Good surgery

1. 1
Fluid And Electrolytes
Emergencies
Prof Shein Myint

2. Volume of Distribution of Water
60%-Males
50%-Females
2
H2O
Solids

3. Intracellular
(2/3)
Solids 40% of Wt
H2O
Extracellular
(1/3)
H2O
Na
3

4. E.C.F. COMPARTMENTS
Interstitial 3/4 Intra-
vascular
1/4
H2O
H2O
Na Na
Colloids
& RBC
4

5. Total body water=60%
=0.6X
body wt
70=42 liters
ECF=1/3
0.3X42=13 liters
ICF=2/3
0.6 X42=25 liters
Blood=1/4 (ECF)
0.25X13=3. 3 liters
Amount of Fluid In Each
5
Compartment in a 70kg Male.

6. Effective circulating volume
6
–Portion of ECF that perfuses organs
–Usually equates to Intravascular
volume

7. “Third Space”
• Acute sequestration in a body compartment
that is not in equilibrium with ECF
• Examples:
– Intestinal obstruction
– Severe pancreatitis
– Peritonitis
– Major venous obstruction
– Capillary leak syndrome
– Burns
7

8. Daily Fluid Balance
Intake:
1-1.5L
Insensible Loss
-Lungs 0.3L
-Sweat 0.1 L
Urine: 1.0 to 1.5L 8

9. Control of Volume
9
Kidneys maintain constant volume and
composition of body fluids
– Filtration and reabsorption of Na
– Regulation of water excretion in response to ADH
Water is freely diffusible
– Movement of certain ions and proteins between
compartments restricted

10. Volume Control
10
• osmoreceptors
• baroreceptors
- day to day control
- respond to pressure
change
neural and hormonal efferents
hormonal mediators

11. Osmoregulation
11
osmolality 289 mOsm/kg H20
osmoreceptor cells in paraventricular/
supraoptic nuclei
osmoreceptors control thirst and ADH
small changes in Posm - large response

12. Osmoregulation
12
 Excess free water
(<Posm 280)
 thirst inhibited
 ADH declines
 urine dilutes to
Uosm 100
Decreased free water
(>Posm 295)
thirst increased
ADH increases
urine
concentrates to
Uosm 1200

13. Baroreceptors
13
• Hormonal effect
 ECF  Na and water reabsorption
• Hormonal mediators
aldosterone
renin
ANP
dopamine
• Neural mechanism
Autonomic nervous system

14. Renin
secreted
when
Angiotensin II
Increases
vascular tone
•increases
Aldosterone
Release
stimutlated by
• Angiotensin II
• increased K
• ACTH
Effect
• Na and water
absorption in distal
tubular segments
14
–drop BP catecolamine
release
–drop Na
delivery to
kidney
•decrease renal
blood flow
•increases Na
reabsorption
–increased
sympathetic
tone
•stimulates
aldosterone release

15. Principles of Treatment
15
• How much volume?
– Need estimate of fluid deficit
• Which fluid?
– Which fluid compartment is predominantly
affected?
– Need evaluation of other
acid/base/electrolyte/nutrition issues.

16. The IV Fluid Supermarket
• Crystalloids
– Dextrose in water
• D5W
• D10W
• D50W
– Saline
• Isotonic (0.9% or “normal”)
• Hypotonic (0.45%, 0.25%)
• Hypertonic
– Combo
• D51/2NS
• D5NS
• D10NS
– Ringer’s lactate “physiologic”.
(K, HCO3, Mg, Ca)
• Colloids
– Albumin
• 5% in NS
• 25% (Salt Poor)
– Dextrans
– Hetastarch
• Blood
16

17. Total body water
ECF=1 liter ICF=0
1 Liter 0.9% saline
Interstitial=3/4
of ECF=750ml
Intravascular
=1/4 ECF=250 ml
17

18. 1 liter 5% Dextose
Total body water=1 liter
ECF=1/3 = 300ml ICF=2/3 = 700ml
Intravascular
=1/4 of ECF~75ml
18

19. 1 liter 5% Albumin
Intravascular=1 liter
19

20. 20
N Engl J Med. 2004 May 27;350(22):2247-56.
A Comparison of Albumin and Saline for Fluid
Resuscitation in the Intensive Care Unit

