1 - Acid/Base Disorders Flashcards
Henderson Hasselbach eqn for physiological pH
pH = 6.1 + log (HCO3-/H2CO3)
=(HCO3-/(0.3xpCO2)
normal PaCo2
35-45 mmHg
normal HCO3
22-26 mEq/L
normal PaO2
95-100 mmHg
normal SaO2
> =95%
What are the adverse CV effects of acidemia?
decr CO
imp’d contractility
incr PVR
arrhythmias
What are the metabolic effects of acidemia?
insulin resis
inhib of anaerobic glycolysis
hyperkal
What are the CNS effecs of acidemia?
coma or AMS
What are misc effects of acidemia?
decr resp musc strength
hypervent
SOB
What are the adverse CV effects of alkalemia
decr coronary BF
arteriolar constriction
decr anginal threshold
arrhytmias
What are the metabolic effects of alkalemia?
decr K, Ca, Mg
stim of anerobic glycolysis
What are the CNS effects of alkemia?
decr cerebral BF
Szs
What are the nonvolatile acids and how are they formed?
anaerobic metab: lactic & pyruvic acid
TG ox: acetoacetic and beta-hydroxybutyric acid
AA metb: sulfuric and phosphoric acids
Describe the buggering capacity of bicarb.
rapid onset w intermediate capacity
Describe the phosphates as a buffer.
intermed onset and capacity.
EC Pi limited actvity
bone relativey inaccessible
Describe proteins as buffer.
alb/hbg: rapid onset, limited: more effective IC
What are the mechanisms by which the kidney regulations acid/base status?
- reabsorb filtered bicarb
- excrete hydrogen ions released from nonvolatile acids
- ammoniagenesis, titratable acidity
most bicarb is reabosbed at the
PCT
limiting H+ secretion into the PCT results in
bicarb losses
How can carbonic anhydrase inhibitors affect a/b status?
cause metabolic acidosis as HCO3- excretion increases
Where does H+ secretion take place?
DCT
H+ secretion in the DCT results in generation of
NEW Bicarb
Describe vent reg of a/b status.
rapid and large cap
chemoreceptors detect incrin PaCO2 and incr rate and depth of vent.
Which chemoreceptors are activated by arterial acidosis, hypercapnia, and hypoxia?
peripheral chemoreceptors in carotid arteries and aorta
Which chemoreceptors are activated by CSF acidosis?
central chemoreceptors in medulla
Describe hepatic regulation of A/b status
Oxidation of protein generations bicarb and ammonium that can be elim’s via urea synthesis or renal ammoniogenesis.
if liver decr urea synthesis–> incr pH
**comp in met acidosis
PaCo2 falls by 1-1.5 x HCO3 fall
**comp in met alk
PaCO2 incr by 0.4-0.6 x rise in plasma HCO3-
**comp in resp acid
acute: HCO3- rise by 0.1 x incr in PaCO2 +/- 3
chronic: 0.4x +/-4
**comp in resp alk
acute: HCO3- fall by 0.1-0.3 x decr in PACO2 but usually not less than 18 mEq/L
chronic: 0.2-0.5, 14 mEq/L
normal anion gap
3-11 mEq/L
anion gap eqn
AG=Na-Cl-HCO3-
nother name of non-anion gap met acidosis
hyperchloremia acidosis
Causes of non-anion gap acidosis
GI bicarb loss
renal wasting/imp’d H+ secr
acid/Cl gain
Examples of GI bicarb loss
diarrhea
pancreatic fistula
biliary drainage
Explain renal bicarbonate loss
type II RTA (PCT)
- cannot reabs
- -incr’d Na and fluid loss –> RAAS
- -2* hyperaldosteronism–>hypokalemia
–> able to acidify urine pH <5.3
what are the causes of reduced renal H+ excretion?
type I RTA (hypokalemia)
type IV RTA (hypoaldosteronism / hyperkalemia)
chronic renal failure
Explain type I RTA
caused by tubule defect, SLE, myeloma, toluene (OD)
H+ cannot be pumped into DCT
- ->urine cannot be acidified
- ->incr K+ excretion d/t Na exchange
Explain type IV RTA
hypoaldosteronism
- ->decr H+ and K+ excretion
- ->acidosis and hyperkalemia
Explain how CRF can cause a metabolic acidosis.
decr H+ secr.
less ammonia production. (less bicarb made)
MULEPAK
methanol uremia lactic acidosis ethylene glycol paraldehyde ingestion aspirin (salicylates) ketoacidosis
MUDPILES
methanol uremia DKA poisoing/propylene glycol ingestion intox/infx lactic acidosis etylene glycol salicylate/sepsis
delta gap
for AG met acidosis add to measured HCO3-
–> if high for HCO3- then mixed disorder (also metabolic alkalosis)
What causes lactic acidosis?
- decr clearance of lactate
- shock (hypoxia, decr hep fxn)
- DRUGs
How does ethanol cause lactic acidosis?
incr lactate and hypoglycemia - impaired gluconeogenesis
How does metformin cause lactic acidosis?
we don’t know
How do NRTIs cause lactic acidosis?
inhibit DNA Pol for mitochondrial DNA synthesis
How do linezolid, isoniazid, and propofol cause lactic acidosis?
simply increase lactic acid
How do Sz cause lactic acidosis?
enhanced met act
self-limiting
How does leukemia cause metabolic acidosis?
packed porly perfused bone marrow caviity
How does hep/RF cause lactic acidosis?
imp’d metab and excr
How does DM cause lactic acidosis?
formation of ketones/lactate; use of metformin
How does ketoacidosis cause met acid?
increase acetoacetic acid and beta-hydroxy butyric acid (KETONE BODIES)
How do salicylates cause AG met acid?
resp alkalosis from stim of resp drive
met acid from accumulation of organic acids
How do methanol/ethylene glycol cause AG met acid?
methanol–>formaldehyde–>formic acid
ethylene glycol–>glycoaldehyde–>glycolate–>glycoxylate–>oxalate
Wht are the Sx of lactic acidosis?
