Presentation abg

‫‪arterial blood gases interpretation‬‬ ‫)‪(ABGs‬‬ ‫محمد رضا رجبی‬ ‫کارشناس بیهوشی‬ ‫کارشناس ارشد مراقبت های ویژه‬ ‫دانشگاه علوم پزشکی تهران‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫1‬

In a survey conducted at a university teaching hospital, 70%of the participating physicians claimed that they were wellversed in the diagnosis of acid-base disorders and that theyneeded no assistance in the interpretation of arterial bloodgases (ABGs). These same physicians were then given a series ofABG measurements to interpret, and they correctlyinterpreted only 40% of the test samples.11/2/2010 mohammad reza rajabi 2

A survey at another teaching hospital revealed that incorrect acid- base interpretations led to errors in patient management in one- third of the ABG samples analyzed This can cause trouble in the ICU, where 9 of every 10 patients may have an acid-base disorder.11/2/2010 mohammad reza rajabi 3

Getting an arterial blood gas sample11/2/2010 mohammad reza rajabi 4

‫شریان های مورد استفاده در نمونه گیری خون شریانی:‬ ‫‪ ‬شریان رادیال ،شریان انتخابی جهت نمونه گیری است.‬ ‫‪‬سایر نواحی: شریان های براکیال،اولنار،فمورال،دورسالیس پدیس و‬ ‫تیبیا.‬ ‫‪‬در نوزادان می توان از شریان نافی استفاده کرد.‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫5‬

‫شریان براکیال: بزرگترین شریان در بازوست و به هنگام سوراخ کردن آن‬ ‫ممکن است به اعصاب و لیگامان های ناحیه صدمه وارد آید.‬ ‫شریان رادیال: راحت و قابل لمس است و به راحتی کنترل می شود.‬ ‫شریان اولنا: لمس آن سخت بوده و اگر بیمار همکاری نکند به سختی می‬ ‫توان از آن خون گرفت.‬ ‫شریان فمورال:شریان بزرگ و راحت در لمس و سوراخ کردن است.‬ ‫اسپاسم شریانی نادر است.استفاده از آن توام با خطراتی نظیر هماتوم و‬ ‫ترومبوس است.‬ ‫شریان دورسالیس پدیس و تیبیا: به ندرت از آنها استفاده میشود،کوچک‬ ‫هستند و هنگام خونگیری خطر تخریب گردش خون انتهایی وجود دارد.‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫6‬

‫اگر نیاز به اندازه گیری مکرر ‪ ABG‬است، یک کتتر شریانی را در‬ ‫شریان رادیال جایگذاری کنید.در طول مدتی که بیمار کتتر شریانی دارد ،‬ ‫انتهاها را از نظر رنگ ،حرارت ،احساس گزگز شدن (پارستزی)به طور‬ ‫مکرر بررسی نمایید.‬ ‫هیچگونه تزریقی از طریق کتتر شریانی انجام نشود و این تذکر را روی‬ ‫پانسمان کتتر شریانی قید نمایید.‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫7‬

11/2/2010 mohammad reza rajabi 8

Ulnar Artery Radial Artery11/2/2010 mohammad reza rajabi 9

ABG Sample Port Blood Pressure Waveform11/2/2010 mohammad reza rajabi 11

Arterial Blood Sample Port Can you identify potential clinical problems with this11/2/2010 mohammad reza rajabi 12

Blood Gas Report Acid-Base Information pH-measures the bloods acidity Normal range 7.35- 7.45 Overall H+ from both respiratory and metabolic factors PCO2 partial pressure of carbon dioxide in the blood Normal range 35-45 mmHg Snapshot of adequacy of alveolar ventilation •HCO3 the amount of bicarbonate in the blood Normal range 22- 26 mEq/L Oxygenation Information •PO2 [oxygen tension] •SO2 [oxygen saturation]11/2/2010 mohammad reza rajabi 14