21. Volume Deficit-Clinical Types
• Total body water:
– Water loss (diabetes insipidus,)
• Extracellular:
– Salt and water loss (secretory diarrhea, ascites, edema)
– Third spacing
• Intravascular:
– Acute hemorrhage
21

22. Clinical Diagnosis
22
• Intravascular depletion(MAP= CO x SVR)
Hemodynamic effects
– BP HR JVP
– Cool extremities
– Reduced sweating
– Dry mucus membranes
• E.C.F. depletion
– Skin turgor, sunken eyeballs
– Weight
– Hemodynamic effects
• Water Depletion
– Thirst
Hypernatremia

23. 23
Example- GI Bleed
A 25 year old patient presents with massive hematemesis
(vomiting blood) x 1 hour. He has a history of peptic ulcer
disease.
Exam: Diaphoretic, normal skin turgor.
Supine BP: 120/70 HR 100
Sitting BP: 90/50 HR=140
Serum Na=140
What is the nature of his fluid deficit ?
What IV fluid resuscitation would you prescribe ?
What do you expect the hematocrit to be :
- at presentation ?
- after 12 hours of Normal Saline treatment?

24. Example-Diarrhea and Vomiting
• A 18 year old previously
healthy medical student
returns from a Caribbean
vacation with a healthy tan
and severe diarrhea and
vomiting x 48 hours.
• Sunken eyeballs, poor skin
turgor and dry mucus
membranes
• BP 80/70 HR 130 supine.
• Labs: Na 130 K=2.8
HCO3 =12
ABG: 7.26/26/100
• What is the nature of
his fluid deficit ?
• What fluid will you
prescribe ?
• What would happen if
D5W were to be used?
24

25. Example-Hyperosmolar State
A 85 year old nursing home resident with dementia, and
known diabetes was admitted with confusion.
Exam: Disoriented
BP: 110/70 supine 90/70 sitting. Decreased skin turgor.
Labs: Na= 150meq/L Wt=50kgs
BUN/Cr=50/1.8 Blood sugar= 1200 mg/dl Hct=45
What is the pathogenesis of her
fluid and electrolyte disorder ?
How would you treat her ?
25

26. Calculation of Water Deficit
Healthy
Osm (P Na) x
volume
Dehydrated
Osm (P Na) x
volume
A 50 kg female with Na=150
•Na x Normal Body Water = Na x Current Body Water
•140 x NBW = 150 x (0.5 x 50=25 liters)
•NBW = 26.8 liters
•Water deficit = NBW-CBW= 26.8-25=1.8 liters
26

27. A Cirrhotic
A 40-year-old patient with known alcoholic cirrhosis, portal
hypertension and ascites is admitted with a rising
creatinine.
Exam: BP 100/70 (no orthostasis), JVP 5cms, +++ascites, no
peripheral edema, +asterixis.
BUN=12mg/dL Creat=2mg/dL Alb=2.0g/dL
Urine lytes: Na=6meq/L, FeNa=0.5%
Urine volume has been 200cc/24h.
1. Comment on his fluid status
2. If volume-depleted how would you treat him?
27

28. Example-Post Op Abdominal Distension
A 60 year old male with pancreatic carcinoma has
undergone total pancreaticoduodenectomy and
gastrojejunal bypass.
On post-operative day-3 he develops abdominal
distension.BP= 110/60 and HR increases from 100 to
130 on sitting. Bowel sounds are absent.
AXR reveals multiple fluid levels in the abdomen. N-G
suction is initiated.
What is the nature of his fluid deficit ?
How will you treat ?
28

29. Surgical Patients
29
prone to disruption
nil orally
anaesthesia
trauma
sepsis

30. Surgical Patients’ Need
30
• Maintenance volume requirements
• On going losses
• Volume deficits

31. 1. Maintenance Requirements
31
• This includes:
– Insensible
– Urinary & stool losses
Body weight
0-10Kg
next 10-20Kg
subsequent Kg
Fluid required
100ml/kg/d
50 ml/kg/d
20ml/kg/d
15ml/Kg/d for elderly

32. 70 Kg Man Needs
32
• 1st 10kg x 100mls = 1000mls
• 2nd 10kg x 50mls = 500mls
• Next 50kg x 20mls=
• TOTAL
1000mls
2500 mls /d

33. 2. On Going Losses
33
• NG
• drains
• fistulae
•third space losses
Concentration is similar to plasma
Replace with isotonic fluids

