ABG 6 Series

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مقاربة الاضطرابات التنفسية في غازات الدم الشرياني

مقاربة الاضطرابات التنفسية في غازات الدم الشرياني

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  • 2. Acid-Base Disorders and the ABG 6
  • 4. Summary of the Approach to ABGs1. Check the pH2. Check the pCO23. Select the appropriate compensation formula4. Determine if compensation is appropriate5. Check the anion gap AG=NA – (HCO3 + CL):12 46. If the anion gap is elevated, check the delta-delta G:G Ratio =Δ AG (12-AG) Δ HCO3 (24-HCO3)7. If a metabolic acidosis is present, check urine pH8. Generate a differential diagnosis
  • 5. EXPECTED CHANGES IN ACID-BASE DISORDERSPrimary Disorder Expected ChangesMetabolic acidosis PCO2 = 1.5 × HCO3 + (8 ± 2)Metabolic alkalosis PCO2 = 0.7 × HCO3 + (21 ± 2) PCO2= 0.9 * HCO3 +16Acute respiratory acidosis delta pH = 0.008 × (PCO2 - 40) ΔHCO3 = 0.1 × (PCO2-40)Chronic respiratory acidosis delta pH = 0.003 × (PCO2 - 40) ΔHCO3 = 0.35 × (PCO2-40)Acute respiratory alkalosis delta pH = 0.008 × (40 - PCO2) ΔHCO3 = 0.2 × (40 – PCO2 )Chronic respiratory alkalosis delta pH = 0.003 × (40 - PCO2) ΔHCO3 2nd × (40 – PCO2) From: THE ICU BOOK - = 0.4 Ed. (1998) [Corrected]
  • 6. PH PH>7,43 PH:7,37-7,43 PH<7,37 MIXED VS ALKALOSIS NORMAL ACIDOSISPCO2>40 PCO2<40 PCO2<40 PCO2>40 M.AL R.AL M.AC R.AC
  • 7. PCO2<36, RES.ALK+ HCO3<21 M.AC PCO2>44, RES.AC +PH(7,37-7,43) HCO3>27 M.ALK PCO2(nor), M.AC +M.ALK HCO3(nor) AG
  • 8. Respiratory system includes:1. CNS (medulla)2. Peripheral nervous system (phrenic nerve)3. Respiratory muscles4. Chest wall5. Lung6. Upper airway7. Bronchial tree8. Alveoli9. Pulmonary vasculature
  • 9. Potential causes of Respiratory Failure
  • 10. RESPIRATORY ACIDOSIS / ALKALOSISCO2 + H2O H2CO3 H+ + HCO3- Respiratory Acidosis Respiratory Alkalosis 10
  • 12. RESPIRATORY ALKALOSIS Normal 20:1 ratio is increased pH of blood is above 7.4H2CO3 HCO3- = 7.4 =0.5 1 : 20 12
  • 13. RESPIRATORY ALKALOSISCause is Hyperventilation Leads to eliminating excessive amounts of CO2 Increased loss of CO2 from the lungs at a rate faster than it is produced Decrease in H+ CO2 CO2 CO2 CO2 CO2 CO2 CO2CO2 CO2 CO2 CO2 CO2 13
  • 14. HYPERVENTILATIONHyper = “Over” Elimination of CO2 H + pH 14
  • 15. RESPIRATORY ALKALOSISCan be the result of: 1) Anxiety, emotional disturbances 2) Respiratory center lesions 3) Fever 4) Salicylate poisoning (overdose) 5) Assisted respiration 6) High altitude (low PO2) 15
  • 16. RESPIRATORY ALKALOSISAnxiety is an emotional disturbance The most common cause of hyperventilation, and thus respiratory alkalosis, is anxietyRespiratory center lesions Damage to brain centers responsible for monitoring breathing rates Tumors Strokes 16
  • 17. RESPIRATORY ALKALOSISFever Rapid shallow breathing blows off too much CO2 17
  • 18. RESPIRATORY ALKALOSIS Salicylate poisoning(Aspirin overdose) Ventilation is stimulated without regard to the status of O2, CO2 or H+ in the body fluids 18
