Acid-Base Physiology & cases
Table of Contents
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Objectives
Examine an arterial blood gas (ABG) and electrolyte panel and recognize the presence of the acid-base disorder and describe pathophysiology
- pH is maintained tightly between 7.35-7.45
- Acid-base balance is maintained by normal pulmonary and renal excretion of CO2 and H+ (respectively)
- Lungs can provide rapid elimination of CO2 and kidneys provide a slower response through elimination of acid (byproduct of protein metabolism)
- ABG measures: pCO2, pH, and HCO3
- Acidosis: process that tends to lower the pH (increase pCO2 and/or decrease HCO3)
- Alkalosis: process that tends to raise the pH (decrease pCO2 and/or increase HCO3)
- Acidemia: low pH
- Alkalemia: high pH
- Kidneys get rid of acid/reabsorb filtered bicarbonate through PCT and CD
- PCT senses acidosis and increase HCO3 reabsorption and ammonium secretion (to trap H in urine) — CA in brush border will convert H2CO3 into H2O + CO2
- Carbonic Anhydrase Inhibitors will cause sodium bicarb loss from PCT
- CD secrete acid through the α-intercalated cells driven by aldosterone
- Secreted acids appear in urine as NH4+
- PCT senses acidosis and increase HCO3 reabsorption and ammonium secretion (to trap H in urine) — CA in brush border will convert H2CO3 into H2O + CO2
- Types of renal tubular acidosis:
- Proximal (Type II): loss of filtered bicarbonate
- Distal (Type I): Failure of α-intercalated cell, leading to favoured K+ excretion by the principal cells. This will cause hypokalemia
- Distal (Type IV): Problem with aldosterone, leading to failure of principal and α-intercalated cells. This will cause hyperkalemia
- Expected Responses
- Metabolic Acid-Base problems:
- Acidosis: Acid gain or bicarb loss should result in 1:1 reduction in pCO2 (compensatory respiratory alkalosis) - can breath as fast as needed
- Alkalosis: Increase in bicarbonate should result in almost 1:1 increase in pCO2 - can reduce breathing, but only to a certain point before hypoxic
- Respiratory Acid-Base problems:
- Acidosis:
- Acute response: cells try to buffer to a small extend, about 1:10 increase in HCO3
- Chronic response: slightly more pronounced due to renal system kicking in (about 4 times stronger, but still not close to equivalent
- Alkalosis:
- Acute response: cells try to shift buffers back to ICF, about 2:10 decrease in HCO3
- Chronic response: renal acid secretion declines, bicarbonate loss increase (about 2 times stronger)
- Acidosis:
- Metabolic Acid-Base problems:
Provide a differential diagnosis for the acid-base abnormality from ABG
- General process:
- Look at ABG, examine pH
- if pH <7.35, metabolic acidosis (low bicarb), or resp acidosis (high pCO2)
- If pH >7.45, metabolic alkalosis (high bicarb), or resp alkalosis (low pCO2)
- Once the primary disorder identified, is the expected compensation adequte? acute/chronic? is there a mixed disorder?
- Compare the calculated anion gap to the expected, given serum albumin
- If metabolic acidosis, determine if AGMA or NAGMA
- If AGMA (MUDMILES!), consider osmolal gap, toxic ingestions, lactate, ketoacids, salicyclates, uremia
- if NAGMA, consider bicarb loss (GI and PCT), vs failure to excrete H+ (CD)
- If alkalosis, is ECF expanded or contracted?
- Metabolic Acidosis
- Pronounced anion gap:
- MUDMILES:
- Methanol
- Uremia (accumulation of phosphates and sulfates)
- Diabetic ketoacidosis
- Metformin
- Iron poisoning
- Lactic acidosis
- Ethylene glycol (antifreeze), or alcoholic ketoacidosis
- Salicylate poisoning or Starvation ketoacidosis
- Very fatal very quickly. Must treat source!!
- Calculate osmolal gap. If wider than expected, suspect toxic alcohols
- MUDMILES:
- Normal anion gap, and bicarb is low (NAGMA):
- Can be a loss of bicarb (PCT didn't reabsorb, or GI loss through diarrhea), or failure to secrete H+ by CD
- To diagnose, must take a history
- HARDUP:
- Hyperalimentation
- Acetazolamide
- Renal tubular acidosis/insufficiency (RTA)*
- Diarrhea* & Diuretics
- Ureteroenterostomy
- Pancreatic fissures
- Examine urin net charge and pH
- If urine Na + K «< Cl, then there is lots of NH4 and the distal nephron is working. Same if urine pH < 5.5
- If urine Na + K ~= Cl, then there is not much NH4, and the distal nephron may be broken
- Pitfall: If there is lots of other anions (e.g. sulfates, hippurate, bicarb, ketoacids), then Cl can be lower, and look like there is not enough H in urine
- Pronounced anion gap:
Describe the appropriate management for the acid-base abnormality
- Acidosis:
- Treat the underlying cause!!
- Alcohol poisoning: emergency dialysis, fermepizole
- Salicylates: hemodialysis
- DM ketoacidosis: insulin
- Provide buffer of Sodium Bicarb
- if patient can't breathe out the excess CO2, this is not a good choice
- If patient is overloaded in the ECF, the added sodium will make it worse
- However, if pH < 7.1, or HCO3 <10-12 mmol/L, then any fall in HCO3 or rise in pCO2 will cause a rapid drop in pH, so should give bicarb!
- Treat the underlying cause!!
- Alkalosis:
- Usually is the body responding to aldosterone
- Primary (rarer): Coon's syndrome, adrenal hyperplasia, reninoma, or exogenous/endogenous compounds with MC actions
- hypokalemia, increased pH are usually associated with hypertension due to aldosterone
- Secondary (more common): Stimulation of the RAAS due to diretics, vomiting, Bartter's and Gitelman's
- Associated with volume contraction
- Primary (rarer): Coon's syndrome, adrenal hyperplasia, reninoma, or exogenous/endogenous compounds with MC actions
- Look at urine lytes, Cl < 10 suggest a secondary cause unless patient on diuretics. Urine K or TTKG (Trans-tubular potassium gradient) high would confirm aldosterone action
- Re-expand ECF with NaCl (secondary cause)
- Ongoing hypokalemia tricks the kidneys into thinking there is acidosis, so must replace K
- Block aldosterone if primary cause
- (ACEi can be used in renal arterial stenosis alkalosis, avoid otherwise)
- Usually is the body responding to aldosterone
Calculate the anion-gap and osmolal gap
- Anion Gap:
- Difference between Na+ and Cl- and HCO3-
- Normally should be 12 (negatively charged proteins are not measured)
- For every 10g/L of albumin lower than 40, the expected AG should be lowered by 3
- Difference between Na+ and Cl- and HCO3-
- Osmolal Gap:
- 2Na + urea + glucose (salty, sweet bunny)
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page revision: 20, last edited: 27 Apr 2012 20:13