abg s final and last touch
TRANSCRIPT
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By.
SYED TABISH REHMAN
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ABGs are indicated if the patient deteriorationin an already critical condition such as:
Decrease in oxygen saturations
ConfusionFall in conscious level (Glasgow ComaScale)Increased respiratory effortCyanosis
Assess the ventilatory status, oxygenation and acidbase status
Assess the response to an intervention
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Bleeding diathesis
AV fistula Severe peripheral vascular
disease, absence of an arterial
pulse Infection over site
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Prepackaged and contains allnecessary equipment 3 5 cc syringe
Pre-heparinized 22ga x 2 needle
Alcohol swap
Gauze pad
Biohazard bag
Misc. items
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The radial artery is superficial, hascollaterals and is easily
compressed. It should almostalways be the first choice.
Other arteries (femoral, dorsalis
pedis, brachial) can be used inemergencies
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Step 1: tight fist x 20 secStep 2: Occlude radial and ulnar arteries
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Step 3: open hand and look forblanching
Step 4: release ulnar artery andlook for capillary refill (5-7 sec)
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Position wrist
Prep skin
Insert needle ~45 degrees,
bevel up Apply pressure x 5min postprocedure
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Hematoma
Arterial laceration
Hemorrhage
Vasovagal reaction Sympathetic nervous system response to pain
Loss of limb
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a) Acidosis
b) Alkalosis
a) Acidosis
b) Alkalosis
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MetabolicAcidosis
HCO3 pCO2
MetabolicAlkalosis
HCO3 pCO2
RespiratoryAcidosis
pCO2 HCO3
RespiratoryAlkalosis
pCO2 HCO3
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Primary lesion
compensation
pH
HCO3
CO2
METABOLIC ACIDOSIS
HYPER VENTILATION
HCO3 changes
pH in same direction
Low
Alkali
LOW HCO3
LOW pH
LOW pCO2 (compensated)
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Primary lesion
compensation
pH
HCO3
CO2
METABOLIC ALKALOSIS
HYPO VENTILATION
BICARB CHANGES
pH in same direction
HIGH HCO3
HIGH pH
HIGH pCO2 (compensated)
High
Alkali
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CO 2 CHANGES
pH in opposite direction
Primary lesion
compensation
pH
CO 2
BICARB
Respiratory acidosis
( Hypoventilation)
HIGH pCO2
LOW pH
HIGH HCO3 (compensated)
High
CO2
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Primary lesion
compensation
pH
CO2
BICARB
Respiratory alkalosis
( Hyperventilation)
Low
CO2
CO 2 CHANGES
pH in opposite direction
LOW pCO2
HIGH pHLOW HCO3 (compensated)
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Bodys physiologic response to Primary disorderin order to bring pH towards NORMAL limit
Partial compensationNo compensation. (uncompensated)
BUT ph never overshoots,
If a overshoot pH is there,
it is a MIXED disorder
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ACUTE pH decreases by 0.08 ORHCO3 increases by 1 mEq/L
CHRONIC pH decreases by 0.03 OR
HCO3 increases by 4 mEq/L
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ACUTE pH increases By 0.08 0rHCO3 decreases by 2 mEq/l
CHRONIC pH increeas by 0.03 ORHCO3 Decreases by 5 mEq/L
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pCO2 will decrease 1.3 mmHg per 1 mEq/Ldecrease in HCO3
WINTERS FORMULA
pCO2= (1.5 *HCO3)+ 8 2
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pCO2 increases 0.7 mmHg per 1 mEq/L
increase in HCO3
pCO2= 0.9[HCO3] +16
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The difference between the commonly measured serumcations (positively charged particles) and the measuredserum anions (negatively charged particles).
