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ACID –BASE DISTURBANCES

University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras. MEDICINE 4 th year English Program Suport de curs. ACID –BASE DISTURBANCES. WATER AND ELECTROLYTES DISTURBANCES Classification ( Shires şi Baxter). V olum e disturbances

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ACID –BASE DISTURBANCES

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  1. University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4th year English Program Suport de curs ACID –BASEDISTURBANCES

  2. WATER AND ELECTROLYTES DISTURBANCESClassification (Shires şi Baxter) • Volume disturbances • Volume contraction • Volume expansion • Concentration disturbances • Hyponatremia • Hypernatremia • Other hyperosmolar states • Composition disturbances • Hypo/hyperpotasemia • Hypo/hypercalcemia • Hypo/hypermagnesemia • Hypo/hyperphosphatemia • Hydrogen ion disturbances (acid-base disturbances)

  3. acidemia – H+ concentration >44nmol/l (pH <7.36) • alcalemia - H+ concentration<36nmol/l (pH > 7.44) • acidosis– the pathological condition which results in acidemia or would result in acidemia in the absence of compensation; • alkalosis - the pathological condition which results in alcalemia or would result in alcalemia in the absence of compensation; Acidosis and alkalosis may coexist and the resultant pH reflects this coexistance. But acidemia and alcalemia are mutuali exclusive conditions.

  4. Respiratory acidosis – the primary (non-compensatory) elevation of PaCO2 • All the other conditions which result in acidosis are termed as metabolic ones (non-respiratory). • Respiratory alkalosis – the primary (non-compensatory) decrease of PaCO2 • All the other conditions which result in alkalosis are termed as metabolic ones (non-respiratory).

  5. RESPIRATORY ACIDOSIS

  6. RESPIRATORY ACIDOSIS • The primary disturbance: ↑ PaCO2 > 45mmHg(hypercapnia) • Compensatory disturbance change: ↑ HCO3> 27mmol/l acute respiratory acidosis forms chronic respiratory acidosis forms

  7. RESPIRATORY ACIDOSIS CAUSES • all conditions resulting in type II respiratory failure • Mechanisms: • alveolar hypoventilation • severe ventilation/perfusion mismatch

  8. RESPIRATORY ACIDOSIS Pathophysiology • ↑ PaCO2 • ↑ CO2 + H2O ↔ H2CO3 ↔ ↑ H+ + HCO3- acidemia • Compensationintra/extracellular buffer systems renal ↑ renal bicarbonate reabsorbtion ↑urinnary H+elimination ↑ urinnary Cl-elimination → ↓Cl-mia • Anticipated HCO3-level (anticipated compensation) • Acute respiratory acidosis: for every ↑ PaCO2of10mmHg → HCO3↑ with 1 mmol/l • Chronic respiratory acidosis: for every ↑ PaCO2of 10mmHg → HCO3↑ with4 mmol/l

  9. RESPIRATORY ACIDOSIS CLINICAL PICTURE • Respiratory system: • respiratory depression ( breathing frequency/amplitude) • rapid shallow breathing • abnormal respiratory pattern • CNS: • headach, visual disturbances • anxiety, drowsiness • sleepyness, coma • cerebral vasodilation→ ICHT • Cardio-vascular system: • Vasodilation (congestive facies, eye congestion, papillary edema) • sympathetic nervous system stimulation– tachycardia, sweating, HTA • negativ inotropic effect • hTA, rhythm disturbances

  10. RESPIRATORY ACIDOSIS TREATMENT • Treatmentul of alveolar hypoventilation (hypercapnia) • Treat causal disease • Respiratory centre stimulation • Ventilatory support (mechanical ventilation) • Treatmentul of hypoxemia • ↑ FiO2(masks or cannulae) • Ventilatory support (mechanical ventilation) • Treatmentul of acidosis • correct settings of artificial ventilation • Acute respiratory acidosis → hyperventilation • Chronic respiratory acidosis: riskof post-hypercapnic metabolic alkalosis

