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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 |
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How are blood gases reported?
___/___/___/___ |
pH/ pCO2/ pO2/ HCO3
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What is the normal pH lab values range?
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7.35-7.45
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What is the normal pCO2 lab values range?
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35-45 mmHg
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What is the normal pO2 lab values range?
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80-100 mmHg
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What is the normal HCO3 lab values range?
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22-26 mEq/L
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What is the normal base excess lab values range?
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-2--+2
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normal pH range?
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7.38-7.42
because ECF contains [H+] b/w 38-42 mEq/L |
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Acidemia defn.
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pH <7.38
below normal blood pH |
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Alkalemia defn.
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pH >7.42
above normal blood pH |
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What problem results from a primary decrease in HCO3?
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metabolic acidosis
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What problem results from a primary decrease in H+?
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respiratory alkalosis
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What problem results from a primary increase in HCO3?
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metabolic alkalosis
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What problem results from a primary increase in H+?
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respiratory acidosis
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What problem results from hypoventilation?
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respiratory acidosis
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What problem results from hyperventilation?
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respiratory alkalosis
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which type of physiological buffer is able to accomodate approximately half of the acid load?
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Intracellular and bone buffers
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which physiological buffers normally buffer a total of 2% of renally excreted H+?
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ammonia-ammonium, and filtered phosphate
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what are the two types of metabolic compensatory mechanisms?
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1. HCO3(base) controlled by carbonic anhydrase (brushborder in PCT of kidney)
2. intravascular-intracellular exchange of H+/K+ |
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During intravascular-intracellular compensatory mechanism, which way do H+ and K+ flow during acidosis? alkalosis?
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Acidosis-->
H+ into cell K+ out of cell into bloodstream Alkalosis--> H+ out of cell into bloodstream K+ into cell |
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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 |
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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) |
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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) |
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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 |
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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 |
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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+ |
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Why is replacing HCO3 controversial in metabolic acidosis?
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1. May induce more acidosis
HCO3+H <--> Co2 +H 2. fluid overload 3. Hemoglobin-O2 curve 4. Ca2+--albumin binding |
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Types of Metabolic Alkalosis
|
Cl responsive
Cl unresponsive |
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Cl Responsive Causes
(metabolic alkalosis) |
increase HCO3 in response to losing Cl
HCl loss(vomiting, suctioning) Diuretics(loop, thiazide) |
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Cl Nonresponsive Causes
(metabolic alkalosis) |
increase in HCO3, irrespective of Cl concentration
Hyperaldosteronism(too much aldosterone) severe hypokalemia Iatrogenic alkali admin (TPN) |
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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) |
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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 |
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treatments for metabolic alkalosis
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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 |
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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) |
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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) |
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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 |
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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!!!! |
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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) |
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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) |