(BQ) Part 2 book Handbook of blood gas/acid-base interpretation has contents: Respiratory acidosis, respiratory alkalosis, metabolic acidosis, the analysis of blood gases, the analysis of blood gases, case examples,... and other contents
Chapter Respiratory Acidosis Contents 7.1 7.2 7.3 7.4 Respiratory Failure The Causes of Respiratory Acidosis Acute Respiratory Acidosis: Clinical Effects Effect of Acute Respiratory Acidosis on the Oxy-hemoglobin Dissociation Curve 7.5 Buffers in Acute Respiratory Acidosis 7.6 Respiratory Acidosis: Mechanisms for Compensation 7.7 Compensation for Respiratory Acidosis 7.8 Post-hypercapnic Metabolic Alkalosis 7.9 Acute on Chronic Respiratory Acidosis 7.10 Respiratory Acidosis: Acute or Chronic? 172 173 174 A Hasan, Handbook of Blood Gas/Acid-Base Interpretation, DOI 10.1007/978-1-4471-4315-4_7, © Springer-Verlag London 2013 171 175 176 176 177 178 179 180 172 7.1 Respiratory Acidosis Respiratory Failure Although four types of respiratory failure have been described, it is usual to classify respiratory failure into Type-1 and Type-2: the latter is associated with hypoventilation and respiratory acidosis (see Sect 7.2) Respiratory failure Type (Hypoxemic respiratory failure) Type (Hypercapnic respiratory failure) PaO2 is low (PaO2 < 50 mmHg) PaO2 is low (PaO2 < 50 mmHg) CO2 is not elevated (PaCO2 < 60 mmHg) CO2 is elevated (PaCO2 > 60 mmHg) See Sect 1.25 See Sect 1.26 Type (Per-operative respiratory failure) FRC falls below closing volume as a result of atelectasis Contributing factors: Supine posture General anesthesia Depressed cough reflex Splinting due to pain Type (Shock with hypo perfusion) The proportion of the cardiac output to the respiratory muscles rises by as much as ten-fold when the work of breathing is high; this can seriously impair coronary perfusion during shock 7.2 7.2 173 The Causes of Respiratory Acidosis The Causes of Respiratory Acidosis In terms of CO2 production and excretion, alveolar hypoventilation is the major mechanism for hypercarbia (See Sects 1.34 and 1.35) Quite often however, increase in dead space is an important mechanism (Sect 1.30) Causes of acute hypercapnia Central depression of respiratory drive Drugs Sedatives, opiates, anaesthetic agents CNS lesions CNS trauma, strokes, encephalitis Neuromuscular Spinal cord lesions or trauma (at or above level of C4) High central neural blockade Tetanus Poliomyelitis Amyotrophic lateral sclerosis Myasthenia gravis Organophosphate poisoning Botulism Muscular relaxants Dyselectreolytemias Airways Upper airway obstruction Aspiration Asthma or COPD Chest wall Flail chest Diaphragmatic dysfunction: Paralysis Splinting Rupture Pleura Pneumothorax Rapid accumulation of a large pleural effusion Lung parenchyma Cardiogenic pulmonary edema ARDS Pneumonia Other Circulatory shock Sepsis Malignant hyperthermia CO2 insufflation into the body Causes of chronic hypercapnia Central depression of respiratory drive Primary alveolar hypoventilation Neuromuscular Chronic neuromyopathies Poliomyelitis Dyselectreolytemias Malnutrition Chest wall Kyphoscoliosis Obesity Thoracoplasty Pleura Chronic large effusions Lung parenchyma Longstanding and severe ILD Airways Persistent asthma Severe COPD Bronchiectasis 174 7.3 Respiratory Acidosis Acute Respiratory Acidosis: Clinical Effects A rapid decrease in alveolar ventilation is poorly tolerated by the body Both acute hypercapnia and acute hypoxemia can be extremely damaging However, surprising degrees of hypercapnia and hypoxemia can be tolerated by the body when chronic Acute Chronic • Poorly tolerated: can result in dangerous fluxes in the acid base status of the body • Relatively well tolerated: due to compensatory mechanisms; patients may remain asymptomatic with very high PaCO2 levels (e.g., over 100 mmHg) Most clinical manifestations of acute hypercapnia are to with the central nervous system Clinical features of Hypercapnia Sympahetic stimulation Tachycardia, arrythmias Sweating Reflex peripheral vasoconstriction Peripheral