fluids.ppt

Fluids and Electrolytes
Ahmed Mayet, Pharm.D., BCPS
Associate Professor
KSU

Learning Objectives
 Total Body Fluid
 Intravascular Volume Depletion
 Fluid resuscitation vs. Maintenance IV Fluid
 Osmolarity of IV Fluids
 Hyponatremia
 Hypernatremia
 Hypokalemia
 Hyperkalemia
 Hypomagnesemia
 Hpermagmesemia

 Hypophosphatemia
 Hyperphosphatemia
 Hypocalcemia
 Hypercalcermia

Fluids
 Body weight of
 adult male 55-60%
 Female 50-55%
 Newborn 75-80%
 Very little in adipose tissues
 Loss of 20% - fatal
 Elderly - decreases to 45-50% of body weight
 Decreased muscle mass, smaller fat stores,
and decrease in body fluids
4

Body Fluid Compartments:
ICF:
28L
Intravascular
plasma
5.6L
Extravascular
Interstitial
Fluid
8.4L
TBW
ECF
3/4
1/4
2/3
1/3

Compartments
 Intracellular (ICF)
 Fluid within the cells themselves
 2/3 of body fluid
 Located primarily in skeletal muscle mass
 High in K, Po4, protein
 Moderate levels of Mg
6

Compartments
 Extracellular (ECF)
 1/3 of body fluid
 Comprised of 3 major components
 Intravascular
 Plasma
 Interstitial
 Fluid in and around tissues
 Transcellular
 Over or across the cells
7

Compartments
 Extracellular
 Nutrients for cell functioning
 Na
 Ca
 Cl
 Glucose
 Fatty acids
 Amino Acids
8

Compartments
 Intravascular Component
 Plasma
 fluid portion of blood
 Made of:
 water
 plasma proteins
 small amount of other substances
9

Compartments
 Interstitial component
 Made up of fluid between cells
 Surrounds cells
 Transport medium for nutrients, gases, waste
products and other substances between blood
and body cells
 Back-up fluid reservoir
10

Compartments
 Transcellular component
 1% of ECF
 Located in joints, connective tissue, bones,
body cavities, CSF, and other tissues
 Potential to increase significantly in abnormal
conditions
11

ICF:
28L
Intravascular
plasma
5.6L
Extravascular
Interstitial
Fluid
8.4L
TBW
ECF
3/4
1/4
 Male 60% of LBW is fluid
 female 50% of LBW is fluid
 70 kg male
 BW x 0.6 = TBW
 70kg x 0.6 = 42 L
 ICF= 2/3 x 42 = 28L
 ECF= 1/3 x 42 = 14L
 ECF
 1/4 is intravascular plasma
 1/4 x 14 = 5.6L
 3/4 is interstitial
 3/4 x 14 = 8.4L
2/3
1/3

Water Steady State
 Amount Ingested = Amount Eliminated
• Pathological losses
vascular bleeding (H20, Na+)
vomiting (H20, H+)
diarrhea (H20, HCO3-).

Fluid Requirement
 The average adult requires approximately 35-
45 ml/kg/d
 NRC* recommends 1 to 2 ml of water for each
kcal of energy expenditure
*NRC= National research council

Fluid Requirement
 1st 10 kilogram 100 cc/kg
 2nd 10 kilogram 50 cc/kg
 Rest of the weight 20 to 30 cc/kg
Example: 50 kg patient
1st 10 kg x 100cc = 1000 cc
2nd 10 kg x 50cc = 500cc
Rest 30 kg x 30cc = 900cc
total = 2400 cc

Fluid
 Fluid needs are altered by the patient's
functional cardiac, hepatic, pulmonary, and
renal status
 Fluid needs increase with fever, diarrhea,
hemorrhage, surgical drains, and loss of skin
integrity like burns, open wounds

Regulation of Fluids:
Response to Decreased volume and Blood pressure

Regulation of Fluids:
Response to increased volume and Blood pressure

Causes of Hypovolemia
 Hypovolemia
 Abnormally low volume of body fluid in
intravascular and/or interstitial
compartments
 Causes
 Vomiting
 Diarrhea
 Excess sweating
 Diabetes insipidus
 Uncontrolled diabetes mellitus

Other Causes of Water Loss
 Fever
 Burns
 N-G Suction
 Fistulas
 Wound drainage

Signs and Symptoms
 Acute weight loss
 Decreased skin turgor
 Concentrated urine
 Weak, rapid pulse
 Increased capillary filling time
 Sensations of thirst, weakness, dizziness,
muscle cramps

