Acid-Base 4.18.58 PM

Acid-Base 4.18.58 PM - Acid Base Disturbances Acid Ian Chan...

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Unformatted text preview: Acid Base Disturbances Acid Ian Chan MS4 Eliza Long R2 10/30/06 ABG analysis ABG Why do we care ? – – – – Critical care requires a good understanding Critical Helps in the differential and final diagnosis Helps in determining treatment plan Treating acid/base disorders helps medications Treating work better (i.e. antibiotics, vasopressors, etc.) work – Helps in ventilator management – Severe acid/base disorders may need dialysis – Changes in electrolyte levels in acidosis Changes (increased K+ and Na+, and decreases in HCO3) (increased Acid buffering Acid The Anion Gap The Na – (Cl + HCO3) NaHCO3 + HCL NaCL + H2CO3 NaHCO3 NaHCO3 + HX NaX+ H2CO3 Unmeasured cations: calcium, Unmeasured magnesium, gamma globulins, potassium. magnesium, Unmeasured anions: albumin, phosphate, Unmeasured sulfate, lactate. sulfate, Gap Acidosis Gap Methanol Uremia Diabetic ketoacidosis Paraldehyde Paraldehyde INH INH Lactic acidosis Ethylene Glycol Salicylate Non Gap Acidosis Non H: hyperalimentation A: acetazolamide R: RTA D: diarrhea U: rectosigmoidostomy P: pancreatic fistula Metabolic Acidosis Metabolic Respiratory compensation process takes 1224 hours to become fully active. Protons are 24 slow to diffuse across the blood brain barrier. In the case of LA this will be faster because LA is produced in the brain. The degree of compensation can be assessed by using Winter’s Formula. It is INAPPROPRIATE to use this formula before the acidosis has existed for 12-24 hours. – PCO2 = 1.5 (HCO3) + 8 +/-2. PCO2 Decreased anion gap Decreased Decrease in unmeasured anions – Hypoalbuminemia Increase in unmeasured cations – Hypercalcemia – Hypermagnesemia – Hyperkalemia – Multiple myeloma – Lithium toxicity Metabolic Alkalosis Metabolic Generation by gain of HCO3 and maintained Generation by abnormal renal HCO3 absorption. This is almost always secondary to volume contraction (low Cl in urine, responsive to NaCl, maintained at proximal tubule) NaCl, – – – – – Vomiting: net loss of H+ and gain of HCO3. Diuretics: ECFV depletion Chronic diarrhea: ECFV depletion Profound hypokalemia Renal failure: if we cannot filter HCO3 we cannot Renal excrete it. Mineralocorticoid excess: increased H secretion, hypokalemia (Na/K exchanger), saline resistant). saline Respiratory Acidosis Respiratory Acute or Chronic: has the kidney had Acute enough time to partially compensate? The source of the BUFFER (we need to produce bicarb) is different in these states and thus we need to make this distinction. Respiratory Acidosis Respiratory Acute : H is titrated by non HCO3 organic tissue Acute buffers. Hb is an example. The kidney has little involvement in this phase. – 10 mm Hg increase in CO2 / pH should decrease by . 08 Chronic: The mechanism here is the renal Chronic: synthesis and retention of bicarbonate. As HCO3 is added to the blood we see that [Cl] will decrease to balance charges. – This is the hypochloremia of chronic metabolic This acidosis. – 10 mm H increase in CO2 / pH should decrease by . 03 Respiratory Acidosis Respiratory Elevation of CO2 above normal with a drop in Elevation extracellular pH. This is a disorder of ventilation. Rate of CO2 elimination is lower than the production production 5 main categories: main – – – – – CNS depression Pleural disease Lung diseases such as COPD and ARDS Musculoskeletal disorders Compensatory mechanism for metabolic alkalosis Respiratory Alkalosis Respiratory Initiated by a fall in the CO2 activate Initiated processes which lower HCO3. Associated with mild hypokalemia. Cl is retained to offset the loss of HCO3 negative charge. Acute response is independent of renal HCO3 wasting. The chronic compensation is governed by renal HCO3 wasting. Causes Causes – – – – – Intracerebral hemorrhage Drug use : salicylates and progesterone Decreased lung compliance Anxiety Liver cirrhosis Sepsis Arterial Blood Gas (ABG) Analysis Arterial ABG interpretation Follow rules and you will always be right !! 