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Vmmc& safdarjung hospital


new delhi
 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.
 PH: it is negative logarithm of H+ concentration
 [H+](n Eq/L)=24 x PCO2 / HCO 3, [24 x 40/24=40]

 PH=Log1/[H+]
 Normal ranges:--
PH=7.36—7.44
PCO2=35-45mmHg
PO2=80-100mmHg
HCO3=22-24mEq/l
BE=- 3 to+3mEq/l
 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 metabolic acidosis


leading to CO2 narcosis lead increase Intracranial hypertension
secondary to increase CBF
CNS DEPRESSION MALIGNANT HYPOTHERMIA
drugs,obesity,trauma
LARGE CARBOHYDRATE LOAD
NEUROMUSCULAR DISORDER
INTENSIVE SHIVERING
FLAIL CHEST THYROID STORM

AIRWAY OBSTRUCTION BURNS

PARENCHYMAL LUNG DISEASE

PNEUMOTHORAX,EFFUSION

ALVEOLAR INCREASED CO2


HYPOVENTILATION PRODUCTION
HIGH AG ACIDOSIS NORMAL AG ACIDOSIS
*Due to fixed acid added to  Due to loss of bicarbonate
ECF. from ECF which
Acid dissc to H+ + anion. counterbalanced by CL-
 Diarrhea
Then H+ combines with HCO3  Isotonic saline infusion
to form carbonic acid which  Early renal insufficiency
leads to ↓ HCO3 & ↑ AG  Renal tubular acidosis
 Acetazolamide carbonic
*Lactic acidosis ‘IMPAIR H+ anhydrase inhibitor that
SECRETIONS’ incr. HCO3 loses in urine.
*Ketocidosis  Ureteroenterostomy
*End stage renal failure
*Methanol ingestion. formic
acid.
* Ethylene glycol → oxalic acid
*Salicyclate toxicity
 Increase the affinity of hemoglobin for oxygen and shift
the dissociation to left. Exchange of the H+ ion with K+
produces HYPOKALEMIA.

 Increase the number of anionic binding sites calcium on


plasma proteins. Therefore decrease ionized plasma Ca
2+, leading to circulatory depression and
‘neuromuscular irritability’.

 Respiratory alkalosis reduces CBF, increases SVR and


may precipitate coronary spasm, increase bronchial
smooth muscle tone (bronco constructer) but decrease
PVR.
CHLORIDE SENSITIVE
.GASTROINTESTINAL – vomiting ,villous adenoma
.RENAL – diuretic ,low cl intake
.SWEAT – cystic fibrosis

CHLORIDE RESISTANT
.INC MINERALOCORTICOID ACTIVITY –
hyperaldosteronism
Cushing syndrome
bartter syndrome

MASSIVE BLOOD TRANSFUSION

HYPERCALCEMIA
CENTRAL STIMULATION
pain, anxiety, stroke, tumor, fever, drugs

PERIPHERAL STIMULATION
hypoxia, High altitude, severe anemia
Pulmonary disease :- CHF, asthma, embolism

SEPSIS

VENTILATOR INDUCED
Primary acid-base disorders and
associated compensatory changes
Primary disorder Primary changes Compensatory
changes
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
Metabolic disorder elicit prompt ventilatory response that are
mediated by peripheral chemo receptors. Metabolic acidosis
stimulate these receptors initiate increase in ventilation.
Metabolic alkalosis silence the receptors and produce prompt
decrease in ventilation.

Compensation for Metabolic Acidosis— ventilatory response to a


metabolic acidosis will reduce PCO2.exp
PaCo2=(1.5×HCO3)+8

For eg. Metabolic acidosis result in serum Hco3 =15meq/L, then


exp Pco2=(1.5×15)+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 respiratory
acidosis in addition to metabolic acidosis. Its is a primary
metabolic acidosis with superimposed respiratory acidosis.
If pco2 < than expected, there is a respiratory alkalosis in
addition to compensated metabolic acidosis and it’s called
primary metabolic acidosis with superimposed metabolic
alkalosis.
Compensation for Metabolic Alkalosis--- if metabolic alkalosis is
associated with plasma HCO3of 40meq/L then expected PCO2
=(0.7×Hco3)+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 it’s a primary metabolic alkalosis with a superimposed resp
alkalosis.
Compensatory response to primary changes in pco2 takes place in
the kidney and involve adjustment of Hco3 reabsorption in the
proximal tubules. An increase in paco2 resp acidosis result in incr
Hco3 reabsorption and subsequently increase in serum Hco3.
while decrease in PCO2(resp alkalosis), result in decrease Hco3
reabsorption subsequently decrease in plasma Hco3.
1.Acute respiratory disorder: before renal compensation, change
in PaCO2of 1 mm of hg will produce change in X ph of 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.
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 a
acute 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.
*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-4.5
Phosphates-2 mag++ 1.5
Sulfates-1
Total=23meq Total=11meq

Anion gap=UA-UC=12 meq


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 it’s called ‘Metabolic acidosis
and co-existence metabolic alkalosis.’
 1.Identify the primary acid base disorder abnormality
present if PCO2 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
then respiratory disorder is primary
 Example PH =7.23 and Pco2 =23…both 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=7.37 and PCO2=55 so it will be combined respiratory
acidosis and metabolic alkalosis.
 4.Evaluate compensatory responses as formula given
previously.Example for primary metabolic
acidosis….PH=7.32 ,PCO2=23,HCO3=15 so primary
metabolic acidosis.exp PCO@=(1.5×15)+8=30.5 . So in
this case final interpretation is primary metabolic acidosis
with a superimposed respiratory alkalosis.
p H 7.35 to
7.45

Incr. Nrml PaCO2 Decr.