Signs of Hypovolemia:
 Diminished skin turgor
 Dry oral mucus membrane
 Oliguria
- <500ml/day
- normal: 0.5~1ml/kg/h
 Tachycardia (100 beats/min)
 Hypotension (SBP < 90 mm Hg)
 Hypoperfusion  cyanosis
 Altered mental status

Clinical Diagnosis of Hypovolemia:
 Thorough history taking: poor intake, GI
bleeding…etc
 BUN : Creatinine > 20 : 1
 Increased specific gravity
 Increased hematocrit
 Electrolytes imbalance
 Acid-base disorder

Labs
 Increased HCT
 Increased BUN out of proportion to Cr
 High serum osmolality
 Increased urine osmolality
 Increased specific gravity
 Decreased urine volume, dark color
26

Complications
 Reduced cardiac function, organ hypo
perfusion and multi-organ failure, renal
failure, shock and death.

Fluid Replacement
 Crystalloids
Normal saline (0.9% NaCl)
Dextrose 5%
 Colloids
Albumin 5%, 25%
Hetastarch

Parenteral Fluid Therapy:
 Crystalloids: (0.9% NaCl)
Contain Na, and Cl as the main osmotically active
particle do not freely cross into cells but they will
distribute evenly in the EC ( IV + IT)
 Crystalloids: (D5W)
D5W - H2O + CO2
Water will distribute in TBW

ICF:
28L
Intravascular
plasma
5.6L
Extravascular
Interstitial
Fluid
8.4L
TBW
ECF
3/4
1/4
2/3
1/3
If 1 liter of NS is given, only 250 ml will
stay in intravascular.
1000ml x 1/4 = 250 ml (Intravascular)
1000ml x 3/4 = 750 ml (Interstitial)
If 1 liter of D5W is given, only
about 100 ml will stay in
intravascular.
1000ml x 2/3 = 667ml (ICF)
1000ml x 1/3 = 333 ml (ECF)
333 ml x 1/4 = 83 ml (IV)
333 ml x 3/4 = 250 ml (IT)

Crystalloids:
 Isotonic crystalloids
- Lactated Ringer’s, 0.9% NaCl
- only 25% remain intravascularly
 Hypotonic solutions
- D5W
- less than 10% remain intra-
vascularly, inadequate for fluid
resuscitation

Colloid Solutions:
 Contain high molecular weight
substances too large to cross capillary walls
 Preparations
- Albumin: 5%, 25%
- Dextran
- Hetastrach

ICF:
28L
Intravascular
plasma
5.6L
Extravascular
Interstitial
Fluid
8.4L
TBW
ECF
3/4
1/4
2/3
1/3
If 1 liter of 5% albumin is given, all will
stay in intravascular because of its large
molecule that will not cross cell
membrance.
1000ml x 1 = 1000 ml
If 100 ml of 25% albumin is given,
it will draw 5 times of its volume in
to intravascular compartment.
100ml x 5 = 500 ml

The Influence of Colloid & Crystalloid on Blood
Volume:
1000cc
500cc
500cc
100cc
200 600 1000
NS or Lactated Ringers
5% Albumin
6% Hetastarch
25% Albumin
Blood volume
Infusion
volume

Fluid Resuscitation
 Calculate the fluid deficit base on serum sodium level
(assume patient Na is 120 mmole/l and patient
weight is 70 kg)
Fluid deficit = BW x 0.5 ( Avg Na – pt Na )
Na avg
= 70 x 0.5 ( 140 – 120)
140
= 5 L

Fluid Resuscitation
 Calculate the fluid deficit base on patient actual
weight
if you know the patient weight before the
dehydration then simply subtract patient current
weight from patient previous weight
Pt wt before dehydration – pt current wt
Exp if pt weight was 70 kg before and now pt weight
65 kg then
70 kg – 65 kg = 5 kg equal to 5 L of water loss (s.g for
water is 1)

Fluid Resuscitation
 Use crystalloids (NS or Lactate Ranger)
 Colloids is not superior to crystalloids
 Administer 500-1000 ml/hr bolus(30-60 mins) and
then 250-500 ml/hr for 6 to 8 hours and rest of the
fluid within 24 hours
 Maintain IV fluid (D5 ½ NS) until vital signs are
normalized and patient is able to take adequate oral
fluid

