Respiratory acidosis and alkalosis

Acid base disorders related to the respiratory system.Blood gas analysis and the renal compensation that happens in respiratory acid base disorders.

1. Respiratory acidosis and alkalosis Presented by: Dr Anwar H Siddiqui Ph.D. Scholar Department of Physiology, J N Medical College, AMU, Aligarh

2. The body and pH.

3. Buffer System Provide or remove H + and stabilize the pH. Include weak acids that can donate H + and weak bases that can absorb H + . Change in pH, after addition of acid, is less than it would be in the absence of buffer .

4. Buffer System

5. Acid base disorder An  acid base disorder  is a change in the normal value of extracellular pH that may result when renal or respiratory function is abnormal or when an acid or base load overwhelms excretory capacity.   Normal acid base values pH pCO2 HCO 3 - Range 7.35- 7.45 36-44 22-26 Optimal Value 7.4 40 24

6. Acid base disorder Clinical disturbances of acid base metabolism classically are defined in terms of the  HCO3-  /CO2  buffer system. Acidosis –  process that increases [H+] by increasing PCO2 or by reducing [ HCO3-] decrease in the blood pH below normal range Alkalosis –  process that reduces [H+] by reducing PCO2 or by increasing [HCO3- ]   Elevation in blood pH above the normal range

7. Respiratory Acid base disorder Respiratory acid-base disorders are those abnormalities in acid-base equilibrium initiated by a change in the arterial carbon dioxide tension (PaCO 2 )--the respiratory determinant of acidity in the following equation : Henderson Hasselbalch equation:   pH = 6.1 + log [HCO3-]/ 0.03 PCO2 Kassirer-Bleich equation:    [ H+] = 24 × PCO2 / [HCO3- ] (Remember this formula !!!!!)

8. Respiratory Acid base disorder There are two respiratory acid-base disorders: respiratory acidosis and respiratory alkalosis.

9. Respiratory Acidosis Respiratory acidosis is the acid-base disturbance initiated by an increase in PaCO 2 . The level of PaCO 2 is determined by the rate of carbon dioxide production (VCO 2 ) and the rate of alveolar ventilation (VA), as follows: PaCO 2 = K x VCO 2 / VA where K is a constant. An increase in arterial pCO 2 can occur by one of three possible mechanisms: Presence of excess CO 2 in the inspired gas Decreased alveolar ventilation Increased production of CO 2 by the body

10. Respiratory Acidosis Overproduction of carbon dioxide is usually matched by increased excretion (due to increased alveolar ventilation) M ost cases of respiratory acidosis reflect a decrease in alveolar ventilation. Alveolar hypoventilation leads to an increased PaCO 2  ( ie , hypercapnia ). The increase in PaCO 2 , in turn, decreases the bicarbonate (HCO 3 – )/PaCO 2  ratio, thereby decreasing the pH.

11. Respiratory Acidosis

12. Respiratory Acidosis In acute respiratory acidosis , the Pa CO 2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis , the Pa CO 2 is elevated above the upper limit of the reference range, with a normal or near-normal blood pH secondary to renal compensation and an elevated serum bicarbonate (HCO 3 − >30 mm Hg ). The expected change in pH with respiratory acidosis can be estimated with the following equations: Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO   2 ) Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO   2 )

13. Aetiology Acute Respiratory Acidosis NORMAL AIRWAY AND LUNGS ABNORMAL AIRWAY AND LUNGS Central nervous system depression GA/ Sedative overdose Head trauma/ Cerebrovascular accident Cerebral edema Brain tumor/Encephalitis Upper airway obstruction Coma induced hypopharyngeal obstruction Aspiration of foreign body or vomitus Laryngospasm or angioedema Obstructive sleep apnea Neuromuscular impairment High spinal cord injury, Guillain-Barre syndrome Status epilepticus , Botulism, tetanus Crisis in myathenia gravis Hypokalemic myopathy Drugs or toxic agents (curare, succinylcholine , aminoglycosides , organophosphates) Lower airway obstruction Generalized bronchospasm Severe asthma Bronchiolitis of infants and adults Ventilatory restriction Rib fractures with flail chest Pneumothorax, Hemothorax Impaired diaphragmatic function Disorders involving pulmonary alveoli Severe bilateral pneumonia Acute respiratory distress syndrome Severe pulmonary edema Iatrogenic events Misplacement of airway cannula during mechanical ventilation Bronchoscopy associated respiratory arrest Increased CO2 production with constant mechanical Ventilation Pulmonary perfusion defect Cardiac arrest, Severe circulatory failure Massive pulmonary thromboembolism, Fat or air embolus

