Positive Airway Pressure in Congestive Heart Failure

Sleep Medicine Clinics 09/2010; 5(3):393-405. DOI: 10.1016/j.jsmc.2010.05.011

ABSTRACT Congestive heart failure (CHF) is an increasingly prevalent condition, which is estimated to affect 23 million people worldwide. 1 Despite significant recent advances in the medical management of this condition with an incidence reaching 12% in those older than 64 years, 2 it remains one of the leading causes of morbidity and mortality in the western world. Rates of hospitalization for CHF increased fourfold between 1971 and 1999, 3 cor-responding with an aging population and greater survival for acute coronary syndromes, valvular disease, and other related conditions. Heart failure (HF) is now the leading cause of hospitalization in developed countries. Positive airway pressure (PAP) delivered nonin-vasively via a mask (noninvasive ventilation [NIV]) has become increasingly used as adjunctive therapy in the acute and chronic settings for CHF. The provision of PAP by means of a face mask avoids the complications of intubation and the need for paralysis, sedation, associated instru-mentation, and tracheostomy. Modern PAP flow generators are lightweight, simple to use, and accessible in hospital ward and outpatient settings. Similarly, today's masks are more comfortable, better fitting, and well tolerated. To understand how PAP works, one needs to look at the pathophysiology of CHF and explore how the various forms of NIV affect CHF. CHF CHF is defined by the inability of the heart to pump sufficient oxygenated blood to meet the metabolic needs of the body. Failure of the heart results in a complex clinical syndrome, which includes dyspnea (at rest and on exertion), fatigue, periph-eral edema, orthopnea, tachypnea, tachycardia, and cardiomegaly. Although CHF may result from valvular disease or disturbances in cardiac rhythm or rate, it is most commonly the result of failure of the cardiac muscle pump. Cardiac muscle pump failure, or cardiomyop-athy, is generally divided into 2 types: systolic and diastolic dysfunction. Systolic dysfunction is defined by impaired left ventricular contractility and is usually the result of ischemic heart disease, long-standing hypertension, or unknown causes (idiopathic). It is defined by a reduced left ventric-ular ejection fraction (LVEF <55%) or impaired left ventricular fractional shortening (<28%). Diastolic dysfunction, recently renamed as HF with normal systolic function (HFNSF), is now recognized as being a significant cause of CHF. 4 It has been esti-mated that 13% to 74% of patients with CHF have normal systolic function, 5 with estimates varying widely depending on diagnostic criteria. The prev-alence of HFNSF increases with age, at 15% in those younger than 50 years, rising to 50% in

Download full-text


Available from: Kirk Kee, Jun 19, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: There is some evidence to suggest that acetazolamide may improve obstructive sleep apnoea (OSA).However, how acetazolamide affects the key traits causing OSA remains uncertain. We aimed to investigate the effect of acetazolamide on the traits contributing to OSA and its severity. Acetazolamide (500 mg twice daily) was administered for 1 week to 13 OSA subjects. Pharyngeal anatomy/collapsibility, loop gain (LG), upper-airway muscle responsiveness (gain) and the arousal threshold were determined using multiple 3 min 'CPAP pressure drops': pharyngeal anatomy/collapsibility was quantified as the ventilation at CPAP=0. LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in ventilation. Upper-airway gain was taken as the ratio of the increase in ventilation to the increase in ventilatory drive across the drop. Arousal threshold was quantified as the level of ventilatory drive associated with arousal. The apnoea-hypopnoea index (AHI)was assessed on separate nights using standard polysomnography. Acetazolamide reduced the median [interquartile range] LG (3.4 [2.4-5.4] versus 2.0 [1.4-3.5]; P <0.05) and NREM AHI (50 [36-57] versus 24 [13-42] events h-1; P <0.05), but did not significantly alter pharyngeal anatomy/collapsibility, upper-airway gain, or arousal threshold. There was a modest correlation between the percentage reduction in LG and the percentage reduction in AHI (r =0.660, P =0.05). Our findings suggest that acetazolamide can improve OSA, probably due to reductions in the sensitivity of the ventilatory control system. Identification of patients who may benefit from reductions in LG alone or in combination with other therapies to alter the remaining traits may facilitate pharmacological resolution of OSA in the future.
    The Journal of Physiology 01/2012; 590(Pt 5):1199-211. DOI:10.1113/jphysiol.2011.223925 · 4.54 Impact Factor