src="http://pagead2.googlesyndication.com/pagead/show_ads.js">
src="http://pagead2.googlesyndication.com/pagead/show_ads.js">
ARTERIAL BLOOD GAS INTERPRETATION
- ACIDOSIS & ALKALOSIS ABG INTERPRETATION CRISBERT I. CUALTEROS, M.D.
- Acidosis – presence of a process which tends to lower pH by virtue of gain of H+ or loss of HCO3
- Alkalosis – presence of a process which tends to raise pH by virtue of loss of H+ or addition of HCO3-
- Respiratory – processes which lead to acidosis or alkalosis through a primary alteration in ventilation and resultant excessive elimination or retention of CO2
- Metabolic – processes which lead to acidosis or alkalosis through their effects on the kidneys and the consequent disruption of H+ and HCO3- control
- Acid Base Balance
- pH is maintained within a narrow range to preserve normal cell function
- Buffers –minimize the change in pH resulting from production of acid -> provides immediate protection from acid
- The primary buffer system is HCO3 -
- HCO3- + H+ H2CO3 H2O + CO2
- Simple acid-base disorder – a single primary process of acidosis or alkalosis
- Mixed acid-base disorder – presence of more than one acid base disorder simultaneously
- Compensation – the normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder
- No overcompensation ( except occasionally primary resp. alkalosis)
- Kidneys slow, lungs fast
- Lack of compensation (or over) determines a second primary disorder
- The degree of appropriate compensation is predictable
- Role of the kidney
- To retain and regenerate HCO3- thereby regenerating the buffer with the net effect of eliminating the acid
- H+ secretion
- HCO3- reabsorption
- Role of the respiratory system eliminate CO2
- Characteristics of the simple acid-base disturbances [HCO3-] Pco2 Respiratory alkalosis [HCO3-] Pco2 Respiratory acidosis Pco2 [HCO3-] Metabolic alkalosis Pco2 [HCO3-] Metabolic acidosis Compensated response Primary Primary pH Disorder
- Combined Alkalosis Alk Respiratory Alkalosis Acid Alkalotic Metabolic Alkalosis Alk Acidotic Alkali Metabolic Acidosis Acid Alkalotic Combined respiratory and metabolic Acidosis Acid Respiratory Acidosis Alk Acidotic Acid Interpretation HCO3 PCO 2 pH
- STEPWISE APPROACH
- Determine primary disorder
- Check the compensatory response
- Calculate the anion gap
- Identify specific etiologies for the acid-base disorder
- Prescribe treatment
- DETERMINE THE PRIMARY DISORDER
- pH = 7.35 – 7.45
- pCO2 = 35 – 45 mmHg lungs
- (Reference Value = 40)
- HCO3 = 22 – 26 mmol/L kidneys
- (Reference value = 24)
- DETERMINE PRIMARY DISORDER
- Check the trend of the pH, HCO 3 , pCO 2
- The change that produces the pH is the primary disorder
- DETERMINE PRIMARY DISORDER
- Check the trend of the pH, HCO 3 , pCO 2
