Haemodynamic Effects of Continuous Positive Airway Pressure in Humans with Normal and Impaired Left Ventricular Function

Abstract

1. Continuous positive airway pressure increases intrathoracic pressure, thereby decreasing left ventricular preload and afterload. We hypothesized that there would be a dose-related alteration in cardiac and stroke volume indices in response to continuous positive airway pressure in normal subjects and patients with congestive heart failure and that the direction of response among those with heart failure would be related to left ventricular preload. 2. Cardiac and stroke volume indices were measured at baseline and after 10 min of continuous positive airway pressure at both 5 and 10 cmH2O (0.5 and 0.99 kPa respectively) in 16 patients with heart failure and five control subjects with normal cardiac function. Among the eight patients with heart failure and elevated pulmonary capillary wedge pressure (≧12 mmHg) (≦ 1.6 kPa), cardiac index increased from 2.47 ± 0.34 at baseline to 2.91 ± 0.32 to 3.12 ± 0.40 l min−1 m−2 (P < 0.025) while on 5 and 10 cm H2O of continuous positive airway pressure respectively. In the same patients stroke volume index increased from 27.8 ± 3.9 to 33.9 ± 4.2 to 36.8 ± 5.5 ml/m2 (P < 0.05). In contrast, in both the control subjects and patients with heart failure and normal pulmonary capillary wedge pressure (< 12 mmHg) there was a dose-related decrease in cardiac and stroke volume indices while on continuous positive airway pressure. 3. Continuous positive airway pressure causes dose-related increases in cardiac and stroke volume indices among patients with chronic heart failure and elevated left ventricular filling pressure. However, it induces dose-related reductions in cardiac and stroke volume indices among normal subjects as well as patients with heart failure and normal left ventricular filling pressures.

Distinct Patterns of Hyperpnea During Cheyne-Stokes Respiration: Implication for Cardiac Function in Patients With Heart Failure

“…16 Because the failing heart is very sensitive to changes in afterload, such an effect could also boost SV and CO by recruiting the respiratory system to assist left ventricular ejection in the face of deteriorating cardiac function. 17,18 This mechanism might be comparable to that from chest compressions during cardio-pulmonary resuscitation for cardiac arrest, 19,20 and to voluntary coughing during conscious cardiac arrest in the cardiac catheterization laboratory where generation of positive P IT augments SV and CO. 21 By this means, in patients with HFrEF and very compromised cardiac function, the respiratory system may be recruited to assist cardiac pumping activity via active expiration and generation of positive P IT during the hyperpnea phase of CSR-CSA.…”

A Nonlinear Model of Cardiac Autonomic Control in Obstructive Sleep Apnea Syndrome

“…For example, in subjects with normal heart function, acute application of CPAP is known to decrease left ventricular preload more than left ventricular afterload, leading to a reduction in cardiac output. 9 However, our OSAS subjects did not show any change in SBP or DBP during sleep relative to wakefulness when only minimal CPAP was applied. The CPAP-induced increase in lung volume itself may have also contributed to some increase in vagal activity and reduction in sympathetic drive.…”

Treatment of sleep disordered breathing in congestive heart failure

“…Bradley et al [12] demonstrated a significant increase in both cardiac index and stroke volume after 10 min of nasal CPAP at 5 cm H 2 O in those patients with a pulmonary capillary wedge pressure [12 mmHg. The presence of an elevated filling pressure appears to be important in regards to the cardiac response to CPAP therapy [55]. Improvements in LVEF have been noted with CPAP therapy when used from 1 to 3 months [11,[13][14][15][16][17][18].…”