Regulation of Fluids in Compartments
 Osmosis
 Movement of water through a selectively
permeable membrane from an area of low solute
concentration to a higher concentration until
equilibrium occurs
 Movement occurs until near equal concentration
found
 Passive process
38

Regulation of Fluids
 Diffusion
 Movement of solutes from an area of
higher concentration to an area of lower
concentration in a solution and/or across a
permeable membrane (permeable for that
solute)
 Movement occurs until near equal state
 Passive process
40

Osmosis versus Diffusion
 Osmosis
 Low to high
 Water potential
 Diffusion
 High to low
 Movement of particles
 Both can occur at the same time
42

Regulation of Fluids
 Active Transport
 Allows molecules to move against
concentration and osmotic pressure to
areas of higher concentration
 Active process – energy is expended
43

Active Transport
 Na / K pump
 Exchange of Na ions for K ions
 More Na ions move out of cell
 More water pulled into cell
 ECF / ICF balance is maintained
44

Active Transport
 Insulin and glucose regulation
 CHO consumed
 Blood glucose peaks
 Pancreas secretes insulin
 Blood glucose returns to normal
46

Osmolarity
 Concentration of body fluids – affects
movement of fluid by osmosis
 Reflects hydration status
 Measured by serum and urine
 Solutes measured - mainly urea, glucose,
and sodium
 Measured as solute concentration/L
47

Osmolarity
 Serum Osm/L = (serum Na x 2) + BUN/3 +
Glucose/18
 Serum Osm/L = (serum Na x 2) + BUN +
Glucose
 Normal serum value - 280-300 mOsm/L
 Serum <240 or >320 is critically abnormal
 Normal urine Osm – 250 – 900 mOsm / L
48

Factors that affect Osmolarity
 Serum
 Increasing Osm
 Free water loss
 Diabetes Insipidus
 Na overload
 Hyperglycemia
 Uremia
49

 Serum
 Decreasing Osm
 SIADH
 Renal failure
 Diuretic use
 Adrenal insufficiency
50

 Urine
 Increasing Osm
 Fluid volume deficit
 SIADH
 Heart Failure
 Acidosis
52

Factors that affect Osmolality
 Urine
 Decreasing Osm
 Diabetes Insipidus
 Fluid volume excess
 Urine specific gravity
 Factors affecting urine Osm affect urine specific
gravity identically
53

Fluid Volume Shifts
 Fluid normally shifts between intracellular and
extracellular compartments to maintain equilibrium
between spaces
 Fluid not lost from body but not available for use in
either compartment – considered third-space fluid
shift (“third-spacing”)
 Enters serous cavities (transcellular)
54

Causes of Third-Spacing
 Burns
 Peritonitis
 Bowel obstruction
 Massive bleeding into joint or cavity
 Liver or renal failure
 Lowered plasma proteins
 Increased capillary permeability
 Lymphatic blockage
55

Assessment of Third-Spacing
 More difficult – fluid sequestered in deeper structures
 Signs/Symptoms
 Decreased urine output with adequate intake
 Increased HR
 Decreased BP, CVP
 Increased weight
 Pitting edema, ascites
57

Osmolarity
 Isotonic solution
 Hypotonic solution
 Hypertonic solution

Osmolarity
 Plasma osmolarity
pOsm = Na + Cl + BUN + Glucose
exp: if pt Serum Na = 145 mmol/l
and Glucose is 6 mmole/l and
B BUN is 6 mole/l, then osmolarity of
serum is
145 + 145 + 6 + 6 = 302

Osmolarity
 Calculate the osmolarity of 1L NS?
MW of Na = 23, Cl = 35.5
0.9% NaCL of 1 L
9 gm NaCl
9/23+35.5 = 0.154 mole (154 mmole)
1 mole of NaCl = 1 mole Na + 1 mole CL
= 2
154 mmole/l x 2 =308

Osmolarity
 Calculate the osmolarity of 1L 3%NaCl?
MW of Na = 23, Cl = 35.5
3% NaCL of 1 L
30 gm NaCl
30/23+35.5 = 0.154 mole (513 mmole)
1 mole of NaCl = 1 mole Na + 1 mole CL
= 2
513 mmole/l x 2 =1026

Osmolarity
 Calculate the osmolarity of 1L D5W?
MW of dextrose 180
D5W of 1 L
50 gm dextrose
50/180 = 0.278 mole (278 mmole)
278 mmole/l x 1 =278 mosm/l

Osmolarity
 Calculate the osmolarity of D5WNS?