ABGs An arterial blood gas (ABG) is a sample of arterial blood that reports:  pH: 7.35 -7.45 (H ion concentration)  PaCO2: 35-45 mm Hg. ( ventilatory effectiveness)  HCO3: 22 to 26 mEq/L (metabolic effectiveness)  PaO2: 80-100 mm Hg (oxygenation of blood)  SaO2 = 95% - 100% (% of hemoglobin saturated)11/2/2010 mohammad reza rajabi 15

Acid-Base Balance within the body CO2 + H2O H2CO3 H+ HCO3- Normal bicarbonate: 22 – 26 mEq/L Normal base excess: -2 mEq/L - + 2 mEq/L Normal Carbon Dioxide: 35 – 45 mmHg11/2/2010 mohammad reza rajabi 17

Evaluate pH and determine acidosis or alkalosis 7.35 7.40 7.45 Acid Normal Base Acidosis Alkalosis11/2/2010 mohammad reza rajabi 18

• Evaluate pCO2 (respiratory) 35 40 45 Base Normal Acid11/2/2010 mohammad reza rajabi 19

• Evaluate HCO3 (metabolic) 22 24 26 Acid Normal Base11/2/2010 mohammad reza rajabi 20

• Determine level of oxygenation (arterial samples only) • Normal = 80 – 100 mmHg • Mild hypoxemia = 60 – 80 mmHg • Moderate hypoxemia = 40 – 60 mmHg • Severe hypoxemia = less than 40 mmHg11/2/2010 mohammad reza rajabi 21

Blood Gas Report Acid-Base Information •pH •PCO2 •HCO3 Oxygenation Information •PO2 [oxygen tension] •SO2 [oxygen saturation]11/2/2010 mohammad reza rajabi 22

PaO2 [oxygen tension]SaO2 [oxygen saturation]a = arterial 11/2/2010 mohammad reza rajabi 23

Pulse Oximeter Measures SaO211/2/2010 mohammad reza rajabi 24

Pulse Oximeter Measures SaO211/2/2010 mohammad reza rajabi 25

pH and [H +] +] (9-pH) [ H in nEq/L = 1011/2/2010 mohammad reza rajabi 27

A normal [H+] of 40 pH [H+]nEq/L corresponds to apH of 7.40. Because 7.7 20the pH is a negative 7.5 31logarithm of the [H+], 7.4 40changes in pH areinversely related to 7.3 50changes in [H+] (e.g., a 7.1 80decrease in pH is 7.0 100associated with an 6.8 160increase in [H+]).11/2/2010 mohammad reza rajabi 28

The left side of the The right side of“H” is the the “H” is therespiratory side metabolic side withwith the “normal” the “normal”values (35 – 45) values (22 – 26)around the around the“midline” of the “midline” of the The “midline” of the “H” is a line which runs between the “normal” values for carbon dioxide and bicarbonate. 11/2/2010 mohammad reza rajabi 29

Hydrogen Ion Regulation The body maintains a narrow pH range by 3 mechanisms: 1. Chemical buffers (extracellular and intracellular) react instantly to compensate for the addition or subtraction of H+ ions. 2. CO2 elimination is controlled by the lungs (respiratory system). Decreases (increases) in pH result in decreases (increases) in PCO2 within minutes. 3. HCO3- elimination is controlled by the kidneys. Decreases (increases) in pH result in increases (decreases) in HCO3-. It takes hours to days for the renal system to compensate for changes in pH.11/2/2010 mohammad reza rajabi 30

 Respiratory acidosis  metabolic alkalosis  Respiratory alkalosis  metabolic acidosis I. Buffers kick in within minutes. II. Respiratory compensation is rapid and starts within minutes and complete within 24 hours. III. Kidney compensation takes hours and up to 5 days11/2/2010 mohammad reza rajabi 31

