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    Acid Base

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    Samantha Deshapriya
    This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers the following key points in 3 sentences: ABG analysis is important for critical care as it helps with diagnosis, treatment plans, and ventilator management. The main steps in interpreting an ABG are evaluating the pH to determine acidosis or alkalosis, calculating the anion gap to identify metabolic acidosis, and using Winter's formula to assess respiratory compensation. Common acid-base disturbances include respiratory acidosis and alkalosis from lung diseases or ventilation issues, and metabolic acidosis and alkalosis which are usually secondary to other processes that impact electrolyte and acid-base balance.

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    Acid Base

    Uploaded by

    Samantha Deshapriya
    41 views28 pages
    This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers the following key points in 3 sentences: ABG analysis is important for critical care as it helps with diagnosis, treatment plans, and ventilator management. The main steps in interpreting an ABG are evaluating the pH to determine acidosis or alkalosis, calculating the anion gap to identify metabolic acidosis, and using Winter's formula to assess respiratory compensation. Common acid-base disturbances include respiratory acidosis and alkalosis from lung diseases or ventilation issues, and metabolic acidosis and alkalosis which are usually secondary to other processes that impact electrolyte and acid-base balance.

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    Acid-Base

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    This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers the following key points in 3 sentences: ABG analysis is important for critical care as it helps with diagnosis, treatment plans, and ventilator management. The main steps in interpreting an ABG are evaluating the pH to determine acidosis or alkalosis, calculating the anion gap to identify metabolic acidosis, and using Winter's formula to assess respiratory compensation. Common acid-base disturbances include respiratory acidosis and alkalosis from lung diseases or ventilation issues, and metabolic acidosis and alkalosis which are usually secondary to other processes that impact electrolyte and acid-base balance.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    41 views28 pages

    Acid Base

    Uploaded by

    Samantha Deshapriya
    This document discusses acid-base disturbances and the interpretation of arterial blood gases (ABGs). It covers the following key points in 3 sentences: ABG analysis is important for critical care as it helps with diagnosis, treatment plans, and ventilator management. The main steps in interpreting an ABG are evaluating the pH to determine acidosis or alkalosis, calculating the anion gap to identify metabolic acidosis, and using Winter's formula to assess respiratory compensation. Common acid-base disturbances include respiratory acidosis and alkalosis from lung diseases or ventilation issues, and metabolic acidosis and alkalosis which are usually secondary to other processes that impact electrolyte and acid-base balance.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 28

    Acid Base Disturbances

    ABG analysis
    Why do we care ?
    Critical care requires a good understanding Helps in the differential and final diagnosis Helps in determining treatment plan Treating acid/base disorders helps medications work better (i.e. antibiotics, vasopressors, etc.) Helps in ventilator management Severe acid/base disorders may need dialysis Changes in electrolyte levels in acidosis (increased K+ and Na+, and decreases in HCO3)

    Acid buffering

    The Anion Gap


    Na (Cl + HCO3) NaHCO3 + HCL NaCL + H2CO3 NaHCO3 + HX NaX+ H2CO3 Unmeasured cations: calcium, magnesium, gamma globulins, potassium. Unmeasured anions: albumin, phosphate, sulfate, lactate.

    Gap Acidosis
    Methanol Uremia Diabetic ketoacidosis Paraldehyde INH Lactic acidosis Ethylene Glycol Salicylate

    Non Gap Acidosis


    H: hyperalimentation A: acetazolamide R: RTA D: diarrhea U: rectosigmoidostomy P: pancreatic fistula

    Metabolic Acidosis
    Respiratory compensation process takes 1224 hours to become fully active. Protons are 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 Winters Formula. It is INAPPROPRIATE to use this formula before the acidosis has existed for 12-24 hours.
    PCO2 = 1.5 (HCO3) + 8 +/-2.

    Decreased anion gap


    Decrease in unmeasured anions
    Hypoalbuminemia

    Increase in unmeasured cations


    Hypercalcemia Hypermagnesemia Hyperkalemia Multiple myeloma Lithium toxicity

    Metabolic Alkalosis
    Generation by gain of HCO3 and maintained by abnormal renal HCO3 absorption. This is almost always secondary to volume contraction (low Cl in urine, responsive to NaCl, maintained at proximal tubule)
    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 excrete it.