Osmolarity
 What happen if you infuse hypotonic
solution?
RBC will
swell and
rapture
Also will
cause brain
edema

Osmolarity
 What happen if you infuse hypertonic solution
to you RBC?
RBC will
shrink and will
not carry
oxygen
properly

Solutions Volumes Na+ K+ Ca2+ Mg2+ Cl- HCO3
- Dextrose mOsm/L
ECF 142 4 5 103 27 280-310
Lactated
Ringer’s
130 4 3 109 28 273
0.9% NaCl 154 154 308
0.45% NaCl 77 77 154
D5W
D5/0.45%
NaCl
77 77 50 406
3% NaCl 513 513 1026
6%
Hetastarch
500 154 154 310
5% Albumin 250,500
130-
160
<2.5
130-
160
330
25%
Albumin
20,50,100
130-
160
<2.5
130-
160
330
Common parenteral fluid therapy

Hypervolemia
 Excess fluid in the extracellular compartment
as a result of fluid or Na retention when
compensatory mechanisms fail to restore
fluid balance or from renal failure

Causes
 Cardiovascular – Heart failure
 Urinary – Renal failure
 Hepatic – Liver failure, cirrhosis
 Other –Drug therapy (i.e., corticosteriods),
high sodium intake, protein malnutrition

Signs/Symptoms
 Physical assessment
 Weight gain
 Distended neck veins
 Periorbital edema, pitting edema
 Adventitious lung sounds (mainly crackles)
 Mental status changes
 Generalized or dependent edema
71

Sign and Symptoms
 Tachycardia
 Tachypnea
 Dyspnea
 S3 gallop (added heart sound)
 Increase CVP and PCWP
 Raise JVP (distended neck vein)
 Weight gain

Lab Abnormalities
Lab data
 ↓ Hct (dilutional)
 Low serum osmolality
 Low specific gravity
 ↓ BUN (dilutional)

Signs / Sympotms
 Radiography
 Pulmonary vascular congestion
 Pleural effusion
 Pericardial effusion
 Ascites
74

Management
 Sodium restriction with no more than 2
grams of salt per day
 Fluid restriction if necessary
 Diuretic
1. Furosemide dose and route depends on
patient condition and underlining diseases

IV Loop diuretic (Furosemide)
 Patient with a cute CHF with pulmonary
edema and difficult in breathing
 Patient with a cute or chronic renal failure
with massive fluid overload
 Patient with liver cirrhosis and refractory to
oral diuretic (furosemide)
 Dose can be range from 80-240 mg/day
 Can be bolus in divided doses or continuous
infusion range from 5-10mg/hour

Monitoring Parameters
 Fluid intake and output (trying to create at
least 1-2 liters of negative fluid balance)
 Patient weight
 Monitor the vital sign BP, RR, PR
 ABG or oxygen saturation
 Chest auscultation If dyspnea or orthopnea
 Urea and electrolytes ( make sure that patient
does not develop renal impairment or
hyponatremia or hypokalemia

Composition of Body Fluids and electrolytes:
Ca+ 2
Mg +2
K+
Na+
Cl-
PO4
3-
Organic
anion
HCO3
-
Protein
0
50
50
100
150
100
150
Cations Anions
ECF
ICF

Sodium
 Normal 135-145 mEq/L
 Major cation in ECF
 Regulates voltage of action potential;
transmission of impulses in nerve and muscle
fibers
 Main factors in determining ECF volume
 Helps maintain acid-base balance

Hyponatremia
 Results from excess Na loss or water gain
 GI losses (vomiting and diarrhea)
 Diuretic therapy
 Severe renal dysfunction (ATN)
 Administration of hypotonic fluid (1/2NS)
 DKA, HHS
 Unregulated production of ADH (pneumonia,
brain trauma, lung cancer etc)
 Some drugs (Li, thiazide)

Sign and Symptoms
 Clinical manifestations
 ↓ BP
 Confusion, nausea, malaise, vomiting
 Lethargy and headache (115-120 mmol/l)
 Seizure and coma (110-115 mmol/l)
 Decreased muscle tone, twitching and tremors
 Cramps