34. 3. Volume Deficit - Acute
34
• vital signs changes
– Blood pressure
– Heart rate
– CVP
• tissue changes not obvious
• urine output low

35. 3. Volume Deficit - Chronic
35
• Decreased skin turgor
• Sunken eyes
• Oliguria
• Orthostatic hypotension
• High BUN/Creatine ratio
• HCT increases 6-8 points per litre deficit
• Plasma Na may be normal

36. 4. Volume Excess
36
• Over hydration
• Mobilisation of third space losses
Signs
weight gain
pulmonary edema
peripheral edema
S3 gallop

37. Fluid and Electrolyte Therapy
37
Goal
normal haemodynamic parameters
normal electrolyte concentration
Method
replace
normal maintenance requirements
ongoing losses
deficits

38. Normal maintenance requirements
use BW formula
On going losses
measure all losses in I/O chart
estimate third space losses
Deficits
estimate using vital signs
estimate using HCT
38

39. The best estimate of the volume
required is the patients response.
39
After therapy started observe
vital signs
Urine output (0.5mls/Kg/hr)
Central venous pressure

40. Time Frame for Replacement
40
• Usually correct over 24 hours
• For ill patients calculate over
shorter period and reassess e.g. 1,
2 hours or 3 hours for e op cases
• Deficits - correct half the amount
over the short period and reassess

41. Preoperative Management
41
• Pre-existing volume and electrolyte
abnormalities should be corrected
before operation whenever possible.
• Consideration of duration and route of
loss provides important information
regarding the extent of fluid and
electrolyte abnormalities.

42. Intraoperative Fluid Management
42
• requires replacement of
– preoperative deficit as well as ongoing losses.
• Intraoperative losses include maintenance
fluids for the duration of the case,
hemorrhage, and “third-space losses.”
• Acute blood loss can be replaced with a
volume of crystalloid that is three to four times
the blood loss or with an equal volume of
colloid or blood.

43. Intraoperative Fluid Management
43
• Intraoperative insensible and third-
space fluid losses depend on
– the size of the incision and
– the extent of tissue trauma and dissection
and
• can be replaced with an appropriate
volume of lactated Ringer's solution.

44. Intraoperative Fluid Management
44
• Small incisions with minor tissue trauma (e.g.,
inguinal hernia repair) result in third-space losses of
approximately 1 to 3 mL/kg/hour.
• Medium-sized incisions with moderate tissue trauma
(e.g., uncomplicated sigmoidectomy) result in third-
space losses of approximately 3 to 7 mL/kg/hour.
• Larger incisions and operations with extensive tissue
trauma and dissection (e.g.,
pancreaticoduodenectomy) can result in third-space
losses of approximately 9 to 11 mL/kg/hour or
greater.

45. 45
Postoperative Fluid Management
• Sequestration of extracellular fluid into the
sites of injury or operative trauma can
continue for 12 or more hours after operation.
• Urine output should be monitored closely and
intravascular volume repleted to maintain a
urine output of 0.5 to 1 mL/kg/hour.
• GI losses that exceed 250 mL/day from
nasogastric or gastrostomy tube suction
should be replaced with an equal volume of
crystalloid.

46. 46
Postoperative Fluid Management
• Mobilization of perioperative third-space
fluid losses typically begins 2 to 3 days
after operation.
• Anticipation of postoperative fluid shifts
should prompt careful evaluation of the
patient's volume status and, if needed,
consideration of diuresis before the
development of symptomatic
hypervolemia

47. Postoperative Fluid Therapy
47
• Check i/v regime ordered in op form
• Assess for deficits by checking I/O chart and
vital signs
• Maintenance requirements calculated
• Usually K not started
• Monitor carefully vital signs and urine output

48. Postoperative Fluid Management
48
• Urine specific gravity may be used
(1.010 - 1.012)
• CVP useful in difficult situations
(5-15 cm H20)
• Body weight measured in special
situation e.g. burns

49. Postoperative Fluid Management
49
• changes in plasma Na are indicative of
abnormal TBW
• losses in surgery are usually isotonic
• hypoosmolar condition usually caused
by replacement with free water

50. Conclusions
50
• Crystalloids are generally adequate for most
situations needing fluid management.
• The composition of the solution and rate of
administration are important when addressing
a specific situation.
• Colloids may be indicated when more rapid
hemodynamic equilibration is required
(inadequate data).

