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acid-base balance
cells function with pH of 7.35-7.45
pH is concentration of H+ ions
pH impacts enzymes, muscle contraction, O2 delivery
buildup of acid → hemoglobin not as effective in carrying O2
sources of acids in the body
acids are normal byproducts of metabolism
body must buffer/eliminate acids to maintain normal pH
excess acid = decreased pH
acid = CO2 or metabolism byproduct
cellular metabolism → carbonic acid (H2CO3)
anaerobic metabolism → lactic acid
fat metabolism → ketoacids
stomach → hydrochloric acid (HCl)
regulation of acid-base balance
kidneys + lungs are compensatory systems
buffer systems
carbonic acid-bicarbonate buffer systems
respiratory system
renal system
buffer systems
primary, MOST EFFICIENT, and acts IMMEDIATELY
change strong acids into weaker ones or bind acids to neutralize them until they can be excreted
carbonic acid-bicarbonate → predominant buffer in the bloodstream
hemoglobin → bind to H+ ions and get ready to excrete them
when pt is more acidic → more hypoxic
instead of RBCs binding O2 → bind H+ instead
not enough O2 carriers thru the bloodstream
carbonic acid-bicarbonate buffer system
CO2 + H2O ←→ H2CO3 ←→ HCO3- + H+
bicarb binds H+ → PREDOMINANT BUFFER
creates carbonic acid: H2CO3
carbonic acid breaks down into H2O + CO2 in the lungs
breathe out O2 and some water, the rest of water remains in bloodstream
if buildup of CO2 → binds to water → turns into carbonic acid → turns into bicarb and H+ → get rid of bicarb thru kidneys
respiratory compensatory system
RCC in brainstem senses changes in CO2 and H+ → adjusts rate and depth of respirations to restore balance
acts within MINUTES
fast but TEMPORARY → lungs can only breathe so fast/slow without having alternate complications
pH low → exhale CO2 → breathe faster and deeper
pH high → retain CO2 → breathe slower
renal compensatory system
SLOWEST compensatory system
acts within HOURS TO DAYS
LONG-TERM REGULATION!!
regulate bicarb and H+
pH low → pee out more H+ and increase bicarb production
pH high → retain more H+ and decrease bicarb production
ABG
venipuncture into an artery (radial/femoral/brachial)
tells overall oxygenation status, acid-base balance, underlying cause of imbalance, body’s ability to compensate/regulate pH
measures:
pH
PaCO2
PaO2
HCO3-
SaO2
PaO2 vs SaO2
PaO2:
measures O2 dissolved in your plasma
pressure measurement
ex) the crows if ppl waiting at the bus stop trying to push their way on
SaO2:
measures how much O2 is actually on hemoglobin
percentage measurement
ex) % of seats on the bus that are occupied by O2 passengers
normal pH value
7.35 - 7.45
normal PaCO2 value
35-45 mmHg
normal PaO2 value
80-100 mmHg
normal HCO3- value
22-26 mEq/L
normal SaO2 value
94-100%
respiratory acidosis causes
hypoventilation
COPD → can’t exhale all air fully
pneumonia → fluid in lungs → can’t get CO2 breathed out as much
pulmonary edema → CO2 not effectively get out
airway obstruction
opioids
sedatives
chest wall injury
neuromuscular weakness
abdominal/chest surgery
anything that will cause retention of CO2 or decreased RR
respiratory acidosis compensation
kidneys → create bicarb and pee out more H+
respiratory acidosis ABGs
pH < 7.35
paCO2 > 45 mmHg
HCO3- = normal or increased if compensating
respiratory acidosis S/S
hypoventilation → hypoxia
rapid, shallow respirations
decreased BP with vasodilation
dyspnea
headache
hyperkalemia
dysrhythmias (d/t incr k+)
drowsiness, dizziness, disorientation
muscle weakness, hyperreflexia
respiratory acidosis management
monitor VS, neuro, respiratory assessment, ABGs, lytes
improve ventilation & oxygenation:
elevate HOB
deep breathing & coughing exercises
IS
CPT
administer O2
suction
non-invasive (CPAP, biPAP) or mechanical ventilation
give O2 and positive pressure to push alveoli partially open for better gas exchange
treat the cause
respiratory alkalosis causes
hyperventilation
blowing off too much CO2
anxiety, fear, pain, fever, hypoxia, brain injury, mechanical over-ventilation
respiratory alkalosis compensation
kidneys → make less bicarb and retain more H+
respiratory alkalosis ABGs
