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162 Cards in this Set
- Front
- Back
What is an acid?
|
substance dissolved in water;
yields H+ ions lowers pH |
|
What is a proton donor?
|
hydrogen
(ie: HCl --> H+ + Cl- |
|
what is one of the most tightly regulated ions in the body?
|
H+
35-45nM/L |
|
what is a base?
|
substance dissolved in water
yields hydroxide ion (OH-) remove H+ ions from a sol'n |
|
what has a strong affinity for H+ ions?
|
hydroxide ions
NaOH --> Na+ + OH- |
|
what is a proton acceptor?
|
bases
remove H+ from a sol'n |
|
what is another way of expressing H+ ions concent
|
pH
|
|
what does pH represent?
|
arterial concentration of H+ ions
|
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what happens w/inc H+ ion concentration
|
acidity
lowers pH |
|
what is pH of ECF
|
7.35 - 7.45
|
|
pH is controlled how?
|
homeostatic process
|
|
what happens w/abnormal fluctuations in pH?
|
break chemical bonds
change shape of proteins alter cellular fxn |
|
pH of <7
|
acidic sol'n
H+ ions prevail |
|
pH of >7
|
alkaline (basic) sol'n
OH- ions prevail (hydroxide) |
|
What is the Henderson-Hasselbach equation?
|
quantitative measurement describing the relationship b/w plasma pH and the ratio of plasma pCO2 and HCO3
|
|
what is the primary determinant of pH
|
ratio of pCO2 to HCO3
not the individual values |
|
when does pH decrease?
|
increase CO2 or
decrease HCO3 |
|
what keeps pH from marked changes
|
the buffering system
dec HCO3 --> dec CO2 |
|
what is the ratio of HCO3 to CO2 at a constant pH
|
20:1
|
|
ratio of HCO3 to CO2 @ 20:1 is = to a pH of?
|
7.4
|
|
is the ratio b/w HCO3 and CO2 directly inversely proportional?
|
directly
|
|
what is the mathematical equation of the Henderson-Hasselbach equation?
|
pH = 6.1 + log(HCO3/0.03 x pCO2)
|
|
what are the buffering systems?
|
bicarbonate buffers
hemoglobin buffers other protein buffers phosphate buffers |
|
what are the 3 systems that keep pH in tight control?
|
buffering systems
ventilatory response renal response |
|
what is the response time of the renal system?
|
12 - 24 hours
|
|
what is the most powerful acid-base regulator system?
|
kidneys
|
|
what are the 2 most important buffering systems?
|
bicarbonate is #1
Hgb is #2 |
|
does the phosphate buffering system include the kidneys?
|
no
|
|
What is the carbonic acid-bicarbonate buffer system?
|
most important in ECF
|
|
what is the phosphate buffer system?
|
buffers ICF and urn
|
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what is the protein buffer system?
|
regulate pH in ECF & ICF
extensive interaction w/other buffer systems |
|
What is carbonic acid?
|
H2CO3
|
|
what is the chemical equation of the bicarbonate buffer system?
|
CO2 + H2O<-->H2CO3<-->H + HCO3
|
|
what does the bicarbonate buffer system depend on?
|
hydration of CO2 to carbonic acid in plasma and erythrocytes
|
|
what is the primary role of the bicarbonate buffer system?
|
prevent pH changes d/t acids in ECF
|
|
what does the bicarbonate system consist of?
|
carbonic acid (weak acid)
and bicarbonate (weak base) |
|
what happens to the CO2 produced throughout the day?
|
converted to carbonic acid; this then dissociates into H+ ion and bicarb ion
|
|
what is the only ICF buffering system?
|
Hgb
has an immediate effect on pH of ECF |
|
what is the Hgb buffering system responsible for?
|
prevents drastic alteration in pH w/inc or dec in pCO2
|
|
what is contained in the cytoplasm of Hgb?
|
large amounts of carbonic andhydrase (enzyme)
|
|
what does Hgb buffering system do?
|
absorbs CO2 from plasma; converts it to H2CO3;
|
|
why is CO2 absorbed into ICF?
|
can diffuse easily across RBC membranes
|
|
what happens when H2CO3 dissociates in the Hgb buffer system?
|
moves into plasma via Cl- shift
|
|
What is the purpose of Cl- in the Hgb buffer system?
|
helps maintain electrical neutrality
|
|
How are H+ ions formed?
|
digestive tract
metabolic activities w/in cells |
|
to preserve homeostasis, what must happen to H+ ions?
