abg s final and last touch

8/4/2019 ABG S Final and Last Touch

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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


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


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


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


HIGH HCO3

HIGH pH

HIGH pCO2 (compensated)

High

Alkali


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CO 2 CHANGES


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


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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abg s final and last touch

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