CENTRAL EQUATION OFACID-BASE PHYSIOLOGYThe hydrogen ion concentration [H+] in extracellular fluid isdetermined by the balance between the partial pressure ofcarbon dioxide (PCO2) and the concentration of bicarbonate[HCO3-] in the fluid. This relationship is expressed asfollows: [H+] in nEq/L = 24 x (PCO2 / [HCO3 -] ) 11/2/2010 mohammad reza rajabi 32

NORMAL VALUES Using a normal arterial PCO2 of 40 mm Hg and a normal serum [HCO3 - ] concentration of 24 mEq/L, the normal + [H ] in arterial blood is 24 × (40/24) = 40 nEq / L11/2/2010 mohammad reza rajabi 33

PCO2/[HCO3- ] Ratio Since [H+] = 24 x (PCO2 / [HCO3-]), the stability of the extracellular pH is determined by the stability of the PCO2/HCO3- ratio. Maintaining a constant PCO2/HCO3- ratio will maintain a constant extracellular pH.11/2/2010 mohammad reza rajabi 34

PCO2/[HCO3- ] Ratio When a primary acid-base disturbance alters one component of the PCO2/[HCO3- ]ratio, the compensatory response alters the other component in the same direction to keep the PCO2/[HCO3- ] ratio constant.11/2/2010 mohammad reza rajabi 35

COMPENSATORY CHANGES When the primary disorder is metabolic (i.e., a change in [HCO3 - ], the compensatory response is respiratory (i.e., a change in PCO2), and vice-versa. It is important to emphasize that compensatory responses limit rather than prevent changes in pH (i.e., compensation is not synonymous with correction).11/2/2010 mohammad reza rajabi 36

Renal Compensation for primary respiratory disorders  Resp.Acidosis: PaCo2 Acute 1meq/L in [Hco3-] for each 10 mmHg in PaCO2 Chronic 3meq/L in [Hco3-] for each 10 mmHg in PaCO2  Resp.Alk: PaCo2 Acute 2meq/L in [Hco3-] for each 10 mmHg in PaCO2 Chronic 5meq/L in [Hco3-] for each 10 mmHg in PaCO211/2/2010 mohammad reza rajabi 38

Respiratory Compensation for primary renal disorders  Metabolic Acidosis: [HCO3] 1.2 mmHg in PaCO2 for each meq in [HCO3]  Metabolic Alk: [HCO3] 0.7 mmHg in PaCO2 for each meq in [HCO3]11/2/2010 mohammad reza rajabi 39

Mixed Acid-Base Abnormalities Case Study No. 3: 56 yo   neurologic dz required ventilator support for several weeks. She seemed most comfortable when hyperventilated to PaCO2 28-30 mmHg. She required daily doses of lasix to assure adequate urine output and received 40 mmol/L IV K+ each day. On 10th day of ICU her ABG on 24% oxygen & VS:11/2/2010 mohammad reza rajabi 40

ABG Results pH 7.62 BP 115/80 mmHg PCO2 30 mmHg Pulse 88/min PO2 85 mmHg RR 10/min HCO3 30 mmol/L VT 1000ml BE 10 mmol/L MV 10L K+ 2.5 mmol/L Interpretation: Acute alveolar hyperventilation (resp. alkalosis) and metabolic alkalosis with corrected hypoxemia.11/2/2010 mohammad reza rajabi 41

Case study No. 4 27 yo retarded  with insulin-dependent DM arrived at ER from the institution where he lived. On room air ABG & VS: pH 7.15 BP 180/110 mmHg PCO2 22 mmHg Pulse 130/min PO2 92 mmHg RR 40/min HCO3 9 mmol/L VT 800ml BE -30 mmol/L MV 32L Interpretation: Partly compensated metabolic acidosis.11/2/2010 mohammad reza rajabi 42

Case study No. 574 yo  with hx chronic renal failure and chronic diuretic therapywas admitted to ICU comatose and severely dehydrated. On40% oxygen her ABG & VS:pH 7.52 BP 130/90 mmHgPCO2 55 mmHg Pulse 120/minPO2 92 mmHg RR 25/minHCO3 42 mmol/L VT 150mlBE 17 mmol/L MV 3.75LInterpretation: Partly compensated metabolic alkalosis withcorrected hypoxemia. 11/2/2010 mohammad reza rajabi 43

