Hemodynamic effects of supplemental oxygen administration in congestive heart failure

Haque, Wasim; Boehmer, John; Clemson, Barry S.; Leuenberger, Urs A.; Silber, David; Sinoway, Lawrence I.

doi:10.1016/0735-1097(95)00474-2

Cited by 187 publications

(131 citation statements)

References 15 publications

Supporting

Mentioning

122

Contrasting

Unclassified

Order By: Relevance

“…Peripheral chemoreflex responses to hypoxia were not enhanced in patients with mild NYHA Class II-III CHF distinguished by dyspnea to mild (III) or moderate (II) exercise (Narkiewicz et al 1999). Similarly, other clinical studies (Haque et al 1996,van de Borne et al 1996 reported that suppression of peripheral chemoreceptor activity by hyperoxia had no effect on muscle sympathetic nerve activity or arterial pressure. By contrast, other groups ,Ponikowski & Banasiak, 2001,Ciarka et al 2006 have found an enhanced ventilatory response to hypoxia in CHF patients, particularly those in more severe stages of heart failure.…”

Section: Chemoreflex Control Of Sympathetic Function In Heart Failurementioning

confidence: 84%

Carotid body function in heart failure

Schultz

2007

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

In this review, we summarize the present state of knowledge of the functional characteristics of the carotid body (CB) chemoreflex with respect to control of sympathetic nerve activity (SNA) in chronic heart failure (CHF). Evidence from both CHF patients and animal models of CHF has clearly established that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in SNA. This adaptive change derives from altered function at the level of both the afferent and central nervous system (CNS) pathways of the reflex arc. At the level of the CB, an elevation in basal afferent discharge occurs under normoxic conditions in CHF rabbits, and the discharge responsiveness to hypoxia is enhanced. Outward voltage-gated K + currents (I K ) are suppressed in CB glomus cells from CHF rabbits, and their sensitivity to hypoxic inhibition is enhanced. These changes in I K derive partly from downregulation of nitric oxide synthase (NOS) / NO signaling and upregulation of angiotensin II (Ang II) / Ang II receptor (AT 1 R) signaling in glomus cells. At the level of the CNS, interactions of the enhanced input from CB chemoreceptors with altered input from baroreceptor and cardiac afferent pathways and from central Ang II further enhance sympathetic drive. In addition, impaired function of NO in the paraventricular nucleus of the hypothalamus participates in the increased SNA response to CB chemoreceptor activation. These results underscore the principle that multiple mechanisms involving Ang II and NO at the level of both the CB and CNS represent complementary and perhaps redundant adaptive mechanisms to enhance CB chemoreflex function in CHF.

show abstract

Section: Chemoreflex Control Of Sympathetic Function In Heart Failurementioning

confidence: 84%

Carotid body function in heart failure

Schultz

2007

Respiratory Physiology & Neurobiology

View full text Add to dashboard Cite

show abstract

“…In healthy persons increased systemic vascular resistance and in dogs increased capacitance vessel tone was observed with hypercapnia [33]. Furthermore, hyperoxia may also increase systemic vascular resistance in heart failure in a dose-dependent way [34]. Hypercapnia increased mean pulmonary artery pressure and pulmonary vascular resistance in a recent study on healthy subjects using Doppler echocardiography [35].…”

Section: Discussionmentioning

confidence: 99%

Treatment of Cheyne-Stokes respiration with nasal oxygen and carbon dioxide

Andreas

Weidel²,

Hagenah³

et al. 1998

Eur Respir J

View full text Add to dashboard Cite

Cheyne-Stokes respiration (CSR) during sleep is common in patients with severe congestive heart failure (CHF). It induces repetitive oxygen desaturations and impairs sleep [1,2]. Disturbed sleep is likely to cause daytime symptoms and the repetitive oxygen desaturations and arousals increase sympathetic activity as well as right and left ventricular afterload [3] and may thus further impede left ventricular function and exercise tolerance [4][5][6]. Effective treatment for CSR is therefore needed. Nocturnal oxygen by nasal prongs reduces CSR by about 50% and consolidates sleep [1,[6][7][8]. Application of 3% CO 2 prevented CSR by increasing the arterial carbon dioxide tension (Pa,CO 2 ) above the apnoeic threshold [9] but sleep was adversely affected, this being attributed to the tight-fitting face mask used [10]. The hypothesis was tested that CO 2 in conjunction with O 2 given by nasal prongs is efficacious in the treatment of CSR. Plasma catecholamines were measured, to evaluate possible effects on sympathetic activity. Methods Subjects and protocolAll patients with severe heart failure admitted to the department of cardiology were candidates for the study.Patients under the age of 75 yrs were eligible if they met the following criteria: at least one episode of cardiac decompensation, ejection fraction ð35%, stable condition on cardiac medication and evidence of CSR by nocturnal polysomnography. Exclusion criteria were myocardial infarction within 1 yr of entry, significant obstructive lung disease as defined by a forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) <70%, primary valvular heart disease, tibial oedema or evidence of obstructive sleep apnoea (more than five obstructive apnoeas·h -1 ). Plasma catecholamines were evaluated in 15 healthy subjects (age 53.2±5.3 yrs) without significant sleep-disordered breathing. The study was approved by the local ethics committee. Informed written consent was obtained from all subjects.The study was designed as a single-blind, placebo-controlled trial. After an accommodation night where no treatment was applied the patients received air as well as O 2 plus CO 2 in a randomized, cross-over fashion on two consecutive nights. Polysomnography was performed during all three nights. Oxygen was given with a flow rate of 2 L·min -1 by nasal prongs and CO 2 was admixed simultaneously with a flow rate of 0.2-1 L·min -1 . Accordingly, the flow rate of the mixture was 2.2-3 L·min -1 . CO 2 flow rate was regulated depending on the transcutaneous carbon dioxide tension (Ptc,CO 2 ), which was not allowed to increase >7.3 kPa (55 mmHg) and on the occurrence of In conclusion, nocturnal O 2 plus CO 2 improves Cheyne-Stokes respiration in patients with congestive heart failure but has adverse effects on the sequel of CheyneStokes respiration, namely sympathetic activation. Eur Respir J 1998; 12: 414-419.

show abstract

“…24 In addition, supplemental oxygen has been suggested to cause hyperoxia, which can have an adverse effect on myocardial function because of the generation of oxygen free radicals. 25,26 We previously conducted a prospective study to elucidate the efficacy of 12 weeks of nocturnal oxygen therapy using a conventional oxygen concentrator on ventricular function, severity of HF, and QOL, together with an improvement in SDB, in ambulatory patients with stable CHF and CSR. 19 That study demonstrated that short-term treatment with nocturnal oxygen significantly improved NYHA functional class, Specific Activity Scale as a measure of QOL, and SDB in CHF patients with CSR-CSA; LVEF also increased from baseline to the end of the study.…”

Section: Discussionmentioning

confidence: 99%