Acid-Base Flashcards
Acid base normal ranges
normal physiological pH: 7.35-7.45
pH < 6.7 or < 7.7 is considered incompatible with life
Acidemia pH
pH < 7.35
Alkalemia pH
pH > 7.45
Carbonic acid/bicarbonate buffer system
H+ + HCO3- <–> H2CO3 <–> CO2 + H2O
left side occurs in “kidney” metabolic side; right side occurs in “lungs”
metabolic disorders involve changes in H+ or HCO3- levels, while repsiratory disorders involve changes in CO2
compensation for a particular disorder involves the opposite part (lungs compensate metabolic disorders, kidneys compensate respiratory disorders)
Henderson-Hasselbach equation
the relationship between pH and the concentration of acid-base pairs in buffer system
pH = pKa + log (base/acid)
pH = 6.1 + log (HCO3-/H2CO3)
pH = 6.1 + log (HCO3-/0.03 x pCO2) - pH of blood determined by ratio of HCO3- to pCO2
Normal blood gas values
PaCO2: 40 mmHg
HCO3: 24 mmHg
arterial blood is the best source for obtaining these readings
Adverse consequences: acidemia
cardiovascular, metabolic, CNS, others
Acidemia - cardiovascular AEs
decreased cardiac output, impairment of cardiac contractility, increase in pulmonary vascular resistance and arrhythmias
Acidemia - metabolic AEs
insulin resistance, inhibition of anaerobic glycolysis, hyperkalemia
Acidemia - CNS AEs
coma or altered mental status
Acidemia - other AEs
decreased respiratory muscle strength, hyperventilaion, dyspnea
Adverse consequences: alkalemia
cardiovascular, metabolic, CNS, others
Alkalemia - cardiovascular AEs
decreased coronary blood flow from arteriolar constriction
decreased anginal threshold; arrhythmias
Alkalemia - metabolic AEs
decrease in K+, Ca, and Mg (all important for electrical activity of the heart)
stimulation of anaerobic glycolysis
Alkalemia - CNS AEs
decrease cerebral blood flow
seizures
Alkalemia - other AEs
decrease respirations
Acid generation - diet
~1mEq/kg/day of acid consumed/day; from oxidation of proteins + fats
aerobic metabolism of glucose produces 15-20K mmol of CO2/day
nonvolatile acids also formed
Nonvolatile acids formed
anaerobic metabolism produces lactic acid and pyruvic acid
triglyceride oxidation produces acetoacetic acid and beta-hydroxybutyric acid
metabolism of sulfur-containing amino acids and phospholipids result in sulfuric and phosphoric acids
0.8 mEq H+ from nonvolatile acids/kg of body weight must be excreted daily
Acid regulation: 3 standard mechanisms
buffering, renal regulation, ventilatory regulation
Extracellular/intracellular buffering systems
first line defense
buffer: ability of a weak acid and its anion (base) to resist change in pH with addition of strong acid or base
buffers: bicarbonate/carbonic acid, phosphate, and protein
Extracellular/intracellular buffering systems -Bicarbonate principle buffer
rapid onset with intermediate capacity to control acid level
HCO3- buffer present in largest concentration extracellulary: supply of CO2 is unlimited, acidity can be controlled by HCO3- or the pCO2
ability of the kidneys + lungs to excrete and retain HCO3- and CO2 respectively
when acid is added, large quantities of CO2 can be exhaled very rapidly; body needs need HCO3- added to system in amount equivalent to H+ load ingested each day
Extracellular/intracellular buffering systems - phosphates
intermediate onset and capacity
extracellular inorganic phosphates limited activity
intracellular organic phosphates
calcium phosphates in bone relatively inaccessible
Extracellular/intracellular buffering systems - proteins
albumin/hemoglobin: rapid onset, limited capacity
more effective intracellular buffer vs extracellular buffer
Renal system regulation
kidney serves 2 main purposes: reabsorb filtered HCO3- and excrete H+ ions released from nonvolatile acids (help generate new HCO3-)
Renal system regulation - bicarbonate reabsorption
most is reabsorbed by proximal tubule, rest is reabsorbed via distal tubule or collecting duct
virtually no HCO3- in urine
Bicarbonate reabsorption
filtered HCO3- combines with a secreted H+ to form H2CO3 –> through the action of carbonic anhydrase (acts in urine), dissasociation occurs to form H2O and CO2 –> H2O and CO2 are reabsorbed into tubular cell (proximal tubule) to form H2CO3 –> H2CO3 dissociates into HCO3-, which is reabsorbed into peritubular capillary (back in bloodstream), and H+ which is secreted into tubular lumen in exchange for Na+
net effect: filtered HCO3- is reabsorbed without net loss of H+!
