arterial blood gas analysis & electrolyte imbalance12

8/7/2019 Arterial Blood Gas Analysis & Electrolyte Imbalance12

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` ABG: Is a blood test that perform using blood

from artery.

` The most common puncture sites: RADIAL

&FEMORAL ARTERY.` The test is used to determine the

PH,

PaO2,

PaCo2,HCO3,

BE in blood.


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` PH: it is negative logarithm of H+ concentration

` [H+](n Eq/L)=24 x PCO2 / HCO3, [24 x 40/24=40]`

PH=Log1/[H+

]` Normal ranges:--

PH=7.367.44

PCO2=35-45mmHg

PO2=80-100mmHgHCO3=22-24mEq/l

BE=- 3 to+3mEq/l


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` Direct & sympathoadrenal activation

` Direct depression of myocardial & smooth muscles contractility&

decreased PVR leading hypotension, tissue hypoxia, both muscles

become less responsive to endogenous& exogenous

catecholamines & threshold of VF decrease

` Hyperkalemia due to exchange H with K become lethal K increase

0.6mEq/Lfor each 0.1decrease in Ph

` CNS depression more in respiratory acidosis than metabolicacidosis leading to CO2 narcosis lead increase Intracranial

hypertension secondary to increase CBF


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ALVEOLAR

HYPOVENTILATION

INCREASED CO2

PRODUCTION

CNS DEPRESSION

drugs,obesity,trauma

NEUROMUSCULAR

DISORDER

FLAIL CHEST

AIRWAY OBSTRUCTION

PARENCHYMAL LUNG

DISEASE

PNEUMOTHORAX,EFFUSION

MALIGNANT HYPOTHERMIA

LARGE CARBOHYDRATE

LOAD

INTENSIVE SHIVERING

THYROID STORM

BURNS


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HIGH AG ACIDOSIS NORMAL AG ACIDOSIS

` Due to loss of bicarbonate

from ECF whichcounterbalanced by CL-

` Diarrhea` Isotonic saline infusion` Early renal insufficiency` Renal tubular acidosis` Acetazolamide carbonic

anhydrase inhibitor thatincr. HCO3 loses in urine.

` Ureteroenterostomy

*Due to fixed acid added to

ECF.Acid dissc to H+ + anion.

Then H+ combines with HCO3

to form carbonic acid which

leads to HCO3 & AG

*Lactic acidosis IMPAIR H+

SECRETIONS

*Ketocidosis

*End stage renal failure

*Methanol ingestion. formicacid.

* Ethylene glycol oxalic acid

*Salicyclate toxicity


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` Increase the affinity of hemoglobin for oxygen and shift thedissociation to left. Exchange of the H+ ion with K+ producesHYPOKALEMIA.

`

Increase the number of anionic binding sites calcium onplasma proteins. Therefore decrease ionized plasma Ca 2+,leading to circulatory depression and neuromuscularirritability.

` Respiratory alkalosis reduces CBF, increases SVR and mayprecipitate coronary spasm, increase bronchial smoothmuscle tone (bronco constructer) but decrease PVR.


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CHLORIDE SENSITIVE

.GASTROINTESTINAL vomiting ,villous adenoma

.RENAL diuretic ,low cl intake

.SWEAT cystic fibrosis

CHLORIDE RESISTANT

.INC MINERALOCORTICOIDACTIVITY

hyperaldosteronism

Cushing syndromebartter syndrome

MASSIVE BLOOD TRANSFUSION

HYPERCALCEMIA


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CENTRAL STIMULATION

pain, anxiety, stroke, tumor, fever, drugs

PERIPHERAL STIMULATIONhypoxia, High altitude, severe anemia

Pulmonary disease :- CHF, asthma, embolism

SEPSIS

VENTILATOR INDUCED


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Primary acid-base disorders and

associated compensatory changes

Primary disorder Primary changes Compensatorychanges

Respiratory acidosis pco2 Hco3

10 mm of Hg 1 meq/L and 4 meq/L

Respiratory alkalosis pco2 Hco3

10 mm of Hg 2 &4 meq /L

Metabolic acidosis Hco3 pco2

1.2 x HCO3 in PCO2

Metabolic alkalosis Hco3 pco2

0.7 HCO3 PCO2

Correlate changes in ph with changes in CO2 or HCO3. In respiratory

disturbance every 10 mmhg change in co2 should change arterial Ph by approx

0.08 units in opp direction. During metabolic disturbance every six mEq changes

in HCO3 also changes arterial ph by 0.1 in same direction. If change in ph

exceed or is less, then predicated, a mixed acid-base disorder.