|
rendered harmless
must be eliminated to preserve homeostasis |
|
Do buffer systems provide total restoration of homeostasis?
|
no, only a temporary sol'n
|
|
What are the 2 mechanisms the body uses to eliminate H+ ions?
|
pulmonary
renal |
|
how does the body maintain heomeostasis?
|
combo of buffering systems
pulmonary renal |
|
What is pulmonary compensation?
|
control of H+ ion concen through the exhalation of CO2
|
|
how is alveolar ventilation mediated?
|
chemoreceptors in the medulla;
they respond to changes in CSF pH |
|
how is pulmonary compensation stimulated?
|
CO2 can easily cross BBB; reacts w/H2O to produce H+ ions to increase respiration
|
|
what is the increase in MV for every inc 1mmHg in PaCO2?
|
1-4L/min
|
|
what does the renal response to pH consist of?
|
increased reabsorption of filtered HCO3
increased excretion of H+ increased production of ammonia (NH3) |
|
What is the goal of the renal system?
|
to reabsorb HCO3
|
|
how much HCO3 is reabsorbed?
where? |
90%
proximal tubule 10% reabsorbed in distal parts of tubule |
|
Is HCO3 normally excreted?
|
No
|
|
What is the fundamental event in renal regulation of acid-base balance?
|
Na+ - H+ exchange
|
|
What happens in the Na+ and H+ exchange?
|
permists bicarboniate ions to be reabsorbed and acids to be excreted
|
|
What is the process by which Na+ and H+ exchange takes place?
|
H+ is actively secreted into the proximal tubule in exchange for Na+
Na+ enters the cell passively |
|
What is the goal of the phosphate buffering system?
|
excrete H+ ions
|
|
What happens in the phosphate buffering system?
|
HCO3 is reabsorbed
H+ is secreted into tubular lumen H+ then combines with phosphorous (HPO4) to create phosphate (H2PO4) |
|
Can H2PO4(phosphate) be reabsorbed?
|
No
r/t charge |
|
What happens to H2PO4?
|
it is excreted from tubual
|
|
What happens when urn pH is 4.4?
|
phosphate saturated;
phosphorous ions no longer available for eliminating H+ ions |
|
What is the buffer system after the phosphate buffer system?
|
Ammonia buffer system.
goal is to form NH3 (ammonia) |
|
Why is this an important buffering system?
|
when phosphate sytem is completely saturated, this the most imporant urinary buffer
|
|
what is the biological process of the ammonia buffer system?
|
deamination of glutamate in the proximal tubule mitochondria
|
|
where is the principal source of NH3 (ammonia) formation
|
proximal tubular cells
|
|
what happens w/acidemia
|
a marked increase in renal NH3 production
|
|
what diffuses easily across the membranes in the ammonia buffer system
|
NH3
enters passively |
|
what is diffusion trapping?
|
NH4 (ammonium) is unable to cross into tubular cells;
trapped in tubules |
|
what does the excretion of NH4 do?
|
effectively eliminates H+
|
|
what does acidosis lead to?
|
release of catecholamines
this offset myocardial depression |
|
what happens w/a pH of 7.2 or less
|
myocardium unable to respond to release of catecholamines
dec SVR/contractility --> dec BP |
|
what is another neg effect of pH 7.2<
|
dec in threshold for vf
|
|
what happens w/pts who have ischemic heart dz or those w/beta blockers/ga
|
detrimental effects of acidemia may be more pronounced
|
|
what happens w/severe acidosis
|
tissue hypoxia even with
shift to right of oxyhgb curve |
|
what happens in lethal hyperkalemia
|
H+ K+ shift across cell membranes
|
|
what happens to plasma k+ concentrations w/change in pH
|
increase 0.6meq/L for each 0.10 decrease in pH
|
|
do H+ ions pass the BBB
|
no
CO2 diffuses more easily |
|
what produces an adverse effect response to acidosis?
|
respiratory (acute)
chronic metabolic is slower process; kidneys are able to keep up w/changes |
|
what is CO2 narcosis?
|
CNS depression
r/t respiratory > metabolic acidosis greatly dec neuronal activity --> coma |
|
what are the vasodilatory effects of acidosis?
|
inc CBF --> inc ICP--> dec CPP--> cerebral ischemia
|
|
what is another CNS effect of acidosis
|
increases szr threshold
|
|
what is acidosis caused by?