vasodilatation (a direct effect of hypercapnia) Headaches, hypotension (if hypercapnia is severe) Central depression (occurs at very high CO2 levels) Drowsiness, flaps, coma Decreased diaphragmatic contractility & endurance Respiratory muscle fatigue Cerebral vasodilatation (results in increased intracranial pressure) Confusion, headache; papilledema, loss of consciousness (if severe); hyperventilation Alberti E, Hoyer S, Hamer J, Stoeckel H, Packschiess P, Weinhardt F The effect of carbon dioxide on cerebral blood flow and cerebral metabolism in dogs Br J Anaesth 1975;47:941–7 Kilburn KH Neurologic manifestations of respiratory failure Arch Intern Med 1965;116: 409–15 Neff TA, Petty TL Tolerance and survival in severe chronic hypercapnia Arch Intern Med 1972; 129:591–6 Smith RB, Aass AA, Nemoto EM Intraocular and intracranial pressure during respiratory alkalosis and acidosis Br J Anaesth 1981;53:967–72 7.4 7.4 Effect of Acute Respiratory Acidosis on the Oxy-hemoglobin Dissociation Curve 175 Effect of Acute Respiratory Acidosis on the Oxy-hemoglobin Dissociation Curve Acute hypercapnia can transiently shift the oxy-hemoglobin dissociation curve to the right Acute hypercapnia The oxy-Hb dissociation curve shifts rightwards When hypercapnia becomes chronic, 2,3 DPG levels within RBC fall The oxy-Hb dissociation curve shifts back towards normal Respiratory acidosis can decrease glucose uptake in peripheral tissues, and inhibit anaerobic glycolysis When severe hypoxia is present, energy requirements can be critically compromised Bellingham AJ, Detter JC, Lenfant C Regulatory mechanisms of hemoglobin oxygen affinity in acidosis and alkalosis J Clin Invest 1971;50:700–6 Oski FA, Gottlieb AJ, Delivoria-Papadopoulos M, Miller WW Red-cell 2, 3-diphosphoglycerate levels in subjects with chronic hypoxemia N Engl J Med 1969;280:1165–6 176 7.5 Respiratory Acidosis Buffers in Acute Respiratory Acidosis The bicarbonate buffer system, quantitatively the most important buffer system in the body, cannot buffer changes produced by alterations in CO2, one of its own components CO2 changes are buffered therefore by non-bicarbonate buffer systems Hemoglobin Intracellular proteins and phosphates About 99 % of the buffering occurs intracellularly Phosphates 7.6 Respiratory Acidosis: Mechanisms for Compensation Hypercapnia CO2 + H2O The elevated PaCO2 stimulates alveolar ventilation Intracellular buffering (rapid) H2CO3 + Hb H+Hb + HCO3– H2CO3 H+ + HCO3– Renal compensation (delayed) H+ is excreted by the kidney Brackett NC Jr, Wingo CF, Mureb O, et al Acid-base response to chronic hypercapnia in man New Eng J Med 1969;280:124–30 7.7 177 Compensation for Respiratory Acidosis 7.7 Compensation for Respiratory Acidosis The following formulae are used to determine the extent of the compensatory processes, or if a second primary acid-base disorder is present Acute respiratory acidosis (24 h) • Δ↓∗pH = 0.008 ì PaCO2 pH = 0.003 ì PaCO2 H+ = 0.8 ì PaCO2 H+ = 0.3 ì ΔPaCO2 • HCO3− increases by up to 0.1 mEq/L for every mmHg rise in CO2 • HCO3− increases by up to 0.4 mEq/L for every mmHg rise in CO2 • H+ = (0.8 ì PaCO2) + H+ = (0.3 × PaCO2) + 27 Limits of compensation for respiratory acidosis • The process of compensation is generally complete within − days • The bicarbonate illy A metabolic alkalosis may be masking the acidosis, and the bicarbonate gap must now be checked B Bicarbonate gap: DAG – DHCO3– = (27–12) – (24–21) = 12 (i.e., >6mEq/L) An associated metabolic alkalosis is present Acute respiratory acidosis: C Colloid gap: Acute respiratory alkalosis: D Disorder, associated primary respiratory: Acute respiratory alkalosis: Expected HCO3– = 24 – [(40 – CO2) × 0.2] = 21 (This identical to the measured HCO3 No associated metabolic disorder is apparent However see anion gap and bicarbonate gap (top left) E Electrolytes, urinary: Chronic respiratory alkalosis: O Clinical correlation: All causes of a wide anion gap metabolic acidosis (Sect 9.8) must be investigated The Bicarbonate gap