3. use low concentration heparin (1000IU/ml) because this would result
in Final Heparin Concentration (FHC) of about 50IU/ml in a fully filled
2ml syringe which would be sufficient for correct BGA results
4. Po2 rise significantly after two minutes' contact with the air
bubble, and PCO2 fell significantly after three minutes'
Air bubbles that exceed 1 to 2 percent of the blood volume
can cause a falsely high PaO2 and a falsely low PaCO2
as PaCO2 rises from
40 to 80 the PAO2
decreases from 100
to approximately 60
and patient will
become hypoxemic
8. Edgar Van Nuys Allen first described the test in 1929.
In 1952, Irving Wright described a
modified version of the Allen test
superior long-term patency in
comparison to the saphenous vein,
9.
10. the equation itself is not frequently used in clinical practice. But looking
at the equation can help us understand the primary acid-base disorder.
Sod.bicarb
15. chloride ion is brought into the cell (in a one-to-one ratio
16.
17.
18. low serum bicarbonate associated with higher mortality in healthy older individuals was
independent of pH, suggesting that this relationship did not depend on whether metabolic acidosis or
respiratory alkalosis was the underlying disorder.
36. intravenous (IV) ammonium chloride is a treatment option for severe cases of metabolic alkalosis.
•Acetazolamide (Diamox). Acetazolamide also appears to be safe and effective in patients with metabolic alkalosis
following treatment of respiratory acidosis from exacerbations of chronic obstructive pulmonary disease (COPD).
54. The accumulated Hydrogen ions stimulate the respiratory centre in brain to cause hyperventilation the
Carbon- di- oxide is reduced
In acute metabolic acidosis the compensation starts within half an hour, is completed within 24 hours
Ph 7.28
Pco2 30
HCO3 14
1.5 (14) + 8 =29
84. SBE can be defined as the amount of strong acid or strong
base that must be added to each liter of fully oxygenated
blood to restore the pH to 7.40 at a temperature of 37°C and
pCO2 kept at 40 mmHg and hemoglobin concentration
standardized to 5 g/dL.
Chronic compensation ….if BE is very low …may be septic
plasma (0.05 l/kg),
interstitial fluid and lymph (0.15 l/kg),
and the transcellular fluids
86. Other anions such as, sulfates, phosphates, lactates, beta
hydroxybutyrates, etc. are not measured routinely. These are
then called as ‘unmeasured anions’
livestock feeds
fertilisers
92. In case of high anion gap use Delta ratio or delta gap
93. However, if the d anion gap is greater than the d HCO3, it suggests that
there is a superimposed metabolic alkalosis leading to higher than
expected HCO3 level.
94.
95. AG 140 – 110 = 30
Delta ratio 30 - 12
24 - 12
= 1.5
Blood sugar 400
102. If the circulation is adequate or only moderately impaired, bicarbonate
administration might be beneficial, and actually improve acid-base parameters
103. it does not generate carbon dioxide. In fact, it might actually lower PaCO2
improving extracellular acid–base parameters with no negative effects
The main advantage of DCA over SB is,, its ability to prevent the intracellular
acidosis development
SB failed to improve lactic acidosis, associated with malignancy. Sepsis- and
phenphormin-associated LA proved to be resistant to SB as well
Complications of its use include intracellular acidification with severe impairment of cardiac function; depression of
ionized Ca2+; volume overload; intracellular acidification is more likely to occur when large amounts of bicarbonate
are administered.
Lean body mass is calculated as
the difference between total
body weight and body fat weigh
110. this patient has arespiratory alkalosis and the elevatedgap metabolic acidosis and the metabolicalkalosis what specific ideologies
couldcause this I always like to start withthe least common or most unexpectedfinding the vast majority of toxicingestions result in a
respiratoryacidosis nots and alkalosis whenever Ihear about a respiratory alkalosis inthe setting of ingestion I think abouttwo things
first this patient aspirateon vomit and now has a hypoxia inducedhyperventilation or second did thispatient ingest aspirin aspirin
directlyactivates the medullary respiratorycenter leading to hyperventilation whenthe ingested dose is extremely high I'dsay this latter
possibility is morelikely since aspirin toxicity can alsolead to uncoupling of oxidativephosphorylation in mitochondria leadingto a lactic
acidosiswhich could be the cause of the elevatedgap metabolic acidosis patient also hasfinally as the girl has bulimia she mayliterally
induce herself to vomitsleading to a loss of hydrogen ions inthe expelled gastric fluids these are ofcourse presumptive diagnosis that
wewould definitely want confirmed withserum drug and lactate levels along witha urine pH and she should also get achest x-ray to roll
an aspirationhowever based on the availableinformation
bulimia she may induce herself to vomits
leading to a loss of hydrogen ions inthe
expelled gastric fluids
ingest aspirin
127. A 24 YEAR-OLD WOMAN IS FOUND DOWN BY SOME BYSTANDERS. THE MEDICS ARE
CALLED AND. UPON ARRIVAL, FIND HER WITH AN OXYGEN SATURATION OF 88% ON ROOM AIR
AND PINPOINT PUPILS ON EXAM. SHE IS BROUGHT INTO THE ER WHERE A ROOM AIR
ARTERIAL BLOOD GAS IS PERFORMED AND REVEALS:
PH 7.25,
PCO2 60,
PO2 65,
HC03 - 26,
BASE EXCESS 1.
ON HIS CHEMISTRY PANEL. HER SODIUM IS 137, CHLORIDE 100, BICARBONATE 27.
