and to hyperoxia