- The change that produces the pH is the primary disorder
- DETERMINE PRIMARY DISORDER
- Check the trend of the pH, HCO 3 , pCO 2
- The change that produces the pH is the primary disorder
- DETERMINE PRIMARY DISORDER
- If the trend is the same, check the percent difference
- The bigger % difference is the 1 0 disorder
- DETERMINE PRIMARY DISORDER
- If the trend is the same, check the percent difference
- The bigger %difference is the 1 0 disorder
- CHECK THE COMPENSATORY RESPONSE
- COMPENSATORY RESPONSE
- HENDERSEN-HASSELBACH EQUATION
- 24 x pCO 2
- H = ----------------
- HCO 3
- COMPENSATORY RESPONSE
- HENDERSEN-HASSELBACH EQUATION
- 24 x pCO 2
- H = ----------------
- HCO 3
- PREDICTION OF COMPENSATORY RESPONSES ON SIMPLE ACID BASE DISORDERS
- Metabolic Acidosis PaCO2 = (1.5 X HCO3) + 8 ± 2
- Metabolic Alkalosis PaCO2 will increase 0.75 mmHg per 1 mmol/L increase in HCO3 (0.7 x HCO3) + 20 ± 1.5
- Respiratory Acidosis
- Acute HCO3 will increase 1 mmol/L per 10 mmHg increase in PaCO2 ( ↓ pH by 0.08/10 mm Hg ↑ PaCO2)
- Chronic HCO3 will increase 4 mmol/L per 10 mmHg increase in PaCO2 ( ↓ pH by 0.03/10 mm Hg ↑ PaCO2)
- Respiratory Alkalosis
- Acute HCO3 will decrease 2 mmol/L per 10 mmHg decrease in PaCO2
- Chronic HCO3 will decrease 4 mmol/L per 10 mmHg decrease in PaCO2
- COMPENSATORY RESPONSE
- METABOLIC ACIDOSIS
- PaCO2 = (1.5 X HCO3) + 8 ± 2
- COMPENSATORY RESPONSE HCO 3 = 35 pCO 2 =11 X 0.75 = 8.25 = 8.25 + 40 = 48.25 pCO 2 = 16 x 0.75 = 12 = 12 + 40 = 52 HCO 3 = 40 METABOLIC ALKALOSIS PaCO2 will increase 0.75 mmHg per 1 mmol/L increase in HCO3
- COMPENSATORY RESPONSE pCO 2 = 55 HCO 3 = 55-40/10= 1.5 1.5 + 24 = 25.5 HCO 3 = 80-40/10= 4 4+24 = 28 pCO 2 =80 ACUTE RESPIRATORY ACIDOSIS HCO3 will increase 1 mmol/L per 10 mmHg increase in PaCO2
- COMPENSATORY RESPONSE pCO 3 = 55 HCO 3 = 55-40/10 x 4 = 1.5 x 4 = 6 6 + 24 = 30 CHRONIC RESPIRATORY ACIDOSIS HCO3 will increase 4 mmol/L per 10 mmHg increase in PaCO2
- COMPENSATORY RESPONSE HCO 3 = 80-40/10 x 4 = 16 + 24 = 40 pCO 3 = 80 CHRONIC RESPIRATORY ACIDOSIS HCO3 will increase 4 mmol/L per 10 mmHg increase in PaCO2
- COMPENSATORY RESPONSE RESPIRATORY ALKALOSIS Acute: HCO3 will decrease 2 mmol/L per 10 mmHg decrease in PaCO2 Chronic: HCO3 will decrease 4 mmol/L per 10 mmHg decrease in PaCO2
- CALCULATE THE ANION GAP
- ANION GAP
- Na – (HCO 3 + Cl) = 10-12 mmol/L
- ANION GAP
- Na – (HCO 3 + Cl) = 10-12
- CHECK THE DELTA / DELTA
- DELTA - DELTA
- If with high AG metabolic acidosis
- 12 – AG
- HCO 3
- If normal AG metabolic acidosis
- 12 – Cl
- HCO 3
- DELTA - DELTA
- / = 1
- / > 1
- / <>
- CASE 1
- 56F with vomiting and diarrhea 3 days ago despite intake of loperamide. Her last urine output was 12 hours ago.
- PE showed BP = 80/60, HR = 110, RR = 28. There is poor skin turgor.
