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Arterial blood gases and oximetry The measurement of hydrogen ion concentration (pH), PaO2 and PaCO2, and bicarbonate concentration in an arterial blood sample is essential in assessing the degree and type of respiratory failure and for measuring acid–base status The pH of the arterial plasma is normally 7.40 Corresponds to a H+ concentration of 40 nmol/L An increase in H+ concentration corresponds to a decrease in pH pH is under tight homeostatic regulation, so that the it does not vary outside the range of 7.44–7.36 under normal circumstances To preserve function of many pH-sensitive enzymes A variety of physiological mechanisms maintain the pH of the ECF The first is the action of blood and tissue buffers, of which the most important involves reaction of H+ ions with bicarbonate to form carbonic acid, which, under the influence of the enzyme carbonic anhydrase dissociates to form CO2 and water CO2+ H2O --H2CO3 --H+ HCO3− This buffer system is important because bicarbonate is present in relatively high concentration in the ECF (21–28 mmol/L) Two of its key components are under physiological control: the CO2 by the lungs, and the bicarbonate by the kidneys Respiratory compensation for acid–base disturbances occurs quickly In response to acid accumulation, pH changes in the brain stem stimulate ventilatory drive, serving to reduce the PCO2 and hence drive up the pH Systemic alkalosis leads to inhibition of ventilation The kidney also provides of defence against disturbances of arterial pH When acid accumulates due to chronic respiratory or metabolic (non-renal) causes, the kidney has the long-term capacity to enhance urinary excretion of acid, & increase the plasma bicarbonate Respiratory acidosis Respiratory acidosis can be due to severe pulmonary disease, respiratory muscle fatigue, or abnormalities in ventilatory control and is recognized by an increase in Paco2 and decrease in pH In acute respiratory acidosis, there is an immediate compensatory elevation (due to cellular buffering mechanisms) in HCO3–, which increases 1 mmol/L for every 10mmHg increase in Paco2 In chronic respiratory acidosis (>24 h), renal adaptation increases the [HCO3–] by 4 mmol/L for every 10-mmHg increase in Paco2. Clinical features Vary according to the severity and duration of the respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia A rapid increase in Paco2 may cause anxiety, dyspnea, confusion, psychosis, and hallucinations and may progress to coma Acute hypercapnia follows sudden occlusion of the upper airway or generalized bronchospasm as in severe asthma, anaphylaxis, inhalational burn, or toxin injury Chronic hypercapnia and respiratory acidosis occur in end-stage obstructive lung disease Restrictive disorders involving both the chest wall and the lungs can cause respiratory acidosis because the high metabolic cost of respiration causes ventilatory muscle fatigue Treatment The management of respiratory acidosis depends on its severity and rate of onset Acute respiratory acidosis can be lifethreatening, and measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation This may include tracheal intubation and assisted mechanical ventilation Oxygen administration should be titrated carefully in patients with severe obstructive pulmonary disease and chronic CO2 retention who are breathing spontaneously The Paco2 should be lowered gradually in chronic respiratory acidosis, aiming to restore the Paco2 to baseline levels To provide sufficient Cl– and K+ to enhance the renal excretion of HCO3– Chronic respiratory acidosis is frequently difficult to correct RESPIRATORY ALKALOSIS Characterized by a primary decrease in Pco2 an increased arterial pH and decreased plasma bicarbonate concentration It is most commonly the result of alveolar hyperventilation rather than underproduction of CO2 Causes Hypoxemia, due to pulmonary disease, congestive heart failure, and high-altitude living, or anemia Mechanical ventilation Primary stimulation of the central chemoreceptor as seen in Endotoxemia Hepatic cirrhosis Salicylate intoxication Correction of metabolic acidosis Hyperthermia Pregnancy Cortical hyperventilation from anxiety and pain Clinical Manifestations Symptoms of acute hypocapnia are largely attributable to the alkalemia and include dizziness, perioral or extremity paresthesias, confusion, asterixis, hypotension, seizures, and coma Symptoms are due to decreased cerebral blood flow or reduced free calcium (because alkalosis increases calcium's protein-bound fraction) Treatment Address the underlying cause of the disturbance Patients who exhibit symptoms, such as tetany and syncope, and do not have more serious causes of hyperventilation can be treated with a rebreathing mask Respiratory failure The term respiratory failure is used when pulmonary gas exchange fails to maintain normal arterial oxygen and carbon dioxide levels Its classification into types I and II relates to the absence or presence of hypercapnia (raised PaCO2) Pathophysiology When disease impairs ventilation of part of a lung (pneumonia), perfusion of that underventilated region results in hypoxic and CO2-laden blood entering the pulmonary veins Increased ventilation of neighbouring regions of normal lung can increase their CO2 excretion, correcting arterial CO2 to normal, but cannot augment their oxygen uptake because the haemoglobin flowing through these normal regions is already fully saturated Causes of Hypoxic ARF(type I) Acute lung injury/ARDS Pneumonia Pulmonary thromboembolism Acute lobar atelectasis Cardiogenic pulmonary edema Causes of Hypercapnic-Hypoxic ARF (type II ) Pulmonary disease COPD Asthma: advanced acute severe asthma Drugs causing respiratory depression Neuromuscular Guillain-Barré syndrome Acute myasthenia gravis Spinal cord tumors Musculoskeletal Kyphoscoliosis