Lecture 51-52 - Acid Base Disorders Flashcards
what are the “rules” of a “simple” acid base disorder?
pH is not brought back to normal by compensation
Bicarb and PCO2 move together
Compensations resolves as primary resolves
metabolic acidosis – characterize the scenarios (what are the values of pH, HCO3 and PCO2)
pH low
Decreased HCO3- (Increased H+, decreased pH)
Compensatory Drop in PaCO2 (hyperventilation; secondary respiratory alkalosis)
If simple – then it’s in the predicted range (on the acid base map)
physiological effects of a metabolic acidosis
- Hb-O2 Dissociation shifts Right and increased O2 to tissues
- Depressed CNS
- Arrhythmias
- Decreased Cardiac Contractility
- Hyperkalemia
- Decreased pulmonary blood flow
3 classes of adaptation to an acid base disorder; time frame for each
Compensation: buffer (immediately)
Compensation: Respiratory/Metabolic response (eg hyperventilate to expel more PCO2, compensating for a metabolic acidosis) (minutes)
Elimination: secretion through the kidney (days)
what three mechanisms are to eliminate extra H+ via the kidney in metabolic acidosis
when does this occur?
3-4 days after onset of metabolic acidosis, increased renal excretion of H+ will take place:
1) PCT: H+ secretion, Bicarb reclamation
2) Titratable acids (Phosphates and sulfates)
3) CD: Buffering with NH3 —> NH4+
what is your differential for a high anion gap metabolic acidosis?
MUDPILES
Methanol -- Formaldehyde Uremia -- creatinine DKA -- ketones Propylene Glycol -- increased Osm Gap/Lactate Iron Tablets; Isoniazid - Check Meds Lactic acidosis -- Lactate Ethylene glycol -- metabolized to Oxalate/Increased Osm Gap; Salicylates -- Level
what is your differential for a normal (hyperchloremic) anion gap metabolic acidosis?
HEARD-CCU
Hyperalimentation – eating too much protein/acid
Expansion
Acetazolamide – (CA inhibiton, blocks H+ excretion)
RTA
Diarrhea
Cholestyramine – exchange resisn bind chol and release H+
Carbonic Anhydrase Inhibition
Uteros Igmoidostomy –
if there is a normal anion gap metabolic acidosis, but the urine is alkaline (ph > 5.5) what should you add to your differential?
Distal Tubule RTA (TYPE 1)
Renal tubular acidosis Type 1 -
What is the defect? Urine ph? what is the plasma K? what is the plasma bicarb? Complication? Causes?
defect in H+ secretion of alpha IC cells of the Collecting Tubule (distal); no new HCO3 is generated; metabolic acidosis
urine ph > 5.5
Low plasma K - not secreting H+, therefore not reabsorbing K+ via IC
Plasma bicarb (<15) - Not secreting H+, therefore not generating new HCO3
Complication: Calcium kidney stones
Causes: Autoimmune (Sjogrens, RA), AmphoB, Hypercalciuria
Renal tubular acidosis Type 2 -
What is the defect? Urine ph? what is the plasma K? what is the plasma bicarb? Complication? Causes?
Defect in PCT reabsorption of HCO3; increased HCO3 excretion; metabolic acidosis
pH < 5.5
Plasma K: Low – wasting of substances that would have otherwise been resorbed in the PCT
Plasma bicarb: > 15
Complication: Rickets
Causes: Fanconi syndrome (generalized PCT dysfunction), Carbonic anhydrase inhibition
RTA type 4 –
what is the defect?
Urine ph?
what is the plasma K?
what is the plasma bicarb?
Defect: hypoaldosteronism; (therefore decreased H+ secretion and decreased NH4+ secretion)
Urine Ph < 5.5
Plasma K: Hyperkalemia; because not upregulating ENAC and ROMK channels wth aldo; more K retention
Bicarb: > 15
What is the only acid base disorder that is “maintained” even when the principle issue is resolved ?
Metabolic alkalosis
Metabolic alkalosis – describe the situation
Primary Problem: Increase of HCO3
PH - increased
Respiratory Compensatory Response: Increased PaCO2 (acidic, eg hypoventilation)
Effects of metabolic alkalosis:
○ Shifts HB-O2 dissociation to the left -- -decreased O2 delivery to the tissues ○ Decreased cerebral blood flow ○ Arrhythmias ○ Tetany ○ Seizures
potential causes of metabolic alkalosis ?
