Acid-base, fluid, and electrolyte disorder Pt.2

normal pH

• 7.35-7.45

normal PaCO2

• 35-45mmHg

• use 40 for calc

normal HCO3

22-26mEq/L

• use 24 for calc

VBG

• often sufficient to eval pH and bicarb in a stbale pt

  • venous pH typically slightly lower than arterial pH

  • venous PCO2 is generally higher, but difference is varaible

ABG

• preferred when accurate PaCO2, oxygenation (PaO2), or precise ventilation assessment is needed

BMP CO2 vs Blood gas PCO2

• BMP= total Co2, mostly bicarb (HCO3-)

• blood gas= idssolved carbon dioxide partial pressure, reflecting vent

pattern of metabolic acidosis

• HCO3 decreases

• pH decreases

pattern of metabolic alkalosis

• HCO3 increases

• pH increases

pattern of respiratory acidosis

• aCO2 icnreases

• pH decreases

pattern of respiratory alkalosis

• PaCO2 decreases

• pH increases

primary pattern clues

• HCO3 moves pH in same direction

• CO2 move pH in opposite direction

compensation limits pH change- metabolic problem

• lungs change Co2 in same direction as HCO3

compensation limits pH change- respiratory problem

• renal adaptation changes HCO3 in the same direction as CO2

compensation limits pH change- mixed disorder

• response falls outside expected range

metabolic disorder compensation

• lungs compensate by changing CO2 (within minutes)

acute respiratory disorder compensation

• immediate chemical buffering causes small HCO3 change

chronic respiratory disorder compensation

• kidneys adust HCO3 over several days (approx 2-5days)

why use winters formula

• in metabolic acidosism HCO3 decreases→ pH decreases; lungs compensate by breathing faster/deeper to remove CO2→ helps raise pH

• WINTERS formula tells us how LOW the CO2 shoudl be if the lungs are compensating appropriately

• if actual CO2 is outside expected range, sus additional respiratory disorder

winters formula

expected PaCO2= (1.5 * HCO3) + 8 ± 2

• within expected range- appropriate resp compensation

• higher than expected- additional resp acidosis

• lower than expected- additional resp alkalosis

what should you check before starting insulin in DKA

K!!

anion gap

AG= Na - (Cl+ HCO3)

high anion gap

• unmeasured anions accumulate as HCO3 falls

normal anion gap

• Cl rises relative to Na as HCO3 falls

what can hide a high gap

• low albumin

high gap acidosis- where does the acid come from

• lactate- shock, severe hypoperfusion, or other causes of lactate excess

• ketones-DKA, etoh- associated ketoacidosis, or starvation ketosis

• retinaed acids- advanced kdiney failure reduces acid excretion

• toxind/drugs- methanol, ethylene glycol, salicylates, ans selected drugs

high anion gap metabolic acidosis (HAGMA)

GOLD MARK

G- glycols

O- oxoproline

L- lactate (hypoperfusion, sepsis)

D- lactate (short bowel syndrome, bacterial overgrowth)

M- methanol

A- aspirin (salicylates)

R- renal failure (uremia)

K- ketoacidosis (diabetic, alcoholic, starvation)

normal gap acidosis- base lost or acid retained

• GI bicarb loss- diarrhea, hgih output intestinal losses, [ancreatic drainage

• renal mech- renal tubularacidosis, earlier CKD, acetazolamide

• chloride load- large amnt of 0.9% saline can cause hyperCl acidosis

what leaves the body/what is result of vomiting or gastric NG suction

• loss of H and Cl

• typical result= metabolic alkalosis

  • often low K and low volume

what leaves the body/typical result of diarrhea and intestinal drainage

• HCO3 and K

• result= normal gap acidosis

  • often low K and volume

why can vomiting sustain in alkalosis

• alkalosis starts- gastric H loss leaves a relative excess of bicarb

• kidney maintains it- low volume, low Cl, and low K limit HCO3 excretion

• tx fits- stop the loss and replace deficits when clinically appropriate

why does vomiting cause hypoK

• vomiting→ metabolic alkalosis + hypoK

  • vomiting causes loss of gastric H and Cl→ metabolic alkalosis

  • fluid depletion activates RAAS/aldosterone

  • aldosterone increases renal K excretion

  • increased distal Na/HCO3 delivery can further increase urinary K loss

• most K loss occurs through kidneys, not directly through vomit

urine Cl- <20

• most likely mech: Cl- depletion; vomiting, remote diuretic use

• clinical direction: often saline responsive; replace KCl as needed

urine Cl- ≥20

• likely mech: ongoing renal Cl- loss or mineralocorticoid effect

• clinical direction: mineralocorticoid excess: usually saline unresponsive

urine chloride pearls

• high BP + high urine Cl: consider mineralocorticoid excess

• recent diuretics can raise urien Cl even when vol depleted

what does high urine CL- mean

• suggests that metabolic alkalosis may not respond to saline alone

respiratory acidosis causes

CO2 clearance is too low

• drive is reduced- opioids, sedatives, or brainstem dz

• pump is weak- neuromuscular dz, chest wall restriction, obesity, hypovent

• airflow limited- COPD or severe asthma with vent failure

• hypercapneia appears- HA, confusionm drowsiness; severe cases: stupor or coma

acute compesation

• kidneys havent had much time to respond → smaller HCO3 change

chronic comprensation

• kideys have had days to adapt→ larger HCO3 change

respiratory alkalosis; excess CO2 removal

• lab pattern: low PaCO2 raises pH. HCO3 may fall with compensation

• impotatnt causes: hypoxemia/PE< spesis, pain, CNS dz, salicylates

• sz: lightheadedness, perioral tingling, hand cramps or spasm

  • why tingle? alkalemia increases calsium binding to albumin, lowering ionized Ca

metabolic acidosis tx

• treat acid prod or base loss

• bicarb is selective

metabolic alkalosis tx

• correct cause and deficits

• assess vol befor esaline

respiratory acidosis tx

• restore adequate ventilation and treat cause

respiratory alkalosis tx

• ID trigger

• avoid paper bag rebreathing!

delta ratio

(AG-12)/ (24-HCO3)

delta ratio <1

• additional nomral gap metabolic acidosis

delta ration 1-2

• compatible wit predom high gap acidosis

delta ratio >2

• additional metabolic alkalosis or elevated baseline HCO3

corrected AG

AG + 2.5 * (4-albumin)