- respiratory - renal - carbonic acid bicarb buffer

Acid-base disorders Flashcards by Emily Hendrickson

How does acid get excreted?

- when combined with urinary buffers:
phosphate 
urate
creatinine
ammonia: major adaptive response is an increase in ammonim excretion in the urine

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Buffers in our body?

respiratory
renal
carbonic acid bicarb buffer

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How does resp buffer work?

pH will trigger an increase or decrease in rate and depth of ventilation until the approp amt of CO2 has been reestablished
compensation may occur within minutes

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Respiratory compensation in metabolic acidosis and alkalosis?

metabolic acidosis: PCO2 will decrease by **1.3 mmHg every 1 mEq/L drop in serum HCO3 (better compensation in acidosis)
metabolic alkalosis: PCO2 will increase 0.7 mmHg for every 1 mEq/L increase in HCO3 (doesn’t increase that much b/c normal RR needs to be overriden to increase CO2)

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Importance of bicarb?

base
buffer for H+ ions
renal system maintains balance of HCO3- and H+
there is small immediate change due to whole body buffering system
kidneys affect changes in pH which take 3-5 days (start chaging within 6-12 hrs with acute problem)

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How much does bicarb buffer compensate in resp acidosis/alkalosis?

acute resp acidosis: HCO3 will increase 1 mEq/L per 10 mmHg increase in PCO2
chronic rep acidosis: HCO3 will increase 3.5 mEq/L per 10 mmHg increase in PCO2
acute resp alkalosis: HCO3 will decrease by 2 mEq/L per 10 mmHg decrease in PCO2
chronic resp alkalosis: HCO3 will decrease by 5 mEq/L per 10 mmHg decrease in PCO2

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Main problem in respiratory acidosis?

too much CO2, resp drive? or CO2 exchange dysfxn

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What are the causes of resp acidosis?

CNS depression: meds - (narcotics, sedatives, or anesthesia), or head injury
impaired resp muscle fxn: spinal cord injury, neuromuscular diseases, neuromuscular blocking drugs
pulm disorders: atelectasis, pneumonia, pneumothorax, pulmonary edema, bronchial obstruction, massive PE, respiratory failure
hypoventilation due to pain, chest wall injury/deformity, abdominal dissension, obesity trauma

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Main problem in respiratory alkalosis?

hyperventilation

- tx by correcting underlying cause

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Causes of resp alkalosis?

psych responses: anxiety or fear, pain
increased metabolic demands: fever, sepsis, pregnancy, or thyrotoxicosis
meds: resp stimulants
CNS lesions

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What is the problem in metabolic acidosis?

not enough HCO3- to buffer acidic state of the body
HCO3- can be lsot: GI or renal losses
or too much acid can build up: excretion problem - renal failure, intake - overdose, metabolism issues: anaerobic, ketone bodies (DKA)
diarrhea, anaerobic metabolism: from tissue hypoxia
starvation
salicylate intoxication

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What should you have at the top of your DDx when a pt has metabolic acidosis?

tissue hypoxia, look for hypoxic tissue

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Anion gap calculation, normal range?

can be used to narrow down etiology of metabolic acidosis
AG = Na-(HCO3+Cl)
traditionally norm range 12+/- 4 mEq/L

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What non acid-base disorders can cause errors in AG interp?

low albumin: for every 1 mEq/L decrease in serum albumin the AG will decrease by 2 mEq/L
hypernatremia
hyponatremia
certain abx

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Why shoudl the AG always be calculated?

possible to have an abnormal AG even if Na+, Cl-, and HCO3- levels are normal
a large AG (greater than 20) suggests a primary metabolic acid-base disturbance regardless of pH or serum bicarb levels (not a resp problem)

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What does a corrected HCO3 indicate?

in an increased AG acidosis there should be a mole for mole decrease in HCO3 as the AG increases
a corrected HCO3 higher or lower than normal (24) indicates the concomitant presence of metabolic alkalosis or normal AG gap metabolic alkalosis or normal AG gap metabolic acidosis

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Causes of increased AG metabolic acidosis?

MUDPILES:
M - methanol intoxication
U - uremia
D - diabetic or alcoholic ketoacdosis
P - paraldehyde
I - isoniazide or Fe overdose
L - lactic acid
E - ethylene glycol intoxication
S - salicylate overdose

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causes of non-AG metabolic acidosis?

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USED CAR:

U - ureteral sigmoid diversions: accum urine in intestine, reabsorb Cl-, H2O in intestine, secrete bicarb in intestine
S - small bowel fistula, saline admin
E - endocrinpathies: addison’s hyperparathyroidism
D - diarrhea
C - carbonic anhydrase inhibitors
A - (hyper) alimentation (TPA)
R - renal tubular acidosis

What is the issue in metabolic alkalosis?

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too much HCO3-: this can occur with excessive H+ loss, this can be GI or renal
or it can be from a gain in HCO3-

Causes of metabolic alkalosis?

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either an excess of base or loss of acid within the body
excess base occurs from ingestion of: antacids, excess use of bicarb, use of lactate in dialysis
loss of acids can occur secondary to:
protracted vomiting, gastric suction, hypochloremia (bicarb isn’t getting exchanged with H+), excess admin of diuretics, high levels of aldosterone

Sxs of alkalosis?

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increased neuromusc irritability: paresthesias of fingers and toes, tetany, seizures
severe alkalosis: pt may become belligerent, CNS depression: confusion - lethargy, death at pH around 7.8

How is H+ lost in metabolic alkalosis through vomiting? What happens normally?