|
hypoventilation and CO2 retention
|
|
what are some causes?
|
drug/dz process that decreases alveolar ventilation --> inc CO2 concent in plasma
|
|
what happens when CO2 crosses BBB
|
dec CSF pH
|
|
what happens w/inc CO2 in CSF
|
dec CSF pH --> stim of medulla --> inc ventilation
|
|
what happens w/inc ventilation
|
dec CO2 content --> restoration of CSF pH
|
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what happens w/peripheral chemoreceptors?
|
carotid bodies/aortic arch respond to changes in CO2 and O2 concent
|
|
what happens to the peripheral chemoreceptors w/GA
|
dec carotid body response to acidemia
|
|
what is the time frame for compensation of acute resp acidosis?
|
varies b/w 6-12 hrs
limited |
|
how is comp of acute resp acidosis accomplished?
|
Hgb buffer
ECF H+ exchanged for Na+/K+ from bone/ICF |
|
what happens w/the renal response to acute resp acidosis?
|
bicarb retention limited
|
|
what happens to the HCO3 plasma concentrations?
|
inc 1meq/L for each 10mmHg inc in PaCO2 >40mmHg
|
|
what does tx consist of ?
|
mechanical ventilation unless a quick tx for a simple etiologic factor can be done
|
|
how long does complete comp for chronic resp acidosis take?
|
12-24 hrs
peak 3-5 days |
|
what happens w/chronic resp acidosis?
|
inc renal secretion of H+ ions --> inc HCO3 plasma concen
|
|
what is the tx for chronic resp acidosis?
|
rarely mech vent
improve pulm fxn --> elim CO2 |
|
what happens when PaCO2 is decreased too quickly in pt w/chronic resp acidosis?
|
metabolic alkalosis
CNS irritability |
|
what is the goal for mech vent pts who have chronic resp acidosis?
|
return PaCO2 to their normal
titrate O2 so resp drive not depressed severe hypovent with overcorrection |
|
what happens w/ metabolic acidosis?
|
inc blood H+ concent d/t loss of bases or inc acids
|
|
what causes the occurrence of met acidosis?
|
accum of acids besides CO2
*inc met prod of H+ ions *dec tubule elim of H+ ions *GI/renal loss of HCO3 *rapid dilution of ECF w/HCO3 free fluid |
|
what happens to met acidosis w/vol anest
|
blunts the carotid body mediated response to acidosis
|
|
what are the pulm response to met acidosis?
|
inc alveolar vent d/t carotid body stim from H+ ions
*max w/in hrs *not able to completely normalize even w/inc vent |
|
what do buffers in bone do?
|
neutralize non-volatile acids in circulation
seen as bone loss in pts w/CRF |
|
What is the formula for the anion gap?
|
(Na + K) - (Cl + HCO3)
|
|
what is the normal range of the anion gap?
|
9-15 meq/L
|
|
what are the major cations?
|
Na
K |
|
what are the major anions?
|
Cl
HCO3 |
|
why do we use the anion gap?
|
determines diff dx of met acid
|
|
what is high anion gap acidosis?
|
> 13 meq/L
SID > 40meq/L |
|
what is high anion gap acidosis d/t?
|
*insufficient renal excretion (CRF or uremia)
*alkali tx r/t ABG *inc pH >7.25 to overcome SE of acidemia *HD in refractory/profound acidemia *correct the cause (DKA, salicylates, other substances) |
|
what is the tx of resp acidosis?
|
*NaHCO3 if pH <7.10 & HCO3 <21
could transiently inc PaCO2 |
|
what should be avoided in cardiac arrest/low flow states?
|
bicarb
no improvement of CV response to catecholamines ICF pH does not improve MAP/ECF pH may improve |
|
what does NaHCO3 reduce in cardiac arrest or low flow states?
|
Ca++
|
|
What is THAM?
|
tromethamine
lacks Na effective ICF buffer |
|
what is the chemical response of NaHCO3?
|
CO2 + H2O<-->H2CO2<-->H + HCO3
|
|
Use of bicarb in pt's w/adequate vent?
|
eliminate inc load of CO2
|
|
when should bicarb be used?
|
best reserved for pts w/adequate vent and pH <7.2
|
|
what is the cause of lactic acidosis?
|
tissue hypoperfusion
volume rescucitation/oxygenation should be first step |
|
what can acidemia potentiate w/GA?
|
depressant effects of most sed and anesth of CNS/CV systems
|
|
what happens to opioids w/acidosis?