Case study No. 643 yo  arrives in ER 20 minutes after a MVA in which heinjured his face on the dashboard. He is agitated, has mottled,cold and clammy skin and has obvious partial airway obstruction.An oxygen mask at 10 L is placed on his face. ABG & VS:pH 7.10 BP 150/110 mmHgPCO2 60 mmHg Pulse 150/minPO2 125 mmHg RR 45/minHCO3 18 mmol/L VT ? mlBE -15 mmol/L MV ?L. Interpretation: Acute ventilatory failure (resp. acidosis) and acute metabolic acidosisreza rajabi corrected hypoxemia11/2/2010 mohammad with 44

Case study No. 7 17 yo, 48 kg  with known insulin-dependent DM came to ER with Kussmaul breathing and irregular pulse. Room air ABG & VS: pH 7.05 BP 140/90 mmHg PCO2 12 mmHg Pulse 118/min PO2 108 mmHg RR 40/min HCO3 5 mmol/L VT 1200ml BE -30 mmol/L MV 48L Interpretation: Severe partly compensated metabolic acidosis without hypoxemia.11/2/2010 mohammad reza rajabi 45

Case No. 7 cont’d This patient is in diabetic ketoacidosis. IV glucose and insulin were immediately administered. A judgement was made that severe acidemia was adversely affecting CV function and bicarb was elected to restore pH to  7.20. Bicarb administration calculation: Base deficit X weight (kg) 3 30 X 48 = 480 mmol/L Admin 1/2 over 15 min & 3 repeat ABG11/2/2010 mohammad reza rajabi 46

Case No. 7 cont’d ABG result after bicarb: pH 7.27 BP 130/80 mmHg PCO2 25 mmHg Pulse 100/min PO2 92 mmHg RR 22/min HCO3 11 mmol/L VT 600ml BE -14 mmol/L MV 13.2L11/2/2010 mohammad reza rajabi 47

Case study No. 8 47 yo  was in PACU for 3 hours s/p cholecystectomy. She had been on 40% oxygen and ABG & VS: pH 7.44 BP 130/90 mmHg PCO2 32 mmHg Pulse 95/min, regular PO2 121 mmHg RR 20/min HCO3 22 mmol/L VT 350ml BE -2 mmol/L MV 7L SaO2 98% Hb 13 g/dL11/2/2010 mohammad reza rajabi 48

Case No. 8 cont’d Oxygen was changed to 2L N/C. 1/2 hour pt. ready to be D/C to floor and ABG & VS: pH 7.41 BP 130/90 mmHg PCO2 10 mmHg Pulse 95/min, regular PO2 148 mmHg RR 20/min HCO3 6 mmol/L VT 350ml BE -17 mmol/L MV 7L SaO2 99% Hb 7 g/dL11/2/2010 mohammad reza rajabi 49

Case No. 8 cont’d What is going on?11/2/2010 mohammad reza rajabi 50

Case No. 8 cont’d If the picture doesn’t fit, repeat ABG!! pH 7. 45 BP 130/90 mmHg PCO2 31 mmHg Pulse 95/min PO2 87 mmHg RR 20/min HCO3 22 mmol/L VT 350ml BE -2 mmol/L MV 7L SaO2 96% Hb 13 g/dL Technical error was presumed.11/2/2010 mohammad reza rajabi 51

Case study No. 9 67 yo  who had closed reduction of leg fx without incident. Four days later she experienced a sudden onset of severe chest pain . Room air ABG & VS: pH 7.36 BP 130/90 mmHg PCO2 33 mmHg Pulse 100/min PO2 55 mmHg RR 25/min HCO3 18 mmol/L BE -5 mmol/L MV 18L SaO2 88% Interpretation: Compensated metabolic acidosis with moderate hypoxemia. Dx: PE11/2/2010 mohammad reza rajabi 52