Anion gap = [Sodium] - ([Chloride] + [Bicarbonate])
The normal anion gap depends on the laboratory set up(usually 12 2)
Anion gap should always be calculated b/c it helps
differentiated b/w causes of metabolic acidosis
A large anion gap (>20) always suggest primarymetaolic acidosis regardless of pH and HCO3 level, b/cbody can not generate large anion gap to compensate
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Na+Cl-
Aniongap
HCO3-
Meta. acidosis: too little baseMore Cl- and anion gap sameDiarrhea, renal acidosis
Meta. acidosis: too little baseMore Cl- and anion gap biggerKetoacidosis, salicylate, lactate
Chronic renal failure
Na+ Cl-
Aniongap
HCO3-
Na+Cl-
Aniongap
HCO3-
electroneutrality
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pHPCO2HCO3 [calculated vsmeasured]
PO2 [oxygen tension]
SO2 [oxygen saturation]
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Assessing a patients acid base statusrequires arterial pH PCO2 and HCO3.
Blood gas analyzers measures PH and PCO2where as HCO3 is calculated fromHanderson Hasselbalch equation.
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Acidemia PH 7.45
Acidosis process which increases H+ions.
Alkalosis process that decreases H+ ions.
Normal values
PH (7.35-7.45)PCO2 (35-45)
HCO3 (22-26)
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Step 1: Acidemic, alkalemic, or normal?
Step 2: Is the primary disturbance respiratory or metabolic?
Step 3: For a primary respiratory disturbance, is it acute orchronic?
Step 4: For a metabolic disturbance, is the respiratory systemcompensating OK?
Step 5: For a metabolic acidosis, is there an increased anion gap?
Step 6: For an increased anion gap metabolic acidosis, are thereother derangements?
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Rule 1:-Look at the pH (whichever side of 7.40 the pH
is on, the process that caused is the primary abnormality)Principle: The body doesn`t fully compensate for anydisorders
RULE 2:-Calculate the Anion Gap (If the anion gap is>20mmol/L the primary metabolic acidosis is presentregardless of pH and HCO3 levels.
Principle: The body doesn`t generate a large anion gap tocompensate forprimary disorder.
RULE 3:- Calculate the Excess anion gap (The total Aniongap minus the normal anion gap) and add the value to
measured bicarbonate concentration.If the sum is greater than a normal Serum HCO3 (>30mmol/L) there is underlying metabolic alkalosis.
If the sum is less than
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pH decreases (< 7.4)
pCO2 Increases Primary defect
HCO3 increases as a Compensatory Response
Results from Hypoventilation and subsequent
hypercapnea
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1. Drugs(anaesthetics,morphine,sedatives
1.obstruction 1. Emphysema 1.Poliomyelitis 1. Obesity
2. Stroke 2. Asthma 2. Pneumoconiosis 2.Khyphoscoliois
2.Hypoventilation
3. infection 3. Bronchitis 3.Myasthenia
4. ARDS 4. Musculardystrophosy
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ACUTE pH decreases by 0.08 ORHCO3 increases by 1 mEq/L
CHRONIC pH decreases by 0.03 OR
HCO3 increases by 4 mEq/L
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Occurs when hyperventilation reduces thepCO2
pH increases
pCO2 decreases primary defect
HCO3 decreases as compensation
Most common cause is Hyperventilation
Other imp causes are bacterial septicemia
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Pain High Altitude,
pCO2 dec
Pregnancy,
progestrone
Hemothorax Septicemia
Anxiety,psychosis
Pneumonia,pulmonaryEdema
Salicylates Flail Chest HepaticFailure
Fever Aspiration Cardiac
Failure
Cardiac
Failure
Heat exposure
CVA Severe Anemia PulmonaryEmbolism
Recovery frommetabolicacidosis
Tumor Mechanical
hyperventilation
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ACUTE pH increases By 0.08 0rHCO3 decreases by 2 mEq/l
CHRONIC pH increeas by 0.03 OR
HCO3 Decreases by 5 mEq/L
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pH decreases
HCO3 decrease- Primary defect
pCO2 also decreases as a Compensatory
response Classified On the basis of anion gap
Base deficit caused by
a) Increase in Endogenous acid production eg:
(Lactic acid, ketoacid)b) Loss of bIcarb from body (Diarrhea)
c) Accumulation of endogenous acid
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Lactic Acidosis
Ketoacidosisa) Diabeticb) Alcoholicc)
Starvation
Toxinsa) Ethylene Glycolb) Methanolc) Salicylatesd) Propylene glycol
Renal Failure
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Gastrointestinal HCO3 loss
Renal Tubular Acidosis
Post Hypocapnea
Hyperalimentation (Arginine and lysine in pareneralnutrition)
Othera) Acid Loads( Ammonium chloride, Hyperalimentation)
b) Expansion acidosis (rapid saline administration)
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Increase Renal NH4Cl excretion to EnhanceH+ removal is a normal physiologicalresponse to metabolic acidosis
Normal daily Urinary excretion of NH4CL isabout 30 mEq/L which can be inc upto 200mEq/l
UAG Reflect the ability of kidney to excrete
NH4ClUAG = [Na +K] [CL]
UAG helps in distinction b/w GI and Renal
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p /Causes of Hyperchloremic acidosis
In GI loss (diarrhea) renal acidification abilityremains normal and NH4Cl excretion increasesin response to acid and UAG becomes Negative ([Cl] > [Na+K]
When UAG is Positive ( [Na+K] > [Cl]) urinaryammonium is low because of inability kidney toexcrete NH4Cl.