  • 19. RESPIRATORY ALKALOSISAssisted Respiration Administration of CO2 in the exhaled air of the care - giver Your insurance won’t cover a ventilator any longer, so Bob here will be giving you mouth to mouth for the next several days 19
  • 20. RESPIRATORY ALKALOSISHigh Altitude Low concentrations of O2 in the arterial blood reflexly stimulates ventilation in an attempt to obtain more O2 Too much CO2 is “blown off” in the process 20
  • 21. Causes of Respiratory Alkalosis CENTRAL RESPIRATORY STIMULATION (Direct Stimulation of Resp Center):Structural Causes Non Structural Causes• Head trauma Pain• Brain tumor Anxiety• CVA Fever• Voluntary PERIPHERAL RESPIRATORY STIMULATION (Hypoxemia  Reflex Stimulation of Resp Center via Peripheral Chemoreceptors)• Pul V/Q imbalance• Pul Diffusion Defects Hypotension• Pul Shunts High Altitude
  • 22. INTRATHORACIC STRUCTURAL CAUSES:1. Reduced movement of chest wall & diaphragm2. Reduced compliance of lungs3. Irritative lesions of conducting airways MIXED/UNKNOWN MECHANISMS:1. Drugs – Salicylates Nicotine Progesterone Thyroid hormone Catecholamines Xanthines (Aminophylline & related compounds)2. Cirrhosis3. Gram –ve Sepsis4. Pregnancy5. Heat exposure6. Mechanical Ventilation
  • 23. RESPIRATORY ALKALOSISKidneys compensate by: Retaining hydrogen ions Increasing bicarbonate excretion HCO3- HCO3- H + H+ HCO3 - HCO3- H + H+ H+ HCO3- HCO - H + 3 H+ HCO3- HCO3- H+ HCO3- H + HCO3- H + H+ 26
  • 24. RESPIRATORY ALKALOSISDecreased CO2 in the lungs willeventually slow the rate of breathing Will permit a normal amount of CO2 to be retained in the lung 27
  • 25. RESPIRATORY ALKALOSIS metabolic balance before onset of - alkalosis pH = 7.4- respiratory alkalosis- pH = 7.7- - hyperactive breathing “ blows off ” CO2 - body’s compensation - kidneys conserve H+ ions and eliminate HCO3- in alkaline urine - therapy required to restore metabolic balance - HCO3- ions replaced by Cl- ions 28
  • 26. RESPIRATORY ALKALOSIS H2CO3 : Carbonic Acid HCO3- : Bicarbonate IonH2CO3 HCO3- (Na+) HCO3- (K+) HCO3- 1 : 20 (Mg++) HCO3- (Ca++) HCO3-metabolic balance before onset of alkalosis- pH = 7.4- 29
  • 27. RESPIRATORY ALKALOSISCO2 CO2 + H2O 0.5 : 20 respiratory alkalosis- pH = 7.7- hyperactive breathing “ blows off ” CO2- 30
  • 28. RESPIRATORY ALKALOSIS HCO3-0.5 : 15 Alkaline Urine BODY’S COMPENSATION - kidneys conserve H+ ions and eliminate HCO3- in alkaline urine31
  • 29. RESPIRATORY ALKALOSISH2CO3 HCO3- Cl- Chloride containing0.5 : 10 solution - therapy required to restore metabolic balance - HCO3- ions replaced by Cl- ions 32
  • 30. RESPIRATORY ALKALOSIS Usually the only treatment needed is toslow down the rate of breathing Breathing into a paper bag or holdingthe breath as long as possible may helpraise the blood CO2 content as theperson breathes carbon dioxideback in after breathing it out 33
  • 31. Treatment of Respiratory Alkalosis Resp alkalosis by itself not a cause of resp failure unless work of increased breathing not sustained by resp muscles Rx underlying cause Usually extent of alkalemia produced not dangerous. Admn of O2 if hypoxaemia If pH>7.55 pt may be sedated/anesthetised/ paralysed and/or put on MV.
