Exam 3 Metabolic Alkalosis Flashcards
What is the PH for metabolic alkalosis? Serum HCO3? Compensatory response?
High PH (>7.45),
High serum HCO3 (>30)
compensatory increase in PaCO2
(High bicarb=metabolic)
Primary rise in HCO3 results from 3 main mechanisms. WHat are they?
Loss of acid from GI tract or urine
Administration of HCO3
Contraction of alkalosis (loss of Cl- rich fluid and HCO3 poor fluid)
What results in maintenance of metabolic alkilosis
impairment of renal function (impairement in renal HCO3 excretion)
What are the two types of metabolic alkalosis?
Saline responsive
Saline resistant
Three main causes of saline responsive alkalosis? Urinary chloride of saline responsive alkalosis
- diuretics (furosemide, torsemide, bumetadine, HCTZ)
- vomiting
- Exogenous HCO3
urinary chloride between 10-20
Normal PCO2 level? Normal HCO3 level? Normal PH level?
PaCO2- 40
HCO3- 24
PH- 7.35- 7.45
acid regulation controlled by
buffering
renal regulation
ventilatory regulation
hepatic regulation (minor)
Main buffers in body
Bicarb
phosphate
proteins
What important roles do the kindeys fulfil?
Reabsorb bicarb (mostly in proximal)
generate new bicarb (h excretion) (mostly in distal tubule)
When we suspect a metabolic acidosis what is the 1st step we do?
always calculate anion gap
What are causes of non anion gap metabolic acidosis
diarrhea- loss of HCO3
Pancreatic fistula- loss of HCO3
Type II RTA- Proximal tubule abnormality. decreased HCO3 reabsorption
Type I RTA- distal tubule abnormality, H+ secretion. Less new HCO3 made
Type IV RTA- hypoaldosteronism, leads to H+ retention
CRF- decreased H+ secretion
increased exogenous acid- TPN, HCl
EXAM! Anion gap metabolic acidosis causes
Methanol intoxication
Uremia
DIabetic ketoacidosis
Poisoning/ propylene glycol
Intoxication/infection
Lactic acidosis
ethylene glycol
salicylates/sepsis
(MUD PILES)
Treatment of acidosis
treatment of underlying cause
acute bicarb therapy for severe cases
When can we give acute bicarb therapy?
PH<7.1
concerns for bicarb use
- Shifting oxygen-hemoglobin saturation to the left where your oxygen wants to hang on to the oxygen instead of releasing it to tissues
- hypernatremia
- CSF ACIDOSIS
- electrolyte changes ( hypokalemia, decreased calcium, decreased magnesium)
most common cause of metabolic alkalosis
Diuretic
3 main causes of saline responsive alkalosis
Diuretic
vomiting
exogenous HCO3 administration or blood transfusion
How do diuretics cause alkalosis
Diuretics enhance excretion of water by resulting in extracellular volume contraction
Volume contraction stimulates aldosterone
Aldosterone increases in distal tubular Na+ reabsoprtion and induces H and K secretion
H secretion is associated with HCO3 reabsorption in proximal tubule and HCO3 generation in distal tubule
What also contributes to saline responsive alkalosis in response to diuretics
Hypochloremic state (they are losing Cl n addition to H20)
What is the 2nd most common cause of saline reponsive alkalosis
Vomiting and NG suction
How much mEq Cl and mEq H+ does 1 L of fluid contain
200 mEq Cl-
25-100 mEq H+
Urinary chloride for saline resistant alkalosis
Urinary chloride >20
Key difference between saline resistant alkalosis and saline responsive alkalosis
No Cl- depletion OR there is an inability to reabsorb Cl-
causes of saline resistant alkalosis
- Increased mineralcorticoid activity (enhances Na and K+ exchange and H+ seretion)
2, hypokalemia (increased H+ secretion)
- renal tubular chloride wasting
How does H+ secretion affect bicarb reabsoption and generation
Absorb more and making more bicarb
What to do about mineralcorticoid induced saline resistant alkalosis
Dx or change to more subtle mineralcorticoid
sx of alkalosis
Muscle crampsT
Treatment of alkalosis
Treat underlying cause
Rapid correction is often not necessary
Treatment of saline responsive alkalosis
- Saline (fluids/electrolytes)
1 L NS with 20-40 mEq/L Kcl over 4 hrs
- Carbonic anhydrase inhibitor (especially for patients that cant tolerate excess fluid or sodium)
adverse effects of CAI
K+ wasting (do not use if K+ is low)
WHen do we use HCl as treatment of akalosis
contraindication to Na replacement (decompensated HF, renal failure)
Failure of previous therapies or
PH>7.55
What are adjunct treatments we always use for saline responsive alkalosis For patients with vomiting or NG suction
H2 antagonist or PPIs
How to treat saline resistant alkalosis
-Correct hypokalemia
- reduce dose of mineralcorticoid or change to one with less mineralcorticoid activity
- add spironolactone
- correct hyperaldosteronism
respiratory acidosis PH? Co2? COmpensatory mechanism?
Low PH <7.35
Hypercapnia >45
compensatory increase in HCO3
Almost always from failure of excretion versus overproduction
causes of respiratory acidosis
-Airway obstruction
-reduced stimulus for respiration from CNS (drug OD, sleep apnea, CNS infections)
- pulmonary embolism
- mechanical ventilation
treatment of respiratory acidosis
-treat underlying cause (if choking get it out)
-Mechanical ventilation or oxygen (use caution with O2 for COPD patient, shuts off their dirve to breathe)
- avoid rapid correction to prevent alkalemia
When do we use bicarb for respiratory acidosis
PH<7.15 (very rare)
For respiratory alkalosis, what is the PH? PaCO2? Compensatory c=mechanism
High PH (>7.45), low PaCO2 (<40)
compensatory decrease in HCO3
treatment of respiratory alkalosis
Treat underlying cause
Ventilation
Sedation
Paralysis
symotoms of Respiratory alkalosis
CNS (lightheadedness, confusion, seizures)
N/V
Muscle cramps
Decreased blood flows
symptoms of respiratory acidosis
Respiratory (dyspne)
CNS (HA drownsiness, confusion/coma)
CV (tachycardia, arrhythmias)
