Expiratory threshold loading impairs cardiovascular function in health and chronic heart failure during submaximal exercise.
We determined the effects of augmented expiratory intrathoracic pressure (P(ITP)) production on cardiac output (Q(TOT)) and blood flow distribution in healthy dogs and dogs with chronic heart failure (CHF). From a control expiratory P(ITP) excursion of 7 +/- 2 cmH2O, the application of 5, 10, or 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 47 +/- 23, 67 +/- 32, and 118 +/- 18% (P < 0.05 for all). Stroke volume (SV) rapidly decreased (onset <10 s) with increases in the expiratory P(ITP) excursion (-2.1 +/- 0.5%, -2.4 +/- 0.9%, and -3.6 +/- 0.7%, P < 0.05), with slightly smaller reductions in Q(TOT) (0.8 +/- 0.6, 1.0 +/- 1.1, and 1.8 +/- 0.8%, P < 0.05) owing to small increases in heart rate. Both Q(TOT) and SV were restored to control levels when the inspiratory P(ITP) excursion was augmented by the addition of an inspiratory resistive load during 15 cmH2O expiratory threshold loading. The highest level of expiratory loading significantly reduced hindlimb blood flow by -5 +/- 2% owing to significant reductions in vascular conductance (-7 +/- 2%). After the induction of CHF by 6 wk of rapid cardiac pacing at 210 beats/min, the expiratory P(ITP) excursions during nonloaded breathing were not significantly changed (8 +/- 2 cmH2O), and the application of 5, 10, and 15 cmH2O expiratory threshold loads increased the expiratory P(ITP) excursion by 15 +/- 7, 23 +/- 7, and 31 +/- 7%, respectively (P < 0.05 for all). Both 10 and 15 cmH2O expiratory threshold loads significantly reduced SV (-3.5 +/- 0.7 and -4.2 +/- 0.7%, respectively) and Q(TOT) (-1.7 +/- 0.4 and -2.5 +/- 0.4%, P < 0.05) after the induction of CHF, with the reductions in SV predominantly occurring during inspiration. However, the augmentation of the inspiratory P(ITP) excursion now elicited further decreases in SV and Q(TOT). Only the highest level of expiratory loading significantly reduced hindlimb blood flow (-4 +/- 2%) as a result of significant reductions in vascular conductance (-5 +/- 2%). We conclude that increases in expiratory P(ITP) production-similar to those observed during severe expiratory flow limitation-reduce cardiac output and hindlimb blood flow during submaximal exercise in health and CHF.
Miller
Jordan D
JD
University of Wisconsin-Madison, John Rankin Laboratory of Pulmonary Medicine, USA. jordan-miller@uiowa.edu
Hemauer
Sarah J
SJ
Smith
Curtis A
CA
Stickland
Michael K
MK
Dempsey
Jerome A
JA
D000818:Animals; D002302:Cardiac Output / Q000502:physiology*; D002303:Cardiac Output, Low / Q000503:physiopathology*; D002319:Cardiovascular System / Q000503:physiopathology*; D004285:Dogs; D045853:Exhalation / Q000502:physiology*; D005260:Female; D005540:Forced Expiratory Flow Rates / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006614:Hindlimb / Q000098:blood supply; D001239:Inhalation / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D015656:Respiratory Mechanics / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D013997:Time Factors