Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
161 Cards in this Set
- Front
- Back
Balanced plasma conc. of what 2 ions regulate acid-base balance?
|
Hydrogen & bicarbonate ions
|
|
Acid-base balance is responsible for what 4 things?
|
1. Enzyme activity
2. Hb saturation 3. Myocardial contractility 4. intracellular reactions |
|
What is an acid?
|
-A subst. that when dissolved in H2O yields H+ ions thereby lowering pH.
-Proton donor (H+) |
|
What is a ptoton donor (H+)?
|
Acid
|
|
What is a base?
|
-A subst. that when dissolved in H2O yields hydroxide ions (OH-)
-Proton acceptors (remove H+ from a solution) |
|
Proton acceptors?
|
Base
|
|
Hrdroxide ions have a stron affinity for what ion?
|
-H+.
-ie. Bases are proton acceptors, they avidly bind to H+ & decrease H+ |
|
What is produced as substrates are oxidized in the production of ATP?
|
Hydrogen ions
|
|
Normal H+ conc. in arterial blood and extracellular fluid at 37c ?
|
35-45nmol/L
|
|
H+ conc. of 35-45nmol/L is equivalent to arterial pH?
|
7.35-7.45
|
|
What is normal plasma bicorbonate ion conc.?
|
22-26mEq/L
|
|
The value of pH is inversely related to ?
|
the level of free H+ ions in the body
|
|
The lower the pH, the higher or lower level of free H+ ions?
|
higher level of free H+ ions
|
|
A change in 1 pH unit represents how much of a change in in free H+ ion conc.
|
10 fold change
|
|
a pH change of 1/10th (7.4-7.3) represents how much of a change in H+ ?
|
a large increase in H+
|
|
Flucuations in normal pH interfere w/ ?
|
-shape & fxn of hormones & enzymes
-distribution of electrolytes -Responses of excitable membranes in heart, nerves, skeletal muscle, & GI tract making them more or less excitable |
|
Acidic solutions have a pH lower than ?
|
7. H+ ions prevail
|
|
Alkaline solutions havs a pH above ?
|
7. Hydroxide ions prevail
|
|
A person could not survive long w/ a pH of ?
|
Below 6.8 or above 7.7
|
|
Quantitative measurement describing the equilibrium b/w plasma pH & ratio of plasma pCO2 & HCO3?
|
Henderson Hasselbach equation
|
|
Primary determinant of pH ?
|
Ratio of pCO2 to HCO3 & not individual values
|
|
An increase in CO2 or decrease in HCO3 will have what kind of change on pH?
|
pH will decrease
|
|
Body tries to maintain a constant pH by maintaining what ratio of HCO3 to dissolved CO2?
|
20:1 which will = a pH of 7.40
|
|
If HCO3 were to drop suddenly what happens to CO2?
|
CO2 will also drop to make body more alkalotic
|
|
3 basic systems to prevnt change in pHa?
|
1. Buffer system
2. ventilatory response 3. Renal response |
|
What 2 buffering systems have quick responses but are incomplete correction?
|
1. Buffering system
2. Ventilatory response |
|
Most powerful system for acid base regulation?
|
Kidneys
|
|
Renal response occurs in what time frame? & is it complete or incomplete correction?
|
-12-48 hrs
-complete correction |
|
Name the 4 buffering systems?
|
1. Bicarbonate buffering system
2. Hb buffering system 3. Proetib buffering system 4. Phosphate buffering system |
|
The most important buffering systen in ECF?
|
Carbonic acid-bicarbonate buffer sys.
|
|
According to lecture, The 2nd most important buffering sys. in ICF? (M&M book says ECF)
|
Hb buffering sys.
|
|
This buffering sys. occurs in ICF (minimal role) & in the urine?
|
Phosphate buffering sys.
|
|
This buffering sys. regulates pH in ECF & ICF?
|
Protein buffering sys.
|
|
How does the bicarbonate buffering sys. work?
|
-Body produces CO2 which gets hydrated in H2O to produce carbonic acid via carbonic anhydrase.