1) determine PH 1) acidemia or alkalemia acidemia 2) calculate the anion gap 2) 3) determine Co2 compensation (winters formula) 4) calculate the delta gap (delta HCO3) ABG analysis ABG Arterial Blood Gas (ABG) –interpretation – Always evaluate PH first Alkalosis – PH > 7.45 Acidosis – PH < 7.35 – Determine anion gap (AG) – AG = NA – (HCO3+ CL) AG metabolic acidosis Non AG acidosis – determined by delta gap – Winters formula Calculates expected PaCO2 for metabolic acidosis PaCO2 = 1.5 x HCO3 + 8 PaCO2 ABG analysis ABG Delta gap – Delta HCO3 = HCO3 (electrolytes) + change in AG Delta gap < 24 = non AG acidosis Delta gap > 24 = metabolic alkalosis – Note: The key to ABG interpretation is Note: following the above steps in order. following ABG analysis ABG 33 y/o with DKA presents with the 33 following: following: – Na = 128, Cl = 90, HCO3 = 4, Glucose = 800 – 7.0/14/90/4/95% – PH = acidemia PH – AG = 128 – (90 + 4) = 34 – Winters formula – 1.5(4) + 8 = 14 – Delta gap = 4 + (34 – 12) = 26 ABG analysis ABG Answer – AG acidosis with appropriate respiratory AG compensation compensation – History c/w ketoacidosis secondary to DKA History with appropriate respiratory compensation with ABG analysis ABG 56 y/o with COPD exacerbation and hypotension 56 and associated diarrhea x 7 days presents with the following ABG: the 139 110 20 – 7.22/30/65/10/90% 7.22/30/65/10/90% 120 4.0 10 1.5 PH(7.22) = acidemia PH(7.22) AG = 139 – (10 + 110) = 19 (nl AG = 8-12) Winters formula – PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23 Delta gap Delta – – – Delta gap = HC03 + change in the AG = 24 Delta gap = 10 + (19 – 12) = 10 + 7 = 17 Delta gap = 17 ABG - example ABG Triple disorder – AG acidosis AG – Incomplete respiratory compensation – Non AG acidosis History would suggest AG acidosis is secondary to History hypotension with lactic acid build up and the patient is not able to compensate with his COPD therefore there is no respiratory compensation and the non AG acidosis is secondary to diarrhea with associated HCO3 loss. diarrhea Look at the pH. Look – pH < 7.35, acidosis – pH > 7.45, alkalosis Look at PCO2, HCO3Look • Main pathology will be the change correlates with Main the pH. the • If alkalosis pCO2 will be low or Bicarb high • If acidosis pCO2 will be high or Bicard low • The other abnormal parameter is the compensator The response response Respiratory or Metabolic • pCO2 - respiratory • Bicarb - metabolic Metabolic Acidosis? Anion Gap? Metabolic • >12 - ketoacidosis, uremia, lactic acidosis, or >12 toxins toxins • Delta ratio to check for gap and non gap Delta disorders , or metabolic alkalosis happening simultaneously simultaneously • Normal anion gap - diarrhea OR unknown. If Normal unknown calculate urine anion gap, if positive likely RTA, if neg liekly diarrhea likely Metabolic Alkalosis If urin Cl is > 20 it is chloride-resistant alkalosis If (increased mineralcorticoid activity (increased If <20 chloride responsive alkalosis (vomitting or If gastric loss) gastric Example # 1 Example 44 yo M 2 weeks post-op from total 44 proctocolectomy for ulcerative colitis. proctocolectomy Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN Na+ 31, Cr 1.5 31, BG: 7.31/ 33 /93 / 16 BG: Example #2 Example 9 yo M presents with N/V. Na 132 , K 6.0, Cl 93, HCO3- 11 glucose Na 650 650 BG: 7.27/23/96/11/-8 Example #3 Example 70 yo M s/p lap chole, on the morning of 70 POD #1. Pt received 2L bolus of crystalloid throughout pm for tachycardia. Now with SOB. 7.24 / 60 / 52 / 27 /+3 7.24 Example #4 Example 54 yo F s/p mult debridements for 54 necrotizing fasciitis, now on vassopressin to maintain blood pressure to BG - 7.29/40/83/17/-6 BG 7.29/40/83/17/-6 Example #5 Example 35 yo M involved in crush injury, boulder 35 vs body. Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38, Cr 1.7, CK 42,346 Cr BG: 7.30/32/96/15/-4 BG: 7.30/32/96/15/-4 Example #6 Example 4 wks M with projectile emesis Na: 140, K:2.9, Cl: 92 Na: 7.49/40/98/30/+6 7.49/40/98/30/+6 ...
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