ACID Base Disturbances Flashcards
what are some possible causes of hypoxia?
- hypoventilation
- V/Q mismatch
- Shunting
- Low inspired fraction of O2
- High altitude
- Diffusion abnromalities e.g. alveolar hemorrhage ( as in goodpastures) , CT disorder (as in Lupus)
A metabolic compensation for acid-base disturbance can take up to _
12-16 hrs; max conc in 1 week.
In determining an acid/base disturbance, what three step approach should be employed?
- Does pt have acidosis or alkalosis?
- Is the acidosis/alkalosis a respiratory or metabolic process?
- If it is a respiratory acidosis/alkalosis, is it a pure respiratory process or is there a metabolic component?
In an acid base disturbance if pH and pCO2 are both up or down in the same direction, then the process is _
metabolic process.
In an acid base disturbance, if the pCO2 and pH move in OPPOSITE direction, the process is _
respiratory process.
if it is a pure respiratory process, for each 10 mmHg change in PaCo2 the pH should move in opposite direction by _
0.08
You suspect a pure respiratory acid/base disturbance and so you calculate the numbers and find that the calculated value does not match the actual pH. what is likely happening?
A second metabolic process is also present referred to as a mixed process.
If the actual pH is not what it should from the measured, and notice the actual pH is higher then what process is also taking place?
Metabolic alkalosis. If it’s lower than what you calculated then it’s metabolic acidosis.
High anion gap causing metabolic acidosis can be due to )
MUDPILES
- Methanol - formic A
- Uremia (renal failure)
- Diabetic ketoacidosis (increased glu; starvation, alcohol abuse, acetoacetic acid, beta-hydroxybutyric acid)
- Paraldehyde (reagent in lab used by chemist)
- INH, iron
- Lactic acid
- Ethylene glycol glycolic (antifreeze)
- S salicylates
Others: CCAT (CO, cynaide, alcohol, toluene)
Differentiate the different types of lactic acidosis
Type A (tissue hypoxia) - shock, severe anemia, heart failure, CO poisoning Type B1 (associated with systemic disorder)DM, liver failure, sepsis, seizures Type B2 (associated with drugs/toxins) ethanol, methanol, ethylene glycol, ASA Type B3 (associated with inborn errors of metabolism ) G6PD deficiency
a 70 yr old with congestive heart failure, difficulty breathing with RR 25, rales, crackles, and wheezes, peripheral edema, cool extremities O2 sat of 80%. Metabolic acidosis with high anion gap. whats are your possible treatment options?
- Oxygen 2-4 L/min N/C
- IV-loop diuretics (furosemide)
- Fluid restriction 1-1.5 L/day
- Na HCO3 - cautiously cuz his pH was really low which can already compromise his cardiac function so added Na may exacerbate it.
- ACEI - cautiously cuz
68yr old african american comes to ER in a lethargic state. Hx of 3-4 weeks of anorexia, confusion, edema and weight gain. PMH: poorly controlled HTN, DM, DJD and hypothryroidism. Meds: HCTZ, Lantus, NSAIDs. 158/88, RR 10, O2 Sat 88%. neck veins 45 degrees, Lungs bilateral crackles, peripheral edema. what are the possible diagnosis?
- Metabolic encephalopahty - R/O hypothryoid (myxedema)
- Likely ischemic cerebral vascular disease due to poorly controlled hypertension
- Electrolyte/acid base disorder
- Fluid overload
- Vulvular heart disease
- HF
- HTN
pH 7.1; pCO2 45, PO2 68, HCO3 8. Based on these numbers what is the acid/base diagnosis?
Metabolic and respiratory acidosis.
68yr old african american comes to ER in a lethargic state. Hx of 3-4 weeks of anorexia, confusion, edema and weight gain. PMH: poorly controlled HTN, DM, DJD and hypothryroidism. Meds: HCTZ, Lantus, NSAIDs. 158/88, RR 10, O2 Sat 88%. neck veins 45 degrees, Lungs bilateral crackles, peripheral edema. electrolytes shows metabolic and respiratory acidosis. Elevated K, TSH, EKG shows significant changes. what is the best form of immediate treatment
- Dialysis - hemodialysis. this is usually done in extreme cases where pt has high K and has significant EKG changes, these are emergent changes and you need to reverse those changes as soon as possible.