14. Aetiology Chronic Respiratory Acidosis NORMAL AIRWAY AND LUNGS ABNORMAL AIRWAY AND LUNGS Central nervous system depression Sedative overdose Methadone/heroin addiction Primary alveolar hypoventilation Obesity-hypoventilation syndrome Brain tumor Bulbar poliomyelitis Upper airway obstruction Tonsillar and peritonsillar hypertrophy Paralysis of vocal cords Tumor of the cords or larynx Airway stenosis post prolonged intubation Thymoma , aortic aneurysm Neuromuscular impairment Poliomyelitis Multiple sclerosis Muscular dystrophy Amyotrophic lateral sclerosis Diaphragmatic paralysis Myxedema Myopathic disease Lower airway obstruction Chronic obstructive lung disease (bronchitis, Bronchiolitis , bronchiectasis , emphysema) Ventilatory restriction Kyphoscoliosis , spinal arthritis Obesity Fibrothorax Hydrothorax Impaired diaphragmatic Function Disorders involving pulmonary alveoli Severe chronic pneumonitis Diffuse infiltrative disease Interstitial fibrosis

15. Compensatory mechanism for Acute respiratory acidosis It is completed within 5-10 min from onset of hypercapnia . It originates exclusively from acidic titration of the body’s non-bicarbonate buffers (hemoglobin, intracellular proteins and phosphates, plasma proteins): CO 2 + H 2 O ↔ H 2 CO 3 ↔ HCO 3 - + H + H + + Buf - ↔ HBuf On average, plasma bicarbonate concentration increases by about 0.1 mEq /L for each 1 mmHg acute increment in PaCO 2

16. Compensatory mechanism for Chronic respiratory acidosis It requires 3-5 days of sustained hypercapnia for completion. It originates from up regulation of renal acidification mechanisms (both in the proximal and distal segments of the nephron) that result in: A transient increase in urinary net H+ excretion; and A persistent increase in the rate of renal bicarbonate reabsorption that maintains the increased plasma bicarbonate level. On average, plasma HCO 3 - concentration increases by about 0.3 mEq /L for each mm Hg chronic increment in PaCO 2

17. Respiratory Alkalosis Respiratory alkalosis is the acid-base disturbance initiated by a reduction in PaCO 2 . This occurs when there is excessive loss of CO 2 by alveolar hyperventilation. Hypocapnia develops when a sufficiently strong ventilatory stimulus causes CO 2 output in the lungs to exceed its metabolic production by the tissues. As a result, partial pressure of CO 2 and H + conc. falls

18. Respiratory Alkalosis By far, most cases of respiratory alkalosis reflect an increase in alveolar ventilation . However, in the presence of constant alveolar ventilation (i.e., mechanical ventilation), decreased carbon dioxide production (e.g., sedation, skeletal muscle paralysis, hypothermia, hypothyroidism) can cause respiratory alkalosis.

19. M ost common acid-base abnormality observed in patients who are critically ill. A common finding in patients on mechanical ventilation.  Acute hypocapnia causes a reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions. A reduction in free serum calcium also occurs due to increased binding of calcium to serum albumin. Many of the symptoms present in persons with respiratory alkalosis are related to hypocalcemia .  

20. Aetiology Respiratory Alkalosis Hypoxemia or tissue hypoxia Decreased inspired O 2 tension/High altitude Bacterial or viral pneumonia Aspiration of food, foreign body, or vomitus Larygospasm , Drowning Cyanotic heart disease, Severe ciurculatory failure Severe anemia,Hypotension Left shift deviation of HbO 2 curve Pulmonary embolism Central nervous system stimulation Voluntarily Pain, Anxiety, Psychosis, Fever Subarachnoid hemorrhage Cerebrovascular accident Meningoencephalitis Tumor, Trauma Stimulation of chest receptors Pneumonia, Asthma Pneumothorax, Hemothorax , Flail chest Infant or adult respiratory distress syndrome Cardiac failure Noncardiogenic pulmonary edema Pulmonary embolism, Interstitial lung disease Drugs or hormones Doxapram , Xanthines Salicylates , Catecholamines Angiotensin II, Vasopressor agents Progesterone, Medroxyprogesterone Dinitrophenol , Nicotine Miscellaneous Pregnancy, Sepsis, Hepatic failure Mechanical hyperventilation Heat exposure, Recovery form metabolic acidosis

