ABG 6 Series

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مقاربة الاضطرابات التنفسية في غازات الدم الشرياني

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<ul><li> 1. ABG seriesANAS SAHLE , MDDAMASCUSE HOSPITAL</li></ul> <p> 2. Acid-Base Disorders and the ABG 6 3. BREIF PREVIEW 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 gapAG=NA (HCO3 + CL):12 46. If the anion gap is elevated, check the delta-deltaG:G Ratio = AG (12-AG) 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 alkalosisPCO2 = 0.7 HCO3 + (21 2) PCO2= 0.9 * HCO3 +16Acute respiratory acidosis delta pH = 0.008 (PCO2 - 40) HCO3 = 0.1 (PCO2-40)Chronic respiratory acidosis delta pH = 0.003 (PCO2 - 40) HCO3 = 0.35 (PCO2-40)Acute respiratory alkalosisdelta pH = 0.008 (40 - PCO2) HCO3 = 0.2 (40 PCO2 )Chronic respiratory alkalosisdelta pH = 0.003 (40 - PCO2) HCO3 2nd (40 PCO2) From: THE ICU BOOK - = 0.4 Ed. (1998) [Corrected] 6. PH PH&gt;7,43PH:7,37-7,43 PH40 PCO27.55 pt may be sedated/anesthetised/paralysed and/or put on MV. 32. RESPIRATORY ACIDOSIS 39 33. RESPIRATORY ACIDOSISCaused by hyperkapnia due tohypoventilation Characterized by a pH decreaseand an increase in CO2pH CO2COCO2 CO2CO CO22 CO2COCO22 CO2 CO2 pH CO2 CO240 34. HYPOVENTILATIONHypo = Under Elimination of CO2H +pH41 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 deeperbreathing44 36. RESPIRATORY ACIDOSISRespiratory acidosisdevelops when thelungs dont expel CO2adequatelyThis can happen indiseases that severelyaffect the lungs, suchas emphysema, chronicbronchitis, severepneumonia, pulmonaryedema, and asthma45 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 emphysema47 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 lung48 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 thebrain which control breathing rates Drug overdose50 42. RESPIRATORY ACIDOSIS3) Decreasedgas exchangebetweenpulmonarycapillaries andair sacs of lungs Emphysema Bronchitis Pulmonaryedema51 43. RESPIRATORY ACIDOSIS4) Collapse of lung Compression injury, open thoracic woundLeft lung collapsed 52 44. Causes of Acute Respiratory AcidosisEXCRETORY 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: CSADrugs (Anesthetics, Sedatives)TraumaStroke2. Spinal Cord &amp; Peripheral Nerves: Cervical Cord injuryLGBS Neurotoxins (Botulism, Tetanus, OPC) Drugs causing Sk. m.paralysis (SCh, Curare,Pancuronium &amp; allied drugs, aminoglycosides) 46. Causes ofChronic Respiratory AcidosisEXCRETORY COMPONENT PROBLEMS:1. Ventilation:COPDAdvanced ILDRestriction of thorax/chest wall:Kyphoscoliosis, ArthritisFibrothoraxHydrothoraxMuscular dystrophyPolymyositis 47. CONTROL COMPONENT PROBLEMS:1. CNS:Obesity Hypoventilation Syndrome Tumours Brainstem infarcts Myxedema Ch sedative abuse Bulbar Poliomyelitis2. Spinal Cord &amp; Peripheral Nerves: Poliomyelitis Multiple Sclerosis ALS Diaphragmatic paralysis 48. RESPIRATORY ACIDOSIS metabolic balance before onset of - acidosispH = 7.4-respiratory acidosis-pH = 7.1- breathing is suppressed holding CO2 in -body bodys compensation- kidneys conserve HCO3- ions to restore -the normal 40:2 ratiokidneys eliminate H+ ion in acidic urine-- therapy required to restore metabolicbalance- lactate solution used in therapy is40 converted to bicarbonate ions in the liver59 49. RESPIRATORY ACIDOSISH2CO3 : 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 ACIDOSISCO2 CO2CO2CO22: 20breathing is suppressed holding CO2 in body-pH = 7.1- 61 51. RESPIRATORY ACIDOSIS H2CO3HCO3- HCO3-+H+2: 30 acidic urine BODYS 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- LIVERLactate HCO3- 2:40 - therapy required to restore metabolic balance- lactate solution used in therapy is converted tobicarbonate ions in the liver 63 53. TREATMENT OFRESPIRATORY ACIDOSIS The goal is to increase the exhalation ofCO2. The treatments are : Based on the underlying causes By providing ventilation therapy Intravenous administration of HCO3- Reversal of sedation or neuromuscularrelaxants Intubation and artificial ventilation (in severecases) 54. CASE -1 A 28 year old woman was admitted electively to aHDU (high dependency unit) following a caesariansection. A diagnosis of fatty liver of pregnancy had beenmade preoperatively. She was commenced on a continuous morphineinfusion at 5 mg/hr and received oxygen by mask. This was continued overnight and she was noted tobe quite drowsy the next day. ABG Arterial blood gases were PH7,16PCO2 61,9PO2115HCO3 21,2 55. ACIDOSIS PH40 HCO3=0,1(62- 40)=2,2(+24) 26,2 21ACUTE.R.AC concomitant M.ACCOMPAG=? ??? 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 PO2214 HCO3 14 58. PH40 RESPIRATORY HCO3=0,1(82- 40)=4,2 (+24)ACUTE.R.AC 28,2 14 concomitant M.ACCOMP 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 7,58K5,2 PCO2 21CL 79PO2154HCO3 20HCO3 19UREA 50,5 mmollCREAT0,38 mmollGLUCO9,5 mmollAG 33Creat = 5 mgdl (0,075) Urea =141,4 (0,357)cNA=128Glucose =171 (*18)Corrected Sodium = Measured sodium + 0.016 * (Serum glucose - 100) 62. PH&gt;7,43 ALKALOSISPCO22) 63. DiscussionThe history suggests the followingpossibilities:Respiratory alkalosis in response to the dyspnoeaassociate with the congestive heart failureA lactic acidosis is possible if cardiac output is lowand tissue perfusion is poorVomiting 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 renalfailure (?prerenal failure) and possibly to lacticacidosis (hypoperfusion due heart failure andhypovolaemia)Metabolic alkalosis due to severe vomitingRespiratory alkalosis due to dyspnoea fromcongestive heart failure.The pO2 is elevated due to administrationof a high inspired oxygen concentration 65. NEXT LECTURE1. Approche to hypoxiemic patient2. Cases</p>