51. 51
Sodium
• The normal individual consumes 3 to 5 g of
NaCl (130 to 217 mmol Na+)/day.
• Balance is maintained primarily by the
kidneys.
• Normal Na+ concentration is 135 to 145
mmol/L (310 to 333 mg/dL).
• Potential sources of significant Na+ loss
include sweat, urine, and gastrointestinal (GI)
secretions.
• The Na+ concentration largely determines the
plasma osmolality (Posm)

52. Hyponatraemia
52
• defined as a serum sodium concentration of
<135 mmol/l after the exclusion of
"pseudo-hyponatraemia".
• The most common electrolyte disorder
• Reported incidence of 15–30%.
• diagnostic and management problems
• Both over-correction and under-treatment can
produce devastating effects on cerebral
function.

53. REGULATION OF SODIUM
53
AND WATER BALANCE

54. • Water homoeostasis is closely related to
– serum osmolarity and
– sodium concentration.
• Water homoeostasis is controlled by thirst,
vasopressin and the kidneys.
• The normal plasma osmolarity is 275–295
mosm/l.
• plasma osmolarity =2 x (Na+K) + urea +
glucose
54

55. Pseudo-hyponatraemia
55
• In this condition, increases in the non-
aqueous components of plasma such
as in hypertriglyceridaemia or
hyperproteinaemia result in a
spuriously low sodium concentration.

56. CLASSIFICATION OF
HYPONATRAEMIA
56
Hyponatraemic disorders are
divided into euvolaemic,
hypovolaemic and hypervolaemic
.

57. Hypovolaemic hyponatraemia:
reduced ECF
57
• Renal loss of sodium
and water; urine Na >20
mmol/day
– Diuretic use
– Salt wasting
nephropathy
– Cerebral salt wasting
– Mineralocorticoid
deficiency/adrenal
insufficiency
– Renal tubular acidosis
• Extrarenal loss of
sodium and water with
renal conservation;
urine Na <20 mmol/day
– Burns
– Gastrointestinal loss
– Pancreatitis
– Blood loss
– 3rd space loss (bowel
obstruction, peritonitis)

58. Hypervolaemic hyponatraemia:
58
expanded ICF & ECF but reduced
effective arterial blood volume
• Causes:
– Congestive cardiac failure
– Cirrhosis
– Nephrotic syndrome

59. Euvolaemic hyponatraemia:
59
expanded ICF & ECF but
oedema absent
• Thiazide diuretics (can be euvolaemic or
hypovolaemic)
• Hypothyroidism
• Adrenal insufficiency (can be euvolaemic or
hypovolaemic)
• SIADH
• Decreased solute ingestion
– (beer potomania/tea and toast diet)

60. SIADH
60
• cancer,
• central nervous system disorders,
• drugs,
• pulmonary disease,
• nausea,
• postoperative pain,
• HIV, infection,
• Guillain-Barre syndrome,
• acute intermittent porphyria

61. SIADH
61
• most common form of hyponatraemia in
hospital patients,
• SIADH is a diagnosis of exclusion.
• Despite the expansion of fluid
compartments, the patient is not
oedematous clinically
• and therefore the term euvolaemic is
applied.

62. The diagnostic criteria for SIADH
62
• hyponatraemia with low serum
osmolarity (<270 mosm/l) and
• an inappropriately high urine osmolarity
of >100 mosm/kg
• in a euvolaemic patient in whom
• hypopituitarism, hypoadrenalism,
hypothyroidism, renal insufficiency and
diuretic use have been excluded.

63. Hyponatremia
63

64. ECF volume
64

65. Postoperative
hyponatraemia
65
• Careful assessment of premedication,
intraoperative records, fluid charts and
anaesthetic records is imperative.
• Drug therapy, surgical procedures and pain
are all causes of SIADH.
• Sodium picosulphate bowel preparation
before colonic surgery
– may cause dehydration and electrolyte disorders,
including hyponatraemia.

66. Postoperative
hyponatraemia
66
• The intravenous administration of
large volumes of
• 5% dextrose
• is a common cause of postoperative
hyponatraemia.