-Carbonic acid (H2CO3) further dissociates into H+ ions & HCO3 -HCO3 enters plasma & H+ ions are buffered by reduced Hb |
|
Explain how the Hb buffering sys. work?
|
-CO2 diffuses into the erythrocytes down a conc. gradient & dissolves in H2O & forms carbonic acid via carbonic anhydrase
-Carbonic anhydrase dissociates into H+ & HCO3 -H+ ions bind to Hb & HCO3 ions are exchanged back into the plasma w/ extracellular Cl- (chloride shift) to maintain electrical neutrality |
|
Extracellular protein buffer?
|
Albumin & globulin
|
|
Intracellular protein buffer?
|
Hb
|
|
Most important extracellular protein buffer?
|
Albumin
|
|
In the ventilatory response this responds to changes in PCO2?
|
Peripheral chemoreceptors in carotid bodies
|
|
During the ventilatory response central chemorecptors in the medulla respond to changes in?
|
CSF pH (b/c HCO3 diffuses back into blood so increase H+ in CSF)
|
|
During ventilatory response, alveolar ventilation increases by how much?
|
Increases 1-4 L/min for every 1 mmHg increase in PaCO2.
|
|
3 important responses that occur during the renal response?
|
1. Increased reabsorption of filtered HCO3
2. Increased excretion of H+ ions 3. Increased production of ammonia |
|
Where in the kidney is HCO3 completely filtered?
|
Glomerulus
|
|
During the renal response, how much HCO3 is reaborbed & where?
|
85-90% HCO3 gets reabsorbed into the blood at the proximal tubule.
|
|
Is HCO3 normally excreted in urine?
|
No
|
|
During the renal response, H+ ions are actively exchanged for what ion ? & where does this occur?
|
H+ is exchanged for Na+ across the luminal membrane into the proximal tubule lumen
|
|
During the renal response in the tubular lumen, H+ ions combine w/ _____ to form _____ ?
|
H+ ions combine w/ HCO3 to form carbonic acid (H2CO3)
|
|
During the renal response in the proximal tubule lumen, H2CO3 is broken down by _____ to form ______ ?
|
H2CO3 is broken down by carbonic anhydrase to form CO2 & H2O.
|
|
Why does filtered HCO3 combine w/ H+ in the proximal tubule lumen?
|
b/c HCO3 alone is not diffusible so it combines w/ H+ to form H2CO3 which is broken down to CO2 & H2O which is diffusible into tubular cell or peritubular capillary
|
|
During the renal response, for each H+ that the kidney excretes there is generation of ?
|
1 new HCO3- ion added to ECF
|
|
Explain Bicarbonate reabsorption during the renal response?
|
Glomerulus secretes HCO3 into proximal tubule lumen. H+ gets secreted by tubular cell into proximal tubule lumen in exchange for 1 Na+. In the tubular lumen HCO3 + H+ = H2CO3. CA breaks up H2CO3 into CO2 & H2O. Now CO2 & H2O can diffuse into tubular cell or peritubular capillary. Inside tubular cell CA catalyze CO2 + H2O= H2CO3 which then dissociates into H+ & HCO3. H+ is again actively excreted into proximal tubule lumen in exchange for 1 Na+ & HCO3 is carried out of tubular cell by Na+ (NaHCO3) into peritubular capillary
|
|
After all the body's HCO3 is exhausted & acidosis is still present, what other 2 ways can the kidney rid of H+ (list in order)?
|
1.In tubular lumen H+HPO4 = H2PO4 which is not diffusible back into tubular cell & gets excreted in urine.
2. In tubular lumen fluid H+NH3=NH4+ which is not diffusible back into tubular cell & gets excreted in urine. |
|
Where is ammonia (NH3)formed? & from what?
|
Mitochondria of proximal tubular cells. Formed from deamination of glutamine
|
|
What increases renal production of NH3?
|
Acidemia b/c kidneys forms more NH3 to bind w/ H+ & form NH4 to be excreted in urine
|
|
What is base excess?
|
Amt. of acid or base required to return pHa to 7.4 & PaCO2 to 40mmHg at 37c & full O2 saturation
|
|
What is the metabolic component of acid-base disturbance?
|
Base excess
|
|
A postive base excess indicates?
|
Metabolic alkalosis
|
|
A negative base excess indiates?
|
Metabolic acidosis
|
|
Acid-base disturbance resulting from changes in ventilation?
|
Resp. acidosis/alkalosis
|
|
Acid-base disturbance unrelated to alveolar ventilation?
|
Metabolic acidosis/alkalosis
|
|
Describes the secondary ventilatory or renal response to the intial disturbance?
|
Compensation
|
|
Adverse response to mild acidemia?
|
Release of catecholamines, increase BP, HR, ect..
|
|
Adverse response to pHa <7.2?
|
Cardiac depression, decreased contractility, Smooth muscle depression, decreased PVR, hypotension, decreased response to catechol.