- CASE 1
- serum Na = 130 pH = 7.30
- K = 2.5 pCO 2 = 30
- Cl = 105 HCO 3 = 15
- BUN = 42 pO 2 = 90
- crea = 2.0
- RBS = 100
- CASE 1
- serum Na = 130 pH = 7.30 ↓
- K = 2.5 pCO 2 = 30 ↓
- Cl = 105 HCO 3 = 15 ↓
- BUN = 42 pO 2 = 90
- crea = 2.0
- RBS = 100
- CASE 1
- serum Na = 130 pH = 7.30 ↓
- K = 2.5 pCO 2 = 30 ↓
- Cl = 105 HCO 3 = 15 ↓
- BUN = 42 pO 2 = 90
- crea = 2.0
- RBS = 100
- CASE 1
- serum Na = 130 pH = 7.30
- K = 2.5 pCO 2 = 30
- Cl = 105 HCO 3 = 15
- BUN = 42 pO 2 = 90
- crea = 2.0
- RBS = 100
- NORMAL ANION GAP METABOLIC ACIDOSIS
- Diarrhea
- Renal Tubular Acidosis
- Interstitial nephritis
- External pancreatic or small-bowel drainage
- Urinary tract obstruction
- CASE 1
- serum Na = 130 pH = 7.30
- K = 2.5 pCO 2 = 30
- Cl = 105 HCO 3 = 15
- BUN = 15 pO 2 = 90
- crea = 177
- RBS = 100
- CASE 1
- 56F with vomiting and diarrhea 3 days ago despite intake of loperamide. Her last urine output was 12 hours ago.
- PE showed BP = 80/60, HR = 110, RR = 28. There is poor skin turgor.
- pH 7.30, HCO 3 =15, pCO 2 =30, Na=130 K=2.5
- CASE 1
- 1) Hydrate
- 2) Hydrate + IV NaHCO 3
- 3) Hydrate + oral NaHCO 3
- 4) Hydrate + correct hypokalemia
- INDICATIONS FOR HCO 3 THERAPY
- pH <>
- When there is inadequate ventilatory compensation
- Elderly on beta blockers in severe acidosis with compromised cardiac function
- Concurrent severe AG and NAGMA
- Severe acidosis with renal failure or intoxication
- COMPLICATIONS OF HCO 3 THERAPY
- Volume overload
- Hypernatremia
- Hyperosmolarity
- Hypokalemia
- Intracellular acidosis
- Causes overshoot alkalosis
- Stimulates organic acid production
- tissue O 2 delivery
- POTASSIUM CORRECTION
- K deficit = { (4.0 – K) X 350 } / 3 + 60
- CASE 2
- 30M with epilepsy has a grand mal seizure. Labs showed:
- pH = 7.14 ↓ Na = 140
- pCO 2 = 45 K = 4
- HCO 3 = 17 ↓ Cl = 98
- CASE 2
- 30M with epilepsy has a grand mal seizure. Labs showed:
- pH = 7.14 Na = 140
- pCO 2 = 45 K = 4
- HCO 3 = 17 Cl = 98
- CASE 2
- 30M with epilepsy has a grand mal seizure. Labs showed:
- pH = 7.14 Na = 140
- pCO 2 = 45 K = 4
- HCO 3 = 17 Cl = 98
- HIGH ANION GAP METABOLIC ACIDOSIS
- Ketoacidosis – DM, alcohol, starvation
- INH, methanol, lactic acid
- Renal failure
- Ethylene Glycol
- CASE 2
- 30M with epilepsy has a grand mal seizure. Labs showed:
- pH = 7.14 Na = 140
- pCO 2 = 45 K = 4
- HCO 3 = 17 Cl = 98
- CASE 2
- 30M with epilepsy has a grand mal seizure. Labs showed:
- pH = 7.14 Na = 140
- pCO 2 = 45 K = 4
- HCO 3 = 17 Cl = 98
- CASE 2
- 1) IV NaHCO 3 using HCO 3 deficit
- 2) oral NaHCO 3 at 1 mEq/kg/day
- 3) intubate
- 4) no treatment
- CASE 2
- HCO 3 DEFICIT = (D – A) x 0.5 x kg BW
- CASE 2
- HCO 3 DEFICIT = (D – A) x 0.5 x kg BW
- PRINCIPLES OF HCO 3 THERAPY
- LACTIC ACIDOSIS
- Primary effort should be improving O 2 delivery
- Use NaCO 3 only when HCO 3 <>
- In states of CO, raising the CO will have more impact on the pH
- In cases of low alveolar ventilation, ventilation to lower the tissue pCO 2
- PRINCIPLES OF HCO 3 THERAPY
- KETOACIDOSIS
- Rate of H + production is slow; NaHCO 3 tx may just provoke severe hypokalemia
- Should be given if…
- 1) severe hyperkalemia despite insulin
- 2) HCO 3 <>
- 3) worsening acidemia inspite of insulin
- CASE 3
- 19F, fashion model, is surprised to find her K=2.7 mmol/L because she was normokalemic 6 months ago. She admits to being on a diet of fruit and vegetables but denies vomiting and the use of diuretics or laxatives. She is asymptomatic. BP = 90/55 with subtle signs of volume contraction.