pH > 7.45
PaCO2 < 35 mmHg
HCO3- = normal or decreased if compensating
respiratory alkalosis S/S
hyperventilation (increased rate & depth)
tachycardia
decreased/normal BP
low CO2 causes blood vessels to dilate
hypokalemia
al-ka-LOW-sis
high pH causes H+ to move out of cells, forcing K+ into cells, out of the bloodstream, to maintain electrical balance
hypocalcemia
al-ca-LOW-sis
numbness & tingling of extremities
hyper-reflexes & muscle cramping
seizures
increased anxiety, increased irritability
respiratory alkalosis management
monitor: VS, ABGs, neuro/muscular & respiratory assessment, lytes (K+ and Ca+2)
treat the cause
reduce hyperventilation:
coached slow breathing
rebreathing techniques - breathe into paper bag and supervise pt
sedation
reassurance
calm environment
metabolic acidosis causes
anything that doesn’t change ventilation but causes increased acid/decreased base
excess acid production:
diabetic ketoacidosis - body doesn’t produce insulin/resistant, fat metabolism, ketones produced, ketones are acidic
lactic acidosis - byproduct of anaerobic metabolism
septic shock - hypoperfusion → anaerobic metabolism → produces lactic acic
loss of bicarb:
AKI & CKD - kidneys stop making bicarb and stop getting rid of H+ thru urine
diarrhea
metabolic acidosis compensation
respiration → increases → get rid of excess CO2
metabolic acidosis ABGs
pH < 7.35
PaCO2 normal or decreased if compensating
HCO3- < 22 mEq/L
metabolic acidosis S/S
headache
decreased BP
hyperkalemia
muscle twitching
warm, flushed skin (d/t vasodilation)
nausea, vomiting, diarrhea
changes in LOC → confusion/drowsiness)
kussmaul respirations → breathing fast and rly deep to compensate
metabolic acidosis management
monitor: VS, ABGs, anion gap (difference between major positive and negative ions in the body → bigger gap d/t H+ build-up in the body), lytes, neuro & respiratory status, UOP, BUN/Cr
treat the cause:
DKA → IV insulin & fluids
diarrhea → rehydration, antidiarrheals
sepsis → antibiotics & IV fluids
shock → IV fluids, vasopressors
renal failure → dialysis
support ventilation & oxygenation
administer sodium bicarb
metabolic alkalosis
loss of acid or gain of base
GI acid loss: vomiting, NG suctioning
excess bicarb intake: antacids, IV sodium bicarb, calcium supplements
diuretics
hypokalemia
when K+ low in blood, H+ lost in blood and blood becomes more basic
metabolic alkalosis compensation
lungs!
respirations slow and shallow
RR decreases
metabolic alkalosis ABGs
pH > 7.45
PaCO2 normal or increased if compensating
HCO3- = >26 mEq/L
metabolic alkalosis S/S
restless followed by lethargy
dysrhythmias (tachycardia)
compensatory hypoventilation
confusion (decreased LOC, dizzy, irritable)
nausea, vomiting, diarrhea
tremors, muscle cramps, tingling of fingers & toes
hypokalemia and hypocalcemia
metabolic alkalosis management
monitor: VS, ABGs, lytes, neuro & resp status
treat the cause:
vomiting → antiemetics
hypokalemia → K+ replacement, avoid K-wasting diuretics
excess bicarbonate → discontinue or reduce intake
support ventilation & oxygenation
breathing slows → not taking in as much O2 → may need external O2 source
mixed acid-base disorders
two or more acid-base disorders present at the same time
pH depends on the type, severity, and compensatory mechanisms involved
common in critically ill or complex medical patients
compensation from one system cannot fully correct abnormalities
pH may appear near normal, so interpretation must include ABGs and clinical context
ABG interpretation
1. acidosis or alkalosis
2. respiratory or metabolic?
3. compensated?
ROME method
Respiratory, opposite → CO2 and pH will be opposite trends
Metabolic, equal → HCO3- and pH will be equal trends
assess for compensation - what is needed to compensate? more CO2 or bicarb?
no compensation: compensating lab value remains within normal range
partial compensation: compensating lab value shifts to correct imbalance, but pH not normal yet
full compensation: compensating lab value shifts to correct imbalance, and pH returned to normal range
if pH returned to normal - look what side closer to - high or low?