Chronic obstructive pulmonary disease (COPD) significantly reduces quality of life and is one of the main causes of chronic morbidity and mortality worldwide. Acute exacerbation of COPD (AECOPD) is a life-threatening condition that causes rapid deterioration of respiratory symptoms (worsening of dyspnea, cough and/or abundant sputum production) requiring urgent treatment. This review article examines the evidence underlying supplemental oxygen therapy and ventilator support during exacerbations of COPD. In the introduction, we discuss the epidemiology and pathophysiology of hypercapnic respiratory failure, and then we explain that the key to achieving appropriate levels of oxygenation is using controlled low-flow oxygen therapy. In patients with risk of hypercapnia a target oxygen saturation (SaO ) range of 88%–92% 2 is now generally accepted unless hypercapnia is disproved by gas analysis of arterial blood. However, if the partial pressure of carbon dioxide in arterial blood (PaCO ) is normal, oxygen therapy may target the usual saturation range of 94%–98%. 2 Many COPD patients may have a lower stable SaO , such that chasing this target (94%-98%) is not usually necessary unless 2 the patient is unwell. Further, we review current recommendations for ventilatory support in patients with AEHOBP. Noninvasive ventilation has assumed an important role in managing patients with acute respiratory failure. The use of invasive ventilation is the last remaining option, associated with a poor outcome.

Scientific research of effects of glucagon on the cardiovascular system have shown that glucagon has some
cardiostimulatory potential. The very interesting fact is that glucagon shows its cardiostimulatory effects by activating its
own, higly specific glucagonic receptors. That is way we wanted to research not only the effects of glucagon on the C.V.S.
but also its effects during the depression of the C.V.S. with high dosses of beta blocators (presolol) expecting a good
hemodinamic response. The experiment has been performed on two groups of 6 dogs. The first group of animal was treated
with i.v. bolus injections of glucagon and other group with presolol (15 mg/kg b.w.) i.v., and after that with i.v. bolus
injection of glucagon. Hemodinamic variables (mean arterial pressure, central venal pressure and hearth frequency) were
registred at the 1-st, 2-nd, 3-rd, 10-th, 20-th, 30-th and 40-th minute. The hearth frequency was registred by continous
monitoring, mean arterial pressure was registred with cateter in the arterial femoralis, while the central venal pressure was
registred over central venal cateter in v. femoralis. After the i.v. bolus injection glukagon shows higly positive effects,
followed by short-term increase of the mean arterial pressure, while the c.v.p. considerably falls. During the administration
of presolol the hearth frequency and mean arterial pressure fall considerably and progressively, while the c.v.p. rises
considerably. Glucagon, in conditions of c.v.s. depresion by high doses of presolol (15 mg /kg b.w.) considerably increases
hearth frequency and mean arterial pressure, while the c.v.p. falls considerably.