Assessment
 Labs
 Decreased Na, Cl, Bicarbonate
 Urine specific gravity ↓ 1.010
Estimated Na deficit (calculation)
Na deficit = 0.6 x LBW (140 – patient serum Na)
Exp: if patient is 70 kg and his serum Na=120
= 0.6 x 70 (140 – 120)
= 42 x 20
= 840 mmole

Pseudohyponatremia
 Na content in the body is not actually
reduced, but rather, it shifts from the eC
compartment into the cells to maintain
plasma osmolarity in a normal range.
 Severe hyperlipidemia
 Severe hyperglycemia
 Every 100 mg above normal glucose add 1.6
mmole to Na value

Treatment
 Interventions
 If patient is normovolemic or edematous
 Fluid restriction
 If patient is intravascular volume depletion
 IV 0.9% NS or LR
 Avoid rapid Na correction
 A change of no more than 10-12 mmole/day
 Raid correction of Na can cause central pontine
myelinolysis and death
 120-125 mmole/l is a reasonable goal and safe

 HS should be given through central
intravenous access because the osmolarity is
greater than 900 mOsm/l.1.
 Some practitioners use 3% Hs through a
peripheral intravenous access site in an
emergency situation because the osmolarity
is close to the cutoff range for peripheral
administration.
 If a peripheral site is used, monitor for
phlebitis and obtain central access as soon
as possible.

Central pontine myelinolysis and death

Hypertonic Saline 3% NaCl
 Use in patient with symptomatic hyponatremia such
as in seizure, comatose patient, or patient with brain
edema
 3% NaCl 250ml with an infusion rate of 1-2ml/kg/hr
exp; 70 kg patient
70kg x 1ml/kg = 70 ml
250ml/70ml = 3.5 hours

Complications of HS
 Central pontine myelinolysis can occur with
rapid correction of hyponatremia.
 Characterized by permanent neurologic
damage such as paraparesis, quadriparesis,
dysarthria, dysphagia, and coma
 More likely to occur with rapid correction of
chronic hyponatremia compared with acute
hyponatremia.
 Advisable not to administer Hs in patients
with chronic asymptomatic

Complications of HS
 Prevent by avoiding changes in serum Na of
more than 10–12 mmol/l in 24 hours or more
than 18 mmol/l in 48 hours.
 Hypokalemia can occur with large volumes of
HS
 Hyperchloremic acidosis can occur because
of the administration of Cl salt
 Phlebitis if administered in a peripheral vein
 Heart failure - Fluid overload can occur
because of initial volume expansion

Hypotonic IV fluid
 Hypotonic fluids administered intravenously
can cause cell hemolysis and patient death.
 Albumin 25% diluted with sterile water to
make albumin 5% has an osmolarity of about
60 mOsm/l and can cause hemolysis
 “Quarter saline” or 0.25% naCl has an
osmolarity of 68 mOsm/l and can cause
hemolysis.

Hypotonic IV fluid
 Avoid using intravenous fluid with an
osmolarity less than 150 mOsm/l.
 Sterile water should never be administered
intravenously.
 Use D5W administered intravenously if only
water is needed.
 Use a combination of D5W and 0.25% NaCl

Q & A
 A 55-year-old man is hospitalized for community-
acquired pneumonia. After 2 days of appropriate anti-
biotic treatment, his WBC has decreased, and he is
afebrile. His BP is 135/85 mm Hg, and he has good
urine output. His laboratory values are normal. His
weight is 80 kg. His appetite is still poor, and he is not
taking adequate fluids. Which of the following is the
best intravenous fluid and rate?

Q & A
 A. 0.9% NaCl + KCl 20 meq/l to infuse at 150
ml/hour.
 B. D5W/0.9% NaCl + KCl 20 meq/l to infuse at 70
ml/hour.
 C. D5W/0.45% NaCl + KCl 20 meq/l to infuse at 110
ml/hour.
 D. 0.9% NaCl 1000-ml fluid bolus.
3

Q & A
 A 72-year-old woman with a history of hypertension has
developed hyponatremia after starting hydrochlo-rothiazide 3
weeks earlier. She complains of dizziness, fatigue, and nausea.
Her serum Na is 116 meq/l. Her weight is 60 kg, her BP is 86/50
mm Hg, and her Hr is 122 beats/minute. Which of the following
initial treatment regimens is recommended?
 A. 0.9% NaCl infused at 100 ml/hour.
 B. 0.9% NaCl 500-ml bolus.
 C. 3% NaCl infused at 60 ml/hour.
 D. 23.4% NaCl 30-ml bolus as needed.
2