-Consider giving HCO3 to this pt (as per lecture) |
|
Which type of acidosis has worse effects on the heart?
|
-Resp. acidosis
-Ventricular threshold for fib is reduced. |
|
Acidosis may lead to hypo/hyper K+ & why?
|
-Potentailly lethal hyperK+ due to H-K shift across cell membrane.
-Movement of K+ out of cell in exchange for extracellular H+ |
|
In acidosis what happens to plasma K+ (increase or decrease & by how much)?
|
Plasma K+ increases by approx. 0.6mEq/L for each 0.10 decrease in pH
|
|
Acidosis effects on Hb affinity for O2?
|
R. shift, less affinity
|
|
CNS depression is more prominent w/ what type of acid-base disturbance & why?
|
-Resp. acidosis.
-CO2 narcosis, greatlt depresses neuronal activity & may lead to coma |
|
What does acidosis do to CBF?
|
Increase CBF via vasodilation which can increase ICP & decrease CPP & cause cerebral ischemia
|
|
What does acidosis do to Sz threshold?
|
Increaes Sz threshold b/c depresses neuronal activity
|
|
What does alkalosis do to Sz threshold?
|
Decrease Sz threshold b/c alkalosis renders all tissues more excitable
|
|
Respirtaory acidosis
|
-Increase in PaCO2
-Drives reaction to R. (forming carbonic acid then H+ & HCO3) causing increase H+ & decrease pHa |
|
Respiratory acidosis is caused by ? (2 things)
|
1. Hypoventilation
2. CO2 retention |
|
Explain central compensatory response to resp. acidosis?
|
-CO2 rapidly crosses BBB leading to decrease CSF pH which stimulates central chemoreceptors in medulla which increase minute ventilation
|
|
Explain peripheral compensatory response to resp. acidosis?
|
Peripheral chemoreceptors in carotid bodies & aortic arch respond to changes in CO2 & O2 conc. If CO2 is high, will increase minute ventilation
|
|
What do volatile anesthetics do to peripheral comp. mech.?
|
Blunt carotid body mediated response to acidemia. (FYI: opioids blunt central response)
|
|
Peripheral chemoreceptors in carotid bodies & aortic arch respond to changes in?
|
CO2 & O2
|
|
Causes of Resp. acidosis r/t alveolar ventilation:
|
CNS depression, neuromuscular disorders, chest wall abn, pleural abn, airway obst. (upper/lower parenchymal lung disease, embolism, aspiration, pneumonia, ect..
|
|
Causes of Resp. acidosis r/t CO2 production?
|
MH, thyroid storm, extensive burn injury, shivering, prolonged sz, lg. caloric loads (b/c carbohydrate breakdown into CO2)
|
|
Compensation of acute resp. acidosis?
|
-Limited resp. compensation
-Buffering (Hb-H, & H ion exchange for Na & K from ICF & bone) -Very limited renal response (plasma HCO3 increases by 1mEq/L for every 10mmHg in PaCO2-above 40) |
|
Limited response in Resp. acidosis? (r/t HCO3 & PaCO2)
|
Plasma HCO3 increases by 1mEq/L for every 10mmHg in PaCO2-above 40.
|
|
Treatment of resp. acidosis?
|
Mech. ventilation, NaHCO3 only if pH <7.10 & HCO3 <15mEq/L
|
|
At what point would you give NaHCO3 during resp. acidosis?
|
pH <7.10 & HCO3 <15mEq/L
|
|
Compensation of chronic resp. acidosis?
|
-Renal compensation (12-24h, may peak at 3-5days)
-Confirmed by normal pH & increased PaCO2 -Increased renal secretion of H+ ions results in increased plasma HCO3 conc. -Treatment rarely involves mech. ventilation |
|
Goal of mech. ventilated pts w/ chronic resp. acidosis?
|
-Return CO2 to their "normal" level & avoid resp. drive depression from excessive O2 therapy
|
|
Metabolic acidosis?
|
pH < 7.35 & HCO3 < 21mEq/L
|
|
Metabolic occurs from (general)?
|
1. Increase in blood H+ ion conc. caused by addition of acids (other than CO2)
2. Loss of bases from body fluid |
|
General causes of metabolic acidosis?
|
-Increased metabolic production of H ions
-Decreased renal tubule elimination of H ions -GI or renal losses -Rapid dilution of ECF compartment w/ bicarbonate free fluid |
|
NS when given in lg. amts. can cause?
|
Hypercholreimc metabolic acidosis
|
|
Compensatory response to metabolic acidosis?
|
-Increased alveolar ventilation(H+ stimulation of carotid bodies)
-Renal tubule secretion of H+ ions into the urine -Buffers in bone neutralize acids in circulation -Ventilatory response is unable to completely normalize pH |
|
What are ions?
|
Molecules w/ a charge (positive or negative)
|
|
What are cations & give 2 examples?
|
Positively charged ions.
