PRINCIPLES OF SURGERY NOVEMBER 2003 FLUID AND ELECTROLYTE BALANCE PART 2: DISORDERS OF ACIDBASE AND

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PRINCIPLES OF SURGERY NOVEMBER 2003FLUID AND
ELECTROLYTE BALANCEPART 2 DISORDERS OF
ACID-BASE AND POTASSIUM BALANCEDr. Bob
Richardson, Toronto General Hospital
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Objectives (1)

• Normal acid-base physiology
• Sources of acid gain from diet
• Renal response to acid gain
• Pathophysiology of acid-base balance
• Effects of vomiting, bile, pancreatic fluid,
  ileostomy losses on acid-base balance
• Effect of renal failure on acid base balance
• Metabolic acidosis from excess acid generation
• Metabolic alkalosis from vomiting

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Objectives (2)

• Therapy of metabolic acidosis
• Why, when, how much bicarbonate
• Normal Potassium homeostasis
• Hyper- and hypokalemia
• causes, manifestations
• emergency treatment

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Normal Acid-Base Physiology-Input

• On a usual North American diet, acid is generated
  from metabolism of sulfur-containing amino acids
  to sulfuric acid
• methionine?, cysteine ? H2SO4
• About 0.8 mmol H/gm of protein ingested
• Typical NA diet generates 50-100 mmol H daily

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Normal Acid-Base Physiology - Buffering

• H added to body water must be buffered
• Without buffering, one days protein intake would
  decrease blood pH to 3!
• Main buffer is bicarbonate
• H HCO3- ? H2CO3 ? CO2 H2O
• Buffering greatly reduces the ? pH
• Buffering would gradually reduce ECF HCO3 if
  new biacrbonate were not generated

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Normal Acid-Base Physiology - Renal Generation of
New Bicarbonate

• In order to restore ECF bicarbonate lost to
  buffering, the kidney excretes acid in the form
  of ammonium (NH4) made from glutamine
• Ammonium excretion increases with metabolic
  acidosis and respiratory acidosis in response to
  the decrease in cell pH
• Urine NH4can increase from 40? 200 mmol/d with
  acidemia

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DIETARY PROTEIN 70 mmol H ( SO4) -
70 mmol HCO3 70 mmol HCO3 KIDNEY URI
NE NET ACID (NH4) 70 mmol
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Corollaries of Normal Physiology

• Low protein diets generate very little acid
• If kidneys fail, acidosis is inevitable
• If kidneys are healthy, chronic acid gain (e.g.
  diarrhea) may cause no acidosis
• If kidneys are not healthy, chronic acid gain
  (diarrhea) may cause severe acidosis

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Acid-Base Impact of Loss of GI Secretions

• Gastric 0.5-2 L/d 100 mM H Alkalosis
• Bile 1 L/d HCO3 40 mM Acidosis
• Pancreatic 2 L/d HCO3 70-120 mM Acidosis
• Ileostomy 0.5-L/d HCO3 30 mM Acidosis
• Colostomy 1 L/d HCO3 20 mM Acidosis
• Diarrhea 1-20 L/d HCO3 up to 75 mM Acidosis

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Causes of Metabolic Acidosis

• Loss of HCO3-containing GI fluid (see table)
• Loss of HCO3 in urine proximal RTA ( rare !)
• Renal failure
• Acid gain
• Lactic acidosis
• Ketoacidosis
• Methanol poisoning (formic acid)
• Ethylene glycol poisoning (a variety of organic
  acids)
• Salicylate poisoning

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The Anion Gap

• Acid gain results in an increase in the anion
  gap
• Na (Cl HCO3)
• Consider lactic acidosis with gain of 10 mmol/L
  H and lactate-
• Before Na 140 After Na 140
• Cl 102 Cl 102
• HCO3 25 HCO3 15
• AG 13 23

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Significance of the Anion Gap

• Anion gap gt 15 indicates accumulation of an
  organic acid anion in plasma
• Almost always means metabolic acidosis
• 5 conditions that cause acid gain with increased
  anion gap are potentially fatal and must be
  recognized

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Differential Dg of Metabolic Acidosis by Anion Gap

• Increased Anion Gap
• Lactic acidosis
• Ketoacidosis
• Methanol poisoning
• Ethylene glycol poisoning
• ASA poisoning

• Normal AG
• Diarrhea or other GI loss
• Renal failure
• Renal tubular acidosis
• Expansion acidosis

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Case History 70 year old woman on hemodialysis
for 5 years. Presents with 6 hour history of
cold left leg. One month earlier her BP was
150/80, Hgb 105 g/L, HCO3 20 mmol/L. For several
weeks she has had abdo pain with bloody
diarrhea. For one week she has been weak and
dizzy and a little confused. On exam confused,
restless atrial fibrillation _at_ 120/min BP
110/70 JVP low mild abdominal tenderness. Left
leg cool and pulseless below knee.
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Lab Values

• Hgb 60 g/L
• WBC 15
• pH 7.22 Na 140
• PCO2 25 K 5.5
• PO2 90 Cl 103
• HCO3 10 AST 300