Hypernatremia (> 145mmol/l)
 Gain of Na in excess of water or loss of water
in excess of Na
 Causes
 Deprivation of water
 Hypertonic tube feedings without water
supplements
 Watery diarrhea
 Increased insensible water loss (burn, fever)
 Renal failure (unable to excrete Na)
 Use of large doses of adrenal corticoids
 Excess sodium intake (NS or HS)

Signs/Symptoms
 Early: Generalized muscle weakness,
faintness, muscle fatigue, headache,
tachycardia, nausea and vomiting
 Moderate: Confusion, thirst
 Late: Edema, restlessness, thirst,
hyperreflexia, muscle twitching, irritability,
seizures, possible coma (Na > 158 mmol/l)
 Severe: Permanent brain damage form
cerebral dehydration and intracerebral
hemorrhage, hypertension (Na > 158 mmol/l)

Labs
 Increased serum Na
 Increased serum osmolality
 Increased urine specific gravity

Treatment (Euvolemic with hypernatremia)
 IV D5W to replace ECF volume if patient is
symptomatic with hypernatremia
D5W need = 0.4 x LBW (pt serum Na – Na normal)
Na
exp: patient 70 kg serum Na = 158, normal Na = 135
= 0.4 x 70 (158 – 135)
135
= 4.77 L
 Gradual lowering with Na level with D5W
 Decrease by no more than 0.5 mmol/l/hr or
12 mmol/l/day

Treatment (Euvolemic with hypernatremia)
Non- symptomatic patient
 Orally (plain water) to replace ECF volume if
patient is not symptomatic with excessive free
water losses

Treatment (hypovolemic with hypernatremia)
Non- symptomatic patient
 Orally (plain water) to replace ECF volume if
patient is not symptomatic with excessive free
water losses
Symptomatic patient
 IV D5W to replace ECF volume if patient is
symptomatic with hypernatremia

Treatment (Hyporvolemic with hypernatremia)
 If hypovolemia is due to osmotic diuretic or
gastroenteritis
 Signs of intravascular depletion
 Treat with 1/2NS or D5 1/4NS

Treatment (Hypervolemic with hypernatremia)
If patient is hypervolemic with hypernatremia
 Loop diuretic is the drug of choice

Evaluation
 Normalization of serum Na level over days
 Resolution of symptoms

Potassium
 Normal 3.5-5.5 mEq/L
 Major ICF cation
 Vital in maintaining normal cardiac and
neuromuscular function, influences nerve
impulse conduction, important in glucose
metabolism, helps maintain acid-base
balance, control fluid movement in and out of
cells by osmosis

Hypokalemia
 Serum potassium level below 3.5 mEq/L
 Causes
 Loss of GI secretions (diarrhea)
 Excessive renal excretion of K
 Movement of K into the cells with insulin (Rx
DKA)
 Prolonged fluid administration without K
supplementation
 Diuretics (some) and beta agonist (albuterol)
 Alkalosis

 Hypokalemia
 Renal excretion –diuretic
 Increased Gi losses of k+ can occur with
vomiting, diarrhea, intestinal fistula or enteral
tube drainage, and chronic laxative abuse
 Asthma treatment salbutamol
 Hypomagnesemia is commonly associated
with hypokalemia caused by increased renal
loss of k+

Signs/Symptoms
 Skeletal muscle weakness, ↓ smooth muscle
function, ↓ respiratory muscle function
 EKG changes, possible cardiac arrest
 Paralytic ileus
 Nausea, vomiting
 Metabolic alkalosis
 Mental depression and confusion

Treatment
 Deficit can be estimated as 200 -400 mmol K
for every 1 mmol/l reduction in plasma K

Treatment
 Patients without EKG changes or symptoms
of hypokalemia can be treated with oral
supplementation.

 Avoid mixing k+ in dextrose, which can cause
insulin release with a subsequent IC shift of
K+. Use NS
 Avoid irritation, no more than about 60-80
meq/l should be administered through a
peripheral vein.
 Recommended infusion rate is 10 meq/hour
up to a maximum of 40 meq/hour
 Patients who receive K+ at rates faster than
10–20 meq/hour should be monitored using a
continuous EKG.

