L ABFE Review

normal blood gas values (pH, pCO2, HOC3-)

pH: 7.35-7.45

pCO2: 35-45

HCO3-: 22-26

what is an unmeasured anion/cation

an ion not reported on a BP

what is the most important unmeasured anion

albumin

anion gap equation

(Na+K)-(Cl+HCO3)

how to adjust anion gap for hypoalbuminemia

calculated anion gap + (2.5*every 1g/dL decline in plasma albumin) (normal albumin 4g/dL)

ex. albumin 2

calculated anion gap + (2.5*2)

workup for pt w electrolyte imbalance

1. clinical status/life threatening

2. EKG

3. Na+: fluid balance, serum/urine osmolality

4. check other electrolytes: (if low K+, or Ca++, check Mg++)

5. is Ca+ low, check PO4 (might be high)

6. check med lists

7. normalize electrolytes at an appropriate rate

8. in pt w severe acidosis (pH <7.20), replace bicarb deficit

s/sx metabolic acidosis

hyperpnea (Kussmaul)

depressed CNS fx

CV symptoms

decreased central and pulmonary vascular compliance predisposes to pulmonary edema

pediatric compensation in metabolic acidosis, how is it different

tachypnea rather than hyperpnea d/t anatomy

causes of AG metabolic acidosis **

CUTE DIMPLES

-Cyanide (HCN, Prussic acid)

-Urea/uremia

-Toluene

-Ethylene glycol (antifreeze)

-DKA

-Iron/INH

-Methanol

-Phenformin/metformin

-Lactic Acid

-Ethanol

-Salicylates (ASA)

physiology of AGMA

increased unmeasured anions and decreased HCO3

physiology NAGMA

anion added is Cl-

diminished renal acid excretion

loss of bicarb

excess/consumption of HCl

causes of NAGMA (acidosis)**

-diarrhea

-RTA 1 and 2

-carbonic anhydrase inhibitors

HARDPUS

-hyperalimentation (IV feeding)

-acetazolamide

-RTA

-Diarrhea

-Pancreatico-intestinal fistula

-ureto-sigmoid fistula

-saline infusion

T/F respiratory compensation for metabolic acidosis is more of a increase in tidal volume (hyperpnea) than an increase in respiratory rate (tachypnea)

t

how to estimate expected pCO2 based on respiratory compensation for metabolic acidosis *

Winter's formula: pCO2=(1.5*[HCO3-] +8 (+/-2)

OR

pCO2~last 2 digits of pH

T/F b/c of the lungs' excellent capacity to excrete excess CO2, increases in pCO2 are always d/t hypoventilation and NEVER increased CO2 production

T

causes of respiratory acidosis

parenchymal pulmonary disease (COPD)

respiratory muscle fatigue (myasthenia gravis)

abnormalities in ventilatory control (CNS problems like drugs, stroke, infx, tumor)

T/F carbonic anhydrase can DIRECTLY buffer preexisting HCO3-

false

the buffering produces an extra H+ which requires an extra HCO3- (2 total)

describe compensation for respiratory acidosis (longer)

cell buffering via carbonic anhydrase, Hb, bone: acute and inefficient

HCO3- generation from kidney: subacute-chronic and efficient

- more protection in the chronic setting

pt w elevated bicarb but ventilating normally, a good PA would suspect ______

COPD or other chronic respiratory acidosis

how to determine if respiratory acidosis/alkalosis is acute or chronic

extent of compensation

if it is well compensated, it's a chronic problem

desrcribe the process of contraction alkalosis

hypovolemic, aldosterone release, sodium resorption in exchange for H+ and K+, worsens alkalosis

kidney will prioritize maintaining blood volume over other functions

what is the maintenance factor in metabolic alkalosis

renal impairment (of some degree, even if just dehydration)