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Metabolic disorder elicit prompt ventilatory response that aremediated by peripheral chemo receptors. Metabolic acidosisstimulate these receptors initiate increase in ventilation.Metabolic alkalosis silence the receptors and produce promptdecrease in ventilation.

Compensation for Metabolic Acidosis ventilatory response to

a metabolic acidosis will reduce PCO2.expPaCo2=(1.5HCO3)+8

For eg. Metabolic acidosis result in serum Hco3 =15meq/L,then exp Pco2=(1.515)+8=30.5

So if measured Pco2 is = Exp Pco2 then respi. compensation is

adequate otherwise,If measured Pco2 is > than expected, there is a respiratoryacidosis in addition to metabolic acidosis. Its is a primarymetabolic acidosis with superimposed respiratory acidosis.

If pco2 < than expected, there is a respiratory alkalosis inaddition to compensated metabolic acidosis and its calledprimary metabolic acidosis with superimposed metabolic

alkalosis.


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Compensation for Metabolic Alkalosis--- if metabolic alkalosis is

associated with plasma HCO3of 40meq/L then expected PCO2

=(0.7Hco3)+21=0.7x40+21=49

If Measured Paco2= Exp Pco2---compensated Metabolic alkalosis

If Measured Paco2> Exp Pco2---there is a resp acidosis in addition to

metabolic alkalosis. This is a primary metabolic alkalosis with

superimposed resp. acidosis.

If Measured Paco2< Exp Pco2 then there is an additional resp alkalosis

then its a primary metabolic alkalosis with a superimposed resp

alkalosis.


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Compensatory response to primary changes in pco2 takes

place in the kidney and involve adjustment of Hco3reabsorption in the proximal tubules. An increase in paco2resp acidosis result in incr Hco3 reabsorption andsubsequently increase in serum Hco3. while decrease inPCO2(resp alkalosis), result in decrease Hco3 reabsorptionsubsequently decrease in plasma Hco3.

1.Acute respiratory disorder: before renal compensation,change in PaCO2of 1 mm of hg will produce change in X phof 0.008 Ph units.

a. Respiratory acidosis-expectd PH=7.4-[.008 (paco2-40)]

b. Respiratory alkalosis-expected PH=7.4+[.008(40-Pco2)]

2 Chronic respiratory disorder; after renal compensation in

the kidney is fully developed, the arterial Ph changes only by

0.003 pH units for every mm change in pco2.


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a. Respiratory acidosis-expectd PH=7.4-[.003 (paco2-40)]

b. Respiratory alkalosis-expected PH=7.4+[.003(40-Pco2)]

For example: Patient with emphysema and chronic CO2 retention with

PaCO2 of 60 mm of hg, expected pH = 7.4-(0.003*20)=7.34 pH units.

Expected pH for acute rise in paco2 to 60, the pH=7.4-(0.008*20)=7.24 pH

units. Therefore the renal compensation for an acute rise in pco2 to 60

is expected to increase arterial pH by 0.1 pH units.

For example. Patient with co2 of 23 mm of hg and pH 7.4 the pco2 and pH

change in opposite direction so primary problem is respiratory and

since the pH is alkalemic this is a primary respiratory alkalosis. Exp

pH= 7.4+0.008*(40-23)=7.54. this the same as measured pH so this aacute uncompensated resp alkalosis. If measured pH was higher than

expected, this will be a superimposed metabolic alkalosis. If measured

pH is less than expected, it should be a metabolic acidosis.