is wide as well The patient has been vomiting, and on account of this, the third disorder—a coexistent met alkalosis-has supervened The hypoxemia is likely on account of the congestive cardiac failure and pulmonary edema 13 13.24 321 Patient X: An 82 year-old woman with Diabetic Ketoacidosis 13.24 Patient X: An 82 year-old woman with Diabetic Ketoacidosis A 82 year old woman was admitted in diabetic ketoacidosis; she had been coughing and breathless for a few days, and a right lower lobe pneumonia was found at admission pH: 7.35, PCO2: 25 mmHg, HCO3−: 18 mEq/L, Na+: 141 mEq/L, Cl−: 89 mEq/L, PaO2 82 mmHg on 50 % O2, 100 7.0 90 12 15 18 21 24 27 7.1 80 sis o cid 70 olic tab Me idosis ac 60 H– (nM/L) ry N onic Chr iratory resp alosis alk 30 20 10 e ut Ac re on Chr Metabolic alkalosis is os e ut kal Ac y al r o at pir 7.2 39 sis 42 45 48 51 57 63 69 75 pH ido y ac r irato sp ic re 33 36 ir sp 50 40 a o at 30 7.3 7.4 7.5 7.6 7.7 7.8 s re [H m CO Eq – /L ] 8.0 8.5 10 20 30 40 50 60 70 80 90 100 PCO2 (mmHg) Patient X Impression: metabolic acidosis with chronic respiratory alkalosis In fact, a triple disorder is present (see discussion opposite) 13 322 13 Case Examples pH 7.36: mildly acidemic A B C D E Is metabolic acidosis present (is the bicarbonate low?) Is respiratory acidosis present (is the PaCO2 high?) Yes, marginally A dominant metabolic acidosis is possibly present: Apply the METABOLIC TRACK No Anion gap: AG=[Na+] – ([Cl–] + [HCO3–]) = 141 – (89 + 18) = 34 The anion gap is widened The acidosis is a WAGMA Bicarbonate gap: Is an associated metabolic alkalosis present? Calculate the bicarbonate gap (delta ratio) Delta ratio= ΔAG – ΔHCO3– Delta ratio= (34 – 12) – (24 – 18)=16 (very high) A coexisting metabolic alkalosis is present Colloid gap: Disorder, associated primary respiratory: Is an associated respiratory disorder present? Actual CO2 = 25 Predicted CO2 = (1.5 × HCO3) + 8±2 = 35±2 mmHg Actual CO2 (25 mmHg) is lower than the predicted CO2 (33–37) A primary respiratory alkalosis is present Electrolytes, urinary: Clinical correlation: DKA presents with a wide anion gap metabolic acidosis However there is a discrepancy: the substantially widened AG suggests a severe metabolic acidosis which is seemingly out of proportion to the mild depression in the serum bicarbonate.A coexisting metabolic alkalosis was suspected and confirmed (see also Sect 9.36) To explain the metabolic alkalosis, dyselectrolytemias (hypochloremia, hypokalemia) should be looked for, and a history of current diuretic therapy etc must be sought The respiratory alkalosis is consistent with the pneumonia 13 323 13.25 Patient Y: A 50 year-old male in Cardiac Arrest 13.25 Patient Y: A 50 year-old male in Cardiac Arrest A 50 year old male suffers a cardiopulmonary arrest in the ICU pH 7.0, HCO3−: 6.0 PCO2: 29 mmHg, PaO2 180 mmHg on FIO2 100 % on ventilator Na+: 144 mEq/L, K+: 5.0 mEq/L, Cl−: 104 mEq/L 7.0 100 90 12 15 18 21 24 27 7.1 80 sis o cid 70 olic tab Me idosis ac 60 H− (nM/L) ry te N onic Chr iratory resp alosis alk 30 20 10 re u Ac on Chr Metabolic alkalosis is os e ut kal Ac y al r o at pir 7.2 39 sis 42 45 48 51 57 63 69 75 pH ido y ac r irato sp ic re 33 36 ir sp 50 40 a o at 30 7.3 7.4 7.5 7.6 7.7 7.8 s re [H m CO Eq − /L ] 8.0 8.5 10 20 30 40 50 60 70 80 90 100 PCO2 (mmHg) Patient Y Severe metabolic acidosis with acute respiratory alkalosis 13 ... ingestion, 23 1 types, 22 3 UAG, 23 3 23 4 WAGMA, 22 5 systemic consequences, 20 8 20 9 TCO2, 21 4 Metabolic alkalosis acute abdomen, 315–316 causes, 25 2 compensation, 24 7, 26 1 diuretic usage, 321 – 322 electrolytes,... in, 21 5 21 7 anion gap in, 26 3 base excess in, 21 9 bicarbonate gap in, 26 3 buffer base in, 21 8 cardiopulmonary arrest and, 329 –330 colloid gap in, 26 3 compensation, 21 2 21 3, 26 1 diarrhea, 323 – 324 ... seizure, 29 5 29 6 hyperkalemia and hypokalemia, 21 1 indicators, 20 4 l-lactic acidosis and d-lactic acidosis, 22 4, 22 7 pathogenesis, 195 renal mechanisms NAGMA, 23 0 renal tubular acidosis, 22 8 22 9 toxin