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Alkalemia, pH increases
Primary defect is a increase in serum Bicarb
Compensatory mechanism leads tohypoventilation
MAK involves a generative phase in which loss of
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g pacid usually causes Alkalosis and then amaintenance phase in which kidney fail tocompensate by excreting HCO3
It is useful to classify Mak in two Groups based on
Saline responsiveness or urinary chloride.
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Renal Alkalosisa) Diuretic Therapyb) Post Hypercapneac) Poorly reabsorbable anion therapy: carbenicillin, penicillin
GASTROIINTESTINAL ALKALOSISa) Loss of HCL from Vomiting , NG suctionb) Chloride Diarrheac) Transfusion
d) Antacids
CONTRACTION ALKALOSIS
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RENAL ALKALOSIS
NORMOTENSIVE
Bartter SyndromeGitelman syndrome
Endogenous mineralocorticoid
a) Primary aldosteronismb) Hyperreninismc) Liddle Syndromed) Adrenal enzyme deficiency :11 and
17 hydroxylase
Severe Potassium depletion Exogenous Alkali
Hypercalcemia Exogenous Mineralocorticoids
Licorice
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METABOLIC ACIDOSIS + RESPIRATORY ALKALOSISHigh or normal AG Mac, prevailing pCO2 below predicted values
METABOLIC ACIDOSIS + RESPIRATORY ACIDOSISHigh or normal AG MAc , prevailing pCO2 above predicted value
METABOLIC ALKALOSIS + RESPIRATORY ALKALOSISpCO2 does not increase as predicted and pH higher than expected
METABOLIC ALKALOSIS + RESPIRATORY AIDOSISpCO2 Higher than predicted ,ph normal
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METABOLIC ACIDOSIS + METABOLIC ALKALOSIS
( eg: uremia with vomiting)
METABOLIC ACIDOSIS + METABOLIC ACIDOSISMixed high AG Normal AG Acidosis( Eg: diarrhea and Lactic acidosis , Treatment of DKA)
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-- pH normal, abnormal PCO2 n HCO3
-- Degree of compensation for primary
disorder is inappropriate-- Combination of respiratory acidosis and
Alkalosis can not coexist
-- Find Delta Delta Gap/ Excess Anion gap
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Equivalent rise of AG and Fall of HCO3
.Pure Anion Gap Metabolic Acidosis
Discrepancy.. in rise & fall
+ Non AG M acidosis, + M Alkalosis
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Delta Delta gap ==AG/HCO3
Delta Delta Gap = 1-2.Pure AG acidosis
< 1 = non AG acidosis(+ AG M Acidosis)
> 2 = metabolic alkalosis(+ AG M
Acidosis)
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CALCULATE EXCESS ANION GAP (EAG)
EAG = Anion Gap - 12 meq/L +bicarbonate
EAG > 30 mEq/L: Metabolic Alkalosispresent
EAG < 23 mEq/L: Non-Anion Gap MetabolicAcidosis
http://www.fpnotebook.com/Renal/Lab/AnGp.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAlkls.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAcds.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAlkls.htmhttp://www.fpnotebook.com/Renal/AcidBase/MtblcAlkls.htmhttp://www.fpnotebook.com/Renal/Lab/AnGp.htm -
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Tripple acid base disorders are not common
Patient develop tripple disorder only if a mixeddisorder coexist with respiratory acidosis or alkalosis
Are usually seen in patient with severe metabolic
disorder AKA-
a) AG gap acidosis+b) Metabolid alkalosis (dehydration)+c) respiratory acidosis (respiratory depression)
DKAa) AG gap Acidosis +b) Metabolic Alkalosis ( dehydration)+c) Respiratory Alkalosis (hyperventilation from
pneumonia or sepsis)
