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Respiratory acidosis treatment

As with the treatment of metabolic acidosis, the role of NaHC03 therapy is not well defined for respiratory acidosis. Realize that administration of NaHC03 can paradoxically result in increased C02 generation (HC03 + H+ —> H2C03 —> H20 + C02) and worsened acidemia. Careful monitoring of the pH is required if NaHC03 therapy is started for this indication. The use of THAM in respiratory acidosis (see metabolic acidosis, above) has unproven safety and benefit. [Pg.428]

The goals of therapy in patients with chronic respiratory acidosis are to maintain oxygenation and to improve alveolar ventilation if possible. Because of the presence of renal compensation it is usually not necessary to treat the pH, even in patients with severe hypercapnia. Although the specific treatment varies with the underlying disease, excessive oxygen and sedatives should be avoided, as they can worsen C02 retention. [Pg.428]

It is imperative to identify serious causes of respiratory alkalosis and institute effective treatment. In spontaneously breathing patients, respiratory alkalosis is typically only mild or moderate in severity and no specific therapy is indicated. Severe alkalosis generally represents respiratory acidosis imposed on metabolic alkalosis and may improve with sedation. Patients receiving mechanical ventilation are treated with reduced minute ventilation achieved by decreasing the respiratory rate and/or tidal volume. If the alkalosis persists in the ventilated patient, high-level sedation or paralysis is effective. [Pg.429]

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. [Pg.860]

In metabolic alkalosis and respiratory acidosis, pH does not usually deviate significantly from normal, but treatment can be required to maintain Pao2 and PaC02 at acceptable levels. Treatment should be aimed at decreasing plasma bicarbonate with sodium and potassium chloride therapy, allowing renal excretion of retained bicarbonate from diuretic-induced metabolic alkalosis. [Pg.861]

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. [Pg.67]

While the fall in serum bicarbonate is asymptomatic in most cases, special caution is required in patients already at risk of metabolic acidosis, such as those with respiratory acidosis, renal disease, frequent severe infections and sepsis, gastrointestinal disorders with recurrent dehydration, inborn errors of metabolism, or treatment with a ketogenic diet (44). [Pg.3451]

The treatment of respiratory acidosis is dependent on the chronicity of the patient s condition. Respiratory decompensation in patients with chronic elevations in PaC02 are frequently seen in those with acute infections and those recently started on narcotic analgesics or oxygen therapy. Aggressive treatment of these conditions can offer considerable benefit and should be initiated. Furthermore, tranquilizers and sedatives should be avoided and supplemental oxygen, if used, should be minimized. [Pg.999]

As a result of the shift, the concentration of carbonic acid in the blood increases, the HCO3 /H2CO3 ratio deCTeases to less than 20 1, and respiratory acidosis sets in. The treatment of respiratory acidosis involves identifying the underlying causes and possibly the intravenous administration of isotonic sodium bicarbonate solution or hemodialysis. [Pg.485]

In cases of acidosis in which correction of the underlying respiratory or metabolic cause will be delayed or prolonged, treatment with infusions of bases such as sodium bicarbonate may be used temporarily. Care should be taken not to overtreat the pH, particularly in respiratory acidosis, because the body s actions to correct the problem in combination with infusion of base can result in a metabolic alkalosis and related complications. [Pg.171]

Chronic pulmonary failure may be further complicated by metabolic disturbances tending to metabolic alkalosis or metabolic acidosis. The mechanism leading to alkalosis is not always clear, but among the factors that may influence it are the loss of hydrogen and Cl ions, because of vomiting or because of selective Cl and potassium depletion as a result of undernourishment, and prolonged treatment with diuretics. It is usually assumed that severe respiratory acidosis is always accompanied by metabolic acidosis. This reasoning is based on the fact that when the same CO2 tensions are achieved in the blood in vivo and in vitro,the plasma concentration of bicarbonate for identical pH s is lower in vivo than in vitro. In reality, this bicarbonate deficit seems to result because (I) the buffer curve of the blood CO2 has a lower slope in vivo than in vitro and (2) hyperventilation in vivo leads to lactic acid accumulation in he blood. [Pg.581]

Figure 6 - Continuous muscle pH data recorded every 5 minutes during treatment of respiratory acidosis in a newborn infant weighing 3.3 kg. (Patient C. H.) with left Bochdalek diaphragmatic hernia. Muscle pH monitoring was started at 2 30 p.m., 2 hours following completion of the operative repair when blood gas data confirmed that the patient had a severe respiratory acidosis (blood pH, 6.78 and PCO2, 160 mm. Hg.). The baby was treated with a ventilator (60 percent oxygen) and muscle pH responded appropriately as confirmed by sampling of central venous blood every 60 to 90 minutes. Figure 6 - Continuous muscle pH data recorded every 5 minutes during treatment of respiratory acidosis in a newborn infant weighing 3.3 kg. (Patient C. H.) with left Bochdalek diaphragmatic hernia. Muscle pH monitoring was started at 2 30 p.m., 2 hours following completion of the operative repair when blood gas data confirmed that the patient had a severe respiratory acidosis (blood pH, 6.78 and PCO2, 160 mm. Hg.). The baby was treated with a ventilator (60 percent oxygen) and muscle pH responded appropriately as confirmed by sampling of central venous blood every 60 to 90 minutes.
The respiratory therapist and physician would be interested in the patient s respiratory acidosis, which is the excess CO resulting from inadequate alveolar ventilation. Respiratory alkalosis is a deficit of COj resulting from alveolar hypersensitivity. The area we will examine is the use of the spirometer and the accompanying charts for comparison. The medical terminology of inhalation therapy is more directed to pulmonary disease treatment, which one is attempting to prevent with the use of respirators. It should be noted that once the worker or person impairs his lungs, modem medicine cannot reinstate previous capacity. At best, present technology can only ease the pain. [Pg.80]

Acidosis occurs when the pH of blood falls below about 7.35. In respiratory acidosis, impaired respiration increases the concentration of dissolved CO2 and lowers the blood s pH. The condition is common in victims of smoke inhalation and patients with asthma, pneumonia, and emphysema. The most efficient treatment consists of placing the patient in a ventilator. Metabolic acidosis is caused by the release of large amounts of lactic acid or other acidic by-products of metabolism (Case study 43), which react with bicarbonate ion to form carbonic acid, thus lowering the blood s pH. The condition is common in patients with diabetes and severe burns. [Pg.173]

Furthermore, pH determination has been used in other clinical research, both alone and in combination with other measurements. This research includes studies into the relationship between extracellular and intracellular pH in an ischemic heart [6, 7], the pH of airway lining fluid in respiratory disease [8], the study of pH as a marker for pyloric stenosis [9], malnutrition in alkalotic peritoneal dialysis patients [10], pH modulation of heterosexual HIV transmission [11, 12], and wound prevention and treatment [13], In addition, pH changes due to blood acidosis have been used to trigger and pace the ventricular rate of an implanted cardiac pacemaker [14], Research using pH measurements... [Pg.285]

Treatment of mixed metabolic acidosis and respiratory alkalosis should be directed at the underlying cause. [Pg.861]


See other pages where Respiratory acidosis treatment is mentioned: [Pg.296]    [Pg.562]    [Pg.102]    [Pg.79]    [Pg.80]    [Pg.999]    [Pg.999]    [Pg.1000]    [Pg.333]    [Pg.259]    [Pg.266]    [Pg.171]    [Pg.642]    [Pg.369]    [Pg.278]    [Pg.269]    [Pg.385]   
See also in sourсe #XX -- [ Pg.428 ]

See also in sourсe #XX -- [ Pg.999 ]




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