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&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
PNEUMOTHORAX,EFFUSION
CHLORIDE RESISTANT
.INC MINERALOCORTICOID ACTIVITY –
hyperaldosteronism
Cushing syndrome
bartter syndrome
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.
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.
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
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=
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
2) GIT loss;
vomiting,diarrhea
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
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%
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
TREATMENT
Acute- IV calcium
Persistent- dialysis
THE END