-Na+ & K+ |
|
What are anions & give 2 examples?
|
Negatively charged ions
Cl- & HCO3- |
|
What accounts for the largest fraction of anion gap?
|
Albumin 11mEq/L
|
|
Anion Gap equation:
|
Na + K + unmeasured cations must = Cl + HCO3 + unmeasured anions
|
|
Anion Gap: unmeasured cations include:
|
Ca2+, Mg+, & minerals
(& K+ as per M&M) |
|
Anion Gap: unmeasured anions include:
|
plasma proteins (albumin), phosphates, sulfates
|
|
Normal anion gap? & how did you come up w/ this value?
|
12mEq/L (7-14)
Na - (Cl+HCO3)= anion gap ie. 140 -(104+24)=12mEq/L |
|
Used in determining differential diagnosis of metabolic acidosis?
|
Anion Gap
|
|
When there are excessive anions (acids) in the plasma, what happens to anion gap?
|
Anion gap increase
|
|
Any condition that increases umeasured anions or decreases unmeasured cations will cause anion gap to_____?
|
Anion gap increase
|
|
Any condition that decreases umeasured anions or increases unmeasured cations will cause anion gap to_____?
|
Anion gap to decrease
|
|
Anion gap > 30mEq/L indicates?
|
A high anion gap acidosis
|
|
High anion gap metabolic acidosis (>30mEq/L) can be due to:
|
-Insufficient renal excretion of acids(ie. CRF decreased GFR<20ml/min)
-Increased endogenous acid production (lactic or ketoacidosis) -Ingestion of exogenous acids (salicytes, methanol, ethylene glycol) |
|
Normal anion gap metabolic acidosis (<13mEq/L)is caused by?
|
-Increased GI loss of HCO3
-Increased renal loss of HCO3 -Rapid expansion of extracellular fluid volume w/ bicarbonate free solution (0.9%NS) -AA infusions (HAL)contain an excess of cations (Cl-) Administration of lg. quantities of ammonium Cl- or arginine HCL |
|
What is normal anion gap metabolic acidosis characterized by?
|
-Hyperchloremia due to plasma chloride replacing HCO3 that is lost due to GI loss of HCO3 (diarrhea, sm. bowel,billiary & pancreatic fluids contain HCO3)
|
|
How does increased renal loss of HCO3 contributes to normal anion gap metabolic acidosis?
|
-Increased renal loss of HCO3 is caused by failure to reabsorb HCO3 in the proximal tubule which then causes failure to secrete H+ ions, so H+ ions can not form H2PO4 & NH4
-Carbonic anhydrase inhibitors ie Acetazolamine (diamox) interfere w/ secretion of H+ ion |
|
How does rapid expansion of extracellular fluid volume w/ bicarbonate free solution (0.9%NS)cause normal anion gap metabolic acidosis?
|
Cl- impairs bicarbonate reabsorption in the kidneys. Produces hyperchloremic metabolic acidosis
|
|
Treatment of metabolic acidosis?
|
-Resp. component should be corrected (lower PaCO2 to low 30's)
-Alkali therapy via ABG's Hemodialysis in refractory or profound acidemia -Correct cause (DKA,ect.) -NaHCO3 if pH <7.10 & HCO3 <21mEq/L -THAM (tromethamine)lacks Na+ & does not regenerate CO2as a byproduct of buffering |
|
Why avoid NaHCO3 in cardiac arrest & low flow states?
|
-May improve MAP and ECF pH but does not improve ICF pH or CV response to catechol.