Anything limiting H+ secretion into proximal tubule lumen results in
urinary bicarbonate losses
ex. carbonic anhydrase inhibitors: inhibit activity of carbonic anhydrase –> decrease entry of CO2 and H2O (decrease HCO3- for reabsorption) –> metabolic acidosis occurs with increased HCO3- excretion secondary to increased urine Na+
Bicarbonate generation/H+ excretion
H+ excretion takes place primarily in the distal tubule
2 processes for bicarb generation
ammonium excretion
titratable activity
Ammonium excretion
secreted H+ combines with NH3 to form NH4+ –> NH4+ can’t cross membranes and ultimately is excreted –> intracellular HCO3- formed during the processed is also reabsorbed in the peritubular capillaries
ammoniagenesis
Titratable acidity
filtered HPO4- combines with secreted H+ and is excreted as H2PO4- –> intracellular HCO3- formed from dissociation of H2CO3 is reabsorbed as new HCO3-
capacity cannot be increased (limited by plasma concentration of HPO4- buffer and by GFR)
Distal tubular hydrogen ion secretion
~50% of net acid excretion
CO2 combines with water in presence of carbonic anhydrase to form H2CO3 which breaks down H+ and HCO3- –> H+ transported back into tubular lumen by ATPase –> HCO3- freely crosses distal tubular membrane and enters peritubular capillary absorption
Acid regulation - ventilatory regulation
rapid onset and large capacity
chemoreceptors detect increase in PaCO2 and increase rate and depth of ventilation
peripheral chemoreceptors in carotid arteries and aorta, and central chemoreceptors in medulla
Hepatic regulation
oxidation of proteins generates HCO3- and NH4+ –> NH4+ can be eliminated via urea synthesis or renal ammoniagenesis; therefore if liver dimishes hepatic urea synthesis, metabolic alkalosis may occur or an acidotic state will be corrected
decrease urea synthesis: more bicarb sitting around
Compensation characteristics for acid-base disorders
respiratory compensation very rapid
renal compensation takes 3-5 days for max effect
compensation moves pH towards normal, but rarely corrects pH to normal
Metabolic acidosis
change: decreased HCO3-
compensation: decreased PaCO2
Metabolic alkalosis
change: increased HCO3-
compensation: increased PaCO2
Respiratory acidosis
change: increased PaCO2
compensation: increased HCO3-
Respiratory alkalosis
change: decreased PaCO2
compensation: decreased HCO3-
1 treatment for all metabolic disorders
fix the cause
Metabolic disorders - metabolic acidosis
low pH (<7.35), low serum HCO3- (<24 mEq/L) and a compensatory decrease in PaCO2 from hyperventilation
classified as either non-anion gap or anion gap metabolic acidosis
If metabolic acidosis present, LOOK AT
anion gap
anion gap = Na - (Cl + HCO3)
normal: 3-11 mEq/L
normal or low: non-anion gap
high: anion gap
Pathophysiology of non-anion gap acidosis (hyperchloremic acidosis)
loss of plasma HCO3- replaced by Cl-
causes: gastrointestinal biacarb losses; renal bicarb loss; reduced renal H+ excretion (distal tubule RTAs); acid and chloride administration
Gastrointestinal bicarb losses
diarrhea very common cause
pancreatic fistulas/biliary drainage
Renal bicarb losses: type II renal tubular acidosis
problem within the proximal tubule (can’t reabsorb bicarb) - can result from various diseases or toxins; reabsorptive threshold for HCO3- is reduced in the proximal tubule
with enhanced bicarb loss –> increase in Na+ and fluid loss –> activates renin-angiotension system leading to secondary hyperaldosteronism –> increased aldosterone –> increased K+ excretion –> hypokalemia
Reduced renal H+ excretion (distal tubule RTAs - most common)
type I RTA (hypokalemia RTA): H+ can’t be pumped into tubule lumen by cells of collecting duct/distal tubule –> urine can’t be maximally acidified –> increase in K+ excretion b/c Na gets interchanged with K+, H+ can’t be secreted in repsonse to Na+ reabsorption
type IV RTA (hypoaldosteronism or hyperkalemia RTA): aldosterone stimulates H+ excretion, with less aldosterone = H+ retention; hyperkalemia also leads to increased H+ retention
chronic renal failure: decreased H+ secretion; less ammonia production ( decreased ability to make new HCO3- via process of ammonium excretion)
Acid and chloride administration
just give too much acid: in TPN or HCl/ammonium Cl adminisitration
Pathophysiology of anion gap acidosis
pts have elevated anion gap
overall HCO3- losses are replaced with another anion besides Cl-
calculate delta gap: difference between pts anion gap and normal anion gap; then add delta gap to pts measured HCO3- –> if you get elevated HCO3-, mixed disorder
Causes of anion gap metabolic acidosis
MUDPILES
methanol intoxication, uremia, diabetic ketoacidosis, poisoning/propylene glycol ingestion, intoxication/infection, lactic acidosis, salicylate/sepsis
Lactic acidosis
increased levels almost always result from decreased clearance vs overproduction
possible causes: shock, drugs/toxins (ethanol, metformin, propylene glycol, linezolid, isoniazid, propofol, topiramate) , seizures, leukemia, hepatic/renal failure, DM, malnutrition, rhadbomyolysis
Drug intoxications
salicylate toxicity: respiratory alkalosis from stimulation of respiratory drive; metabolic acidosis from accumulation of organic acids
Treatment of anion gap acidosis
treat underlying cause!