- Na HCO3. The guideline is if pts pH is less than 7.2, give some
- Synthryroid - she had high TSH
- aerosol tx w/ nubulizers to make sure she gets the appropriate bronchodilation
37 yr old female with 6days hx of diarrhea.
NO recent travels. Family hx of inflammatory bowel disease (Crohn’s). No hx of abx.
BP 80/50, R18, temp 100, Sat 94%.
appears pale, poor skin turgor, dry mucous, neck veins are flat, tachycardia, abd: hyperactive, mildly tender. extremities cool to touch.
1. whats the possible diagnosis?
- Diarrhea (secretory, infectious, consider IBD)
what are some possible causes of normal anion gap metabolic acidosis - HCO3 falls and Cl rises (hyperchloremic metabolic acidosis)
HARDUPS
H-hyperalimentation
A-Acid infusion, acetazolamide
R - RTA - renal loss of HCO/or decreased H sec
D- Diarrhea (loss of Bicarb)
U - Ureteral sigmoid or ileal diversion - losing HCO3/inc Cl and H resorption
P - Pancreatic fistula - losing HCO3, decreased K
S- spironolactone
In this type of renal tubular acidosis, H+ secretion is decreased, thus can’t get rid of acid, ie “failure to acidify urine”
what are possible causes of this type of RTA?
Type 1. - Distal tubule
Causes: SLE, Sjogren’s, toluene
A defect that leads to decreased absorption of HCO3 in PCT thus not absorbing buffer is known as _
renal tubular acidosis type II. Possible causes include: MM, heavy metal poisoning, Wilson’s disease, amyloidosis.
what is Type IV renal tubular acidosis characterized by?
Defect is in distal tubule.
it’s also known as Hyperkalemic RTA - hyporenin and hypoaldosterone - decreased NH4 excretion and decreased HCO production.
Possible causes include: analgesic nephropathy, sickle cell disease and SLE.
46yr hispanic male with one week of vomiting. Can’t eat or drink anything! no diarrhea, no hematemesis. Has chills, malaise, felt hot. His past med hx unremarkable. BP 90/52, P119, R20, temp 101, O2 90. dry mucous, poor skin turgor, neck veins flat, AbD: vitiligo areas on abd, no distention, No edema, neuro normal. what’s the differential diagnosis?
What can you give to treat?
- Volume depleted (dehydration) Vomiting complicated by volume contraction; hypotension; infection
- Rx underlying cause, NaCl, KCL, Mg, spironolactone for mineralocorticoid excess
For every 1 unit increase in HCO3, how much paCO2 also increase to compensate?
.7
what are some causes of metabolic alkalosis causes?
CLEVER PD C- contraction of volume L - licorice E- endocrine (conn's cushing) V- vomiting E- Excess alkli R - refeeding alkalosis P-Post hypercapnia D- diuretics
Chloride unresponsive metabolic alkalosis can be due to what endocrine causes?
Bartters, severe K depletion, hyperalo, Cushings.
Urine Cl > 10-20. These patients do not respond to saline.
52 yr old female: i feel weak all over. Has HTN, BP has been more resistant to control despite meds. She is taking beta blocker, ACEI and a vasodilator.
BP 168/104, O2sat 94%
Diffuse muscle weakness is noted in hands, arms and legs.
1. what are possible DDX?
2. Pts ABGs are pH7.5; PCO 48, PO2 90, HCO3 29. What is the acid base disorder
3. Urine Cl: >20; ALd high. Plasma renin level is low. what’s the ddx based on these
4. possible tx?
- A) Diffuse muscle weakness –> hypothyroidism, electrolyte disorder - low Na, K, mg, Ca; B) HTN becoming resistant
- Metabolic alkalosis
- Hyperaldosteronism (combo of HTN and hypokalemia should indicate hyperalodsteronism (conn’s syndrome) until proven otherwise); metabolic alkalosis
- Adenoma - laparoscopic excision; bilateral hyperplasia - spironolactone to inhibit hyperplasia and ald production; correct hypokalamia
