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How does acid get excreted?

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


Buffers in our body?

- respiratory
- renal
- carbonic acid bicarb buffer


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


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)


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)


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


Main problem in respiratory acidosis?

- too much CO2, resp drive? or CO2 exchange dysfxn


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


Main problem in respiratory alkalosis?

- hyperventilation
- tx by correcting underlying cause


Causes of resp alkalosis?

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


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


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

- tissue hypoxia, look for hypoxic tissue


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


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


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)


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


Causes of increased AG metabolic acidosis?

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


causes of non-AG metabolic acidosis?


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?

- 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?

- 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?

- 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?

- 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?

- 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?

- 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