Plasma K levels
Mmol/l
Treatment Comments
3 – 3.5 Oral KCl 60-80
mmol/d if no sign or
symptoms
Plasma K level rise
by about 1.5 mmol/l
2.5 -3 Oral KCl 120
mmol/d or IV 10 -20
mmol/hr if sign or
symptoms
Plasma K level rise
by about 2.0 mmol/l
2 -2.5 IV KCl 10 -20
mmol/hr
Consider continous
EKG monitoring
Less than 2 IV KCl 20 -40
mmol/hr
Requires continous
EKG monitoring

Caution
 Don’t mix K in dextrose
 No more than K 10 mmol/hr to be infused in
general ward
 If rate exceed more than 10 mmol/hr, then
consider EKG monitor

Monitoring
Monitor
 Potassium level
 EKG
 Bowel sounds
 Muscle strength

Hyperkalemia
 Serum potassium level above 5.3 mEq/L
 Causes
 Excessive K intake (IV or PO) especially in renal
failure
 CRF
 Tissue trauma
 Acidosis
 Catabolic state
 ACE inhibitors, K-sparing diuretics, B blockers

Signs/Symptoms
 ECG changes – tachycardia to bradycardia to
possible cardiac arrest
 Peaked, narrowed T waves
 Cardiac arrhythmias (VF
 Muscle weakness and paralysis
 Paresthesia of tongue, face, hands, and feet
 N/V, cramping, diarrhea
 Metabolic acidosis

Treatment
Asymptomatic elevation of plasma K
 Use cation exchange resin (calcium or sodium
polystyrene sulfonate Kayexalate )
 15- 30 grams 3 to 4 times/day as orally or
rectal enema
 Specially used in chronic renal failure patient
with hyperkalemia.
 Avoid K containing food

Treatment (symptomatic)
Urgent immediate treatment is needed if patient
1. Plasma K+ of 8mmol/l
2. Severe muscle weakness
3. ECK changes
10% Ca gluconate 20ml should be given
immediately if a patient has hyperkalemia -
induced-arryhymias (2 grams IV bolus)

Treatment (symptomatic)
 Sodium bicarbonate 1 mmol/kg can be given if
patient has acidosis (pH of < 7)
 50% glucose solution 50 ml (25 gm) with 10 units of
insulin  push K+ intracellular and lower serum K+
level by 1 to 1.5 mmol/l in one hour
 B2 adrenergic agonist  salbutamol 10 -20 mg in NS
as nebulizer over 10 mins  lower K+ level by 1 to
1.5 mmol/l in one hour to two hours
 Kayexalate PO or PR
 Hemodialysis
 Avoid K in foods, fluids, salt substitutes

Evaluation
 Normal serum K values
 Resolution of symptoms
 Treat underlying cause if possible

Calcium
 Normal 2.25-2.75 mmol/L
 99% of Ca in bones, other 1% in ECF and soft
tissues
 ECF Calcium – ½ is bound to protein – levels
influenced by serum albumin state
 Ionized Calcium – used in physiologic
activities – crucial for neuromuscular activity

Calcium
 Required for blood coagulation,
neuromuscular contraction, enzymatic
activity, and strength and durability of bones
and teeth
 Nerve cell membranes less excitable with
enough calcium
 Ca absorption and concentration influenced
by Vit D, calcitriol (active form of Vitamin D),
PTH, calcitonin, serum concentration of Ca
and Phos

Causes of Hypocalcemia
 Hypoparathyroidism (depressed function or
surgical removal of the parathyroid gland)
 Hypomagnesemia
 Hyperphosphatemia
 Administration of large quantities of stored
blood (preserved with citrate)
 Renal insufficiency
 ↓ Absorption of Vitamin D from intestines

Signs/Symptoms
 Abdominal and/or extremity cramping
 Tingling and numbness
 Positive Chvostek or Trousseau signs
 Tetany; hyperactive reflexes
 Irritability, reduced cognitive ability, seizures
 Prolonged QT on ECG, hypotension, decreased
myocardial contractility
 Abnormal clotting

Treatment
 Asymptomatic hypocalcaemia associated with
hypoalbuminemia check for corrected Ca++
Corrected Ca = Serum Ca + (normal S albumin – pt
serum albumin x 0.02
Exp: if patient serum Ca is 1.8 mmol/l and albumin is
20 gm/l then corrected Ca is (assume Normal Ca is
45 gm/l
= 1.8 + (45 – 20) x 0.02
= 1.8 + 25 x 0.02
= 1.8 + 0.5
= 2.3