acute bicarb therapy: consider if pH <7.10-7.15
dose (mEq) = [0.5 L/kg (IBW)] x (desired HCO3 - actual HCO3)
use 12 mEq/L for desired HCO3-
give 1/3-1/2 the calculated dose
during cardiac arrests, ~1 mEq/kg may be given
chronic bicarb therapy for chronic metabolic acidosis: 1-3 mEq/kg/day
Hazards of bicarb therapy
overalkanization can impair oxygen release from Hgb to tissues
hypernatremia/hyperosmolality
CSF acidosis
electrolyte shifts: hypokalemia and hypocalcemia
Metabolic alkalosis
increased pH (>7.45), increased HCO3- (>30 mEq/L) and a compensatory hypoventilation resulting in increased PaCO2
Metabolic alkalosis pathophysiology
primary rise in plasma HCO3- from: loss of acid from GI tract or urine; administration of HCO3- or a bicarb precursor; contraction alkalosis
Saline responsive alkalosis (urinary chloride < 10-20 mEq/L)
diuretic therapy
vomiting and NG suction
exogenous HCO3- administration or blood transfusions (contain citrate, which is broken down to HCO3-)
maintenance of alkalosis
Diuretic therapy
enhances excretion of sodium chloride and water –> volume contraction –> aldosterone release –> aldosterone increased distal tubular Na+ reabsorption and induces H+ and K+ secretion (H+ secreation associated with HCO3- reabsorption in proximal tubule and HCO3- generation in distal tubule)
in response to the hypokalemia –> H+ moves intracellularly and K+ moves extracellularly –> in exchange for the K+, Na+ gets reabsorbed
hypochloremic: without Cl-, Na+ is reabsorbed with HCO3-
Saline resistant alkalosis (urinary chloride > 20 mEq/L)
enhanced renal H+ excretion and HCO3- reabsorption
key difference: no chloride depletion or inability to reabsorb chloride
Causes of saline resistant alkalosis
increased mineralcorticoid activity: stimulates H+ secretion and increases ammoniagenesis by causing hypokalemia
hypokalemia
renal tubular wasting: impaired NaCl reabsorption –> volume depletion activates RAA system –> increase aldosterone which leads to H+ secretion and hypokalemia
Treatment of saline resistant alkalosis
correct underlying cause!
Treatment of saline responsive alkalosis
treat with saline (fluid electrolyte replacement with NaCl or KCl) - allows more Na+ to be reabsorbed with Cl- vs getting exchanged with H+ or reabsorbed with HCO3-; caution in pts with HF or hepatic/renal failure
carbonic anhydrase inhibitors for pts who can’t tolerate excess fluids or sodium (acetohexamide)
Persistent metabolic alkalosis
HCl acid in either D5W or NS: indicated for pts with contraindication to Na replacement (HF, renal failure), failure of previous therapies, or confirmed severe metabolic alkalosis
ammonium chloride: avoid in hepatic/renal failure
arginine monohydrochloride
Adjunct therapy:
H2 antagonists or PPIs in pts with vomiting or NG suction
Saline resistant alkalosis
urinary chloride concentration > 20 mEq/L
correct hypokalemia with potassium sparing diuretic or KCl supplementation; decrease dose of mineralcorticoid; administer spironolactone; correct hyperaldosteronism
Respiratory disorders - respiratory acidosis
characterized by low pH (<7.35), hypercapnia (>45 mmHg) and a compensatory increase in HCO3- concentration
Pathophysiology of respiratory acidosis
results from a failure of excretion versus overproduction
causes: airway obstruction, reduced stimulus for respiration from CNS, failure of heart or lungs, neuromuscular defects affecting nerves or skeletal muscles required for ventilation, mechanical ventilation
Treatment of respiratory acidosis
correct underlying cause
mechanical ventilation or oxygen (caution giving O2 in COPD pt)
avoid rapid correction to prevent alkalemia
Respiratory disorders - respiratory alkalosis
increased pH (>7.45), decreased PaCO2 (<40 mmHg), and a compensatory decrease in HCO3- concentration
Respiratory alkalosis pathophysiology
causes: central/peripheral stimulation of respiration, mechanial ventilation, pulmonary, salicylate intoxication
Treatment of respiratory alkalosis
correct the underlying cause!
ventilation, sedation, paralysis