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each mEq of H+ lost generates 1 mEq of HCO3-
normally H+ is secreted into the stomach: when acidic chyme enters small intestine HCO3- is secreted into the lumen
person vomiting: H+ is being lost so HCO3- isn’t secreted
Cl- also secreted with H+ so lost with vomiting
so HCO3- doesn’t have H+ to bind to in the small intestine so it stays in the blood

How is H+ lost with loop or thiazide diuretics with metabolic alkalosis?

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increased flow to DCT and CT- increased reabsorption of Na+
as Na+ reabsorbed increased secretion H+ and increase HCO3- reabsorption
may also get volume contraction

How does excess aldosterone cause increased H+ loss?

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excess aldosterone is going to promote Na+ reabsorbtion and kick out H+ and increase HCO3- reabsorption

What is contraction alkalosis? Causes?

- loss of large volumes of fluid - contraction of extracellular vol around relatively quantity of bicarb causes: IV loop diuretics with rapid fluid removal, thiazides, vomiting (prolonged), sweat losses in pts with CF

How can metabolic alkalosis be further characterized by urinary chloride?

- can be diff in terms of response to tx with NaCl- | - by the level of urinary Cl as determined by ordering a spot or random UCI

What does it mean if UCl is less than 10 mEq/L?

- renal loss of chloride: diuretics, CF, posthypercapnia - GI loss of H+, Cl-: 1. NG suctioning 2. Vomiting 3. chloride wasting diarrhea a. congenital in children b. villous adenoma

What does it mean if UCl is greater than 10 mEq/L?

- excess mineralocorticoid: 1. adrenal: cushings, hyperaldosteronism (Conn's syndrome) 2. exogenous steroid admin 3. bartter's syndrome

What is the initial problem in chloride sensitive metabolic alkalosis? What does this result in?

- initial problem: sustained loss of chloride out of proportion to loss of Na (either by renal or GI) - this chloride depletion results in renal Na+ conservation leading to a corresponding reabsorption of HCO3- by the kidney - in this category of met. alkalosis: UCl - is less than 10 mEq/L - the disorders respond to tx with IV NaCl

What is problem in chloride insensitive (resistant) metabolic alkalosis?

- direct stim of kidneys to retain HCO3- irrespective of electrolyte intake and losses - UCl is greater than 10 mEq/L and these disorders don't respond to NaCl admin

What is the tx of metabolic alkalosis?

- correct the underlying disorder 1. chloride responsive: replace volume with NaCl if depleted correct hypokalemia if present admin of NH4Cl and HCl should be reserved for extreme cases 2. chloride resistant: tx underlying problem, such as stopping exogenous glucocorticoids

What can alklali admin cause?

- milk-alkali syndrome - post correction metabolic alkalosis by admin of NaHCO3 to tx lactic acidosis or ketoacidosis - admin of large quantities of citrate (ex: with infusion of 8 or more units of blood or giving FFP in plasmapheresis) each mmol of citrate generates 3 mEq of bicarb (for a total of 23 meq of bicarb in each unit of blood) - metabolic alkalosis can occur if the renal ischemia or underlying renal disease prevents the excess bicarb from being excreted in the urine

What does normal value of anion gap represent? range?

- reflects concentration of nonbicarb buffers: albumin, phosphate, sulfate, organic acids - range 12+/- 4 but can be depending on the instrument used to measure serum electrolytes

What is a high serum anion gap usually due to?

- due to an increase in unmeasured anions and this is almost always caused by one of the organic metabolic acidoses (lactic acidosis, ketoacidosis, alcoholic acidosis)

When should you use the delta gap equation?

- only if anion gap is elevated for metabolic acidosis - it is the ratio of the increase in anion gap compared to the decrease in HCO3 concentration - AG measure - 12= delta AG * only will work with elevated AG - 24-measured HCO3= delta bicarb

What does it mean if delta AG is greater than delta BC in metabolic acidosis?

- metabolic alkalosis is present | - if equal (=/-2) then NO add disturbance)

What does it mean if delta AG is less than delta BC?

- then non-AG metabolic acidosis (for example: an add non-AG metabolic acidosis ( lactic acidosis superimposed on severe diarrhea) - if equal (=/-2) then no add disturbance

How does normal rep compensation work in metabolic acidosis?

- PCO2 should decrease by 1.3 mmHg for every 1 meq/L decrease in serum HCO3 - PCO2 can only fall to 8-12 mmHg

When do you use winter's formula? Why is it used?

- used in metabolic acidosis to predict the PaCO2 you should have if there is approp resp compensation for the metabolic acidosis - predicted PaCO2 = 1.5x(HCO3-)+8(+/-2) - rough est is HCO3+15 or PCO2 should be similar to decimal digits of pH (pH 7.25 the PCO2 should be about 25)

What does a higher and lower than predicted winter's formula mean?

- higher than predicted: concomitant respiratory acidosis | - lower than predicted: concomitmant resp alkalosis

How does norm. resp compensation work in metabolic alkalosis?

- for every 1 meq/L elevation in HCO3 the PCO2 should increase by about 0.7 mmHg - upper limit for increasing the CO2 is about 55mmHg

When is summer's formula used? What do these values mean? Formula?

- in metabolic alkalosis - it is used to calculate resp compensation (CO2) for metabolic alkalosis - if calculated CO2 is higher than actual= concomitant respiratory alkalosis - if calculated CO2 is lower than actual = concomitant respiratory acidosis - formula: PCO2 = 0.7(HCO3+21)+/-2 - if normal than no resp compensation occurring

When might it be helpful to measure a urine chloride?

- metabolic alkalosis

How long does it take for renal system to compensate by increasing the HCO3-?

- 3-5 days, starts compensating in acute cases 6-12 hrs

Acid-base disorders Flashcards

(44 cards)