2. A metabolic condition in which the arterial pH is
elevated beyond the normal range ( 7.35-7.45 )
Result of decreased hydrogen ion concentration,
leading to increased bicarbonate and increased PaCo2
As a result of compensatory alveolar hypoventilation
3. Often associated with hypochloremia and
hypokalemia.
Often occurs in association with other disorders like
respiratory acidosis or alkalosis or metabolic acidosis.
Arterial pH makes the diagnosis as it is increased in
metabolic alkalosis and may b normal or decreased in
respiratory acidosis.
11. Vomiting or nasogastric suction
Results in the loss of hydrochloric acid with the
stomach contents.
Loss of fluid and Nacl in vomitus results in contraction
of ECF and increased secretion of renin and
aldosterone.
Severe vomiting also causes loss of potassium
(hypokalaemia) and sodium (hyponatremia).
The kidneys compensate for these losses by retaining
sodium in the collecting ducts at the expense of
hydrogen ions by the action of aldosterone, leading to
metabolic alkalosis
12. Congenital chloridorrhea
Rare autosomal recessive disorder which causes severe
diarrhea, fecal acid loss and HCO3 retention
The main mechanism is loss of ileal HCO3/Cl anion
exchange mechanism which results in decreased Cl
reabsorption.
Na/H exchange mechanism remains normal so normal
H+ is secreted in stool which causes Na and HCO3 to
be retained
This results in metabolic alkalosis
13. Villous adenoma
High adenoma derived K secretory rate
Colonic secretion is alkaline
K and volume depletion most probably causes
alkalosis
14. Diuretics
Loop diuretics and thiazide reduce the ECF
without affecting the total body bicarbonate
content.
Diuretics blocks Na+ and Cl- channels
More Na is delivered to DCT
15. Na exchange with K+ under the effect of
aldosterone
Kaliuresis and hypokalemia occurs
Depleted ECF causes contraction alkalosis
Hypokalemia augments renal ammoniagenesis
16. Posthypercapnia
During respiratory acidosis prolonged co2 retention
occurs (chronic hypoventilation and hypercapnia)
resulting in increased plasma HCO3 concentration
Due to increased reasbsorption and generation of
HCO3
When hypercapnia resolves increased HCO3 content
and associated ECF contraction will cause metabolic
alkalosis
Alkalosis persists until chloride supplementation is
given
17. Nonreabsorbable anions
Administration of large amount of non reabsorbable
anions like penicillin or carbenicillin can enhance
distal acidification and K+ excretion
H+ secretion occurs without Cl- dependant HCO3
secretion.
Mg deficiency also results in hypokalemic alkalosis by
enhancing distal acidification by stimulation of renin
and hence aldosterone secretion.
18. Bartter’s syndrome
Autosomal recessive disorder involving impaired Thick
Ascending Limb salt reabsorption
Results in salt wasting, volume depletion, and
activation of renin-angiotensin system
It is associated with metabolic alkalosis, hypokalemia
and normal to low blood pressure
19. Gitelman syndrome
autosomal recessive disorder
characterised by metabolic alkalosis, hypokalemia,
hypocalciuria and hypomagnesemia
It is caused by loss of function of the thiazidesensitive
sodium-chloride symporter located in the distal
convoluted tubule.
21. High renin
States with high renin may be accompanied by
hyperaldosteronism and alkalosis
Renin levels may be increased due to increased renin
secretion or decreased circulating blood volume
Examples of high renin HTN are Accelerated
hypertension and renovascular hypertension
Estrogen increase renin substrate and hence
angiotensin II formation
Primary tumor overproduction of renin can also cause
Metabolic alkalosis
22. Low renin
I. Hyperaldosternism
Adenoma, carcinoma and hyperplasia of adrenal gland
results in aldosterone overproduction
Adrenal enzyme defects (11 B hydroxylase deficiency, 17 a-
hydroxylase deficiency)
Aldosterone causes hypokalemia which results in an
increased indirect reabsorption of HCO3 via the rise in
proximal tubular intracellular H+
Hypokalemia reduces GFR and thereby maintains the
elevated blood HCO3
23. II. Cushing’s syndrome or disease
Abnormally high glucocorticoid hormone
production caused by adrenal gland adenoma or
carcinoma or ectopic corticotrophin production can
cause metabolic alkalosis
24. Liddle’s syndrome
Autosomal dominant disorder
Characterized by early, and frequently severe,
hypertension associated with low plasma renin
activity, metabolic alkalosis, hypokalemia, and normal
to low levels of aldosterone
Liddle syndrome involves abnormal kidney function,
with excess reabsorption of sodium and loss of
potassium from the renal tubule
25. CYSTIC FIBROSIS
Cystic fibrosis
Mutation in CF gene on CHR-7
(del 3 bp in CFTR protein )
Na+ & Clˉ loss
Volume depletionHrponatremia (rare)
alkalosis hypokalemia
26. Milk-Alkali syndrome
Ingestion of large amount of milk and absorbable
antacids: CaCO3
Patient excrete large amount of Ca and HCO3 in the
urine
Ca deposits more in alkaline urine
Deposition of Ca leads to renal function impairment
Thus HCO3 increased in plasma
28. COMPENSATION
Respiratory compensation for metabolic alkalosis is
less predictable than that for metabolic acidosis
PCO2 can be estimated by adding 15 to the HCO3
when HCO3 range is from 25 to 40 meq/l
Further elevation in PCO2 is limited by hypoxemia and
to some extent hypokalemia, which normally
accompanies metabolic alkalosis
29. Compensation for metabolic alkalosis occurs mainly in the
lungs, which retain carbon dioxide (CO2) through
hypoventilation.
