Hypoxemia chronic

In advanced COPD, caution should be used since overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. In these patients, mild hypoxemia, rather than carbon dioxide accumulation, triggers their drive to breathe. 

Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI) other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm). 

In a patient with chronic respiratory acidosis (e.g., chronic obstructive pulmonary disease), treatment is essentially similar to that for acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia. 

Significant changes in arterial blood gases are not usually present until the FEV is less than 1 L. At this stage, hypoxemia and hypercapnia may become chronic problems. Hypoxemia usually occurs initially with exercise but develops at rest as the disease progresses. 

Some patients lose the ability to increase the rate or depth or respiration in response to persistent hypoxemia. This decreased ventilatory drive may be due to abnormal peripheral or central respiratory receptor responses. This relative hypoventilation leads to hypercapnia in this situation the central respiratory response to a chronically increased PaC02 can be blunted. Because these changes in Pa02 and PaC02 are subtle and progress over many years, the pH is usually near normal because the kidneys compensate by retaining bicarbonate. 

In conditions that lead to chronic hypoxemia, such as smoking and chronic obstructive pulmonary disease, an increased concentration of BPG In the RBCs promotes O2 dissociation from hemoglobin in tissues to support cellular function. 

R, Brouet, J.C., Adnot, S., Akoun, G.M. Severe hypoxemia-associated intrapulmonary shunt in a patient with chronic liver disease improvement after medical treatment. Amer. Rev. Resp. Dis. 1992 146 526—527... 

Almitrine is a respiratory stimulant that improves hypoxemia in about 80% of patients with severe chronic obstructive pulmonary disease (SEDA-17, 212). Oral almitrine bimesilate (100 mg/day) increased Pa02 in patients with severe chronic obstructive pulmonary disease without altering mean pulmonary artery pressure (1). Adverse effects were rarely observed and it was concluded that long-term treatment was safe. In other studies, respiratory, digestive, and neurological symptoms have been noted but were often pre-existent (2,3). 

Chronic bronchitis is a persistent inflammation of the bronchi because of excess mucous production that irritates the bronchial and results in a persistent productive cough. Smoking is a common cause of chronic bronchitis and is aggravated by air pollution, infection, and allergies. Patients with chronic bronchitis have rhonchi (a gurgling sound) on inspiration and expiration, caused by airway blockage from excess mucus. This excess results in hypercapnia (buildup of carbon dioxide in the blood) and hypoxemia (decreased oxygen in the blood). The patient experiences respiratory acidosis. 

The consequences of long-standing COPD and chronic hypoxemia include the development of secondary pulmonary hypertension that progresses slowly if appropriate treatment of COPD is not initiated. Pulmonary hypertension is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. ... 

The elevated pulmonary artery pressures are attributed to vasoconstriction (in response to chronic hypoxemia), vascular remodeling, and loss of pulmonary capillary beds. If elevated pulmonary pressures are sustained, cor pulmonale can develop, characterized by hypertrophy of the right ventricle in response to increases in pulmonary vascular resistance. 

The use of supplemental oxygen therapy increases survival in COPD patients with chronic hypoxemia. Although long-term... 

Respiratory acidosis may produce neuromuscular symptoms, including altered mental status, abnormal behavior, seizures, stupor, and coma. Hypercapnia may mimic stroke or CNS tumors by producing headache, papilledema, focal paresis, and abnormal reflexes. Carbon dioxide acts as a vasodilator in the brain, thus causing an increase in cerebral blood flow. This increase in cerebral blood flow is thought to be partially responsible for the CNS symptoms. The CNS response to hypercapnia is extremely variable between patients and is also influenced by the acuity of presentation. Chronic hypercapnia blunts the usual respiratory stimulus resulting from increased PaC02. In patients with severe chronic respiratory acidosis, hypoxemia rather than hypercapnia provides the primary ventilatory stimulus. ... 

Patients with a history of chronic respiratory acidosis (e.g., those with chronic obstructive pulmonary disease) may experience an acute worsening of their respiratory acidosis. This may result in severe life-threatening hypoxemia. As with acute respiratory acidosis, the goals... 

Another study has shown a significant association between the severity of pulmonary inflammation/fibrosis induced by IP, as well as other particulate compounds including nickel oxide, nickel subsulfide, cobalt sulfate, and talc, and increased incidences of adrenal pheochromocytoma in rats (Ozaki et al. 2002). The systemic hypoxemia and reduced gas exchange induced by chronic pulmonary lesions from IP exposures may result from stimulated catecholamine secretion from the adrenal medulla and this chronic endocrine hyperactivity may lead to hyperplasia and neoplasia of the adrenal gland. 

Nitroprusside can worsen hypoxemia in patients with chronic obstructive pulmonary disease because the drug interferes with hypoxic pulmonary vasoconstriction and thereby promotes ventilation/perfusion mismatch. 

Although the reversibility of airways obstruction is an important characteristic of asthma, those asthmatics with chronic symptoms do not reverse completely. The chronic airways obstruction is probably related to mucus plugging of bronchi and hypertrophy of the bronchial smooth muscle. These changes are not reversible by bronchodilators, and it is not clear that they can be reversed with any specific therapy. Both types of obstruction contribute to an imbalance of the ventilation to perfusion ratio in the lung and can result in hypoxemia and hypocarbia. The decreased carbon dioxide content of the blood is the result of the asthmatic s hyperventilation and will persist until the respiratory muscles fatigue and hypoventilation becomes prominent. Asthmatics can die quite quickly when this occurs. 

B. Low-level chronic exposure may produce dyspnea, wheezing, and other signs and symptoms consistent with asthma. Interstitial lung injury, with radiographic infiltrates and hypoxemia, may occur less commonly. 

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