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*Anion gap is an estimate of relative abundance of unmeasured

anions, and it is used to determine if a metabolic acid is due to an

accumulation of non volatile acids (lactic acid) or a net loss of bi-

carbonate (diarrhea)

*Use the Gap to evaluate metabolic acidosis:

Anion gap=Na+UC=(CL+HCO3)+UA

So the equation is Na-(CL+HCO3)=UA-UC

Normal anion gap=12 4 meq/l

Unmeasured anions Unmeasured Cations

Albumin-15 calcium-5

Organic acids-5 potassium-4.5Phosphates-2 mag++ 1.5

Sulfates-1

Total=23meq Total=11meq

Anion gap=UA-UC=12 meq


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Interpretation of gap-gap AG excess /HCO3 DEFICIT=

(MEASURED AG-12)/(24-MEASURED HCO3)

Mixed Metabolic Acidosis- in the presence of high AG metabolic

acidosis gag-gap (AG excess /HCO3 DEFICIT ) ratio of

less than 1 indicates the co-existence of normal AG metabolic

acidosis. If gap-gap ratio>1, then its called Metabolic acidosisand co-existence metabolic alkalosis.


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` 1.Identify the primary acid base disorder abnormality present ifPCO2 or PH is outside of normal range` 2.if changes in PCO2 or PH in same direction then primary

disorder is metabolic and changes in opposite direction thenrespiratory disorder is primary

` Example PH =7.23 and Pco2 =23both are reducing so primary

metabolic acidosis.` 3.If either PH or PCo2 is normal then it will be mixed

disorder(one is acidosis and other is alkalosis).Example PH=7.37and PCO2=55 so it will be combined respiratory acidosis andmetabolic alkalosis.

` 4.Evaluate compensatory responses as formula givenpreviously.Example for primary metabolic acidosis.PH=7.32,PCO2=23,HCO3=15 so primary metabolic acidosis.expPCO@=(1.515)+8=30.5 . So in this case final interpretation isprimary metabolic acidosis with a superimposed respiratoryalkalosis.


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p H 7.35 to

7.45

Incr. PaCO2 Nrml PaCO2 Decr.

PaCO2

Incr HCO3

Nrml HCO3

Decr HCO3 incr. HCO3

Respiratory acidosis +

metabolic alkalosis No acid-base

disturbance

Chronic

metabolic

acidosis (renal

disease)

Chronic

metabolic

alkalosis

(pulmonary

dysfunction)


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increased

Paco2norPaco2 DecrPaCO2

Incre

HCO3

Unch or

dec HCO3Dec HCO3 Dec HCO3

PH below 7.35

Respiratoryacidosis

Respiratoryplus metabolic

acidosis

Metabolic plusrespiratory

acidosis

Metabolicacidosis


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P H Above 7.45

Increase Pco2 Decrease Paco2

Increased HCO3Deceased

HCO3

Increased HCO3

Metabolic AlkalosisRespiratory

Alkalosis

Respiratory plus

Metabolic Alkalosis


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` To reverse imbalance between CO2 production& alveolar

ventilation

` Reduced production CO2 by dantroline, muscle paralysis

,anti thyroid drugs, reduced carbohydrate intake

` Improve alveolar ventilation by bronchodilators, reversal

of narcosis, respiratory stimulant (doxapram) or improve

lung compliance (diuretics)

` Mechanical ventilation & increase inspiratory O2

NaHCO3=base deficit0 .3body weight


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` Correction of underlying process for respiratory alkalosis

(intravenous HCl, arginine chloride or ammonium

chloride may be indicated).

` Controlled ventilation if respiratory alkalosis is there.

` Intravenous NaCl and KCl and H2 blocker therapy.

` Acetazolamide in edematous patient.

` If it is associated with primary increase in

mineralocorticoid activity readily responses to

aldosterone antagonist (spirinolactone).


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` Impaired Thrist

` Coma

` Essential hypernatremia

` Solute diuresis` Osmotic diuresis DKA, nonketotic

hyperosmolar coma,mannitol admin

` Excessive water loss

` Renal:pitutitary DI ,Nephrogenic DI

` Extrarenal:sweating


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` CF:restlessness,lethargy,hyperreflexia,,seizures.coma

` Tt Hypernatremia

`

water & Na+ loss water loss incr Na content

Replace isotonic loss replace water deficit loop diuretic

replace water deficit replace any water

deficit


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` 70 kg man with pl. Na 160mEq/l .Calculate water

deficit?

Normal TBW X140 = present TBW X PL.Na

(70x0.6) x 140= present TBW X160Present TBW = (70X0.6)X140 /160 =36.7L.

