Metabolic Alkalosis causes, clinical features, diagnosis, and management.

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Metabolic Alkalosiscauses, clinical features,
diagnosis, and management.

• Alex Yartsev
• Derived largely from Brandis

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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
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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 Sorensens
  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 131304. Nørby JG. (2000) The origin and
meaning of the little p in pH. Trends in
Biochemical Sciences 25 36-37.
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The physiological range of pH

• 7. 45
• 7.35

• Above 7.45 alkalosis
• 7.45 to 7.35 normal range
• Below 7.35 acidosis

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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
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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

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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

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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

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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

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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 (pseudohyperaldostero
  nism)
• 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
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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

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Another classification of metabolic alkalosis

• Urinary chloride classification
• Based on measured urinary chloride concentration
  (which can be elevated with diuretic infusion)
• Chloride responsive alkalosis - lt 20mEq/L
• Loss of hydrogen ions, eg. vomiting
• Loss of bicarbonate-poor water, (concentration of
  bicarbonate, contraction alkalosis)
• Chloride resistant alkalosis - gt 20mEq/L
• Retention of bicarbonate
• Shift of hydrogen ions into the intracellular
  space (eg. in hypokalemia)
• Administration of alkalotic agents, eg.
  bicarbonate

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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
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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
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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 198780729-33
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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)

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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
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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

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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.

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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.
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Management of metabolic alkalosis in the
Intensive Care Unit

• More basic management
• REPLACE POTASSIUM / OTHER ELECTROLYTES
• AVOID HYPERVENTILATION

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Management of metabolic alkalosis in the
Intensive Care Unit

• Advanced management strategies
• Hydrochloric acid infusion
• Via a central line just make sure it doesnt
  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 CL-
• Increases 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
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Questions?