APPROACH TO RESPIRATORY ACIDOSIS AND ALKALOSIS Prof.S.SHIVAKUMAR’S UNIT. K.VASANTH.M.D.P.G

This session will cover… Basic principles of CO 2 transport. Physiology of respiratory control. Aetiologies and management of Respiratory Acidosis. Aetiologies and management of Respiratory Alkalosis. Conclusion. 25 slides.

Clinical scenario 1 Miss.B, a 24 year old female had consumed 25 tablets of Pethidine and was brought to the Emergency department in a drowsy state with irregular shallow breathing pattern. Her ABG showed pH – 7.26 p CO 2 – 60 mmHg HCO 3 – 26 mEq / L p O 2 – 70 mmHg Values are consistent with Acute Respiratory acidosis.

Why was she normal before ? Determinants of CO 2 tension in body fluids CO 2 production CO 2 elimination CO 2 production Cellular metabolism produces mmol of volatile acid per day – CO 2 Non volatile acids – 100 mmol, excreted by kidneys Ratio – 150 : 1 This imbalance leads to immediate derangement in acid – base balance that follows pulmonary dysfunction.

CO 2 transport.. CO 2 loading at tissue level – pCO 2 46 mmHg CO 2 unloading at alveolar level – pCO 2 40 mmHg Haldane effect : At any given level of pCO 2 reduced blood displays enhanced capacity to transport CO 2 than oxygenated blood Transport forms of CO 2 HCO 3 – 82 % Carbamino compounds – 10 % Dissolved CO 2 – 8 %

C0 2 elimination PCO 2 gradient. Rate of alveolar ventilation. Alveolar perfusion.

What controls her alveolar ventilation? Medullary respiratory center Respiratory muscles Chest wall Airways Gas exchange system

How does it control ? Hypoxemia – through carotid bodies Hypercapnia – brain stem.powerful stimulus

What is respiratory acidosis ? It is an acid-base disorder initiated by an increase in CO 2 tension in body fluids. Characterised by elevation of pCO 2 more than 45 mm Hg at rest and at sea level. Caused almost always by reduction in effective alveolar ventilation. Always accompanied by hypoxemia.

What happens in CO 2 retention ? CO 2 + H 2 0 ↔ H 2 CO 3 ↔ H + HCO 3 - Decrease in pH Compensatory rise in [ Hco 3 ] acute – Hco 3 ↑ by 1 mmol / 10 mmhg ↑ in pCO 2 chronic – Hco 3 ↑by 3.5 mmol / 10 mmhg ↑ in pCO 2 Dilates cerebral vessels.

How does it manifest ? Acute - anxiety,dyspnea,confusion,psychosis leading to coma and death. Chronic – sleep disturbances,loss of memory,day time somnolence,tremors,myoclonic jerks,signs of raised ICT. - Respiratory centers become less sensitive to CO 2 and therefore the acidemic drive to ventilation. - Hypoxemia becomes the primary stimulus to respiration.

Aetiology ? Brain stem – drugs,stroke, infection. Respiratory muscles – GBS,MS,Myasthenia,snake bite,OPC poisoning Chest wall – kyphoscoliosis, AS, obesity Airways – COPD, acute severe asthma Gas exchange system – ARDS, ILD Mechanical ventilation

How to diagnose ? ABG – pH,pCO 2 and HCO 3. Detailed history and complete physical examination. Pulmonary function tests. Imaging. Toxicological analysis.

How to manage ? Acute Ensure patent airway PO 2 7.1, pCO 2 < 60 and an alert patient - administer O 2 via nasal mask - correct reversible causes – antibiotics, bronchodilators and steroids Monitor Consider mechanical ventilation if pO 2 60

Cont… Obtunded patient pO 2 < 60 pH < 7.1 pCO 2 > 60 Consider endotracheal intubation and mechanical ventilation. Provide sufficient chloride and potassium to enhance renal excretion of HCO 3

Chronic respiratory acidosis Alert patient and vitals stable PO 2 < 55 PO 2 < with P pulmonale PO 2 < 60 with cardiac arrhythmias Administer nasal O 2 Correct reversible causes

Cont… PO 2 < 55, worsening hypercapnia, vitals stable - Consider NIPPV PO 2 < 55 with vitals unstable - Proceed to mechanical ventilation.

Our patient ? Assess airway Assess vitals Samples for toxicological analysis Endo tracheal intubation and mechanical ventilation Opioid antagonists

Clinical scenario 2 Miss.C a 20 year old female,a known case of Anxiety disorder developed sudden dyspnea,tightness of chest and was brought to the ED.she was tachypneic and had carpopedal spasm.Her ABG showed pH – 7.51 pCO 2 – 22 mmHg HCO 3 – 20 mmHg Values are consistent with acute respiratory alkalosis.

What is respiratory alkalosis ? It is an acid base disturbance initiated by a reduction in CO 2 tension of body fluids. Characterised by pCO 2 < 35 mmHg determined at rest and at sea level. It is the most common acid base disorder in critically ill patients. Many cardio-pulmonary disorders manifest as R.A. and the finding of normocapnia with hypoxemia in a hyperventilating patient may herald the onset of rapid respiratory failure.

What are the adverse effects ? Decreased pCO 2 Decreased [ H ] Decreased reabsorption of HCO 3 Intracellular shift of Na,k,PO4 Reduced free [Ca ] Compensation Acute – HCO 3 ↓ by 2 mmol / 10 mm hg ↓ pCO 2 Chronic – HCO 3 ↓ by 5 mmol / 10 mm hg ↓pCO 2 Significant reduction in cerebral blood flow.

Clinical manifestations ? Acute dizziness, mental confusion, cardiac arrhythmias paresthesias tetany seizures Chronic – usually asymptomatic

What are the causes ? Alveolar hyperventilation. Stimulation of ventilatory apparatus. CNS-pain,meningo-encephalitis, CVA, tumour, fever drugs – progesterone, salicylate poisoning, methyl xanthines Lungs ( hypoxemia ) – acute pulmonary edema,pulmonary embolism,high altitude,pneumonia Miscellaneous – sepsis, mechanical ventilation,pregnancy,hyper-ventilation syndrome

How to diagnose ? Measurement of arterial pH and pCO 2 Serum electrolytes – Na,K, Ca Cause should be investigated.

How to manage ? Acute - Alleviation of the underlying disorder - pH > 7.55 and vitals stable rebreathing into a closed bag. - pH > 7.55 and pCO 2 < 20 mm hg, vitals unstable consider skeletal muscle paralysis with mechanical ventilation Chronic – treatment of the underlying disorder

Our patient ? Reassurance Rebreathing from a paper bag β – blockers Attention to underlying psychological stress.

Conclusion.. Respiratory acid – base disorders are common in clinical practice. Respiratory acidosis is almost always due to alveolar hypoventilation. Always search for reversible causes like poisoning, infection and broncho constriction before invading the patient. Respiratory alkalosis is the most common acid base disorder in critically ill patients. Presence of normocapnia with hypoxemia in a hyper ventilating patient may herald the onset of rapidly developing respiratory failure.