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Primary lesion
compensation
pH
HCO3
CO2
METABOLIC ACIDOSIS
HYPER VENTILATION
HCO3 changes
pH in same direction
Low
Alkali
LOW HCO3
LOW pH
LOW pCO2 (compensated)
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Primary lesion
compensation
pH
HCO3
CO2
METABOLIC ALKALOSIS
HYPO VENTILATION
BICARB CHANGES
pH in same direction
HIGH HCO3
HIGH pH
HIGH pCO2 (compensated)
High
Alkali
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CO 2 CHANGES
pH in opposite direction
Primary lesion
compensation
pH
CO 2
BICARB
Respiratory acidosis
HIGH pCO2
LOW pH
HIGH HCO3 (compensated)
High
CO2
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Primary lesion
compensation
pH
CO2
BICARB
Respiratory alkalosisLow
CO2
CO 2 CHANGES
pH in opposite direction
LOW pCO2
HIGH pHLOW HCO3 (compensated)
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pH 7.24
pCO2 24 mmHg
[HCO3] 10 mEq/L
Na 130K 4
Cl 94
STEP 1: Evaluate the ph and narrow down to twoibil
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possibilty
pH < 7.36= Acidosis (met or resp)
STEP 2:Evaluate the pCO2 and narrow down to one
definite process
pCO2 < 40 mmHg
Atleast metabolic acidosis is present
STEP 3: Apply Compensation formula and compare
predict pCO2 with actual pCO2Expected pCO2= 1.5[HCO3]+82 = 21-
25
Actual pCO2 = 24 (compensated)
STEP 4: Determine if any other process existTh d CO2 A l C 2
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The expected pCO2 = Acual pCo2
A pure Metabolic acidosis With no other
process
STEP 5: Evaluate Anion Gap
AG= 130- (94+10)
26
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pH 7.52pCO2 20mmHg[HCO3] 19 mEq/l
Na 136
Cl 103
STEP 1: Evaluate the ph and narrow down to twopossibilities
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possibilities
pH > 7.44 = Alkalosis ( metab or Resp)
STEP 2: Evaluate the pCO2 and narrow down to
definite process
pCO2 < 40 (atleast resp alkalosis is present)
STEP 3: Apply compensation formula for resp
alkalosis ( based on history apply for acute)
For every decrease of 10mmhg pCO2 [HCO3]
decrease 2 meq (from 24)bec pco2 dec by 20 [HCO3] should dec by 4
Expected [HCO3]= 20 meq,
Actual [HCO3] = 19 meq
STEP 4: Determine if any other process is thereth t l d t d [HCO3] l l
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the actual and expected [HCO3] closely
matches.
No other disorder STEP 5: Evaluate Anion Gap
AG = 136- (103+19) = 14 (normal)
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pH 7.47
pCO2 21
[HCO3] 15 mEq/l
Na 136Cl 110
STEP 1: pH > 7.44 = Alkalosis( meta or resp)
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STEP 2: pCO2 < 40 = atleast Resp Alkalosis
STEP 3: Apply compensation formula For chronic
Resp Alkalosis (as u know the history)
For every decrease of 10mmhg pCO2
[HCO3] expect to dec 5 mEq/lBec pCO2 dec by 20 HCO3 should dec
10 mEq (24-10 =14)
Expected HCO3 = 14Actual = 15
STEP 4: Determine if any other processare presentBoth the act al and [HCO3] match the
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Both the actual and [HCO3] match the
expected changes closely
No other Acid base disorder
STEP 5: Evaluate the Anion Gap
AG= 136-(110+15) = 11 (normal)
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pH 7.47
pCO2 21 mmHg[HCO3] 15 mEq/l
Na 136
Cl 109
STEP 1: pH> 7.44 = Alkalosos (metab or Resp)
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STEP 2: pCO2 < 40 = Atleast metab. Alkalosis
STEP 3: Apply formula for compensation, now u
dont know acute or chronic, Therefore
apply Both formulas.