Water deficit= Normal TBW Present TBW

= 70X0.6 - 36.7L = 5.3L

This amount should be replaced in 48 hrs with 5%

dextrose.


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` Serum Na


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` Progressive cerebral edema lead to

lethargy,confusion,seizures coma may lead to

death.

` Management;-is directed at correcting both theunderlying disorder as well as plasma Na.isotonic

saline is generally Tt of choice for hyponatremic pt

with decrease total body sodium content.

Na deficit=TBW (desired Na-present Na)/stren


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HYPONATREMIA`

extracellular volume normal extra cellular extracellular

Renal extrarenal adrenal or thyroid

hypofunction CCF,Cirrhoosis renalneph synd.

Una>20 meq Una


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` Correction of plasma sodium to > 125 meq/l or 3-

7meq/l is usually sufficient

` Na deficit=

TBW x (desired Na- present Na)` Very rapid correction results in CPM

` Rapidity of correction tailored to needs: Mild symptoms: 0.5meq/l/hr or less

Mod. Symptoms: 1meq/l/hr or less Severe symptoms: 1.5meq/l/hr or less


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` 80kg women having plasma Na 118mEq/l

` How much NaCl must be given to raise pl. Na

130 mEq/l ?

Na deficit= 80x 0.5 (130- 118 ) = 480mEqIsotonic saline contains 154 mEq/l, saline to be

infused will be 480 / 154 =3.12L in 24 hrs.


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` Plasma k


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` K>5.5` CausesPseudohyperkalemia

` hemolysis` Leukocytosis

` ThrombocytosisIntercompartment shift` Acidosis` Rhabdomyolysis

` periodic paralysisDecrease renal potassium clearance

` Renal failure` Adrenal insufficiency

` Drugs;-ACE inhibitor,cyclosporine digitalis K sparing diuretics,NSAID,scolene

Increased potassium intake


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` Clinical manifestation;-most serious consequence is slowing the

electrical conduction in the heart

` ECG changes begin K 6.0meq/l With a tall and tapering T

wave,as the hyperkalemia progress Peaked T wave

widening of QRS complex prolongation of P-R interval

loss of P wave loss of R wave amplitude - ST segment

depression - resem ble sine wave - VF and Asystole.


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` 1. membrane antagonism;- calcium gluconate

10% 10ml IV

` 2.Transcellular shift

` A. insulin-dextrose` B. Sod bicarbonate

` 3.Enhanced clearance

` A. exchange resin

` B. loop diuretics

` C. hemodialysis


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` Normal ca++ conc. in plasma is 8.5-10.5` Causes:---HypoparathyroidismVitamin D deficiency` Nutritional` MalabsorptionHyperphosphatemia` Precipitation of calcium` Pancreatitis` Rhabdomyolysis` Fat embolismchelation of calcium` Blood transfusion


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` Paresthesia,confusion,laryngeal stridor,carpopedal

spasm(Trousseaus sign)massator

spasm(chvosteks sign),and seizures.

`

Cardiac irritability can lead to arrythmia` Decrease cardiac contractility may result in heart

failure.

` Treatment: Calcium chloride(3-5 ml of a 10%

solution) or calcium gluconate(10-20 ml of a 10%solution) IV


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` Serum calcium >5.5mEq/L

` SIGN AND SYMPTOMS

.sedation, vomiting, polyurea

. Cardiac conduction disturbance

. Renal calculi

TREATMENT

Hydration with normal saline

IV Furosemide 40- 80 mg

bisphosphonates


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` Most patients are asymptomatic butanorexia,weakness ,fasciculationparesthesia,confusion,ataxia,and seizures may beencountered

` It is frequantly associated with hypocalcemia andhypokalemia

` Associated with incidence of electrical irritability, atrialfibrillation,

` Treatment: asymptomatic can be treated with orally

magnesium sulphate.` Symptomatic:--IV Mg so4 1-2 gm over 15-60 min.


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` Serum magnesium concentration >2.5 mEq/L

` SIGN AND SYMPTOMS

. CNS depression hyporeflexia, sedation

. Cardiac depression

.Skeletal muscle weakness

TREATMENT

Acute- IV calcium

Persistent- dialysis


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`

` THE END

arterial blood gas analysis & electrolyte imbalance12

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