21. Compensatory mechanism for respiratory alkalosis Acute adaptation It is completed within 5-10 min from onset of hypocapnia It originates principally from alkaline titration of the body’s nonbicarbonate buffers (hemoglobin, intracellular proteins and phosphates, plasma proteins ) Bicarbonate (HCO  3   - ) falls 2 mEq /L for each decrease of 10 mm Hg in the PCO  2 ;

22. Compensatory mechanism for respiratory alkalosis Chronic adaptation It requires 2-3 days of sustained hypocapnia for completion. It originates from downregulation of renal acidification mechanisms (both in the proximal and distal segments of the nephron) that result in A transient decrease in urinary net acid excretion (mostly a fall in ammonium excretion and an early component of increased bicarbonate excretion) that reduces the body’s bicarbonate stores; and A persistent decrease in the rate of renal bicarbonate reabsorption that maintains the decreased plasma bicarbonate level.

23. Compensatory mechanism for respiratory alkalosis Bicarbonate (HCO  3   - ) falls 5 mEq /L for each decrease of 10 mm Hg in the PCO  2 ; that is, ΔHCO  3  = 0.5(ΔPCO  2 ) The expected change in pH with respiratory alkalosis can be estimated with the following equations: Acute respiratory alkalosis: Change in pH = 0.008 X (40 – PCO  2 ) Chronic respiratory alkalosis: Change in pH = 0.017 X (40 – PCO  2 )

24. Identify ? Respiratory Acidosis o r Respiratory alkalosis Compensated o r Uncompensated

25. A rterial B lood G as Analysis

26. 5 Steps for Successful Blood Gas Analysis

27. Is this ABG authentic ? Henderson- Hasselbalch equation pH = 6.1 + log HCO 3 - 0.03 x PCO 2 pH expected = pH measured = ABG is authentic [ H+] meq /l = 24 X (PCO 2 / HCO 3 ) H + ion pH 100 7.00 79 7.10 63 7.20 50 7.30 45 7.35 40 7.40 35 7.45 32 7.50 25 7.60

28. ACIDEMIA or ALKALEMIA? pH < 7.35  acidemia pH > 7.45  alkalemia This is  usually  the primary disorder Remember:  an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 – 7.45)

29. RESPIRATORY or METABOLIC? IS PRIMARY DISTURBANCE RESPIRATORY OR METABOLIC? pH HCO 3 or pH HCO 3 METABOLIC pH PCO 2 or pH PCO 2 RESPIRATORY In primary respiratory disorders, the pH and PaCO2 change in  opposite directions ; in metabolic disorders the pH and HCO 3-  change in the same direction. RULE- If either the pH or PCO 2 is Normal, there might be mixed metabolic and respiratory acid base disorder.

30. If Respiratory – ACUTE or CHRONIC? Acute respiratory disorder - ∆pH (e-acute) = 0.008x ∆Pco 2 Chronic respiratory disorder - ∆pH (e-chronic) = 0.003x ∆pCO 2 .08 change in pH ( Acute ) .03 change in pH ( Chronic ) 10 mm Change PaCO 2 =

31. Is COMPENSATION adequate? Usually, compensation does  not  return the pH to normal (7.35 – 7.45). If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present.

32. Case: 6 year old male with progressive respiratory distress Muscular dystrophy . Blood Gas Report Measured 37.0 o C pH 7.301 PaCO 2 76.2 mm Hg PaO 2 45.5 mm Hg Calculated Data HCO 3 act 35.1 mmol / L O 2 Sat 78 % PO 2 (A - a) 9.5 mm Hg D PO 2 (a / A) 0.83 Entered Data FiO 2 21 % pH <7.35 : acidemia Res. Acidemia : High PaCO 2 and low pH Hypoxemia Normal A-a gradient D CO 2 =76-40=36 Expected D pH for ( Acute ) = .08 for 10 .08 × 3.6= 0.29 Expected ( Acute ) pH = 7.40 - 0.29=7.11 Chronic resp. acidosis Hypoventilation Chronic respiratory acidosis With hypoxia due to hypoventilation With renal compensation HCO3 elevated D HCO 3 (e) = 3.5 ( D CO 2 /10) = 3.5 (3.6) = 12.6 HCO3 expected =24+12.6 = 36.6 ± 2