Metabolic Alkalosis causes, clinical features, diagnosis

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Transcript Metabolic Alkalosis causes, clinical features, diagnosis

Metabolic Alkalosis
causes, clinical features, diagnosis, and management.
Alex Yartsev
Derived largely from Brandis
The concept of pH
pH = - log10 aH+
Where aH+ is the activity of the H+ ion
at the glass electrode in the ABG machine
• “ a dimensionless representation of the H+
concentration”
• i.e. the higher the pH, the lower the H +
concentration.
• Pure water is neutral: pH of 7
• Thus, it has 0.0000001 moles of hydrogen ion
per litre
'Acid-base pHysiology' by Kerry Brandis - from http://www.anaesthesiaMCQ.com
What does pH mean anyway?
• 1909, Dr. Søren Peder Lauritz Sørensen–
used the term to refer to the negative
log of the hydrogen ion concentration,
hence the H.
• He decided to call it
“Wasserstoffionenexponent”
• To this day, there is debate as to what
the “p” in pH actually means – looks like
Dr Sorensen’s electrodes were
arbitrarily named “p” and “q”
Sørensen, S. P. L. (1909). Enzymstudien. II: Mitteilung. Über die Messung und die Bedeutung der
Wasserstoffionenkoncentration bei enzymatischen Prozessen; Biochemische Zeitschrift 21: 131–304.
Nørby JG. (2000) The origin and meaning of the little p in pH. Trends in Biochemical Sciences 25: 36-37.
The physiological range of pH
Above 7.45 = alkalosis
7. 45
7.45 to 7.35 – normal range
7.35
Below 7.35 = acidosis
Definition of alkalosis
• an abnormal process or condition which would raise arterial
pH if there were no secondary changes in response to the
primary aetiological factor.
Definition of metabolic alkalosis
• a primary acid-base disorder which causes the plasma
bicarbonate to rise to a level higher than expected
The severity of a metabolic alkalosis is determined by the difference
between the actual [HCO3] and the expected [HCO3].
Definitions from the findings of the Ad-Hoc Committee of the New York Academy of
Sciences in 1965.
Cited in 'Acid-base physiology' by Kerry Brandis
Physiology
• Kidneys are responsible for maintaining a
stable bicarbonate concentration
• Too much bicarb and it is rapidly excreted in
the urine (eg. when you inject sodium bicarb
into a healthy person, the pH only rises very
briefly)
• Too little bicarb, and all of it gets reabsorbed
from the urine
• THUS: for alkalosis to persist, there needs to be an
additional process which impairs renal bicarb regulation
How a metabolic alkalosis is initiated
• Gain of alkali
– From the outside, eg. infusion of sodium bicarb
– From the inside, eg. metabolism of ketoanions to
produce bicarbonate – like lactate in Hartmanns,
acetate in Plasmalyte, citrate in transfused blood
• Loss of acid
– Through the kidneys, eg. use of diuretic
– Through the gut , eg. vomiting or NG suction
How a metabolic alkalosis is maintained
Whatever maintains the alkalosis has to cause a massive decrease
in the kidneys ability to handle bicarbonate and hydrogen ions.
These causes can be divided into 4 groups:
• Chloride depletion
• Potassium depletion
• Reduced glomerular filtration rate
• Extracellular volume depletion
Chloride depletion alkalosis
• The most common form: 90% of clinical cases
• Chloride and bicarb are the only anions present in any significant
quantity in the ECF: decrease in one leads to an increase in the other
• Gastric acid loss eg. due to NG suction or vomiting:
– If the acid from the stomach is lost, pancreatic secretions are not stimulated,
and there is no loss of bicarbonate.
• Enteric chloride loss eg. due to villous adenoma
• Diuretic use, eg. frusemide infusion
– These patients lose chloride in excess of bicarbonate , because loop diuretics
increase sodium (and thus chloride) excretion
– Those patients who develop alkalosis from diuretic use are also volume
depleted and have reduced chloride intake.
• Administration of chloride is required to correct these disorders
Potassium depletion alkalosis
• Bicarbonate resorption in the proximal and distal tubule is
increased in the presence of potassium depletion
• Potassium depletion also decreases aldosterone release by the
adrenal cortex
• Examples:
• Primary or secondary hyperaldosteronism – increased
aldosterone causes increased K+ and H+ losses
• Cushings syndrome, or COPD on IV hydrocortisone –
corticosteroids have some mineralocorticoid effect
• Potassium-depleting diuretics eg. frusemide
• Also Bartter syndrome ( inherited juxtaglomerular
hyperplasia), licorice abuse (pseudohyperaldosteronism)
• Severe potassium depletion alone
Iida R, Otsuka Y, Matsumoto K, Kuriyama S, and Hosoya T. Pseudoaldosteronism due to the concurrent use of two herbal medicines containing
glycyrrhizin: interaction of glycyrrhizin with angiotensin-converting enzyme inhibitor. Clin Exp Nephrol 2006 Jun; 10(2) 131-5.