Case study No. 10 76 yo  with documented chronic hypercapnia secondary to severe COPD has been in ICU for 3 days while being tx for pneumonia. She had been stable for past 24 hours and was transferred to general floor. Pt was on 2L oxygen & ABG &VS: pH 7.44 BP 135/95 mmHg PCO2 63 mmHg Pulse 110/min PO2 52 mmHg RR 22/min HCO3 42 mmol/L BE +16 mmol/L MV 10L SaO2 86% . Interpretation: Chronic ventilatory failure (resp. acidosis) with uncorrected hypoxemia11/2/2010 mohammad reza rajabi 53

Case No. 10 cont’d She was placed on 3L and monitored for next hour. She remained alert, oriented and comfortable. ABG was repeated: pH 7.36 BP 140/100 mmHg PCO2 75 mmHg Pulse 105/min PO2 65 mmHg RR 24/min HCO3 42 mmol/L BE +16 mmol/L MV 4.8L SaO2 92% . Pt’s ventilatory pattern has changed to more rapid and shallow breathing. Although still acceptable the pH and CO2 are trending in the wrong direction. High-flow oxygen may be better for this pt to prevent intubation11/2/2010 mohammad reza rajabi 54

Respiratory Acidosis • Excessive CO2 retention • Causes – Airway obstruction – Depression of respiratory drive • Sedatives, analgesics • Head trauma – Respiratory muscle weakness resulting from muscle disease or chest wall abnormalities – Decreased lung surface area participating in gas exchange11/2/2010 mohammad reza rajabi 55

Respiratory Acidosis • Clues – Confusion, restlessness – Headache, dizziness – Lethargy – Dyspnea – Tachycardia – Dysrhythmias – Coma leading to death11/2/2010 mohammad reza rajabi 56

Respiratory Acidosis • Solutions – Improve ventilation • Ensure adequate airway; positioning, suctioning • Encourage deep breathing and coughing • Frequent repositioning • Chest physio/ postural drainage • Bronchodilators • Decrease sedation/analgesia • Oxygen therapy11/2/2010 mohammad reza rajabi 57

Respiratory Alkalosis • Excessive CO2 loss due to hyperventilation • Causes – CNS injury: brainstem lesions, salicylate overdose, Reye’s Syndrome, hepatic encephalopathy – Aggressive mechanical ventilation – Anxiety, fear or pain – Hypoxia – Fever – Congestive heart failure11/2/2010 mohammad reza rajabi 58

Respiratory Alkalosis • Clues – Light headedness – Confusion – Decreased concentration – Tingling fingers and toes – Syncope – Tetany11/2/2010 mohammad reza rajabi 59

Respiratory Alkalosis • Solutions – Decrease respiratory rate and depth • Sedation/analgesia as appropriate • Rebreather mask • Paper bag • Emotional support/encourage patient to slow breathing • Calm, soothing environment11/2/2010 mohammad reza rajabi 60

Metabolic Acidosis • Excessive HCO3 loss, or acid gain • Causes – Diabetic ketoacidosis – Sepsis/shock – Diarrhea (fluid losses below gastric sphincter) – Renal Failure – Poison ingestion – Starvation – Dehydration11/2/2010 mohammad reza rajabi 61

Metabolic Acidosis • Clues – Stupor – Restlessness – Kussmaul’s respirations )air hunger( – Seizures – Coma leading to death11/2/2010 mohammad reza rajabi 62

Metabolic Acidosis • Solutions – Replace HCO3 while treating underlying cause – Monitor intake and output – Monitor electrolytes, especially K+ – Seizure precautions11/2/2010 mohammad reza rajabi 63

Physiologic Effects of Acidosis  Reduced cardiac contractility  Increased PVR  Reduced SVR  Impaired response to catecholamines  Compensatory hyperventilation11/2/2010 mohammad reza rajabi 64