- CASE 3
- serum Na 138 63
- K 2.7 34
- Cl 96 0
- HCO 3 30 0
- pH 7.45 5.6
- pCO 2 45
- CASE 3 Expected PCO 2 = 6 x 0.75 = 4.5+40 = 44.5 CompensatedMetabolic Alkalosis serum Na 138 63 K 2.7 34 Cl 96 0 HCO 3 30 0 pH 7.45 5.6 pCO 2 45 Plasma Urine PaCO2 will increase 0.75 mmHg per 1 mmol/L increase in HCO3 from 24
- CASE 3 Anion Gap = Na – (HCO3+Cl) 138 – (30+96) = 12 NAG Plasma Urine serum Na 138 63 K 2.7 34 Cl 96 0 HCO 3 30 0 pH 7.45 5.6 pCO 2 45
- CASE 3 Plasma Urine serum Na 138 63 K 2.7 34 Cl 96 0 HCO 3 30 0 pH 7.45 5.6 pCO 2 45 What is the cause of the acid base disorder?
- CASE 3 What is the cause of the acid base disorder? 1) diuretic intake 2) surreptitious vomiting 3) Bartter’s syndrome 4) Adrenal tumor 5) nonreabsorbable anion
- CASE 3 How should her acid-base disorder be managed? 1) correct hypokalemia 2) hydrate with NSS 3) administer acidyfing agent 4) give carbonic anhydrase inhibitor
- METABOLIC ALKALOSIS
- Vomiting
- Remote diuretic use
- Post hypercapnea
- Chronic diarrhea
- Cystic fibrosis
- Acute alkali administration
- METABOLIC ALKALOSIS
- Bartter’s syndrome
- Severe potassium depletion
- Current diuretic use
- Hypercalcemia
- Hyperaldosteronism
- Cushing’s syndrome
- Gastric aspiration
- MANAGEMENT OF METABOLIC ALKALOSIS
- Chloride repletion
- Potassium repletion
- Tx hypermineralocorticoidism
- Dialysis
- Carbonic anhydrase inhibitors
- Acidyfing agents
- HCl, NH 4 Cl
- INDICATIONS OF HCl
- pH > 7.55 and HCO 3 > 35 with contraindications for NaCl or KCl use
- Immediate correction of metabolic alkalosis in the presence of hepatic encephalopathy, cardiac arrhythmias, digitalis intoxication
- When initial response to NaCl, KCl, or acetalozamide is too slow or too little
- USE OF HCl
- HCL requirement = (A – D) x 0.5 x kg BW
- 0.1 – 0.2 N HCl solution = 100 – 200 mEq
- Do not exceed 0.2 mEq/kg/hour of HCl
- CASE 4
- 73M with long standing COPD (pCO 2 stable at 52-58 mmHg), cor pulmonale, and peripheral edema had been taking furosemide for 6 months. Five days ago, he had anorexia, malaise, and productive cough. He continued his medications until he developed nausea. Later he was found disoriented and somnolent
- CASE 4
- PE: BP 110/70, HR 110, RR 24, T=40
- respiratory distress
- prolonged expiratory phase
- postural drop in BP
- drowsy, disoriented
- scattered rhonchi and rales BLFs
- distant heart sounds
- trace pitting edema
