Heart-lung interaction in a model of COPD: importance of lung volume and direct ventricular interaction

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 311; no. 6; pp. H1367 - H1374
• Main Authors: Cheyne, William S, Williams, Alexandra M, Harper, Megan I, Eves, Neil D
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.12.2016
• Subjects: Adult; Chronic obstructive pulmonary disease; Echocardiography; Female; Healthy Volunteers; Heart Ventricles - diagnostic imaging; Heart Ventricles - physiopathology; Hemodynamics; Humans; Hypoxia; Hypoxia - diagnostic imaging; Hypoxia - physiopathology; Integrative Cardiovascular Physiology and Pathophysiology; Lung - physiopathology; Male; Models, Cardiovascular; Pressure; Pulmonary Disease, Chronic Obstructive - physiopathology; Stroke; Stroke Volume; Thorax; Tidal Volume; Ultrasonic imaging; Vascular Resistance; Ventricular Dysfunction, Left - diagnostic imaging; Ventricular Dysfunction, Left - physiopathology; Ventricular Function, Left; Ventricular Septum - diagnostic imaging; Ventricular Septum - physiopathology; Young Adult; dynamic hyperinflation; direct ventricular interaction; intrathoracic pressure; echocardiography; chronic obstructive pulmonary disease
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00458.2016

Chronic obstructive pulmonary disease (COPD) is associated with dynamic lung hyperinflation (DH), increased pulmonary vascular resistance (PVR), and large increases in negative intrathoracic pressure (nITP). The individual and interactive effect of these stressors on left ventricular (LV) filling, emptying, and geometry and the role of direct ventricular interaction (DVI) in mediating these interactions have not been fully elucidated. Twenty healthy subjects were exposed to the following stressors alone and in combination: 1) inspiratory resistive loading of -20 cmH O (nITP), 2) expiratory resistive loading to cause dynamic hyperinflation (DH), and 3) normobaric-hypoxia to increase PVR (hPVR). LV volumes and geometry were assessed using triplane echocardiography. LV stroke volume (LVSV) was reduced during nITP by 7 ± 7% (mean ± SD; P < 0.001) through a 4 ± 5% reduction in LV end-diastolic volume (LVEDV) (P = 0.002), while DH reduced LVSV by 12 ± 13% (P = 0.001) due to a 9 ± 10% reduction in LVEDV (P < 0.001). The combination of nITP and DH (nITP+DH) caused larger reductions in LVSV (16 ± 16%, P < 0.001) and LVEDV (12 ± 10%, P < 0.001) than nITP alone (P < 0.05). The addition of hPVR to nITP+DH did not further reduce LV volumes. Significant septal flattening (indicating DVI) occurred in all conditions, with a significantly greater leftward septal shift occurring with nITP+DH than either condition alone (P < 0.05). In summary, the interaction of nITP and DH reduces LV filling through DVI. However, DH may be more detrimental to LV hemodynamics than nITP, likely due to mediastinal constraint of the heart amplifying DVI.