67. Isotonic hyponatremia
67
• Hyperlipidemic and hyperproteinemic states result in
– an isotonic expansion of the circulating plasma volume and
cause a decrease in serum Na+ concentration,
– although total body Na+ remains the same.
• The reduction in serum sodium (mmol/L) can be
estimated by multiplying the measured plasma lipid
concentration (mg/dL) by 0.002 or the increment in
serum protein concentration above 8 g/dL by 0.25.
• Isotonic, sodium-free solutions of glucose, mannitol,
and glycine are restricted initially to the extracellular
fluid and may similarly result in transient
hyponatremia

68. Hypertonic hyponatremia
68
• Hyperglycemia may result in transient fluid
shift from the intracellular to the extracellular
compartment, thus diluting the serum Na+
concentration.
• The expected decrease in serum Na+ is
approximately 1.3 to 1.6 mmol/L (2.99 to 3.68
mg/dL) for each 100-mg/dL increase in blood
glucose above 200 mg/dL.
• Rapid infusion of hypertonic solutions of
glucose, mannitol, or glycine may have a
similar effect on Na+ concentration

69. Hypotonic hyponatremia
69
• is classified on the basis of extracellular
fluid volume.
• generally develops as a consequence of
the administration and retention of
hypotonic fluids [e.g., dextrose 5% in
water (D5W), 0.45% NaCl] and
• rarely from the loss of salt-containing
fluids alone.

70. Hypotonic hyponatremia
70
• Hypovolemic hypotonic hyponatremia
– in the surgical patient most commonly results from
replacement of sodium-rich fluid losses (e.g., from
the GI tract, skin, or lungs) with an insufficient
volume of hypotonic fluid (e.g., D5W, 0.45%
NaCl).
• Hypervolemic hypotonic hyponatremia.
– The edematous states of congestive heart failure,
liver disease, and nephrosis occur in conjunction
with inadequate circulating blood volume.
– This serves as a stimulus for the renal retention of
sodium and of water. Disproportionate
accumulation of water results in hyponatremia.

71. Hypotonic hyponatremia
71
• Isovolemic hypotonic hyponatremia
• Water intoxication
• K+ loss
• Reset osmostat
• SIADH

72. Clinical manifestations
72
• predominantly neurologic and result from
hypoosmolality.
• A decrease in Posm causes intracellular water influx,
increased intracellular volume, and cerebral edema.
• lethargy, confusion, nausea, vomiting, seizures, and
coma.
• Chronic hyponatremia is often asymptomatic until the
serum Na+ concentration falls below 110 to 120
mEq/L (253 to 276 mg/dL).
• An acute drop in the serum Na+ concentration to 120
to 130 mEq/L (276 to 299 mg/dL), conversely, may
produce symptoms.

73. Treatment
73
• Isotonic and hypertonic hyponatremia
– correct with resolution of the underlying disorder.
• Hypovolemic hyponatremia
– 0.9% NaCl to correct volume deficits and replace
ongoing losses.
• Water intoxication
– responds to fluid restriction (1,000 mL/day).
• SIADH
– water restriction (1,000 mL/day) should be
attempted initially.
– a loop diuretic (furosemide) or an osmotic diuretic
(mannitol) may be necessary in refractory cases.

74. • Hypervolemic hyponatremia
– may respond to water restriction (1,000 mL/day) to return
Na+ to greater than 130 mmol/L (299 mg/dL).
• In cases of severe congestive heart failure,
optimizing cardiac performance may assist in Na+
correction.
– plasma Na+ can be increased to a safe level by the use of a
loop diuretic (furosemide) while replacing urinary Na+ losses
with 3% NaCl.
– A reasonable approach is to replace approximately 25% of
the hourly urine output with 3% NaCl.
• Hypertonic saline should not be administered to
these patients without concomitant diuretic therapy.
74

75. • In extreme hyponatremia [Na+ <110 mmol/L (253
mg/dL)]
– hypertonic saline (3% NaCl) is indicated
– Each liter of 3% NaCl provides 513 mmol Na+
– Serum Na+ should be corrected to approximately 120
mmol/L (276 mg/dL).
• The quantity of 3% NaCl can be estimated by
calculating the Na+ deficit:
• Na+ deficit (mmol) = 0.60 ×lean body weight (kg)
×[120 - measured serum Na+ (mmol/L)].
75

76. Central pontine demyelination
76
• The serum Na+ should be increased by no more than
12 mmol/L (27.6 mg/dL) in 24 hours of treatment [i.e.,
Na+ <0.5 mmol (1.15 mg/dL)/hour].
• For acute hyponatremia (<48 hours), the serum Na+
may be corrected more rapidly [i.e., Na+ = 1 to 2
mmol (2.3 to 4.6 mg/dL)/hour].
• The patient's volume status should be carefully
monitored and the serum Na+ should be determined
frequently (every 1 to 2 hours).
• Once the serum Na+ concentration reaches 120
mmol/L (276 mg/dL) and symptoms have resolved,
administration of hypertonic saline can be
discontinued.