Loss of H+
Extra Renal –
GI: Bicarbonate ingestion, Vomiting (most commonly)
H+ Trancellular shift – Hypokalemia
Renal:
Diuretics
Gain Bicarb
An actual bicarb injection
Citrate infusions (with blood) – converts to bicarb
difference between transient and maintained metabolic alkalosis?
Transient –metabolic alkalosis resolves after the increased bicarbonate loading has stopped
Extra Bicarb is lost by the kidney (bicarbinaturia)
Bicarb reclamation is not increased;
H+ secretion is not increased
Maintained: Alkalosis persists even after the increased bicarb has resolved
Increased H+ secretion
Which is manifested by a paradoxical Aciduria
three scenarios that can lead to maintained metabolic alkalosis
what will be the clue for maintained metabolic alkalosis?
which is the common scenario
Clue: paradoxical aciduria in setting of alkalosis
Three scenarios:
Volume Depletion
CL Depletion – most commonly
K Depletion
How does Volume Depletion lead to a maintained metabolic alkalosis?
how do you treat this?
Volume Deplete –> increased Na reabsorption
Na initially absorbed with Cl
When CL runs out Na is absorbed with organic acids
When Organic acids run out, Na is exchanged for H+
Increased H+ excretion = paradoxical aciduria and maintenance of alkalosis
Treat: saline
How does Chloride depletion lead to a maintained metabolic alkalosis?
how can you treat this ?
Beta IC cells function: Dump HCO3- in exchange for Cl -
When the body is Chloride deplete, the function of the alpha IC cell takes over
Alpha IC function: secrete H+, resulting in HCO3- reabsorption
Treat: Saline
How does K depletion lead to maintained metabolic alkalosis?
How do you treat this?
Really really low K – the renal tubular cells will resorb as much K as possible into the blood, but this is in exchange for H+
Results in an intracellular acidosis
Cells dump H+ into the urine
CANNOT TREAT WITH SALIDE
describe the clinical algorithm for a maintained metabolic alkalosis ?
Check Urine Chloride -
§ If low – treat with saline
§ If normal — check urine potassium
Urine Potassium
§ If low – suggest K loss from somewhere else (GI)
§ If high — suggest K loss from kidney (possible +/- hyperaldo)
□ Treat: K+ & Anion
In regards to respiratory disorders, what is different about the compensatory adaptations?
In light of this difference, what is always important to consider when evaluating the acid/base graphs for predicted ranges of values?
No respiratory compensation (bc there is something wrong with the lungs)
There is only: extraceullar buffering, intracellular buffering, and renal secretion changes (but the latter takes days to reach maximally)
acute vs chronic respiratory acidosis/alkalosis
Describe the profile of respiratory acidosis
Increased PaCO2 (due to poor gas exchange)
Decreased PH
Increased bicarb – Compensatory
This is simple secondary increase in bicarb if withn the appropriate confidence bands (acute, chronic, or btw)
Increased H+ occurs days later (kidey dumps H+ and reclaims HCO3)
Causes of respiratory acidosis
§ CNS Depression – Narcotics
§ Respiratory Muscle Dysfunctions – myopathies
§ Airway obstruction –
§ Poor Gas exchange – pulmonary edema
Impaired lung motions – Pneumothroax, hemothorax, flail chest
Describe the profile of respiratory alkalosis
Decreased PaCO2 Increased PH Decreased HCO3 -- compensatory Simple -- if within the confidence bands Acute, chronic or in btw
§ Decreased renal H+ secretion (increase H+ resorbtion)
Causes of respiratory alkalosis
Hypoxemia Lung disease Sepsis -- some patients hyperventilate Salicylates CNS stimulants
what clues might lead you to a dx of a mixed acid base disturbance?
□ Take H&P
□ Compensation back to normal PH
□ Compensation maps outside the confidence bands
□ Presumed compensatory responses do not resolve
what should be the first step for any patient with presumed acid base disturbance?
CALCULATE THE ANION GAP
if high, then at least one of the acid base disturbances is a anion gap metabolic acidosis (MUDPILES)
what is Winter’s formula and how is it used?
PaCO2 = [1.5 x HCO3] + 8
only used in metabolic acidosis to determine if there is appropriate respiratory compensation