Manifestations usually being when serum pH goesbelow 7.2  Tachycardia (until pH less than 7.0, than bradycardia)  Kussmaul’s respirations  Dysrhythmias  CNS depression11/2/2010 mohammad reza rajabi 65

Metabolic Alkalosis • HCO3 retention, or loss of extracellular acid, • Causes – GI losses above gastric sphincter • Vomiting • Nasogastric suction – Antiacids – Diuretic therapy causing electrolyte loss11/2/2010 mohammad reza rajabi 66

Metabolic Alkalosis • Clues – Weakness, dizziness – Disorientation – Hypoventilation – Muscle twitching – Tetany11/2/2010 mohammad reza rajabi 67

Metabolic Alkalosis • Solutions – Control vomiting – Replace GI losses – Eliminate overuse of antacids – Monitor intake and output – Monitor electrolytes11/2/2010 mohammad reza rajabi 68

Effects of Metabolic Alkalosis  Decreased serum potassium  Decreased serum ionized calcium  Dysrhythmias  Hypoventilation / hypoxemia  Increased bronchial tone / atelectasis  Left shift of the Oxygen curve11/2/2010 mohammad reza rajabi 69

‫‪Anion Gap‬‬ ‫) ] -3‪ [Na+ ] – ([Cl- ] + [Hco‬‬ ‫‪ difference between the concentrations of the measured‬‬ ‫‪cations and the measured anion‬‬ ‫‪ approximately 8 to 12 mEq/L in healthy individuals‬‬ ‫فقط بعضی از آنیون ها و کاتیون ها در آزمایشگاه تعیین می شوند.‬ ‫‪‬‬ ‫کاتیون ها وآنیون های تعیین شده : سدیم،بیکربنات،کلر‬ ‫‪‬‬ ‫کاتیون های تعیین نشده: پتاسیم،منیزیم،کلسیم‬ ‫‪‬‬ ‫آنیون های تعیین نشده: فسفات،آلبومین،سولفات،الکتات‬ ‫‪‬‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫07‬

‫شکاف آنیونی طبیعی (هیپرکلرمی)‬ ‫شکاف آنیونی افزایش یافته‬ ‫(نورموکلرمی)‬ ‫اسهال‬ ‫کتواسیدوز‬ ‫اسیدوز توبولی کلیوی‬ ‫اسیدوز الکتیک‬ ‫نارسایی کلیوی مزمن‬ ‫سالیسیالت ها‬ ‫مسمومیت با متانول‬ ‫مسمومیت با اتیلن گلیکول‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫17‬

‫مواردی که باعث کاهش شکاف آنیونی می شوند‬ ‫‪ ‬هیپرکالمی‬ ‫‪ ‬هیپوآلبومینمی‬ ‫‪ ‬هیپوناترمی‬‫0102/2/11‬ ‫‪mohammad reza rajabi‬‬ ‫27‬

increase the anion gap in the absence of metabolic acidosis  renal failure  volume depletion  metabolic alkalosis  some penicillins11/2/2010 mohammad reza rajabi 73

How to Analyze an ABG 1. PO2 NL = 80 – 100 mmHg 2. pH NL = 7.35 – 7.45 Acidotic <7.35 Alkalotic >7.45 3. PCO2 NL = 35 – 45 mmHg Acidotic >45 Alkalotic <35 4. HCO3 NL = 22 – 26 mmol/L Acidotic < 22 Alkalotic > 2611/2/2010 mohammad reza rajabi 74

Four-step ABG Interpretation Step 1:  Examine PaO2 & SaO2  Determine oxygen status  Low PaO2 (<80 mmHg) & SaO2 means hypoxia  NL/elevated oxygen means adequate oxygenation11/2/2010 mohammad reza rajabi 75

Four-step ABG Interpretation Step 2:  pH acidosis <7.35 alkalosis >7.4511/2/2010 mohammad reza rajabi 76