  • 33. RESPIRATORY ACIDOSISCaused by hyperkapnia due tohypoventilation Characterized by a pH decrease and an increase in CO2 pH CO2 CO CO2 CO2 CO CO2 2 CO2 COCO2 2 CO2 CO2 pH CO2 CO2 40
  • 34. HYPOVENTILATIONHypo = “Under” Elimination of CO2 H + pH 41
  • 35. RESPIRATORY ACIDOSISThe speed and depth of breathing control theamount of CO2 in the bloodNormally when CO2 builds up, the pH of theblood falls and the blood becomes acidicHigh levels of CO2 in the blood stimulate theparts of the brain that regulate breathing,which in turn stimulate faster and deeperbreathing 44
  • 36. RESPIRATORY ACIDOSISRespiratory acidosisdevelops when thelungs dont expel CO2adequatelyThis can happen indiseases that severelyaffect the lungs, suchas emphysema, chronicbronchitis, severepneumonia, pulmonaryedema, and asthma 45
  • 37. RESPIRATORY ACIDOSISRespiratory acidosis can also develop whendiseases of the nerves or muscles of the chestimpair the mechanics of breathingIn addition, a person can develop respiratoryacidosis if overly sedated from narcotics andstrong sleeping medications that slowrespiration 46
  • 38. RESPIRATORY ACIDOSISThe treatment of respiratory acidosisaims to improve the function of the lungsDrugs to improve breathing may helppeople who have lung diseases such asasthma and emphysema 47
  • 39. RESPIRATORY ACIDOSISDecreased CO2 removalcan be the result of:1) Obstruction of air passages2) Decreased respiration (depression of respiratory centers)3) Decreased gas exchange between pulmonary capillaries and air spacs of lungs4) Collapse of lung 48
  • 40. RESPIRATORY ACIDOSIS1) Obstruction of air passages Vomit, anaphylaxis, tracheal cancer 49
  • 41. RESPIRATORY ACIDOSIS2) Decreased Respiration Shallow, slow breathing Depression of the respiratory centers in the brain which control breathing rates Drug overdose 50
  • 42. RESPIRATORY ACIDOSIS3) Decreasedgas exchangebetweenpulmonarycapillaries andair sacs of lungs Emphysema Bronchitis Pulmonary edema 51
  • 43. RESPIRATORY ACIDOSIS4) Collapse of lung Compression injury, open thoracic wound Left lung collapsed 52
  • 44. Causes of Acute Respiratory Acidosis EXCRETORY COMPONENT PROBLEMS:1. Perfusion: Massive PTE Cardiac Arrest2. Ventilation: Severe pul edema Severe pneumonia ARDS Airway obstruction3. Restriction of lung/thorax: Flail chest Pneumothorax Hemothorax
  • 45. 4. Muscular defects: Severe hypokalemia Myasthenic crisis5. Failure of Mechanical Ventilator CONTROL COMPONENT PROBLEMS:1. CNS: CSA Drugs (Anesthetics, Sedatives) Trauma Stroke2. Spinal Cord & Peripheral Nerves: Cervical Cord injury LGBS Neurotoxins (Botulism, Tetanus, OPC) Drugs causing Sk. m.paralysis (SCh, Curare, Pancuronium & allied drugs, aminoglycosides)
  • 46. Causes of Chronic Respiratory Acidosis EXCRETORY COMPONENT PROBLEMS:1. Ventilation: COPD Advanced ILD Restriction of thorax/chest wall: Kyphoscoliosis, Arthritis Fibrothorax Hydrothorax Muscular dystrophy Polymyositis
  • 47. CONTROL COMPONENT PROBLEMS:1. CNS: Obesity Hypoventilation Syndrome Tumours Brainstem infarcts Myxedema Ch sedative abuse Bulbar Poliomyelitis2. Spinal Cord & Peripheral Nerves: Poliomyelitis Multiple Sclerosis ALS Diaphragmatic paralysis
  • 48. RESPIRATORY ACIDOSIS metabolic balance before onset of - acidosis pH = 7.4- respiratory acidosis- pH = 7.1- breathing is suppressed holding CO2 in - body body’s compensation- kidneys conserve HCO3- ions to restore - the normal 40:2 ratio kidneys eliminate H+ ion in acidic urine- - therapy required to restore metabolic balance - lactate solution used in therapy is 40 converted to bicarbonate ions in the liver 59
  • 49. RESPIRATORY ACIDOSIS H2CO3 : Carbonic Acid HCO3- : Bicarbonate IonH2CO3 HCO3- (Na+) HCO3- (K+) HCO3- 1 : 20 (Mg++) HCO3- (Ca++) HCO3-- metabolic balance before onset of acidosis - pH = 7.4 60
  • 50. RESPIRATORY ACIDOSIS CO2 CO2 CO2 CO22 : 20breathing is suppressed holding CO2 in body- pH = 7.1- 61