CO2 is then consumed toward the formation of the
carbonic acid, thus decreasing pH.
The decrease in H+ suppresses the peripheral
chemoreceptors, which are sensitive to pH.
But, because respiration slows, there's an increase in PCO2
which offsets the depression because of the action of the
central chemoreceptors which are sensitive to the partial
pressure of CO2 in the cerebral spinal fluid.
So, because of the central chemoreceptors, respiration rate
would be increased.
30. Renal compensation for metabolic alkalosis consists of
increased excretion of HCO3
-
Filtered load of HCO3
- exceeds the ability of the renal
tubule to reabsorb it.
The development of metabolic alkalosis hence means
the failure of kidneys to eliminate HCO3 at normal
capacity
31. CLINICAL PRESENTATION
Symptom of metabolic alkalosis are not specific.
Include changes in central and peripheral nervous
system function
Hypoventilation develops because of inhibition of the
respiratory center in the medulla.
Mental confusion, obtundation, predisposition to
seizure is common
32. Aggravation of arrhythmia and hypoxemia in COPD
may also be seen
Symptoms of hypokalemia like muscle cramps,
myalgia and muscle weakness may also be seen
Symptoms of hypocalcemia (eg, jitteriness, perioral
tingling, muscle spasms) may be present.
35. Chloride-Sensitive (Responsive) Metabolic
Alkalosis:
The initial problem is a sustained loss of chloride out
of proportion to the loss of sodium (either by renal or
GI )
This chloride depletion results in renal sodium
conservation leading to a corresponding reabsorption
of [HCO3 -] by the kidney.
In this category of metabolic alkalosis, the urinary
[Cl-] is <10 mEq/L,
and the disorders respond to treatment with
intravenous NaCl.
36. Chloride-Insensitive (Resistant) Metabolic
Alkalosis:
The pathogenesis in this category is direct stimulation
of the kidneys to retain bicarbonate irrespective of
electrolyte intake and losses.
The urinary [Cl-] >15-20 mEq/L, and these disorders
do not respond to NaCl administration.
37. ynm dduh new delhi 64
HISTORY
vomiting,
medication diuretics in CHF
Salty sweats CYSTIC FIBROSIS
Intake of sodabicarbonate
Massive blood transfusion, (citrate bicarbonate)
Total parenteral nutrition (TPN) ( acetate bicarbonate)
POLYHYDRAMNIOS IN MOTHER antenatal Bartter
syndrome
Deafness , Recurrent dehydration Bartter syndrome
Hypertension hypermineralocorticoid state
39. The anion gap is frequently elevated to a modest degree
in metabolic alkalosis because of the increase in the
negative charge of albumin and the enhanced
production of lactate.
Serum bicarbonate concentration can be calculated
from a blood gas sample using the Henderson-
Hasselbalch equation, as follows:
pH = 6.10 + log (HCO3
- ÷ 0.03 × PaCO2)
Alternatively, HCO3
- = 24 × PaCO2 ÷ [H+]
40. Normally, arterial PaCO2 increases by 0.5-0.7 mm Hg
for every 1 mEq/L increase in plasma bicarbonate
concentration
If the change in PaCO2 is not within this range, then a
mixed acid-base disturbance occurs.
if the increase in PaCO2 is more than 0.7 times the
increase in bicarbonate, then metabolic alkalosis
coexists with primary respiratory acidosis.
If the increase in PaCO2 is less than the expected
change, then a primary respiratory alkalosis is also
present.
42. MANAGEMENT
chloride- Responsive metabolic alkalosis
Re-expand volume with Normal Saline ( Primary
Therapy)
Supplement with Potassium to treat hypokalemia
(alkalosis associated with severe hypokalemia will be
resistant to volume resuscitation until K is repleted)
H+ blockers or PPIs if vomiting/NG suction to prevent
further losses in H+ ions
43. Discontinue diuretics
Acetazolamide if NS contraindicated due to CHF.
(Monitor for hypokalemia)
HCl or NH4Cl in emergency. (HCl can cause
hemolysis, NH4Cl should not be used in liver disease)
Hemodialysis in patients with marked renal failure
