Respiratory Acidosis Respiratory acidosis is characterized by a

Respiratory Acidosis

Ø Respiratory acidosis is characterized by a primary rise in PCO 2 and is invariably due to alveolar hypoventilation. Ø CO 2 retention is invariably associated with hypoxemia and may even cause death before PCO 2 levels reach over 80 mm. Hg. Ø In acute respiratory acidosis, for every 10 mm. Hg increase in PCO 2, the bicarbonate will increase by 1 mmol/L. Ø In chronic respiratory acidosis, the renal mechanisms play a role and cause elevation of HCO 3 by 4 m. Eq/L for every 10 mm. Hg rise in PCO 2.

Causes of Respiratory Acidosis 1. Neurologic causes: a. Inhibition of respiratory center (central) General anesthesia Sedative overdose Head injury/cerebrovascular accident/tumours Encephalitis/brainstem lesions b. Neuromuscular causes: Spinal cord injury Poliomyelitis Multiple sclerosis Muscular dystrophy Guillain-Barré syndrome Status epilepticus Amyotrophic lateral sclerosis

2. Respiratory muscle paralysis: Tetanus, botulism Myasthenic crisis Periodic paralysis Diaphragmatic paralysis Myopathies Succinyl choline administration Organophosphorus poisoning

3. Upper and lower airway obstruction Obesity Sleep apnea Aspiration Laryngeal edema / vocal cord palsy Bronchoconstriction Emphysema Chronic interstitial lung disease Pleural thickening/ lung stiffening Thymoma/ aortic aneurysm

Clinical Features Ø Hypercarbia (CO 2 retention) and hypoxemia (low Pa. O 2) often coexist. Ø The usual symptoms include severe breathlessness, disorientation, confusion, tremor, myoclonus, headache, asterixis, incoherence and drowsiness. Ø Blurring of optic disc, papilledema and symptoms of increased intracranial pressure are due to vasodilatory effects of CO 2. Sometimes, injudicious administration of high flow O 2 may precipitate coma. Ø The vascular manifestations are due to vasodilatation. Ø Congestive cardiac failure and cardiac arrhythmias may occur. These patients may also develop salt and fluid retention.

Treatment Ø Hypoxemia is mainly responsible for the mortality. Ø Therefore, careful O 2 administration is the mainstay in the treatment. Injudicious O 2 administration may lead to worsening of hypoxemia due to suppression of respiratory drive particularly in patients with chronic obstructive airway disease. Ø In acute respiratory acidosis, the treatment principles include maintenance of airway, administration of oxygen and judicious use of antibiotics, bronchodilators and corticosteroids. Ø Noninvasive ventilation or intubation and mechanical ventilation may be used for more severe cases with p. H<7. 0 and PCO 2 > 80. Ø Bicarbonate administration may be necessary to bring the p. H to 7. 2.

Respiratory Alkalosis

Ø Respiratory alkalosis is characterised by a primary fall in PCO 2. Ø The rate of production of CO 2 in the body is relatively constant. Therefore, any fall in PCO 2 can only be due to alveolar hyperventilation. Ø It is a common acidbase disorder and occurs in normal pregnancy and at high altitude. Ø It also occurs in critically ill patients as a simple disorder or as a part of mixed disorder. Ø The primary fall in PCO 2 does not increase p. H to levels above 7. 55 and severe alkalemia is unlikely.

Causes of Respiratory Alkalosis A. CNS stimulation and hyperventilation Voluntary/psychogenic/ anxiety/pain Pregnancy Brainstem lesions Encephalitis Salicylate intoxication Sepsis Cirrhosis of liver.

B. Stimulation of intrathoracic receptors Pneumothorax, hemothorax, flail chest, pneumonia, asthma, pulmonary edema, pulmonary embolism, pulmonary fibrosis, acute respiratory distress syndrome. C. Stimulation of peripheral chemoreceptor High altitude hypoxemia, Hypotension, severe anemia, Drowning, aspiration, pneumonia. D. Drugs Respiratory stimulants (doxapram, nikethamide) Salicylates Nicotine Epinephrine/nor-epinephrine.

Clinical Features Ø The clinical features are variable and depends on the primary disorder, rate of onset and severity of the respiratory alkalosis. Ø The usual initial symptoms include tingling sensation in the extremities, and circumoral region, lightheadedness and confusion. Ø Later, muscle cramps, carpopedal spasm and brisk deep tendon reflexes may be noted. Ø Cardiac arrhythmias and seizures may also occur in severe cases. Ø The occurrence of symptomatic respiratory alkalosis or PCO 2< 2025 mm. Hg in critically ill patients suggests a grave prognosis.

Diagnosis and Treatment Ø The diagnosis can be established by the history, physical examination and laboratory data including ABG. Ø The treatment is directed towards the underlying cause. Ø Often, no treatment is required for mild respiratory alkalosis if it is not associated with symptoms.

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