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a decrease in the oxygen content of the blood as a result of disruption of blood circulation, increased tissue requirements for oxygen (due to excessive muscular exertion, for example), decreased exchange of gases in the lungs when they are diseased, decreased hemoglobin content of the blood (for example, in anemias), and decreased partial pressure of oxygen in inhaled air (altitude sickness). The consequence of hypoxemia is hypoxia.

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5] Pulmonary arterial hypertension develops late in the course of COPD with the development of hypoxaemia (Pa[O.
This study showed that arterial hyperoxaemia was independently associated with increased in-hospital mortality compared with either hypoxaemia or normoxaemia and that there was a dose-dependent association between supra-normal oxygen levels and the risk of in-hospital mortality23.
The aetiopathogenesis of cor pulmonale in COPD patients is complex and includes several mechanism such as hypoxaemia, polycythaemia, inflammation and endothelial dysfunction that promote pulmonary hypertension (15).
The classic clinical presentation includes respiratory distress, cyanosis, hypoxaemia and acidosis.
Calculation for the presence of hypoxaemia or decreased lung compliance was rarely done.
Respiratory depression and hypoxaemia appear as the most common respiratory events, in contrast with the information available from ASA where the most common events associated with the respiratory system were difficult intubation, inadequate ventilation and aspiration.
COPD is a slow progressive disease that is characterised by a reduction in airflow that is not fully reversible which may lead to severe disabling breathlessness on minimal exertion and often leads to chronic hypoxaemia and respiratory failure, increased hospital admission and premature death.
Gas exchange is impaired as airflow obstruction and alveolar destruction worsen, leading to various degrees of hypoxaemia and hypercapnia.
With worsening anaemia, the resulting hypoxaemia initially causes redistribution of blood flow to the brain and coronary arteries, but ultimately tissue hypoxia leads to metabolic acidosis and myocardial dysfunction, manifesting as right atrial enlargement and placentomegaly due to congestion, and later overt fetal hydrops and demise due to high-output cardiac failure.
Clinical signs of hypercapnia and hypoxaemia are simple to detect by an observant nurse.
A number of studies have now confirmed the association of COPD and peripheral neuropathy with hypoxaemia being a dominant etiopathogenic factor among others.
The included children comprised those with hypoxaemia, severe respiratory distress (respiration rate > 70 breaths/minute) and children with associated illnesses, such as ventricular septal defect (VSD), underlying pulmonary tuberculosis, heart failure, etc.