Kussmaul respiration periph vasodil causes flushing and tachycardia --> arrhythmias, decr contractility hyperkalemia lethary/coma N/V bone demineralization if chronic
When to use bicarb therapy?
pH <7.1-7.15
ind: hyperkalemia, pH <7.1 w/ cardiac arrest after defib, vent, and meds have been utilized, ODs
How to dose bicarb
dose (mEq)=[0.5L/kg x IBW] x (goal bicarb - actual bicarb)
use 12 mEq/L for goal
give 1/3-1/2 calc’d dose
monitor ABG
Tips for bicarb therapy
monitor ABG
supplement K+, if needed
don’t overalk–>left shift hypoxia, hypernatremia, CSF acidosis
What electrolyte shifts can bicarb therapy cause?
K+ –> shifts IC –> hypokalemia
Ca2+–>decr Cai so decr contractility
Dose of chronic bicarb therapy.
1-3 mEq/kg/d (up to 10+)
What is tromethamine?
Tx for acidosis
combines with H+ from H2CO3 to form bicarb
–osmotic diuretic
What are some drugs to treat met acidosis?
bicarb
tromethamine
carbicarb
dichloroacette (DCA): lactate metab
What are the mechanisms of metabolic alk?
loss of acid
admin of HCO3- or precursor
contraction alkalosis
What the heck does contraction alkalosis mean?
loss of Cl- rich, HCO3- poor fluid
How do volume and chloride depletion maintain a met alk?
decr in blood vol
decr ability to excr bicarb
incr reabs of PCT reabs of bicarb
What are the two types of met alkalosis?
saline responsive saline resistance (Cl in urine >20 mEq/L)
What are the causes of saline responsive met alk?
diuretic therapy
vomting and NG suction
exogenous HCO3- admin or blood transfusions
How is a saline responsive met alk maintained?
reduced GFR (incr HCO3 reabs w Na+)
- incr PCT HCO3- abs w Na+ (hypochloremia)
- hypokalemia: more H+ secreted and new bicarb
How does diuretic therapy cause saline responsive met alk?
volume contraction –> ALDOSTERONE –> incr Na reabs in DCT
- -> incr H+/K+ sec
- -> incr BICARB made
–>HYPOKALEMIA–> K+ moves EC –> H+ moves IC –> basic EC
–>HYPOCHLOREMIA (d/t diuresis) –> increase bicarb reabs
Why do blood products cause alkalosis?
contain citrate–>breaks down into bicarb
What is the pathology of saline resistant met alk?
enhanced renal H+ excr and bicarb reabs
urinary chloride >20 mEq/L
–> no Cl depletion or there is inability to reabsorb Cl
What are the causes of saline res mmet alk?
incr mineralcorticoid activity
hypokalemia
renal tubular chloride wasting (Bartter’s syndrome)
How does increased mineralcorticoid acitivyt cause saline res met alk?
stim CD H+ secr
–>incr ammoniagenesis
How does hypokalemia cause saline res met alk?
incr H+ secr w bicarb reabs and ammoniagenesis
How does Bartter’s syndrome cause saline res met alk?
chloride wasting:
imp’s NaCl reabs
–>fluid loss –> RAAS –> incr aldosterone
What are the Sx of metabolic alkalosis?
msucle cramps, weakness, paresthesias
cellular hypoxia, confusion, coma, Sz
myocardial suppression, CV collapse, arrhytmias (low K)
How to treat saline responsive alkalosis?
fluid/elyte replacement w NaCl or KCl
- -> less bicarb reabs
- ->increase volume
- ->increase K+ –> decr H+ secr
or CAI
Example fluid treatment for saline responsive met alk
0.9% NaCl w 20-40 mEq/L KCl over 4-6 hrs
What to monitor for met alk?
I/O BP HR lung sounds elyes edema
How do carbonic anhydrase inhibitors help treat saline resp met alk?
decr bicarb reabs in PCT
SE: K+ wasting
carbonic anhydrase inhibitor dose
acetohexamide 250-375 once or bid
Rare therapeutic options of met alkalosis
HCl acid
Ammonium chloride
arginine monohydrochoride
adjunct therapy for pts for met alk d/t NG suctioning or vomitting
H2 antagonists or PPIs
How to treat saline resistant alkalosis?
correct hypokalemia w K-sparing diuretic or KCl supplementation
- decrease mineralcorticoids
- spironolactone (mincortR antag, inhib aldosterone-stim of H+ secr)
–correct hyperaldosteronism-> give fluids but not first line
What are the causes of respiratory acidosis?
airway obstruction reduced stimulatus for resp from CNS (OD, sleep apnea, CNS infx) -failture of heart or lungs -neuromusc defects (can't breathe) -mech vent
Sx of resp alk?
SOB
CNS: HA, drowsy, confusion, coma, Sz
CV: tachycardia, arrhythmias, hypoTN
Tx of resp acidosis
underlying cause
- mech vent or O2 (caution in COPD)
- avoid rapid correction (alk)
- rarely use bicarb (only high arrhythmia risk)
What are the causes of resp alk?
central stim of resp periph stim of resp mech vent pulmonary salicylate intox
What are the Sx of resp alk?
CNS: lightheadedness, confusion, Sz
decr cerebral BF
tetany/cramps
N/V
How is resp alk treated?
correct underlying cause
vent, sedate, paralyze
