Resp Care
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Tracheotomy has been used to assist in weaning patients from mechanical ventilation. Some patients fail to be weaned from the ventilator despite tracheostomy. We hypothesized that removing the inner cannula from the tracheostomy tube would decrease the tube's imposed work of breathing (WOB(IMP)). ⋯ There was a significant decrease in WOB(IMP) with each tube when the inner cannula was removed. WOB(IMP) increased with an increase in inspiratory flow demand (ie, increase in V(T) and/or frequency), as well as when tube size decreased. In weaning a tracheostomized patient from mechanical ventilation, increasing the internal diameter of the tube by removing the inner cannula may be beneficial. Further study is needed to determine if these findings are clinically important.
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Acid-base homeostasis involves chemical and physiologic processes responsible for the maintenance of the acidity of body fluids at levels that allow optimal function of the whole individual. The chemical processes represent the first line of defense to an acid or alkali load and include the extracellular and intracellular buffers, whereas the physiologic processes modulate acid-base composition by changes in cellular metabolism and by adaptive responses in the excretion of volatile acids by the lungs and fixed acids by the kidneys. The need for the existence of multiple mechanisms involved in acid-base regulation stems from the critical importance of the hydrogen ion (H+) concentration on the operation of many cellular enzymes and function of vital organs, most prominently the brain and the heart. ⋯ We review the determinants of the acidity of body fluids, the mechanisms that maintain normal acid-base composition, and the overall defense to disruption in acid-base equilibrium. Specific topics include an examination of the scales of acidity, buffer systems, intracellular acid-base regulation, excretion of acids, alkali and acid loading, and normal acid-base composition. The limitations of arterial blood sampling in the assessment of acid-base status are also evaluated.
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Respiratory acidosis, or primary hypercapnia, is the acid-base disorder that results from an increase in arterial partial pressure of carbon dioxide. Acute respiratory acidosis occurs with acute (Type II) respiratory failure, which can result from any sudden respiratory parenchymal (eg, pulmonary edema), airways (eg, chronic obstructive pulmonary disease or asthma), pleural, chest wall, neuromuscular (eg, spinal cord injury), or central nervous system event (eg, drug overdose). ⋯ Although the symptoms, signs, and physiologic consequences of respiratory acidosis are numerous, the principal effects are on the central nervous and cardiovascular systems. Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology.
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Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation, mainly in the proximal tubule, and bicarbonate generation, predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na(+)-H(+) antiporter and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase). ⋯ The effects of metabolic alkalosis on the body are variable and include effects on the central nervous system, myocardium, skeletal muscle, and liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.