- CASE 4 admission after 48 hrs pH = acidosis pCO 2 =acidosis, HCO 3 = alk Respiratory Acidosis serum Na 136 139 K 3.2 3.9 Cl 78 86 HCO 3 40 38 pH 7.33 7.42 pCO 2 78 61 pO 2 43 56
- CASE 4 serum Na 136 139 K 3.2 3.9 Cl 78 86 HCO 3 40 38 pH 7.33 7.42 pCO 2 78 61 pO 2 43 56 admission after 48 hrs Expected HCO 3 = 78-40/10 = 3.8 + 24 = 27.8 Respiratory Acidosis & M. Alkalosis
- CASE 4 serum Na 136 139 K 3.2 3.9 Cl 78 86 HCO 3 40 38 pH 7.33 7.42 pCO 2 78 61 pO 2 43 56 How should this patient be managed? admission after 48 hrs
- CASE 4 1) intubation and mechanical ventilation 2) low flow oxygenation by nasal prong 3) oxygen by face mask 4) sodium bicarbonate infusion with KCl How should this patient be managed?
- RESPIRATORY ACIDOSIS
- CHRONIC: COPD, intracranial tumors
- ACUTE: pneumonia, head trauma, general
- anesthetics, sedatives
- MANAGEMENT OF RESPIRATORY ACIDOSIS
- Correct underlying cause for hypoventilation
- effective alveolar ventilation intubate, mechanically ventilate
- Antagonize sedative drugs
- Stimulate respiration (e.g. progesterone)
- Correct metabolic alkalosis
- CASE 5
- 42M, alcoholic, brought to the ER intoxicated. He was found at Rizal park in a pool of vomitus. PE showed unkempt and incoherent patient with a markedly contracted ECF volume. T=39 0 C with crackles on the RULF.
- serum Na = 130 pH = 7.53
- K = 2.9 pCO2 = 25
- Cl = 80 HCO3 = 20
- BUN = 34 pO2 = 60
- crea = 1.4 alb = 38
- RBS = 15 mmol/L
- serum Na = 130 pH = 7.53 ↑
- K = 2.9 pCO2 = 25 ↓
- Cl = 80 HCO3 = 20 ↓
- BUN = 34 pO2 = 60
- crea = 1.4 alb = 38
- RBS = 120 mmol/L
- serum Na = 130 pH = 7.53
- K = 2.9 pCO2 = 25
- Cl = 80 HCO3 = 20
- BUN = 12 pO2 = 60
- crea = 120 alb = 38
- RBS = 120 mmol/L
- serum Na = 130 pH = 7.53
- K = 2.9 pCO2 = 25
- Cl = 80 HCO3 = 20
- BUN = 12 pO2 = 60
- crea = 120 alb = 38
- RBS = 15 mmol/L
- serum Na = 130 pH = 7.53
- K = 2.9 pCO2 = 25
- Cl = 80 HCO3 = 20
- BUN = 12 pO2 = 60
- crea = 120 alb = 38
- RBS = 15 mmol/L
- 1) aspiration pneumonia
- 2) alcohol ketoacidosis
- 3) vomiting
- RESPIRATORY ALKALOSIS
- Hyperventilation, Pregnancy, Liver failure, Methylxanthines
- MANAGEMENT OF RESPIRATORY ALKALOSIS
- Correct underlying cause of hyperventilation
- Rebreathe carbon dioxide
- Mechanical control of ventilation
- increase dead space
- decrease back up rate
- decrease tidal volume
- paralyze respiratory muscles
- QUESTIONS?
- Thank You