-normal kidney should never develop alkalemia bc it can always excrete extra bicarb

causes of metabolic alkalosis

vomiting

NG suction

diuretics

excessive antacid consumption

compensation for metabolic alkalosis

reducing alveolar ventilation

respiratory alkalosis causes

hyperventilation

-CVA

-trauma

-pregnancy

-hyperthyroidism

-non cardiovascular compromising PE

-liver disease (hepatopulmonary syndrome)

-recovery from metabolic acidosis

-mechanical hyperventilation

how long does it take for renal compensation for metabolic disorders to start

starts after 2-6hrs

complete after 2-3hrs

delta ratio <0.4

hyperchloremic NG metabolic acidosis

delta ratio <1:1

non gap AND gap acidosis

ie. lactic acidosis and severe diarrhea

delta ratio btwn 1-2:1

pure anion gap acidosis

ie. lactic acidosis, DKA, alcoholic acidosis

delta ratio near 1.6

lactic acidosis

delta ratio near 1:1

acidosis alcoholic or DKA, lower d/t ketone loss

delta ratio 2:1

gap acidosis AND concurrent metabolic alkalosis

OR

pre-existing compensated respiratory acidosis (COPD)

ie. sepsis and DKA OR chronic resp acidosis (COPD) w compensated metabolic alkalosis

what % of body wt is water

60%

what % of body water is extracellular volume

33%

what % of body water is intracellular volume

66%

Normal Input/Output adult male

2600cc each

breakdown of normal intake

ingested water: 1500cc

food: 800cc

oxidation: 300cc

breakdown of normal water output

urine: 1500cc

skin: 500cc

respiratory tract: 400cc

stool: 200cc

clinical signs that mean you should use 5% for volume depletion calculations

thirsty

decreased tears

normal mental status

skin recoil <2s

clinical signs that mean you should use 10% for volume depletion

apathetic, lethargic, unconscious

tachycardia

deep breathing

deeply sunken eyes

tenting skin turgor

absent tears

minimal cap refill

cold, cyanotic extremities

s/sx fluid overload

edema

JVD

rales, SOB

S3 heart sound

wt gain

CHF

normal urine output by wt

men: 20cc/kg/day

women: 15cc/kg/day

oliguria classifications by urine output

<0.5 cc/kg/hr adult

<1cc/kg/hr in infant

how to calculate the fluid deficit and % dehydration

take pts wt loss in L

divide that by euvolemic TBW

ex. normal wt 70kg (TBW 42L bc body is 60% water), dehydrated wt is 67kg

TBW loss = 3L

dehydration = 3L/42L = 7% dehydration

isotonic IV fluids

0.9% normal saline

lactated ringer's (more close to normal than NS)

Hypotonic IV solutions

1/2 NS

5DW

1/4 NS

Hypertonic IV fluids

3% NaCl

maintenance water requirement order

1.5cc/kg/hr

maintenance Na+ requirement

1.5meq/kg/days

K+ requirement

1 meq/kg/day

glucose requirement

2g/kg/day

FINAL IV ORDER for maintenance fluids, electrolytes, glucose

D5 1/2 NS w 20meq KCl/L at 1.5cc/kg/hr (rate changes w body wt)

Daily water requirement for pediatrics

- 1st 10kg: 100ml/kg/day

- next 10 kg: add 50ml/kg/day (to previous 100)

- next 1-40kg: add 20ml/kg/day

IV infusion rate for pediatrics fluid management

- 1st 10kg: 4ml/kg/hr

- next 10kg: add 2ml/kg/hr (to previous 4)

- next 1-40kg: add 1ml/kg/day

what fluid to use in children vs infants

children: use D5 1/2 NS

infants: D5 1/4 NS

main intracellular cation

potassium

describe how K+ interacts with digitalis

digitalis toxicity can cause hyperkalemia (inhibits Na/K ATPase pump)

HYPOkalema also potentiates digitoxicity

how much glucose is in a L of D5W

L of D5W

50g

how much free water is in a L of NS

none

how much free water is in a L of 1/2 NS

500cc

how much free water is in a L of 1/4 NS

800cc

pt is extremely hypernatremic, what fluid do you give?

