Metabolic Alkalosis

OVERVIEW

  • Metabolic alkalosis is a a primary acid-base disorder that causes the plasma bicarbonate to rise to an abnormally high level
  • the severity of a metabolic alkalosis is determined by the difference between the actual [HCO3] and the expected [HCO3]

CAUSES

  • the persistence of a metabolic alkalosis requires an additional process which acts to impair renal bicarbonate excretion
  • this means that the initiation and maintenance must be considered when analysing a metabolic alkalosis

The Initiating Process

GAIN OF ALKALI IN THE ECF

  • from an exogenous source (e.g. IV NaHCO3 infusion, citrate in transfused blood)
  • from an endogenous source (e.g. metabolism of ketoanions to produce bicarbonate)

LOSS OF H+ FROM ECF

  • via kidneys (e.g. use of diuretics)
  • via gut (e.g. vomiting, NG suction)

Maintenance of Alkalosis

  • maintenance of the alkalosis requires a process which greatly impairs the kidney’s ability to excrete bicarbonate and prevent the return of the elevated plasma level to normal.
  • the four factors that cause maintenance of the alkalosis (by increasing bicarbonate reabsorption in the tubules or decreasing bicarbonate filtration at the glomerulus) are:
  1. chloride depletion
  2. potassium depletion
  3. reduced glomerular filtration rate (GFR)
  4. ECF volume depletion (volume contraction)

CHLORIDE DEPLETION

  • the commonest cause
  • administration of chloride is necessary to correct these disorders
  • two commonest causes: (1) loss of gastric juice and (2) diuretic therapy

Gastric loss alkalosis

  • most marked with vomiting due to pyloric stenosis or obstruction because the vomitus is acidic gastric juice only
  • vomiting in other conditions may involve a mixture of acid gastric loss and alkaline duodenal contents and the acid-base situation that results is more variable

Diuretics

  • diuretics such as frusemide and thiazides interfere with reabsorption of chloride and sodium in the renal tubules
  • urinary losses of chloride exceed those of bicarbonate
  • the patients on diuretics who develop an alkalosis are those who are also volume depleted (increasing aldosterone levels) and have a low dietary chloride intake (‘salt restricted’ diet)
  • hypokalaemia is common in these patients
  • it is high while the diuretic is acting, but drops to low levels afterwards

Other rare causes

  • chloride diarrhoea
  • villous adenomas excreting chloride

POSTASSIUM DEPLETION

  • potassium depletion occurs with mineralocorticoid excess
  • bicarbonate reabsorption in both the proximal and distal tubules is increased in the presence of potassium depletion
  • potassium depletion decreases aldosterone release by the adrenal cortex

Primary Hyperaldosteronism

  • the increased aldosterone levels lead to increased distal tubular Na+ reabsorption and increased K+ & H+ losses
  • increased H+ loss is matched by increased amounts of renal HCO3- leaving in the renal vein
  • the net result is metabolic alkalosis with hypochloraemia and hypokalaemia, often with an expanded ECF volume

Cushing’s Syndrome

  • the excess corticosteroids have some mineralocorticoid effects and because of this can produce a metabolic alkalosis
  • the alkalosis is most severe with the syndrome of ectopic ACTH production

Severe K+ depletion

  • cases have been reported of patients with metabolic alkalosis and severe hypokalaemia ([K+] < 2 mmol/l) due to severe total body potassium depletion
  • aetiology is not understood but correction of the alkalosis requires correction of the potassium deficit – urinary chloride losses are high (>20mmol/l)

Bartter’s syndrome

  • syndrome of increased renin and aldosterone levels due to hyperplasia of the juxtaglomerular apparatus
  • an inherited as an autosomal recessive disorder usually found in children
  • the increased aldosterone levels usually result in a metabolic alkalosis
  • patients present with hypokalaemic alkalosis of uncertain cause are often suspected of having this condition but other causes which may be denied by the patient should be considered (eg surreptitious vomiting and/or use of diuretics for weight loss or psychological problems)
  • rare genetic disorders such as Gitelmann’s syndrome should also be considered

URINARY CHLORIDE

  1. Urine Cl- < 10 mmol/l
  • often associated with volume depletion (increased proximal tubular reabsorption of HCO3)
  • respond to saline infusion (replaces chloride and volume)
  • causes: previous diuretic therapy, vomiting
  1. Urine Cl- > 20 mmol/l
  • often associated with volume expansion and hypokalaemia
  • resistant to therapy with saline infusion
  • causes: excess aldosterone, severe K+ deficiency, diuretic therapy (current), Bartter’s syndrome
  • a high urinary chloride in association with hypokalaemia suggests mineralocorticoid excess
  • the urinary chloride/creatinine ratio may occasionally be useful as it is elevated if there is an extra-renal cause of alkalosis

EFFECTS

CVS

  • decreased myocardial contractility
  • arrhythmias

RESP

  • impaired peripheral oxygen unloading (due shift of oxygen dissociation curve to left) – hypoxaemia may occur and oxygen delivery to the tissues may be reduced
  • hypoventilation (due respiratory response to metabolic alkalosis)
  • pulmonary microatelectasis (consequent to hypoventilation)
  • increased ventilation-perfusion mismatch (as alkalosis inhibits hypoxic pulmonary vasoconstriction)

CNS

  • decreased cerebral blood flow
  • confusion
  • mental obtundation
  • neuromuscular excitability

COMPENSATION

  • the hypoventilation causes a compensatory rise in arterial pCO2 but the magnitude of the response has generally been found to be quite variable
  • the expected pCO2 due to appropriate hypoventilation in simple metabolic alkalosis can be estimated from the following formula:

Expected pCO2 = 0.7 [HCO3] + 20 mmHg

  • maximum value of arterial pCO2 55 to 60mmHg although much higher values have been reported
  • failure of hypoventilation may be attributed to hyperventilation for any reason

TREATMENT

  • correct cause (eg correct pyloric obstruction, cease diuretics)
  • correct the deficiency which is impairing renal bicarbonate excretion (ie give chloride, water and K+)
  • expand ECF volume with normal saline (and KCl if K+ deficiency)
  • if the diagnosis is not obvious, spot urine chloride is useful: low levels suggest Cl- depletion and need for replacement; high levels suggest adrenocortical excess and need for K+ replacement
  • rare ancillary measures: HCl infusion, acetazolamide, oral lysine hydrochloride
  • supportive measures (eg. O2, monitoring and observation)
  • avoid hyperventilation as this worsens the alkalaemia

References and Links


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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