'Acid-base pHysiology' by Kerry Brandis -from http://www.AnaesthesiaMCQ.com
Extracellular volume depletion and
reduced GFR alkalosis
• Hypovolemia  increased Na+ and fluid reabsorption
• Chloride and bicarbonate should be reabsorbed
together with the sodium, but bicarbonate is
absorbed in preference to chloride
• In this situation, chloride depletion is the single most
significant cause
• Correcting volume without correcting chloride deficit
will not correct the alkalosis
• THUS: these should be treated with normal saline
infusion
Another classification of metabolic
alkalosis:
• Urinary chloride classification:
Based on measured urinary chloride concentration (which can be elevated
with diuretic infusion)
– Chloride responsive alkalosis - < 20mEq/L
• Loss of hydrogen ions, eg. vomiting
• Loss of bicarbonate-poor water, (concentration of
bicarbonate, “contraction alkalosis”)
– Chloride resistant alkalosis - > 20mEq/L
• Retention of bicarbonate
• Shift of hydrogen ions into the intracellular space (eg. in
hypokalemia)
• Administration of alkalotic agents, eg. bicarbonate
Urinary classification of metabolic
alkalosis
• Why is is this useful?
– If urinary chloride is low,
• The alkalosis is likely due to volume depletion and/or
gastric losses
• will respond to saline infusion
- If urinary chloride is high,
- Likely the alkalosis is due to hypokalemia or
aldosterone excess
- Will not respond to saline infusion
'Acid-base pHysiology' by Kerry Brandis
Common causes of metabolic alkalosis
in the INTENSIVE CARE UNIT
•
•
•
•
•
•
•
Frusemide infusion, use of thiazides
High volume NG aspirates
Diarrhoea
Severe hypokalemia (eg. insulin infusion)
Corticosteroid therapy
Overcorrection of chronic respiratory acidosis
Recovery phase post organic acidosis (excess
regeneration of HCO3)
• Large doses of IV penicillin-based drugs
“ Acid Base Disorders “ - in Principles of Critical Care Medicine, Mc Graw Hill
Consequences of metabolic alkalosis
• In critically ill patients, = significant increase in morbidity and
mortality
– Decreased myocardial contractiity
– Arrhythmias
– Decreased cerebral blood flow (vasoconstriction)
– Neuromuscular excitability  tetany  difficult ventilation
– Impaired peripheral oxygen unloading (oxygen-hemoglobin
dissociation curve shifts to the left, thus hemoglobin is less
inclined to part with oxygen in the tissues)
– Confusion, obtundation, seizures
– Hypoventilation, thus atelectasis
– Increased V/Q mismatch (alkalosis inhibits hypoxic pulmonary
vasoconstriction)
Anderson LE, Henrich WL. Alkalemia-associated morbidity and mortality in medical and surgical patients. South Med J
1987;80:729-33
Compensation for metabolic alkalosis
• The normal response is hypoventilation
• The key is to compensate by increasing pCO2
• How much pCO2 is enough?
Expected pCO2 = 0.7 [HCO3] + 20 mmHg (range: +/- 5)
Clinical features of metabolic alkalosis
• Hypoventilation, even hypoxia
• Other changes are similar to those of
hypercalcemia:
– confusion, obtundation, seizures
– paraesthesia
– Muscle cramps, tetany
DuBose, Jr. Thomas D, "Chapter 48. Acidosis and Alkalosis" (Chapter). Fauci AS, Braunwald E, Kasper DL,
Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison's Principles of Internal Medicine, 17e:
Diagnosis of metabolic alkalosis in the
ICU
• SUSPICION:
– Is the patient vomiting, is the NG sucking?
– Is the pt on frusemide? Whose week is it?
– Has there recently been a massive transfusion?
• ABGS: routine and frequent
Management of metabolic alkalosis in
the Intensive Care Unit
• Its usually something we did.
• Stop doing that.
• If it is a side-effect of a greater therapeutic
strategy, and cannot be avoided, then one can
focus on managing the alkalosis and
ameliorating its ill effects.
Management of metabolic alkalosis in
the Intensive Care Unit
Basic management:
• GIVE OXYGEN: the tissues are not getting enough
– Unless the patient is a CO2 retainer with severe compensatory
hypercapnea
• GIVE CHLORIDE: in chloride-responsive alkalosis this
will reverse the alkalosis
– “give chloride” means “give saline”
• GIVE PROTON PUMP INHIBITOR: if you reduce the
rate of H+ excretion by the gastric mucosa, the NG
aspirates will cause less of a
Hixson R and Christmas D. Use of omeprazole in life-threatening metabolic alkalosis. Intensive Care Med 1999
Oct; 25(10) 1201.
Management of metabolic alkalosis in
the Intensive Care Unit
More basic management:
• REPLACE POTASSIUM / OTHER ELECTROLYTES
• AVOID HYPERVENTILATION
Management of metabolic alkalosis in
the Intensive Care Unit
Advanced management strategies:
•
Hydrochloric acid infusion
–
–
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Via a central line; just make sure it doesn’t extravasate
The H+ will consume HCO3 – then its all about blowing off enough of
the created CO2
Acetazolamide
–
–
Carbonic anhydrase inhibitor: forces kidneys to excrete HCO3 and H+
to enter the bloodstream together with CLIncreases losses of Na+, K+, and water.
Buchanan IB, Campbell BT, Peck MD, and Cairns BA. Chest wall necrosis and death secondary to hydrochloric
acid infusion for metabolic alkalosis. South Med J 2005 Aug; 98(8) 822-4.
Worthley LI. Intravenous hydrochloric acid in patients with metabolic alkalosis and hypercapnia. Arch Surg 1986 Oct;
121(10) 1195-8.
Marik PE, Kussman BD, Lipman J, and Kraus P. Acetazolamide in the treatment of metabolic alkalosis in critically ill
patients. Heart Lung 1991 Sep; 20(5 Pt 1) 455-9
Questions?