EVALUATING USING FORMULA FOR CHRONIC
for every dec. Of 10mmHg in pCO2 [HCO3] decby 5
mEq/lExpected [HCO3] = 14
Actual [HCO3] = 15
SIMPLE CHRONIC RESPIRATORY ALKALOSIS
EVALUATE USING FORMULA FOR ACUTE PROCESSFor every dec of pCO2 expect [HCO3] to dec By
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For every dec of pCO2, expect [HCO3] to dec By
2mEq/l
Expected [HCO3] = 20Actual [HCO3] = 15
STEP 4: Determine if any other process existActual HCO3 is lower than expected
Now which process can lower HCO3
from expected, answer is MetabolicAcidosis, as two Respiratory cant coexist
STEP 5 : Evaluate the Anion GapAG 136 (109+15) 12 (normal)
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AG= 136- (109+15) = 12 (normal)
Without the clinical history we canconclude Either
a)
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pH: 7.01
pCO2: 70 mmHg
[HCO3]: 19 mEq/L
Na 140
CL 99
STEP 1: Evaluate the pH
H 7 35
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pH < 7.35
Acidosis (resp or Metabolic)
STEP 2: Evaluate the pCO2pCO2 > 40
Atleast Respiratory Acidosis
STEP 3: Apply compensatory formula For acute respacidosis
For every increase of 10 mmHg in pCO2,[HCO3]
expected to increase 1 mEq/l
Bec pCO2 inc. By 30, [HCO3] should inc by 3 to
27 mEq/l (from 24)
EXPECTED [HCO3] = 27 mEq/L
ACTUAL [HCO3] = 19 mEq/L
STEP 4: Determine if any other process existActual [HCO3] is lower than predicted this
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Actual [HCO3] is lower than predicted, thissuggest other than resp acidosis there ismetabolic acidosis which is lowering [HCO3]
STEP 5: Evaluate the Anion GapAG = 140 (99+19)= 22An Elevated gap Metabolic acidosis
STEP 6: Calculate delta delta change= AG- Normal AG/ HCO3- calculated HCO3= 22-12 = 10 / 24- 19= 5= 2
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pH: 7.27
pCO2: 62
[HCO3]:28
Na 134
Cl 85
STEP 1: Evaluate the pH
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pH < 7.35 = Acidosis (metab or resp)
STEP 2: Evaluate the pCO2pCO2 > 40
Atleast Respiratory acidosis is present
STEP 3: Apply formula of compensation for acuteresp. Acidosis
for every increas of 10 mm in pCO2, [HCO3]
expected to inc 1 mEq/l
Bec pCO2 inc by 20 HCO3 should inc by 2
Exected HCO3 = 26
Actual HCO3 = 28
STEP 4: Determine if any other process
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Since Actual HCO3 slightly higher thanexpected, a small metabolic alkalosis
maybe present
STEP 5: Evaluate the Anion Gap
AG= 134- (85+28) = 23Elevated AG Metabolic acidosis also
present
STEP 6: Calculate Delta Delta Gap= (23-12)/ (28-24) = 11/4= > 2Metabolic Alkalosis is present
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The resp acidosis is due to respiratory
depression from Alcohol Intoxication and BZoverdose
The mild met. Alkalosis is due to emesis and
resultant volume Depletion
The Elevated AG met. Acidosis is likely causedby Alcoholic ketoacidosis
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THANKYOU
FORYOUR TIME
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HARRISONS MEDICINE 17 EDITION
CMDT 2010
E-MEDICINE
RED BOOK
FRED FERRI
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