|
they are weak bases
*inc fraction of drug in nonionized form *penetrate into brain |
|
why is aspiration a risk w/an acidotic pt and GA?
|
*inc sedation
*dec airway reflexes |
|
what is the CV effects of acidosis and GA?
|
*exaggeration of agents d/t cv dec
*inc response to CV dec w/anesth *dec sympathetic tone |
|
what happens to halothane in acidosis?
|
inc arrhythmogenesis
|
|
what GA agent should be avoided in acidosis?
|
succs
|
|
what augments NMB?
|
resp acidosis
*may prevent antagonism w/reversal agents |
|
what happens to K in alkalosis?
|
K dec as H+ is exchanged for K
|
|
what happens to K w/alkalosis?
|
K dec 0.6meq/L w/each 0.10 inc in pH
|
|
what happens to the oxyhgb dissociation curve in alkalosis?
|
shifts left
|
|
what happens to Ca binding sites in alkalosis?
|
increases
*NB irritability *circulatory depression |
|
what are adverse effects of alkalosis?
|
*hypokalemia
*CV dysrhythmia *dig toxicity inc *inc SVR; poss coronary vasospasm *resp alkalosis: inc bronchial tone, dec vent effort *atelectasis |
|
what happens to CBF in resp alkalosis?
|
dec CBF
*normal CBF 50ml/100g/min w/a PaCO2 40mmHg |
|
what are vent effects of alkalosis?
|
compensatory hypoventilation
(can dec PaO2) |
|
what are the lab values in resp alkalosis?
|
pH >7.45
PaCO2 always <35 |
|
what happens in respiratory alkalosis?
|
*inc MV > metabolic prod CO2
|
|
what does resp alkalosis signify?
|
*mech vent
*anxiety *CNS injury *hyperthermia *pain *hypoxemia *CNS dz *sepsis NEEDS TO BE EVALUATED IMMED |
|
How can you tell if it is resp acid/alk?
|
can be completely compensated
|
|
can met acidosis/alk be compensated
|
Not completely
|
|
What are the lab values in met alkalosis?
|
pH >7.45
hypercarbonatemia >26meq/L |
|
does met alk have a resp component?
|
no
|
|
what is the result of met alk?
|
dec plasma H+ conc d/t loss of acids or inc body fluid bases
|
|
What are some causes of met alkalosis?
|
*N/V
*NG suction *diuretic use (hypokalemia) *renal hypoperfusion d/t cont stimulus *Cl- & K+ depletion inc H secretion |
|
what is one way to tx met alkalosis a/w resp acid?
|
IVF of KCl instead of mech hyperventilation
|
|
ABG determination of met alk?
|
serum CO2 1meq > than ABG HCO3
(look for serum CO2 >29) |
|
What is WNL of ABG HCO3 and serum CO2?
|
24meq
25meq (ABG HCO3 >28) |
|
what happens if these measurements >4meq/L above normal?
|
primary met alkalosis
conserved HCO3 r/t chronic hypercarbia |
|
What can hyperbicarbonatemia indicate?
|
hypovolemia
hypokalemia |
|
what is the tx for met alk?
|
*IVF bolus --> inc renal perf
*KCL bolus *use NS instead of LR (increases Cl/dec HCO3) |
|
what should be considered tx w/severe met alkalosis?
|
*IV hydrochloric acid (CVL)
*arginine chloride *ammonium chloride *HD *acetazolamide (Diamox) |
|
when should H2 blockers be considered in met alkalosis?
|
w/inc GI losses
|
|
During postop period: resp acidosis?
|
d/t residual GA and NMB which blunt response to rising CO2
|
|
during postop period met acidosis?
|
*surgical blood loss
*3rd spacing *inadequate fluid rescucitation |
|
what is cause of resp alk in postop period?
|
pain and anxiety
|
|
how do you determine resp/met acid-base balance by ABG?
|
*resp if PaCO2 ~ w/change in pH
*met if HCO3 ~ w/change in pH |
|
what is an alternative to ABG draws?
|
vein in back of hand
|
|
VBG can be helpful in determining what?
|
PCO2 and pH during GA
(0.05u < ABG pH) |
|
what is the relationship b/w PaCO2 and VBG CO2?
|
PaCO2 4-6mmHg >
|
|
HCO3 ABG vs VBG?
|
2meq < VBG
|
|
what can cause false decreases in pH when taking ABG?
|
heparin
PCO2 is directly proportional |