  • 51. RESPIRATORY ACIDOSIS H2CO3 HCO3- HCO3- + H+2 : 30 acidic urine BODY’S COMPENSATIONkidneys conserve HCO3- ions to restore the - normal 40:2 ratio (20:1) kidneys eliminate H+ ion in acidic urine- 62
  • 52. RESPIRATORY ACIDOSIS LactateH2CO3 HCO3- LIVER Lactate HCO3- 2 : 40 - therapy required to restore metabolic balance - lactate solution used in therapy is converted to bicarbonate ions in the liver 63
  • 53. TREATMENT OF RESPIRATORY ACIDOSIS The goal is to increase the exhalation of CO2. The treatments are : – Based on the underlying causes – By providing ventilation therapy – Intravenous administration of HCO3- – Reversal of sedation or neuromuscular relaxants – Intubation and artificial ventilation (in severe cases)
  • 54. CASE -1 A 28 year old woman was admitted electively to a HDU (high dependency unit) following a caesarian section. A diagnosis of fatty liver of pregnancy had been made preoperatively. She was commenced on a continuous morphine infusion at 5 mg/hr and received oxygen by mask. This was continued overnight and she was noted to be quite drowsy the next day. ABG Arterial blood gases were PH 7,16 PCO2 61,9 PO2 115 HCO3 21,2
  • 55. • ACIDOSIS PH<7,37 • RESPIRATORY PCO2>40 • ∆HCO3=0,1(62- 40)=2,2(+24) • 26,2 ≠21ACUTE.R.AC • concomitant M.AC COMP AG=? • ??? Normal AG (12 4)
  • 56. CASE-2A 69 year old patient had a cardiac arrestsoon after return to the ward following anoperation.Resuscitation was commenced andincluded intubation and ventilation.Femoral arterial blood gases werecollected about five minutes after thearrest.
  • 57. LAB :Anion gap 24,Lactate 12 mmol/l. ABG PH 6,85 PCO2 82 PO2 214 HCO3 14
  • 58. PH<7,37 • ACIDOSIS PCO2>40 • RESPIRATORY • ∆HCO3=0,1(82- 40)=4,2 (+24)ACUTE.R.AC • 28,2 ≠14 • concomitant M.AC COMP AG=24 • High AG M.AC Normal AG (12 4) • NO other metabolic disordersGAP:gap=1,2
  • 59. DiscussionCardiac arrest with low cardiac output and tissuehypo-perfusion causing a:– severe lactic acidosis.Ventilation is depressed causing a:– respiratory acidosis.Inadequate ventilation in this pre-arrest phase mayhave been related to several factors, in particular :– inadequate reversal of neuromuscular paralysis,– airway obstruction in a supine sedated patient or– acute pulmonary oedema.
  • 60. CASE-3A 70 year old man was admitted with severecongestive cardiac failure.He has been unwell for about a week andhas been vomiting for the previous 5 days.He was on no medication.He was hyperventilating and was verydistressed. Admission biochemistry is listed below.He was on high concentration oxygen bymask.
  • 61. LAB: BIOCHEMISTRY ABGNA 127 PH 7,58K 5,2 PCO2 21CL 79 PO2 154HCO3 20 HCO3 19UREA 50,5 mmollCREAT 0,38 mmollGLUCO 9,5 mmollAG 33Creat = 5 mgdl (0,075) Urea =141,4 (0,357)cNA=128 Glucose =171 (*18) Corrected Sodium = Measured sodium + 0.016 * (Serum glucose - 100)
  • 62. PH>7,43 • ALKALOSISPCO2<40 • RESPIRATORY • ∆HCO3=0,4(40 -21)=24 – 7,6C,R .ALK • 16,4 ≠19 • concomitant M.ALK COMP AG=28 • HIGH AG M.ACNormal AG (12 4) GAP:gap • concomitant M.ALK (=4 >2)
  • 63. DiscussionThe history suggests the followingpossibilities: Respiratory alkalosis in response to the dyspnoea associate with the congestive heart failure A lactic acidosis is possible if cardiac output is low and tissue perfusion is poor Vomiting suggests metabolic alkalosisThe renal failure could be associated witha high anion gap acidosis
  • 64. DiscussionThis patient has a triple acid-basedisorder: Acute metabolic acidosis probably due to renal failure (?prerenal failure) and possibly to lactic acidosis (hypoperfusion due heart failure and hypovolaemia) Metabolic alkalosis due to severe vomiting Respiratory alkalosis due to dyspnoea from congestive heart failure.The pO2 is elevated due to administrationof a high inspired oxygen concentration
  • 65. NEXT LECTURE1. Approche to hypoxiemic patient2. Cases