77. Hypernatremia
77
• uniformly hypertonic and typically the
result of water loss in excess of solute

78. 7
8
Diagnostic approach to
hypernatremia

79. Clinical manifestations
79
• Symptoms of hypernatremia that are
related to the hyperosmolar state are
primarily neurologic.
• lethargy, weakness, and irritability and
• may progress to fasciculations,
seizures, coma, and irreversible
neurologic damage.

80. Treatment
80
• Water deficit associated with hypernatremia:
• Water deficit (L) = 0.60 ×total body weight (kg) ×[(serum Na+
in mmol/L/140) = 1].
• Rapid correction- cerebral edema and permanent neurologic
damage.
• Consequently, only one half of the water deficit should be
corrected over the first 24 hours, with the remainder being
corrected over the following 2 to 3 days.
• Serial Na+ determinations
• Oral fluid intake is acceptable for replacing water deficits.
• If oral intake is not possible, D5W or D5/0.45% NaCl can be
substituted.

81. Potassium
81

82. • major intracellular cation,
• with only 2% of total body K+ located in
the extracellular space.
• The normal serum concentration is 3.3
to 4.9 mmol/L (12.9 to 19.1 mg/dL).
82

83. Hypokalaemia
83
• GI losses (e.g., diarrhea, persistent vomiting,
nasogastric suctioning),
• renal losses (e.g., diuretics, fluid mobilization,
amphotericin B), and
• cutaneous losses (e.g., burns).
• acute intracellular K+ uptake
– associated with insulin excess, metabolic alkalosis,
myocardial infarction, delirium tremens, hypothermia,
and theophylline toxicity).
• in the malnourished patient after initiation of total
parenteral nutrition (refeeding syndrome),
– caused by the incorporation of K+ into rapidly dividing
cells.

84. Clinical manifestations.
84
• Mild hypokalemia [K+ >3 mmol/L (11.7
mg/dL)] is generally asymptomatic.
• The symptoms present with severe K+
deficiency [K+ <3 mmol/L (11.7 mg/dL)]
– Early ECG manifestations- ectopy, T-wave
depression, and prominent U waves.
– Severe depletion increases susceptibility to
reentrant arrhythmias.

85. Treatment
85
• In mild hypokalemia, oral replacement is
suitable.
• 40 to 100 mmol (156 to 390 mg) KCl orally in
single or divided doses.
• Parenteral therapy is indicated in the
presence of severe depletion, significant
symptoms, or oral intolerance.
– in peripherally administered intravenous fluids
should not exceed 40 mmol/L (156 mg/dL),
– the rate of administration should not exceed 20
mmol (78 mg)/hour.

86. • higher K+ concentrations [60 to 80 mmol/L (234 to
312 mg/dL)] administered more rapidly (with cardiac
monitoring)
– are indicated in cases of severe hypokalemia, for cardiac
arrhythmias, and in the management of diabetic
ketoacidosis.
• Administration of high K+ concentrations via
subclavian, jugular, or right atrial catheters should be
avoided because local K+ concentrations may be
cardiotoxic.
• Hypomagnesemia frequently accompanies
hypokalemia and generally must be corrected to
successfully replenish K+. 86

87. Hyperkalemia
87

88. Causes
88
• Abnormal redistribution of K+ from the
intracellular to the extracellular
compartment may occur as a result of
– insulin deficiency,
– β-adrenergic receptor blockade,
– acute acidemia,
– rhabdomyolysis, cell lysis (after
chemotherapy),
– digitalis intoxication,
– reperfusion of ischemic limbs, and
– succinylcholine administration.

89. 89
Clinical manifestations.
• Mild hyperkalemia [K+ = 5 to 6 mmol/L is
generally asymptomatic.
• Signs of significant hyperkalemia [K+ >6.5
mmol/L are, most notably, ECG
abnormalities:
• symmetric peaking of T waves, reduced P-
wave voltage, and widening of the QRS
complex.
• If untreated, severe hyperkalemia ultimately
may cause a sinusoidal ECG pattern.