    Mineralocorticoid excess: increased H secretion, hypokalemia (Na/K exchanger), saline resistant).

    Respiratory Acidosis
    Acute or Chronic: has the kidney had 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
    Acute : H is titrated by non HCO3 organic tissue 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 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 acidosis. 10 mm H increase in CO2 / pH should decrease by .03

    Respiratory Acidosis
    Elevation of CO2 above normal with a drop in extracellular pH. This is a disorder of ventilation. Rate of CO2 elimination is lower than the production 5 main categories:
    CNS depression Pleural disease Lung diseases such as COPD and ARDS Musculoskeletal disorders Compensatory mechanism for metabolic alkalosis

    Respiratory Alkalosis
    Initiated by a fall in the CO2 activate 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
    Intracerebral hemorrhage Drug use : salicylates and progesterone Decreased lung compliance Anxiety Liver cirrhosis Sepsis

    Arterial Blood Gas (ABG) Analysis


    ABG interpretation Follow rules and you will always be right !! 1) determine PH acidemia or alkalemia 2) calculate the anion gap 3) determine Co2 compensation (winters formula) 4) calculate the delta gap (delta HCO3)

    ABG analysis
    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

    ABG analysis
    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 following the above steps in order.

    ABG analysis
    33 y/o with DKA presents with the following:
    Na = 128, Cl = 90, HCO3 = 4, Glucose = 800 7.0/14/90/4/95% PH = acidemia AG = 128 (90 + 4) = 34 Winters formula 1.5(4) + 8 = 14 Delta gap = 4 + (34 12) = 26

    ABG analysis
    Answer
    AG acidosis with appropriate respiratory compensation History c/w ketoacidosis secondary to DKA with appropriate respiratory compensation

    ABG analysis
    56 y/o with COPD exacerbation and hypotension and associated diarrhea x 7 days presents with the following ABG: 139 110 20 7.22/30/65/10/90% 120
    4.0 10 1.5 PH(7.22) = acidemia AG = 139 (10 + 110) = 19 (nl AG = 8-12) Winters formula
    Delta gap
    Delta gap = HC03 + change in the AG = 24 Delta gap = 10 + (19 12) = 10 + 7 = 17 Delta gap = 17

    PaCO2 = 1.5 (HCO3) + 8 = 1.5 (10) + 8 = 23

    ABG - example
    Triple disorder AG acidosis Incomplete respiratory compensation Non AG acidosis
    History would suggest AG acidosis is secondary to 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.

    Look at the pH. pH < 7.35, acidosis pH > 7.45, alkalosis Look at PCO2, HCO3 Main pathology will be the change correlates with the pH. 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 response Respiratory or Metabolic pCO2 - respiratory Bicarb - metabolic

    Metabolic Acidosis? Anion Gap? >12 - ketoacidosis, uremia, lactic acidosis, or toxins Delta ratio to check for gap and non gap disorders , or metabolic alkalosis happening simultaneously Normal anion gap - diarrhea OR unknown. If unknown calculate urine anion gap, if positive likely RTA, if neg liekly diarrhea Metabolic Alkalosis

    If urin Cl is > 20 it is chlorideresistant alkalosis (increased mineralcorticoid activity

    Example # 1
    44 yo M 2 weeks post-op from total proctocolectomy for ulcerative colitis. Na+ 134, K+ 2.9, Cl- 108, HCO3- 16, BUN 31, Cr 1.5

    BG: 7.31/ 33 /93 / 16

    Example #2
    9 yo M presents with N/V. Na 132 , K 6.0, Cl 93, HCO3- 11 glucose 650 BG: 7.27/23/96/11/-8

    Example #3
    70 yo M s/p lap chole, on the morning of POD #1. Pt received 2L bolus of crystalloid throughout pm for tachycardia. Now with SOB. 7.24 / 60 / 52 / 27 /+3

    Example #4
    54 yo F s/p mult debridements for necrotizing fasciitis, now on vassopressin to maintain blood pressure BG - 7.29/40/83/17/-6

    Example #5
    35 yo M involved in crush injury, boulder vs body. Na 135 , K 5.0, Cl 98, HCO3- 15 BUN 38, Cr 1.7, CK 42,346 BG: 7.30/32/96/15/-4

    Example #6
    4 wks M with projectile emesis Na: 140, K:2.9, Cl: 92 7.49/40/98/30/+6

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