Hypoventilation acute

In order to effectively treat respiratory acidosis, the causative process must be identified and treated. If a cause is identified, specific therapy should be started. This may include naloxone for opiate-induced hypoventilation or bronchodilator therapy for acute bronchospasm. Because respiratory acidosis represents ventilatory failure, an increase in... 

High concentration oxygen therapy is reserved for a state of low PaOj in association with a normal or low PaCO (type I respiratory failure), as in pulmonary embolism, pneumonia, pulmonary oedema, myocardial infarction, and young patients with acute severe asthma. Concentrations of up to 100% may be used for short periods, since there is little risk of inducing hypoventilation and CO retention. 

In theory, there are three causes for the occurrence of HPS (since hypoventilation is not deemed a possible cause) (1.) arteriovenous shunts, (2.) disturbed alveolo-capillary oxygen diffusion in terms of impaired diffusion-perfusion, and (3.) mismatches between ventilation and perfusion. Consequently, there are numerous liver diseases which are associated with HPS. Transient HPS in acute viral hepatitis A and B has recently been reported. (17, 38) (s. tab. 18.1)... 

Respiratory acidosis may be acute or chronic. Acute conditions occur within minutes or htnirs. They are uncompensated. Renal compensation has no time to develop as the mechanisms which adjust bicarbonate reabsorption take 48-72 h to become fully effective. The primary problem in acute respiratory acidosis is alveohir hypoventilation. If airflow is completely or partially reduced, the PCO, in the bltHtd will rise immediately and the H ) will rise quickly (Fig. 2). A resulting low PO, and high PCO. causes coma. If this is not reliev ed rapidly, death results. 

If acute hypercapnia does not constitute a threat to normal individuals with good blood circulation and normal renal function, in a surgical patient in shock with reduced renal blood flow, hypoventilation may mean death as a result of rapidly worsening acidosis. When blood pH falls to low values, the neuromuscular impulses that control heart beats are distorted, and ventricular fibrillation may develop. 

This nomenclature is now applied to the sequence of events in hypoventilation. Within half an hour, the subject moves to a point which is described as acute or uncompensated respiratory acidosis . There is acidaemia. Over the course of the ensuing days, renal compensation occurs and the patient s blood is represented by a point which is described as compensated respiratory... 

Respiratory acidosis Hypoventilation of acute onset results in a change of blood biochemistry (along the normal, to a different) blood line, as shown by arrow. .. In the resultant uncompensated respiratory acidosis the alveolar PCO2 is... 

Chloride, Cl 100-106 hyperchloremia (anemia heart conditions dehydration) hypochloremia (acute infection burns hypoventilation)... 

Hypercapnic respiratory failure is due to failure of the ventilatory pump caused by acute (drug overdose, acute neuromuscular diseases) or chronic (chest wall abnormalities, chronic neuromuscular diseases) disorders. It is characterized by alveolar hypoventilation, which leads to hypercapnia with coexistent, usually mild, hypoxemia. The central drive may be globally reduced with the fall in Pa02 resulting from the increase in alveolar CO2. More commonly, the drive remains high, but the mechanical load on the respiratory systan is too great or the capacity of the muscles too low to ensure efficient CO2 elimination (Fig. 1). 

The respiratory patient evaluation includes a survey for symptoms of chronic and/or acute alveolar hypoventilation, medical history, physical examination, cough evaluation, and simple pulmonary function tests. Measurement of mucous transport through the bronchial tree by radiolabeled tracers is a technique that has been used above all to study mucociliary clearance, as well as the measurement of the volume of expectorated mucous (32). 

The hypoventilation situation can vary depending on a patient s medical history (COPD, asthma, CF, NMD) and the phase in which the patient s condition is evaluated. At the positive end of the continuum will be patients who consider their cough to be satisfactory and productive. At the negative end will be those who are unable to generate even minimal coughing, either in cases of acute bronchial disease or after minor aspirations of food fragments. This situation of loss of control is evident both for patients and for those around them and should be considered a potential emergency (4,8,9,12). 

Figure 6 Ventilatory management in OHS and ARF. Abbreviations OHS, obesity hypoventilation syndrome ARF, acute respiratory failure. Source From Ref. 47.

Ventilatory impairment results from inspiratory muscle weakness, central hypoventilation, thoracic restriction, upper airway narrowing, extreme obesity, abdominal distension, and improperly fitting thoracolumbar orthoses. In NMD, pulmonary infiltrates and respiratory failure are precipitated by mucus plugging due to an ineffective secretion clearance, especially during acute respiratory infections (2,7). 

Many patients with NMD develop CO2 narcosis with supplemental oxygen. Hypoventilation is often first recognized during a respiratory infection when bronchial mucus plugging triggers acute respiratory failure. Ventilatory failure can also develop suddenly or over a period of hours or days in patients with acute cervical myelopathies, Guillain-Barre syndrome, myasthenia gravis, acute poliomyelitis, or exacerbations of multiple sclerosis. 

In a recent study, 25 patients with ALS became dependent on NIPPV, including 13 who became continuously dependent for 19.7 16.9 months without developing acute respiratory distress or oxyhemoglobin desaturation. For another 76 patients, the daytime Sa02 baseline persistently decreased to <95%, 78 times because of some combination of alveolar hypoventilation and airway congestion. For 41 patients, the baseline was corrected by some combination of NIPPV and MAC for 11.1 8.7 months before desaturation recurred in 27. Of the latter, 11 underwent tracheostomy, 14 died in less than two months, and two were again corrected by the addition of MAC to NIPPV. Thirty-three of the 35 patients for whom the Sac>2 could not be normalized required tracheostomy or died within two months. The difference between the patients who could be spared respiratory... 

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