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39 Cards in this Set

  • Front
  • Back
T/F
Blood gas readings are used primarily for prophylaxis?
False.
Blood gases are used for DIAGNOSTIC purposes
How are blood gases reported?

___/___/___/___
pH/ pCO2/ pO2/ HCO3
What is the normal pH lab values range?
7.35-7.45
What is the normal pCO2 lab values range?
35-45 mmHg
What is the normal pO2 lab values range?
80-100 mmHg
What is the normal HCO3 lab values range?
22-26 mEq/L
What is the normal base excess lab values range?
-2--+2
normal pH range?
7.38-7.42
because ECF contains [H+] b/w 38-42 mEq/L
Acidemia defn.
pH <7.38
below normal blood pH
Alkalemia defn.
pH >7.42
above normal blood pH
What problem results from a primary decrease in HCO3?
metabolic acidosis
What problem results from a primary decrease in H+?
respiratory alkalosis
What problem results from a primary increase in HCO3?
metabolic alkalosis
What problem results from a primary increase in H+?
respiratory acidosis
What problem results from hypoventilation?
respiratory acidosis
What problem results from hyperventilation?
respiratory alkalosis
which type of physiological buffer is able to accomodate approximately half of the acid load?
Intracellular and bone buffers
which physiological buffers normally buffer a total of 2% of renally excreted H+?
ammonia-ammonium, and filtered phosphate
what are the two types of metabolic compensatory mechanisms?
1. HCO3(base) controlled by carbonic anhydrase (brushborder in PCT of kidney)
2. intravascular-intracellular exchange of H+/K+
During intravascular-intracellular compensatory mechanism, which way do H+ and K+ flow during acidosis? alkalosis?
Acidosis-->
H+ into cell
K+ out of cell into bloodstream

Alkalosis-->
H+ out of cell into bloodstream
K+ into cell
How do you equate an anion gap?
What do the results mean?
AG= (Na + K) - (Cl +HCO3)
normal AG = 6-12 mEq/L
AG if > or = 20 mEq/L
Anion Gap Causes
(metabolic acidosis)
Methanol(A)
Uremia(A/C)
Diabetic ketoacidosis(A)
Paraldehyde(A), protease inhibtor(C)
Isonazid(INH)(A/C), iron(A)
Lactate(A)
Ethanol(A), ethylene glycol(A)
Salicylates(A), starvation(C)
Non-Anion Gap Causes
(metabolic acidosis)
Hyperalimentation(C)
Acid ingestion(A), Addison's
Renal tubular acidosis(C)
Diarrhea(A), diuretics(A/C), drugs(A/C)
Uretosigmoidostemy/(C)
Pancreatitis(A/C)
Metabolic Acidosis Compensation Mechanisms:
respiratory
metabolic
positive Osm Gap
Respiratory: hyperventilation to decrease pCO2(24 hrs)

Metabolic: 1. increase renal production of HCO3(5 days)
2. intracellular exchange H+/K+(fast)

Osm Gap with MeOH, ethylene glycol, paraldehye. calculated
2Na + BUN/2.8 + glucose/18 + EtOH/4.3
Metabolic Acidosis Treatment
Chronic
acetate in TPN(if they don't have enough acetate)
***sodium bicarb tablets*** to replenish HCO3
325-650 mg (12mEq HCO3/g) or Shol's soln.(1mEq/ml) in divided doses. Total daily dose 24-48 mEq
Metabolic Acidosis Treatment
Acute
IV Sodium Bicarb if.....
pH < 7.2 orHCO3 < 15 mEq/L
3 amps NaHCO3 per 1 L D5W @ 75 ml/hr
OR...
THAM buffer--IV proton binder that does not supply Na+
Why is replacing HCO3 controversial in metabolic acidosis?
1. May induce more acidosis
HCO3+H <--> Co2 +H
2. fluid overload
3. Hemoglobin-O2 curve
4. Ca2+--albumin binding
Types of Metabolic Alkalosis
Cl responsive
Cl unresponsive
Cl Responsive Causes
(metabolic alkalosis)
increase HCO3 in response to losing Cl
HCl loss(vomiting, suctioning)
Diuretics(loop, thiazide)
Cl Nonresponsive Causes
(metabolic alkalosis)
increase in HCO3, irrespective of Cl concentration
Hyperaldosteronism(too much aldosterone)
severe hypokalemia
Iatrogenic alkali admin (TPN)
Metabolic alkalosis compensation:
Respiratory
Metabolic
respiratory: hypoventilation to increase pCO2 (fast)

Metabolic: 1. increase renal excretion of HCO3 (fast)
2. intravascular exchange of H+ for K+ (fast)
Main treatment for metabolic alkalosis
acetazolamide
(carbonic anhydrase inhibitor)
250-500 mg po/IV q 8 hrs for 3-4 doses
promotes renal excretion of HCO3
treatments for metabolic alkalosis
1. correct hypokalemia(20-60 mEq K+ infused over 3 hrs)
2. vol. replacement w/ NS or Cl replacement(if Cl responsive). Kidney will excrete HCO3 to preserve neutrality w/ Cl.
3. acetazolamide(see other card)
4. H2 antagonists or PPI to prevent HCl secretion, reduce HCl loss assoc. w/ vomiting/suctioning
5. severe/emergency: IV HCl or arginine HCl (142.5 mEq HCl/300 ml) or ammonium Cl if pH > 7.6
Respiratory Acidosis Causes:
increased pCO2 due to decreased ventilation/ventilation-perfusion mismatch
COPD(C)
PE(A)
Interstitial Lung Disease
Over sedation/NM blockade
Hypothyroidism(C)
NM Disorders(Myasthenia gravis, GB syn., CNS injury)
Hypoventilation w/ ventilator
Pickwickian syn.--obesity(C)
Respiratory acidosis compensation:
respiratory
metabolic
Respiratory: limited, since diseases freq. assoc. w/ irrev. lung damage

Metabolic: 1. increased renal H+ secretion(onset12-24 hrs, max effect 5 days)
2. intracellular shift of H+ for K+(fast)
Respiratory Acidosis treatment
O2 replacement w/w/out intubation
Increase ventilatory rate as long as O2 not adversely affected
***replace HCO3 if pH < 7.2 but use caustiously b/c increased HCO3 will worsen hypoventilation to promote retention of pCO2
NEVER GIVE BICARB TO TREAT ACUTE Resp. Acidosis
why shouldn't you give bicarb to treat ACUTE respiratory acidosis???
7.11/70/50/23
(low pH, high pCO2, norm HCO3)

--give pt. HCO3---->
7.2/70/50/30
lab values shift further
---> 7.11/90/40/30
Acidosis worsens!!!!
Respiratory Alkalosis Causes
Decreased pCO2 due to increased ventilation

Hypoxia(C/A)
nervousness/anixiety/pain(A)
PE(A)
interstitial lung disease(C)
Hyperventilation w/ ventilator
Hyperthyroidism(C)
pregnancy(C)
CNS injury(A)
Fever(A)
severe anemia(C)
CHF, hepatic insuff.(C)
Stimulants(A)
Respiratory Alkalosis Compensation:
Respiratory
Metabolic
respiratory: need removal of exacerbating stimulus

metabolic: 1. decrease renal production of HCO3(2 wks) 2. intravascular shift of H+ for K+(fast)