PaCO2 PaCO2

Incr HCO3 Decr HCO3 incr.


Nrml HCO3
HCO3
Respiratory acidosis
No acid-base Chronic Chronic
+ metabolic
disturbance metabolic metabolic
alkalosis
acidosis alkalosis
(renal (pulmonary
disease) dysfunction
)
PH below 7.35

increased norPaco2 DecrPaCO2


Paco2

Incre Unch or Dec HCO3 Dec HCO3


HCO3 dec HCO3

Respiratory Respiratory Metabolic plus Metabolic


acidosis plus respiratory acidosis
metabolic acidosis
acidosis
P H Above 7.45

Increase Pco2 Decrease Paco2

Deceased Increased HCO3


Increased HCO3
HCO3

Respiratory Respiratory plus


Metabolic Alkalosis
Alkalosis Metabolic
Alkalosis
 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 deficit×0 .3×body weight


 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).
 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
 CF:restlessness,lethargy,hyperreflexia,,seizures.c
oma
 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
 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 X160
Present 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.
 Serum Na <135
 Classification

Decrease total Na content


 Renal-diuretics,minralocorticoid def,osmotic
diuresis,renal tubular acidosis
 Extrarenal;-vomiting diarrhea

Normal total Na content


 SIADH,glucocorticoid def,hypothyroidism,drug
induced
Increased total Na content;-CHF,Cirrhosis,nephrotic
syndrome
 Progressive cerebral edema lead to
lethargy,confusion,seizures coma may lead to
death.
 Management;-is directed at correcting both

the underlying 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
HYPONATREMIA

↓ extracellular volume normal extra cellular ↑ extracellular

Renal extrarenal adrenal or thyroid


hypofunction CCF,Cirrhoosis renal
neph synd.
Una>20 meq Una<10
meq/l Una <20 una>20

cortisol or
REPLACE ISOTONIC & NA DEFICIT thyroid harmone RESTRICT WATER & LOOP
DIURETIC RESTRICTWATER
water restricted
 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
 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 ) = 480mEq
Isotonic saline contains 154 mEq/l, saline to
be infused will be 480 / 154 =3.12L in 24
hrs.
 Plasma k <3.5

CAUSES

1) Excess renal loss


 Mineralocorticoid
 chr metabolic alkalosis
 Diuresis
 Antibiotics;carbenicillin,gentamicin.amphotericin B
 Renal tubular acidosis

2) GIT loss;
vomiting,diarrhea

3) ECF ICF shifts


 Acute alkalosis ,insulin ,vitamin B12 Therapy,thyrotoxicosis

4) Inadequate intake
 Mild hypokalemia usually asymptomatic and
may associated with ECG changes including
prominent U wave,flattening or T wave
inversion.
 Severe form K<2.5 produce skeleton muscle
weakness and augment arrhythmias.
 Management;
 1 oral replacement with potassium chloride
solution(60-80meq/l)
 2.intravenous potassium chloride .max rate
of@20meq/hr
 K>5.5
 Causes

Pseudohyperkalemia
 hemolysis
 Leukocytosis
 Thrombocytosis

Intercompartment shift
 Acidosis
 Rhabdomyolysis
 periodic paralysis

Decrease renal potassium clearance


 Renal failure
 Adrenal insufficiency
 Drugs;-ACE inhibitor,cyclosporine digitalis K sparing
diuretics,NSAID, scolene
Increased potassium intake
 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.
 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
 Normal ca++ conc. in plasma is 8.5-10.5
 Causes:---
Hypoparathyroidism
Vitamin D deficiency
 Nutritional
 Malabsorption

Hyperphosphatemia
 Precipitation of calcium
 Pancreatitis
 Rhabdomyolysis
 Fat embolism

chelation of calcium
 Blood transfusion
 Paresthesia,confusion,laryngeal
stridor,carpopedal spasm(Trousseau’s
sign)massator spasm(chvostek’s 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
 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
 Normal plasma 1.7-2.1 meq/l
 Hypomagnesemia is common & frequent overlooked
problem

Causes;--
Inadequate intake---nutritional
Reduced GI absorption
 Malabsorption syndrome,
 Small bowel or biliary fistulas
 Prolonged nasogastric suctioning
 Severe diarrhea

Increased renal loss


 Diuresis
 Diabetic ketoacidosis,
 Hyper parathyroidism,hypophosphatemia,drugs
 Most patients are asymptomatic but
anorexia,weakness ,fasciculation
paresthesia,confusion,ataxia,and seizures may be
encountered
 It is frequantly associated with hypocalcemia and
hypokalemia
 Associated with incidence of electrical irritability,
atrial fibrillation,
 Treatment: asymptomatic can be treated with
orally magnesium sulphate.
 Symptomatic:--IV Mg so4 1-2 gm over 15-60
min.
 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

 THE END

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