Small Group 2 Acid Base Flashcards
- Explain metabolic acidosis and differentiate non-anioin gap from anion gap acidosis.
metabolic acidosis= deficiency of bicarbonate because it is excessively used, not generated or excessively excreted
anion gap in the case of MUDPALES (methanol, uremia, DKA, paraldehyde, alcohol, lactic acidosis ethylene glycol and salicylate)
Note: methanol, ethylene glycol and alcohol can produce an increased osmolar gap
- Explain metabolic alkalosis and differentiate generation from maintenance cause.
generation: the initial insult to cause an imbalance in the system: i.e.. vomitting and loss of HCl
maintenance: volume contraction, hypokalemia, hypochloremia
make sure to check urine chloride to access whether the metabolic alkalosis is saline responsive
note in vomiting or gastric suctioning, bicarbonate is generate at the same rate as H+ is lost (half rate of HCl)
- Interpret data from arterial blood gases and serum and urine studies in the diagnosis of acid-base disorders.
access:
pH
bicarb, anion gap
pCO2
determine primary disorder,
determine if the compensation is appropriate
- Describe clinical conditions associated with different types of acid-base disorders.
vomiting or gastric suctioning: metabolic alkalosis
COPD: chronic respiratory acidosis
DKA: ketoacidosis, can be complicated by septic shock with kidney function
metabolic alkalosis from diuretic induced volume contraction and hypokalemia
- Describe how acid-base disorders are associated with alterations in volume status and alterations in serum potassium concentration .
metabolic alkalosis can lead to loss of bicarb in the urine which can decrease volume due to concurrent Na+ loss to maintain
electroneutrality, K+ and Cl- move passively into tubule
What things are important to consider if trying to estimate the ICF
Na+ osmolarity
keep an eye for other factors like glucose that could cause a shift in osmolality
remember the equation Na x 2 + glucose/18 +BUN/2.8
List conditions that will result in high serum potassium.
acidosis
lack of insulin, B agonists
increased aldosterone from ECV contraction
What is pre-renal azotemia?
in a patient that is volume contracted, their kidneys are hypo perfused and reabsorb salt, water and BUN (active reabsorption)