NS IV

why? fix fluid deficit

how much free water is in a L of D5W

1 L

% TBW that is interstitial fluid

15%

% TBW that is plasma

5%

examples of transcellular fluid

CSF, bowel secretions, joint fluid, intraocular fluid, pleural fluid, pericardial fluid, peritoneal fluid

normal serum Na+

135-145 meq/L

normal serum K+

2.5-5.5 meq/L (or 3-5.5)

normal serum MG

1.7-2.2 mg/dl

normal serum total calcium

9-10.5mg/dl

normal serum phosphate

2.5-4.5 mg/dl

EKG changes in hyperkalemia

1. Tall peaked T waves

2. Flat P waves

3. Prolonged PRI

4. Widened QRS complexes, deep S

5. Lengthening of QT interval

6. Sine Wave

7. Vfib and death

EKG findings in hypokalemia

-U waves

-Flattened T waves

-ST segment changes

-prolonged QT, then PVC, torsades, and Vfib

what other electrolyte should you check if there is hypokalemia

Mg++ (K+ won't correct unless MG++ deficit is corrected)

when to suspect pseudohyponatremia

-severe hyperglycemia

-sever hyperproteinemia

-severe hyperlipidemia

(under reporting of the [Na+] bc serum volume is overreported d/t big heavy molecules like glucose, lipids, protein)

calculation of Na+ deficit

(0.6wt in kg) (125-actual Na)

if using hypertonic saline, 125 is target
if not, use 140 for calculation instead

Na replacement if [Na+] >127

oral: chips or salt tabs

NA+ replacement if [Na]>120

NS

Na replacement if [Na] <118

3% hypertonic saline

what is the risk of correcting (raising) Na+ levels too quickly

central pontine myelinolysis

clinical uses of Mg++ **

-tx hypokalemia

-tx torsades

-tx asthma

-tx tension HA

-repletion of Mg++ in alcoholic, malnourished pts

-preeclampsia/eclampsia (lowers BP/prevents seizures)

-tocolytic

common cause of hypomagnesemia

chronic alcoholism

difference btwn total and ionized calcium

total Ca++ varies w albumin

ionized Ca++ does not vary w albumin

s/sx hypercalcemia

stones, bones, groans, moans, thrones, psychiatric overtones

EKG changes hypercalcemia

-shortend QTc secondary to shortened ST

-wide or flattened T wave

-J point elevation

-Osborn (J) wave

tx options hypercalcemia

-saline diuresis

-lasix

-calcitonin (IV/SQ, NOT nasal)

-denosumab

-zolendronic acid

-mithramycin

-surgical removal or parathyroids

early s/sx hypocalcemia

-peri oral numbness

-paresthesias of hands/feet

-muscle cramps

s/sx sever hypocalcemia

tetany 9carpopedal spasm, laryngospasem, seizures)

Trousseau's sign: crapopedal spasm after infaltion of BP cuff above SBP for 3 min

Chvostek's sign: contraction of ipsilateral face muscles after tapping on facial nerve as it passes through parotid gland

what should you check if Ca++ is low

intact PTH

(PTH high - primary, PTH low, secondary)

EKG changes hypocalcemia

prolonged QTc secondary to shortened ST

what form of calcium should be given IV

calcium gluconate (less irritating to veins than calcium chloride)

tx hyperphosphatemia, esp in CKD

phosphate binders

s/sx hyperphosphatemia

calcium phosphate precipitates and hypocalcemia

MC cause hyperphosphatemia

CKD

what is in lactated ringers

NaCl, KCl, CaCl, lactate (metabolized to bicarb in liver)

what pts can't get lactated ringers

liver disease/alcoholic

contains lactate, metabolized to bicarb in liver - bad liver means worsenes acidosis, rather than fix

normal serum osmolarity

280mOsm/L

90% of extracellular cations are _

sodium

low potassium is most dangerous in what scenario?

sudden and quick diuresis (loss of fluid)

electrolytes vs. nonelectrolytes, which has a greater osmotic power?

electrolytes

→ can shift fluids more