Acid-Base Imbalance (CHP 8) Flashcards
Describe the intracellular and extracellular mechanisms for buffering changes in body pH. Compare the roles of the kidneys and respiratory system in regulation of acid-base balance. Differentiate between respiratory and metabolic alkalosis; and respiratory and metabolic acidosis. Describe causes of respiratory and metabolic acidosis; and metabolic and respiratory alkalosis. Compare and contrast the etiology and clinical manifestations of metabolic and respiratory acidosis and of metabolic and re
______ and ________ = ECF
interstitial
plasma
intracellular water is found in …
cells
what is the body’s extracellular pH
7.35 - 7.45
acids and bases exist as _________ pairs/systems
buffer
acids are generated as ___________ of metabolic processes
byproducts
how do volatile acids exit the body?
lungs
how do nonvolatile/ fixed acids exit the body?
kidneys
the pH is regulated by: (3)
- chemical buffer systems (combine As and Bs to neutralize)
- lungs (get rid of CO2)
- kidneys (eliminate H+ & reabsorb/eliminate HCO3-)
the chemical buffer systems in the body, don’t do well with _______ changes
big
where are chemical buffer systems located?
within the ICF and ECF
buffer systems trade a strong acid for a ______ base OR trade a weak ______ for a strong base
weak
acid
what are the 3 main buffer systems?
bicarbonate buffer system
proteins
transcellular H+/K+ exchange system
the bicarbonate buffer system acts by __________ combining _____ & ______ to prevent changes in ____
immediately
A B
pH
transcellular H+/K+:
1. if plasma is acidic (too much _____)
2. H+ moves _____ cells, as ____ moves out
3. at risk for _________
why?
H+
in, K+
hyperkalemia
the ICF can be acidic (temporarily) but the ECF needs to stay between 7.35 - 7.45
________________ recognize changes in pH and tell the respiratory system to fix changes
chemoreceptors
pH above 7.45
alkalotic
pH below 7.35
acidic
increased ventilation = _______ PCO2
decreased
decreased _______ = increased PCO2
ventilation (RR)
lungs are the ___________ response, but can not be maintained indefinitely
fastest
what are the 3 roles of the kidneys in regulating pH?
- excretion of H+ (urine)
- reabsorption of HCO3-
- production of new HCO3-
pH changes with the kidneys take _______ but continue for ______ until pH returns to normal
hours
days
if the pH is too high, the kidneys will _________ or produce new ________ to lower the pH to normal
reabsorb
HCO3-
why does the body excrete H+?
to prevent hyperkalemia
(get rid of excess H+, K+ can go back into cell)
what are the 4 renal control mechanisms?
- H+ elimination and HCO3- conservation
- tubular buffer system
- K+/H+ exchange
- Cli-/HCO3- exchange
the tubular buffer system stops eliminating _____ (dangerous to kidneys) and pairs them with _______ and then restarts excretion
H+
buffers
pH < 7.35 (acidosis)
H+ elimination:
K+ elimination:
plasma [K+]
_______kalemia
increases
decreases
increases
hyper
pH > 7.45 (alkalosis)
H+ elimination:
K+ elimination:
plasma [K+]
_______kalemia
decreases
increases
decreases
hypo
pH > 7.45 (alkalosis)
Cl- elimination:
HCO3- elimination:
decreases
increases
pH < 7.35 (acidosis)
Cl- elimination:
HCO3- elimination:
increases
decreases
why is renal regulation of pH more efficient?
they have more mechanisms that can be tailored to fixing the issue
what is the range for PCO2?
this is the _______ component
35 - 45 mmHg
respiratory
what is the range for HCO3-?
this is the _______ component
22 -26 mmol/L
kidney
why do we use an artery for ABGs?
more accurate to the systemic issues of the body
(venous is dependent on the metabolic demands of surrounding tissue)
base excess =
metabolic alkalosis
base deficit =
metabolic acidosis
what does the anion gap measure?
difference between plasma concentrations of major cations (Na/K) and sum of measured anions (Cl- /HCO3-)
what is the normal anion gap value?
8 - 16 mEq/L
if the anion gap is high …
there are more negative ions in the body, which means the body has kidney issues
metabolic
kidneys
R
O
M
E
respiratory
opposite
metabolic
equal
pH and HCO3- for: metabolic acidosis
low and low
respiratory compensation for metabolic acidosis:
increase RR (to decrease PCO2)
pH and HCO3- for: metabolic alkalosis
high and high
respiratory compensation for metabolic alkalosis:
decrease RR (to increase PCO2)
renal compensation for metabolic alkalosis:
decrease H+ excretion
decrease HCO3- reabsorption
renal compensation for metabolic acidosis:
increase H+ excretion
increase HCO3- reabsorption
pH and PCO2: respiratory acidosis
low pH
high PCO2
pH and PCO2: respiratory alkalosis
high pH
low PCO2
renal compensation for respiratory acidosis:
increase in H+ excretion
increase in HCO3- reabsorption
renal compensation for respiratory alkalosis:
decrease in H+ excretion
decrease in HCO3- reabsorption
__________ mechanisms: Provides a means to control pH when correction is impossible or cannot be achieved immediately
compensatory
what is an example of mixed acid-base disorders?
someone having COPD
and then
getting into a car crash and injuring a kidney
(both systems are impaired and can’t regulate pH)
what is an example of a single acid-base disorder?
getting into a car crash and injuring a kidney
(lungs still available to regulate pH)
etiology of metabolic acidosis: (4)
- increased production of acids (meds)
- inability of kidneys to excrete acids
- excessive loss of bicarb through kidneys or GI tract (upper GI all alkaline)
- increased plasma [Cl-] (high Cl = low HCO3)
causes of metabolic acidosis: (3)
lactic acidosis
ketoacidosis (alcoholic + diabetic)
kidney failure/destruction
manifestations of metabolic acidosis (6)
N and V
weakness
confusion
peripheral vasodilation
decreased HR
cardiac arrhythmias
signs of metabolic acidosis compensation
increased RR (kussmaul)
hyperkalemia
acid urine
increased ammonia in urine
etiology of metabolic alkalosis: (3)
- gain of base (oral or IV = antacids)
- loss of fixed acids from the stomach (vomiting)
- maintenance of increased bicarbonate levels by contraction of ECF volume, hypokalemia, hypochloremia (excessive diuretics)
causes of metabolic acidosis: (3)
excessive gain of bicarb (antacids)
excessive loss of H+ ions (vomiting or gastric suction)
diuretic therapy
manifestations of metabolic acidosis (5)
confusion
hyperactive reflexes
tetany
hypotension
arrhytmias
signs of metabolic alkalosis compensation (2)
decreased rate and depth
increased urine pH
etiology of respiratory acidosis: (2)
acute or chronic conditions (decreased respiratory drive, lung disease, disorders of chest wall and respiratory muscles)
causes of respiratory acidosis: (4)
depression of respiratory center
lung disease
airway obstruction or disorders of chest wall (paralysis of resp m, chest injuries)
breathing air with high CO2
manifestations of respiratory acidosis (3)
dilation of cerebral vessels
depression of neural function
stupor and coma
etiology of respiratory alkalosis (1_
hyperventilation
causes of respiratory alkalosis (2)
hyperventilation and fever
manifestations of respiratory alkalosis (3)
CONSTRICTION of cerebral vessels
dizziness, panic, light-headed
numbness and tingling of fingers/toes