-It also reduces plasam ionized Ca2+ levels -Increases CO2 |
|
Treament goal for metabolic acidosis?
|
Raise pH to at least above 7.25 to over come adverse effects of acidemia
|
|
Bicarb is best reserved for what kind of pts?
|
Pts w/ adequate ventilation & pH <7.20
|
|
Lactic acidosis from inadequate tissue perfusion should be treated w/ ?
|
Volume resusitation & oxygenation
|
|
How do you calculate NaHCO3 dose?
|
Body wt x BD(deviation of plasma HCO3 from 24mEq/L)x ECF volume as a fraction of body (0.3); then give 1/2 of this.
ie. 70kg pt w/ HCO3 of 12mEq/L (70)(24-12)(0.3) = 252mEq; give 126mEq |
|
Anesthetic considerations in acidosis w/ opioids?
|
Opioids are weak bases & may have increased fraction of drug in non-ionized form & increase penetration into brain
|
|
Anesthetic considerations in acidosis?
|
Acidemia can potentiate depressant effects of most sedtaives & anesthetic agents on CNS & circulatory
|
|
Anesthetic considerations in acidosis r/t airway?
|
Increased sedation & depression of airway reflexes predispose pulm. aspiration
|
|
Anesthetic considerations in acidosis w/ PIA's & IV anesthetics?
|
Circulatory depressants effects of PIA's & IV anesthetics can be exaggerated
|
|
Which PIA is more arrhythmogenic in acidosis?
|
Halothane
|
|
Anesthetic considerations in acidosis w/ NMB's
|
-Avoid SCh in hyperkalemia (acidosis causes hyperkalemia by exchanging H+ & K+)
-Respiratory (not metabolic)acidosis may augment NDNMB & prevent antagonsim by reversal agents. |
|
Adverse effects of alkalosis on K+ ? How much?
|
-Hypokalemia=cardiac dysrhythmias
-With alkalosis, serum K+ decreases as H+ diffuses out of cell in exchange for K+ -Plasma k+ decreases 0.6mEq/L for each 0.10 increase in pH |
|
Adverse effects of alkalosis on oxyHb dissociation curve?
(shift right or left) |
Left b/c alkalosis increases affinity of Hb for O2
|
|
Adverse effects of alkalosis on Ca2+ ?
|
-Enhanced binding for Ca+ on plasma proteins, decreasing ionized plasma Ca levels
-incr. # of anionic binding sites for Ca on plasma proteins=decr. iCa -circulatory depression & neuromuscular irritability |
|
Adverse effects of resp. alkalosis on bronchial tone & ventilatory effort? & PVR as per M&M?
|
-Increases bronchial tone (bronchoconstriction) & decreases ventilatory effort contributing to atelectasis
-Decrease pulm. vascular resistance (M&M p720) |
|
Adverse effects of alkalosis on SVR?
|
Increase SVR & possibly coronary vasospasm
|
|
Adverse effects of Resp. alkalosis on CBF?
|
Decrease CBF (norm:50ml/100g/min @ 40mmHg PaCO2)
|
|
Metabolic alkalosis may trigger compensatory hypo/hyperventilation?
|
-Compensatory hypoventilation (to incr.PaCO2) causing hypoxemia.
|
|
Resp. Alkalosis is characterized by pH____ & PaCO2____?
|
-pH >7.45 & PaCO2 <35
|
|
What does resp. alkalosis do to minute ventilation?
|
-Increase in minute ventilation to a level greater than required to excrete the metabolic production of Co2
|
|
pH of severe alkalemia?
|
pH >7.6
|
|
During resp. alkalosis, what happens to plasma HCO3 for every 10mmHg acute decrease in PaCO2 below 40mmHg?
|
Plasma HCO3 will decrease 2-5mEq/L for each 10mmHg acute decrease in PaCo2 below 40mmHg (M&M p720)
|
|
Treament for resp. alkalosis?
How about severe alkalemia pH >7.6? |
-Correction of underlying problem
-Severe alkalemia: IV HCL acid, arginine Cl, or NH4 Cl(M&M p720) |
|
Causes for resp. alkalosis r/t incr. Co2 elimination?
|
-Incr. Co2 elimination (mech., self induced, dx, preg, pain, anxiety, decr. barometric pressure,CNS injury, art. hypoxemia, pulm. emboli, liver cirrhosis, sepsis
|
|
Causes for resp. alkalosis r/t decr. Co2 production?
|
hypothermia, hypothyroidism, skeletal muscle paralysis by NBA
|
|
Causes of metabolic alkalosis?
|
1. Increased in plasma HCO3
2. Cl sensitive (NaCl deficiency & ECF depletion) 3. Cl resistant (enhanced mineralocorticoid activity) |
|
Explain metabolic alkalosis due to Cl sensitive?
|
-Depletion of ECF (diuretic tx)enhances Na reabsorption at renal tubules back into blood so that H2O can follow. B/c there is not enough Cl to accompany all the Na ions reabsorbed, incr. H+ is secreted to maintain electroneutrality & those extra H+ ions bind HCO3 in tubule lumen. HCO3 ions that should have been excreted are reaborbed into blood.
