17,18) Administration of DIDS (4,4-diisothiocyanostilbene 2,2-disulfonic acid, anion exchanger inhibitor), a potent and relatively specific inhibitor of anion exchanger or acetazolamide, a carbonic anhydrase inhibitor or induction the Na-free medium decrease pulmonary vascular tone during hypercapnia
in the isolated pulmonary artery.
Mathematical models easily demonstrated the critical importance of minute ventilation in driving dynamic hyperinflation, and gave a potent rationale for pursuing a strategy of permissive hypercapnia
in the ventilatory support of severe airflow obstruction--long before its use in ARDS.
Portner and colleagues have investigated the effects of hypercapnia
and reduced extracellular pH on the marine invertebrate Sipunculus nudus and on Antarctic fishes (Langenbuch and Portner, 2003; Langenbuch et al.
2003) it is possible that the adaptation to hypercapnia
could be the result of RBF training.
On the other hand, short-term exposure to hypercapnia
elicits acidosis of body fluids that remains almost uncompensated in the deep-sea crab Chionoecetus tanneri, but is fully recovered by bicarbonate accumulation in the shallow-water crab Cancer magister (Pane & Barry 2007).
However, outcomes were significantly better with surgery than with watchful waiting on measures of obstructive apneahypopnea, oxygen desaturation index, hypercapnia
, sleep arousal index, and percentage of sleep time in fight sleep.
This relaxation increases the upper airway resistance during inspiration, leads to paralaryngeal collapse and hypoventilation, which end up with hypoxia and hypercapnia
The authors note that there is little evidence that hypercapnia
is harmful to critically ill patients; indeed, there is much evidence that hypercapnia
can aid lung-repair mechanisms in certain circumstances (7).
In addition the hypercapnia
(pCO2) that develops with periods of apnoea will result in acidosis, which in turn compromises myocardial contractility as hydrogen ions bind to calcium receptors on the actin-myosin mechanism within cardiac muscle fibres (Devlin 2011).
At the most recent presentation, the patient exhibited marked respiratory distress, and she was in an acute state of confusion secondary to hypercapnia
Patients with post-hyperventilation central apnoea are typically free of neuromuscular or pulmonary disorder and have a normal or exaggerated response to hypercapnia
These include nocturnal hypoxemia, hypercapnia
, a tremendous increase in sympathetic nerve activity, hypertensive surges, endothelial dysfunction, vascular oxidative stress, inflammation, hypercoagulability, and markedly elevated left ventricular wall stress.