Transcript PRINCIPLES OF SURGERY NOVEMBER 2001 FLUID AND …

PRINCIPLES OF SURGERY
November 2011
FLUID AND ELECTROLYTE BALANCE
PART 2: DISORDERS OF ACID-BASE
AND POTASSIUM BALANCE
Dr. Bob Richardson
Toronto General Hospital
Objectives (1)
Normal acid-base physiology
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Acid from diet
Renal response to acid
Pathophysiology of acid-base balance
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Effects of vomiting, bile, pancreatic fluid,
ileostomy losses on acid-base balance
Effect of kidney disease on acid base balance
Metabolic acidosis from excess acid generation
Metabolic alkalosis from vomiting
Objectives (2)
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Therapy of metabolic acidosis
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Why, when, how much bicarbonate
Normal Potassium homeostasis
Hyper- and hypokalemia
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causes, manifestations
emergency treatment
Normal Acid-Base Physiology
Input
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On a usual North American diet, acid is
generated from metabolism of sulfurcontaining amino acids to sulfuric acid:
methionine , cysteine  H2SO4
Typical NA diet generates 50-100 mmol
H+ daily
Normal Acid-Base Physiology Buffering
H+ added to body water must be buffered:
 Without buffering, one day’s 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 bicarbonate were not generated
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Normal Acid-Base Physiology
Kidney Generation of New HCO3
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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 NH4+ can increase from 40 200 mmol/d
with acidemia
DIETARY PROTEIN
70 mmol H+ (+ SO4)
- 70 mmol HCO3
+ 70 mmol HCO3
KIDNEY
URINE NET ACID
(NH4+) 70 mmol
Corollaries of Normal Physiology
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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
Acid-Base Impact of Loss of GI
Secretions
Gastric
0.5-2 L/d 100 mM H+
Bile
1 L/d
HCO3 40 mM
Pancreas 2 L/d
HCO3 70-120 mM
Ileostomy 0.5-1 L/d HCO3 30 mM
Colostomy 1 L/d
HCO3 20 mM
Diarrhea 1-20 L/d HCO3 up to 75 mM
Alkalosis
Acidosis
Acidosis
Acidosis
Acidosis
Acidosis
Causes of Metabolic Acidosis
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Loss of HCO3-containing GI fluid (see table)
Loss of HCO3 in urine: proximal RTA ( rare !)
Kidney failure (GFR< 30 ml/min)
Acid gain
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Lactic acidosis
Ketoacidosis
Methanol poisoning (formic acid)
Ethylene glycol poisoning (a variety of organic
acids)
Salicylate poisoning
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 lactateBefore: Na
140 After:Na
140
Cl
102
Cl
102
HCO3
AG
25
13
HCO3
15
23
Significance of the Anion Gap
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Anion gap > 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
Differential Dg of Metabolic Acidosis
by Anion Gap
Normal AG
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Diarrhea or other GI
loss
Kidney failure
Renal tubular acidosis
“Expansion” acidosis
Increased Anion Gap
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Lactic acidosis
Ketoacidosis
Methanol poisoning
Ethylene glycol
poisoning
ASA poisoning
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
@ 120/min BP 110/70; JVP low; mild abdominal
tenderness. Left leg cool and pulseless below knee.
Lab Values
Hgb 60 g/L
WBC 15
pH
PCO2
PO2
HCO3
7.22
25
90
10
Na
K
Cl
AST
140
5.5
103
300
Diagnosis
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Lactic acidosis
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Anemia
Hypotension (atrial fib)
Ischemic leg
Ischemic bowel/liver
Therapy of Metabolic Acidosis
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Metabolic acidosis is more important for
diagnosis than therapy
No trials proving bicarbonate therapy
alters outcome
Generally try and maintain pH > 7.00
and bicarbonate > 8 mmol/L
Amount needed = [HCO3] X BWt
(assuming severe acidosis)
Metabolic Alkalosis from vomiting or
gastric suction
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Bicarbonate generation:
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Loss of HCl from stomach
Volume depletion (concentration)
Renal bicarbonate retention
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Hypokalemia (from urine loss of K+ with
bicarbonaturia and high aldosterone)
Increased angiotensin II – stimulates
proximal bicarbonate reabsorption
How to Prevent Metabolic Alkalosis in a
Patient on Gastric Suction
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Prevent volume depletion
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Prevent hypokalemia
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Replace gastric losses with normal saline
Replace KCl
Prevent HCl secretion
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Use PPI or H2 blocker
Potassium
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Normal potassium homeostasis
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Hyperkalemia
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shift into and out of cells
kidney regulation of potassium excretion
cardiac effects
cell shift
impaired K+ excretion
Hypokalemia
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cell shifts
urine and GI losses
Normal Potassium Distribution
ICF
K=140 mM
ECF
Na+
K+
K=4 mM
Normal Potassium Balance
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ECF [K] 4 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+
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insulin promotes K+ uptake by cells
 P[K+] stimulates aldosterone
Aldosterone stimulates K+ secretion and
excretion
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.
K+ Excretion by Kidney
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Regulated at cortical collecting duct
Aldosterone stimulates Na+
reabsorption
Makes lumen negatively charged
Negative charge attracts K+ from cell
Flow rate also very important (volume)
since excretion = concentration X flow
Flow depends on GFR, volume state
Major Factors Affecting K
excretion
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Aldosterone
Flow
Hyperkalemia Cardiac Effects
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Life-threatening arrhythmias when
P[K+] > 7 mM
Abnormal ECG when P[K+] > 6.0
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peaked T waves
broad QRS
flat P waves
sine wave
ECG
ECG post acute treatment
ECG post dialysis
Hyperkalemia - Role of Kidney
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ALWAYS impaired K+ excretion as cause of
hyperkalemia - usually both:
Low flow to CCD:
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advanced renal failure
severe ECF volume depletion
oliguria, anuria
Low aldosterone activity
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adrenal insufficiency (mineralocorticoid)
impaired renin secretion or AII generation
Drugs Promoting Hyperkalemia
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Block aldosterone generation by angII
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Block aldosterone action on CCD
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ACE inhibitors, angiotensin receptor
blockers
spironolactone
amiloride, triamterene
high dose Septra
Multiple effects
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cyclosporine
Case of Hyperkalemia
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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
Diagnosis
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Shift of K out of cells
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Rhabdomyolysis
Reduced renal excretion
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Very low CCD flow
Hypotensive shock – reduced GFR,
increased proximal reabsorption
Oliguric ATN
Management of Hyperkalemia
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Urgent: for P[K+]>7, arrhythmia or ECG
changes:
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1 amp calcium gluconate bolus
20 units insulin bolus (+ 1 amp 50% D/W)
2-4 puffs of ventolin or ventolin inhalation
Semi-urgent
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increase urine flow - saline if appropriate
furosemide
hemodialysis
Hypokalemia- Effects
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Cardiac:
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VPB’s, u-waves, VF and VT if cardiac
ischemia
Muscle weakness
Metabolic alkalosis
Impaired insulin secretion
Hypokalemia - causes
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Shift into cells
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insulin
high catecholamines - endogenous or
exog.
Increased loss
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GI - diarrhea, vomiting, fistulas, ostomies
Urine:
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diuretics
polyuria
primary aldosteronism
Treatment of Hypokalemia
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Oral KCl - 8 or 20 mmol/tablet or liquid
IV KCl if urgent or unable to take orally
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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
Potassium and IV Fluids
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Most hospitals committed to removing
KCl from wards
Prefer standard IV fluids with added KCl
Usually 10 or 20 mmol/L
High concentrations (20 mmol/100 ml)
only in monitored setting using pumps
and central lines