  11. RESPIRATORY ALKALOSIS

  12. RESPIRATORY ALKALOSIS • Primary disturbance: ↓ PaCO2 < 35mmHg (hypocapnia) • Compensatory change: ↓ HCO3 < 24mmol/l

  13. RESPIRATORY ALKALOSIS CAUSES • Hypoxemia • Pulmonary diseases: ARDS, pneumonia, pulmonary edema, pulmonary embolism, pulmonary fibrosis •  FiO2 – high altitude, closed spaces • Congenital cardiac diseases • Anemia, blood hypotension • Stimulation of respiratory center • psychogenic hyperventilation (fear, effort) • CNS diseases: trauma, tumors, ICHT, brain stem diseases • Pulmonary deseases: pneumonia, asthma, pulmonary embolism • Other causes • salicilate intoxication • SIRS, sepsis • liver failure • pregnancy • Hyperventilation during mechanical ventilation

  14. RESPIRATORY ALKALOSIS Pathophysiology •  PaCO2 • Compensatory mechanism→  HCO3 • Buffer systems • Renal mechanism: →  renal HCO3reabsorbtion → ↑ renal HCO3 formation alkaline urine • Intracellular compartment H+goes out K+goes in hypopotasemia • ↑ bonding of ionized Ca to albumine → plasma ionized Ca→ hypocalcemia • Anticipated HCO3-level (anticipated compensation) • Acute respiratory alkalosis: for every ↓PaCO2of10mmHg → HCO3↓with2 mmol/l • Chronic respiratory alkalosis: for every ↓PaCO2of 10mmHg → HCO3↓with5 mmol/l

  15. RESPIRATORY ALKALOSIS CLINICAL PICTURE • Respiratory system: • Hyperventilation (↑breathing frequency/amplitude) • CNS: • Cerebral vasoconstriction • Dizziness, confusion • Loss of conscienceness • Neuro-muscullar system: • ionized Ca → hyperexcitability • parestesias of the lips, tongue and extremities • muscle twiching • Chvostek sign, Trousseau sign • laryngeal spasm, rhythm disturbances • convulsions

  16. RESPIRATORY ALKALOSIS TREATMENT • Treat the causative condition • Rebreathing masks – psychogenic hyperventilation (rebreathing normalizes CO2 ) • correct setting of ventilatory parameters during artificial ventilation

  17. METABOLIC ACIDOSIS

  18. METABOLIC ACIDOSIS =increased H+concentration due to acids acumulation or alkali loss (base deficit BE > -2mEq/l) • Primary disturbance: ↓ HCO3< 24mmol/l • Compensatory change: ↓ PaCO2< 35mmHg

  19. METABOLIC ACIDOSIS Sum of cations= sum of anions Na + K + unmeasured cations= Cl +HCO3 + unmeasured anions Na + ....... = Cl +HCO3 + unmeasured anions Anion gap =Unmeasured anions Anion gap = Na – (Cl + HCO3 ) Normal value= 3-11mEq/l

  20. METABOLIC ACIDOSIS CLASSIFICATION • With increased anion gap (acids acumulation) • With normal anion gap (alkali loss)

  21. METABOLIC ACIDOSIS Metabolic acidosis with increased anion gap CAUSES • Lactic acid accumulation • Type A: all shock classes, cardio-respiratory arrest. hypoxia, effort • Type B: liver failure, leukemia, ereditary lactic acidosis, drugs, toxins (biguanide, alcohool) • Keto-acids acumulation • Diabetus melitus, starvation, alcohool ingestion • Phosphate and sulphate acumulation • renal failure • Acumulation of other substances (intoxications) • Metanol, salicilaţes, etilenglicol

  22. METABOLIC ACIDOSIS Metabolic acidosis with normal anion gap CAUSES • With hypopotasemia • Digestive HCO3 loss • diarheea • pancreatic/billiary fistulas/drainage • uretero-sigmoidostomy • RenalHCO3 loss • Renal tubullar acidosis type 1 and type 2 • acetazolamid • With normo/hyperpotasemia • Acidifying agents - HCl, parenteral feeding • Hypoaldosteronism • Renal tubullar acidosis type 4

  23. METABOLIC ACIDOSIS Pathophysiology Metabolic acidosis with increased anion gap • Acids acumulation→ H+ excess • H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O HCO3- consumption→  HCO3- • Acidemia → stimulation of respiratory center → ↑ CO2 elimination →  PaCO2

  24. METABOLIC ACIDOSIS Pathophysiology Metabolic acidosis with normal anion gap • Digestive/urinnary alkaki loss H+ excess •  HCO3- → ↑ Cl- (hyperchloremic metabolic acidosis)

  25. METABOLIC ACIDOSIS Pathophysiology • Compensation: PCO2= (1,5 x HCO3) + 8 PCO2=the last two digits of pH • Acidosis→ excess of extracelular H+ intracellular compartment H+ goes in K+ goes out hyperpotasemia