Four-step ABG Interpretation Step 3:  study PaCO2 & HCO 3  respiratory irregularity if PaCO2 abnl & HCO3 NL  metabolic irregularity if HCO3 abnl & PaCO2 NL11/2/2010 mohammad reza rajabi 77

Four-step ABG Interpretation Step 4: Determine if there is a compensatory mechanism working to try to correct the pH. ie: if have primary respiratory acidosis will have increased PaCO2 and decreased pH. Compensation occurs when the kidneys retain HCO3.11/2/2010 mohammad reza rajabi 78

~ PaCO – pH Relationship 2 0.08 change in PH for every 10 mmHg change in PaCO2 ~ [HCO3] – pH Relationship 0.1 change in PH for every 1 meq/L change in bicarbonate11/2/2010 mohammad reza rajabi 79

Respiratory Compensation The ventilatory control system provides the compensation for metabolic acid-base disturbances, and the response is prompt. The changes in ventilation are mediated by H+ sensitive chemoreceptors located in the carotid body (at the carotid bifurcation in the neck) and in the lower brainstem.11/2/2010 mohammad reza rajabi 80

Respiratory Compensation A metabolic acidosis excites the chemoreceptors and initiates a prompt increase in ventilation and a decrease in arterial PCO2. A metabolic alkalosis silences the chemoreceptors and produces a prompt decrease in ventilation and increase in arterial PCO2.11/2/2010 mohammad reza rajabi 81

 Recall that for acute respiratory disturbances (where renal compensation does not have much time to occur) each arterial PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.08, while for chronic respiratory disturbances (where renal compensation has time to occur) each PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.03.11/2/2010 mohammad reza rajabi 82

CENTRAL EQUATION OF ACID- BASE PHYSIOLOGY The hydrogen ion concentration [H+] in extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO2) and the concentration of bicarbonate [HCO3-] in the fluid. This relationship is expressed as follows: [H+] in nEq/L = 24 x (PCO2 / [HCO3 -] ) where [ H+] is related to pH by [ H+] in nEq/L = 10 (9-pH)11/2/2010 mohammad reza rajabi 83

Case report  Very sick 56 year old man being evaluated for a possible double lung transplant  Dyspnea on minimal exertion  On home oxygen therapy (nasal prongs, 2 lpm)  Numerous pulmonary medications arterial blood gas sample is taken, revealing the following: pH 7.30 PCO2 65 mm Hg11/2/2010 mohammad reza rajabi 84

What is the hydrogen ion concentration? [H+] = 10 (9-pH) = 10 (9-7.3) = 10 (1.7) = 50.1 nEq/L11/2/2010 mohammad reza rajabi 85

What is the bicarbonate ion concentration? Remember that [H+] = 24 x (PCO2 / [HCO3 -] ) Thus, [HCO3 -] = 24 x (PCO2 / [H+] ) [HCO3 -] = 24 x (65 / 50.1 ) [HCO3 -] = 31.1 mEq/L11/2/2010 mohammad reza rajabi 86

What is the acid-base disorder?Recall that for acute respiratory disturbances (whererenal compensation does not have much time to occur)each arterial PCO2 shift of 10 mm Hg is accompaniedby a pH shift of about 0.08, while for chronicrespiratory disturbances (where renal compensationhas time to occur) each PCO2 shift of 10 mm Hg isaccompanied by a pH shift of about 0.03.11/2/2010 mohammad reza rajabi 87

What is the acid-base disorder?In our case an arterial PCO2 shift of 25 mm Hg (from 40 to 65mm Hg) is accompanied by a pH shift of 0.10 units (from 7.40to 7.30), or a 0.04 pH shift for each PCO2 shift of 10 mm. Since0.04 is reasonably close to the expected value of 0.03 for anchronic respiratory disturbance, it is reasonable to say that thepatient has aCHRONIC RESPIRATORY ACIDOSIS.11/2/2010 mohammad reza rajabi 88

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