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Diagnosis

• Lactic acidosis
• Anemia
• Hypotension (atrial fib)
• Ischemic leg
• Ischemic bowel/liver

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Therapy of Metabolic Acidosis

• Metabolic acidosis is more important for
  diagnosis than therapy
• No trials proving bicarbonate therapy alters
  outcome
• Generally try and maintain pH gt 7 and bicarbonate
  gt 8 mmol/L
• Amount needed ?HCO3 X BWt (assuming severe
  acidosis)

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Metabolic Alkalosis from vomiting or gastric
suction

• Bicarbonate generation
• Loss of HCL from stomach
• Volume depletion (concentration)
• Renal bicarbonate retention
• Hypokalemia (from urine loss of K with
  bicarbonaturia and high aldosterone)
• Increased angiotensin II stimulates proximal
  bicarbonate reabsorption

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How to Prevent Metabolic Alkalosis in a Patient
on Gastric Suction

• Prevent volume depletion
• Replace gastric losses with normal saline
• Prevent hypokalemia
• Replace KCl
• Prevent HCl secretion
• Use PPI or H2 blocker

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Potassium

• Normal potassium homeostasis
• shift into and out of cells
• kidney regulation of potassium excretion
• Hyperkalemia
• cardiac effects
• cell shift
• impaired K excretion
• Hypokalemia
• cell shifts
• urine and GI losses

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Normal Potassium Balance

• ECF K 3.5-5.0 mM ICF 140 mM
• 2 in ECF 98 in ICF
• Daily intake 30-80 mmol (fruits, veggies)
• Note one large K meal total ECF K
• insulin promotes K uptake by cells
• ? PK stimulates aldosterone
• Aldosterone stimulates K secretion and excretion

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K Shift

• K shift into cells
• insulin
• catecholamines (?2 receptor) - e.g. ventolin
• anabolic state (growth, refeeding etc)
• K shift out of cells
• insulin deficiency - diabetes, fasting
• cell ischemia, necrosis (e.g. rhabdomyolysis),
  red cell lysis etc.

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K Excretion by Kidney

• Regulated at cortical collecting duct
• Aldosterone stimulates Na reabsorption
• Makes lumen negatively charged
• Negative charge attracts K from cell
• Aldosterone and plasma K set lumen K
• Flow rate also very important (volume) since
  excretion concentration X flow
• Flow depends on GFR, volume state

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Hyperkalemia Cardiac Effects

• Life-threatening arrhythmias when PK gt 7 mM
• Abnormal ECG when PK gt 6.0
• peaked T waves
• broad QRS
• flat P waves
• sine wave

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ECG
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ECG post acute treatment
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ECG post dialysis
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Hyperkalemia - Role of Kidney

• ALWAYS impaired K excretion as cause of
  hyperkalemia - usually both
• Low flow to CCD
• advanced renal failure
• severe ECF volume depletion
• oliguria, anuria
• Low aldosterone activity
• adrenal insufficiency (mineralocorticoid)
• impaired renin secretion or AII generation

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Drugs Promoting Hyperkalemia

• Block aldosterone generation by angII
• ACE inhibitors, angiotensin receptor blockers
• Block aldosterone action on CCD
• spironolactone
• amiloride, triamterene
• high dose Septra
• Multiple effects
• cyclosporine

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Case of Hyperkalemia

• 40 year old construction worker falls three
  stories from scaffold
• Multiple fractures - femur, ribs, humerus
• Compartment syndrome in thigh, calf
• Hypovolemic shock
• Serum potassium 5.2 ? 6.5 over 2 hours
• Urine flow 10 ml/h
• CK 12,000

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Diagnosis

• Shift of K out of cells
• Rhabdomyolysis
• Reduced renal excretion
• Very low CCD flow
• Hypotensive shock reduced GFR, increased
  proximal reabsorption

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Management of Hyperkalemia

• Urgent for PKgt7, arrhythmia or ECG changes
• 1 amp calcium gluconate bolus
• 20 units insulin bolus ( 1 amp 50 D/W)
• 2-4 puffs of ventolin or ventolin inhalation
• Semi-urgent
• increase urine flow - saline if appropriate
• furosemide
• hemodialysis

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Hypokalemia- Effects

• Cardiac
• VPBs, u-waves, VF and VT if cardiac ischemia
• Muscle weakness
• Metabolic alkalosis
• Impaired insulin secretion

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Hypokalemia - causes

• Shift into cells
• insulin
• high catecholamines - endogenous or exog.
• Increased loss
• GI - diarrhea, vomiting, fistulas, ostomies
• Urine
• diuretics
• polyuria
• primary aldosteronism

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Treatment of Hypokalemia

• Oral KCl - 8 or 20 mmol/tablet or liquid
• IV KCl if urgent or unable to take orally
• 40 mmol/L max concentration, 40 mmol/h maximum
  rate
• most hypokalemic patients have high losses and
  volume depletion
• in monitored setting and central line can give
  boluses of 40/100 mL if volume a concern