  26. METABOLIC ACIDOSIS CLINICAL PICTURE Acidosis→ generalized celullare dysfunction • Respiratory system: • Küssmaul breathing • CNS: • Sleepiness, coma • Cardio-vascular system: • Vasodilation • Stimulation of SNS • Negative inotropic effect • rhythm disturbances • Digestiv system: • Nausea, vomiting, diarheea • Physiological effects: • Hi\yperpotasemia • Right shift of hemoglobin dissociation curve • ↑ ionized Ca

  27. METABOLIC ACIDOSIS PRINCIPLES of TREATMENT • Treatment of the causative disease • Treatment of acidemia • Sodium bicarbonate is indicated when pH <7,15-7,10 • Goal of bicarbonate administration is pH ~ 7,20 ( NOT normal pH) • Estimation of needed bicarbonate amount: mEq = 0,5 x kg x (14 – HCO3) mEq = 0,5 x kg x (10 – BE) • Side effects of bicarbonate administration: sodium overload, hyperosmilarity, metabolic alkalosis by over-compensation, paradoxic intracellular acidosis, hypopotasemia • Monitoring of treatment: pH, K • During correction of acidosis K administration may be needed (when the patient has potasium depletion)

  28. METABOLIC ALKALOSIS

  29. METABOLIC ALKALOSIS =base accumulation (base exces BE > + 2,5 mEq/l) • Primary disturbance primary increase of HCO3 > 27mmol/l • Compensatory change secondary increase of PaCO2> 45mmHg

  30. METABOLIC ALKALOSIS CAUSES • Excessive alkali intake/administration • Milk-alkali syndrome • Massive blood transfusion • Bicarbonate administration (overcompensation of metabolic acidosis) • Volume and chloride depletion • Gastric losses (vomiting, fistula, piloric stenosis, …) • Renal losses (diuretics, Bartter sdr, posthypercapnic metabolic alkalosis) • Mineralo-corticoids excess • Primary hyperaldosteronism • Cushing syndrome • Corticoids administration

  31. METABOLIC ALKALOSIS CLASIFICATION • Chloride-responsive metabolic alkalosis Urinary Cl< 10mEq/l Gastric losses or diarrheea Diuretics • Chloride-unresponsive metabolic alkalosis Urinary Cl> 20mEq/l Primary hyperaldosteronism Corticoids administration Excessive alkali intake/administration

  32. METABOLIC ALKALOSIS PATHOPHYSIOLOGY • ↑ HCO3- + H+ ↔ H2CO3 ↔ ↑ CO2 + H2O (minutes) ↑ PaCO2 •  externalventilation → ↑ PaCO2 (hours) limited by PaO2regulation limitedcompensation • Intracellular compartment H+ out K+ in hypopotasemia • ↑ albumin-bound ionized Ca →  plasma ionized Ca → hypocalcemia

  33. METABOLIC ALKALOSIS PATHOPHYSIOLOGY the most frequent acid-base disturbance Hypochloremic contraction metabolic alkalosis Hypovolemia→ RAA system→ ↑ Na, water and bicarbonate reabsorption Compensation: PaCO2= (0,7 x HCO3) + 21

  34. METABOLIC ALKALOSIS CLINICAL PICTURE • Respiratory system • Alveolar hypoventilation • Hypoxemia • Cardio-vascular system • Hypovolemia/blood hypertension • Arhythmia • CNS • Lethargy, coma • Convulsions • Metabolic • Hypopotasemia • Hypocalcemia

  35. METABOLIC ALKALOSIS DIAGNOSIS • Intravascular volume evaluation • Presence/absence of blood hypertension • Plasma K evaluation • Urinary Cl evaluation

  36. METABOLIC ALKALOSIS TREATMENT mild/moderate form (BE <12, HCO3<40) • Contraction alkalosis • Volume repletion with chloride rich isotonic /colloid solutions • Potasium administration (20mEq / 500ml) • Causative treatment • Mineralo-corticoid excess • Causative treatment • Spironolactone for correction of potasemia • Exogenous alkali excess • Stop the administration severe form (BE >12, HCO3>40) • Acidifying treatment to alleviate alkalosis • HCl – for immediate pH neutralization; 0,1N solution (100mEq/l) • Amoniu chloride – metabolized to release H+; 2,4% solution (400mEq/l) • Start with 50% of BE; pH monitoring

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