This happens b/c maint. of ECF has priority over acid-base balance -K+ secretion is also enhanced to maintain electroneutrality during ECF depletion. -Hypokalemia(due to ECF depletion)enhances H+ secretion & HCO3 reabsorption |
|
Causes of metabolic alkalosis due to Cl sensitive?
|
-diuretics(furosemide & thiazide)incr. Na,Cl, & K+ excretion=decr.NaCl & hypokalemia
-Loss of GI fluids H+, Na+, K+, & Cl depletion(vomiting NG sx) |
|
Explain metabolic alkalosis r/t Cl resistant?
|
-Incr. mineralocorticoid activity cause Na retention & expansion of ECF volume
-Kidneys secrete H+ & K+ to balance neutrality |
|
Co2 in blood is carried as?
|
Bicarbonate
|
|
Measurement of total Co2 on electrolyte reports should be ____ greater/lower than HCO3 & why?
|
Total Co2 should be about 1mEq greater than HCO3 b/c Co2 in blood is carried by bicarbonate
|
|
If normal HCO3 on ABG is 24,
what is normal Co2 on serum electrolyte? |
tCo2=25 on serum electrolyte
|
|
If pt's HCO3 or serum Co2 exceeds normal by >4 what would you suspect?
|
-primary metabolic alkalosis
-conserved HCO3 in response to chronic hypercarbia |
|
If pts serum HCO3 level is elevated, what do you suspect?
|
-hypovolemia(body trying to conserve Na & as a result due to incr. H+ will have incr. HCO3 reabsorption
-hypokalemia(augments H+ secretion & HCO3 reabsorption) |
|
Treatment of metabolic alkalosis?
|
-Expansion of intravascular volume to incr. renal perfusion
-Administration of K+ to reverse hypokalemia -Intraop infusion of NS instead of LR to incr. Cl & decr. HCO3 |
|
Treatment of metabolic alkalosis due to Cl resistant?
|
-Spirinolactone (aldosterone antagonist) treats incr. mineralcortiocoid activity
|
|
Treatment of metabolic alkalosis due to Cl sensitive?
|
-NS (NaCl) & KCl(M&M p721)
|
|
Can resp. acidosis/alkalosis be completely compensated?
|
Yes
|
|
Can metabolic acidosis/alkalosis be completely compensated?
|
No
|
|
Acid base disturbances in post op period?
|
-Resp. acidosis
-Metabolic acidosis -Resp. alkalosis |
|
Why would post-op pt. develop Resp. acidosis?
|
-Residual anesthetics & NMB which blunt response to Co2
|
|
Why would post-op pt. develop Metabolic acidosis?
|
-Surgical blood loss or 3rd space losses are under appreciated & volume resuscitation is inadequate
|
|
Why would post-op pt. develop Resp. alkalosis?
|
-Pain & anxiety
|
|
For every 10mmHg decr. in PaCo2 what will happen to pH & HCO3? & by how much?
|
-pH will incr. by 0.10
-HCO3 will decr. by 2mEq/L |
|
What will happen to pH & HCO3 w/ chronic 10mmHg decr. in PaCo2? & by how much?
|
-pH will normalize
-HCO3 will decr. by 5-6mEq/L |
|
For every acute 10mmHg incr in PaCo2 what will happen to pH & HCO3? & by how much?
|
-pH will decr. by 0.05
-HCO3 will incr. by 1mEq/L |
|
What will happen to pH & HCO3 w/ chronic 10mmHg incr. in PaCo2? & by how much?
|
-pH will normalize
-HCO3 will incr.by 4-5mEq/L |
|
Venous blood pH is usually ___ lower/higher than arterial blood pH?
|
-0.05U lower
|
|
Venous Co2 is usually ___ lower/higher than PaCo2?
|
4-6mmHg higher than PaCo2
|
|
Calculated bicarbonate is ___ lower/higher than arterial bicarbonate?
|
2mEq/L higher than arterial bicarb
|
|
How can heparin coated syringes used for ABG sample affect results?
|
False decreases in pH b/c acidic
|
|
How do air bubbles affect ABG sample?
|
Prevent equilibration of O2 & Co2 Pp
|