90. 90
Treatment
• Mild hyperkalemia [K+ = 5 to 6 mmol/L
– reduction of daily K+ intake
– loop diuretic e.g., furosemide
• Any medication that is capable of impairing
K+ homeostasis should be discontinued, if
possible.
– nonselective β-adrenergic antagonists,
– angiotensin-converting enzyme inhibitors,
– K+-sparing diuretics,
– nonsteroidal anti-inflammatory drugs

91. • Severe hyperkalemia K+ >6.5 mmol/L
• NaHCO3 [1 mmol/kg or 1 to 2 ampules (50
mL each) of 8.4% NaHCO3]
– intravenously over a 3- to 5-minute period.
– can be repeated after 10 to 15 minutes if ECG
abnormalities persist.
• Dextrose (0.5 g/kg body weight) infused with
insulin (0.3 unit of regular insulin/g of
dextrose)
– transiently lowers serum K+ (the usual dose is 25
g dextrose, with 6 to 10 units of regular insulin
given simultaneously as an intravenous bolus)
91

92. • Inhaled β-agonists [e.g., albuterol sulfate, 2 to
4 mL of 0.5% solution (10 to 20 mg) delivered
via nebulizer]
– lower plasma K+, with a duration of action of up to
2 hours.
• Calcium gluconate 10% (5 to 10 mL
intravenously over 10 minutes)
– to patients with profound ECG changes
– who are not receiving digitalis preparations.
– Calcium functions to stabilize the myocardium.
92

93. Increasing potassium
excretion
93
– Sodium polystyrene sulfonate (Kayexalate), a
Na+-K+ exchange resin,
• orally or rectally to promote K+ elimination.
• A decrease in serum K+ level typically occurs 2 to 4
hours after administration.
– Hydration with 0.9% NaCl in combination with a
loop diuretic
• furosemide, 20 to 100 mg IV to patients with adequate
renal function to promote renal K+ excretion.
– Dialysis is definitive therapy in severe, refractory,
or life-threatening hyperkalemia.

94. Guidelines for Treatment of
94
Adult Patients With
Hyperkalemia
• Stop all infusion of potassium
• ECG EVIDENCE OF PENDING ARREST:
– Loss of P wave and broad slurring of QRS;
• immediate effective therapy indicated
• 1. IV infusion of calcium salts 10 mL of 10%
calcium chloride over a 10-minute period or 10 mL of
10% calcium gluconate over a 3- to 5-minute period
• 2. IV infusion of sodium bicarbonate 50-100 mEq
over a 10- to 20-minute period; benefit proportional to
extent of pretherapy acidemia

95. • ECG EVIDENCE OF POTASSIUM
EFFECT:
• Peaked T waves;
• prompt therapy needed
• 1. Glucose and insulin infusion IV
infusion of 50 mL of D50W and 10 units
of regular insulin; monitor glucose
• 2. Immediate hemodialysis
95

96. 96
• Biochemical evidence of hyperkalemia
and no ECG changes:
• Effective therapy needed within hours
• 1. Potassium-binding resins into the
gastrointestinal tract, with 20%
sorbitol
• 2. Promotion of renal kaliuresis by
loop diuretic D50W, 50% dextrose in
water

97. 97

98. ISOTONIC SOLUTIONS
98
• 0.9% Normal Saline
• D5W 5 % Dextrose*
• D51/4NS 5% Dextrose 0.2% NS
• D51/3NS 5% Dextrose 0.3% NS
• LR or RL Lactated Ringers Solution

99. HYPERTONIC SOLUTIONS
99
• 3% N S
• 5 % N S
• D 10 W
• D 20 W
• D5 ½ NS
3% Normal saline
5% Normal Saline
Dextrose 10% in water
Dextrose 20% in Water
5%Dextrose,with 0.45% Normal
Saline
5% Dextrose with 0.9% Normal
• D5NS
Saline
• D5LR
Ringers
5% Dextrose with Lactated

100. HYPOTONIC SOLUTIONS
100
• 1/3 N S
• 1/2 N S
• D 2.5 W
0.33% Normal
Saline
0.45% Normal
Saline
Dextrose 2.5%
in water

101. QUESTIONS
101