Effects of Nifedipine on Ventilation/Perfusion Matching in Primary Pulmonary Hypertension

Exercise testing in pulmonary arterial hypertension and in chronic heart failure

“…An increase in physiological dead space is a probable explanation. Previous studies on pulmonary gas exchange using the multiple inert gas elimination technique in patients with either primary or thromboembolic pulmonary hypertension showed only mild ventilation/perfusion (V9/Q9) inequality limited to lower-than-normal-V9/Q9 regions, with no high V9/Q9 modes and no increase in dead space [27][28][29]. Exercise, in these studies, did not alter V9/Q9 distributions, and, in particular, was shown not to be associated with an abnormal increase in dead space [29].…”

Clinical relevance of autonomic nervous system disturbances in pulmonary arterial hypertension

“…The respective contributions of physiological dead space and chemosensitivity to hyperventilation in PAH are difficult to assess from reported expired and arterial blood respiratory gases. Studies using the independent multiple inert gas elimination technique have shown that the distribution of ventilation/perfusion (V9A/Q9) relationships in PAH patients is actually close to normal, with a low-to-normal arterial oxygen tension explained by a low mixed venous oxygen tension, a consequence of a low cardiac output, at rest [8,9] as well as during exercise [10]. A proportion of patients with PAH present with a cardiac right-to-left shunt, which causes more consistent hypoxaemia [9], and also a peripheral chemoreflex-mediated additional increase in ventilation at exercise [11].…”

Treatment of right heart failure on pulmonary arterial hypertension: is going left a step in the right direction?

“…Furthermore, studies using the sophisticated multiple inert gas elimination technique have shown that their distributions of ventilation-perfusion (V/Q) relationships are close to normal, at rest [12,13] as well as during exercise [14]. The mean V/Q is shifted to higher V/Q, which decreases the efficiency of gas exchange and increased physiological dead space, but the resulting arterial partial pressure of oxygen (PO 2 ) often remains normal or low to normal [12][13][14]. Hypoxaemia is explained by a low mixed venous PO 2 , a result of a low cardiac output [12][13][14].…”

“…The mean V/Q is shifted to higher V/Q, which decreases the efficiency of gas exchange and increased physiological dead space, but the resulting arterial partial pressure of oxygen (PO 2 ) often remains normal or low to normal [12][13][14]. Hypoxaemia is explained by a low mixed venous PO 2 , a result of a low cardiac output [12][13][14]. In some patients, hypoxaemia is caused by right to left shunting through a patent foramen ovale [13].…”

“…Hypoxaemia is explained by a low mixed venous PO 2 , a result of a low cardiac output [12][13][14]. In some patients, hypoxaemia is caused by right to left shunting through a patent foramen ovale [13]. In spite of vascular obliteration, dead space remains normal or near-normal, and increased physiological dead space only partly accounts for a resting and exercise hyperventilation that does not limit exercise capacity [14][15][16].…”