Treatment
Asymptomatic hypocalcemia
 Oral calcium salts (mild) – 2 – 4 gm of elemental
Ca++/day with Vit D supplementation
Symptomatic hypocalcemia
 IV calcium as 10% calcium chloride 10 ml or 10%
calcium gluconate 20ml (270 mg elemental Ca)– give
with caution over 5-10 mins followed by continous
infusion of Ca at a rate of 0.5 – 2 mg/kg/hr
 Don’t exceed infusion rate 60 mg/min
 Close monitor for hypotension and bradycardia
 Vitamin D supplementation

Monitoring
 Close monitoring of serum Ca++
 Phosphorus level
 Magnesium level
 Vitamin D level
 Albumin level

Hypercalcemia
 Causes
 Mobilization of Ca from bone
 Malignancy (non-small cell and small cell lung
cancer, breast cancer, lymphomas, renal cell)
 Hyperparathyroidism
 Immobilization – causes bone loss
 Thiazide diuretics and hormonal therapy
 Thyrotoxicosis
 Excessive ingestion of Ca or Vit D

Signs/Symptoms
 Anorexia, constipation
 Generalized muscle weakness, lethargy, loss
of muscle tone, ataxia
 Depression, fatigue, confusion, coma
 Dysrhythmias and heart block
 Deep bone pain and demineralization
 Renal calculi
 Pathologic bone fractures

Hypercalcemic Crisis
 Emergency – level of 4-4.5 mmol/L
 Intractable nausea, dehydration, stupor,
coma, azotemia, hypokalemia,
hypomagnesemia, hypernatremia
 High mortality rate from cardiac arrest

Treatment
 NS IV infusion 3 – 6 L over 24 hours followed by
loop diuretic to prevent over load
 I and O hourly to avoid over hydration
 Biphosphonate- pamindronate 60mg IV once (inhibit
bone resorption)
 Corticosteroids (HC 100 q6 hr) and Mithramycin in
lymphomas and myeloma patient
 Calcitonin 2-8 IU/kg IV or SQ q6 to q12 to inhibit
PTH effect
 Phosphorus in patient with hypophosphatemia
 Encourage fluids
 Dialysis in renal patient with hypercalcemia

Evaluation
 Normal serum calcium levels
 Improvement of signs and symptoms
specially heart block, PVC, tachycardia,
mental status

Magnesium
 Normal 0.7 to 1.25 mmol/l
 Important in CHO and protein metabolism
 Plays significant role in nerve cell conduction
 Important in transmitting CNS messages and
maintaining neuromuscular activity
 Causes vasodilatation
 Decreases peripheral vascular resistance

Hypomagnesemia
 Causes
 Decreased intake or decreased absorption or
excessive loss through urinary or bowel
elimination
 Acute pancreatitis, starvation, malabsorption
syndrome, chronic alcoholism, burns,
prolonged hyperalimentation without
adequate Mg supplement
 Hypoparathyroidism with hypocalcemia
 Diuretic therapy

Signs/Symptoms
 Tremors, tetany, ↑ reflexes, paresthesias of
feet and legs, convulsions
 Positive Babinski, Chvostek and Trousseau
signs
 Personality changes with agitation,
depression or confusion, hallucinations
 ECG changes (PVC’S,
V-tach and V-fib)

Treatment
 Mild
 Diet – Best sources are unprocessed cereal
grains, nuts, green leafy vegetables, dairy
products, dried fruits, meat, fish
 Magnesium salts (MgO 400mg/d)
 More severe
 MgSO4 IM
 MgSO4 IV slowly

Treatment of Severe Symptomatic
Hypomagnesemia
 Treated with 2gm Mg sulfate (4mmol/ml) IV over
15 min, followed by infusion of 6g Mg sulfate in 1L
or more IV fluid over 24hrs or 0.5 meq/kg/day
added to intravenous fluid and administered as a
continuous infusion.
 Need to replenish intracellular stores, the infusion
should be continued for 3-7 days
 Serum Mg should be measured q24h and the
infusion rate adjusted to maintain a serum Mg level
of <1.25 mmol/L
Singer G: Fluid and electrolyte management. In: The Washington Manual of Therapeutics.
Lippencott. 30th edition, 2001. p68-69.

Treatment of Severe Symptomatic
Hypomagnesemia
 In patient with normal renal function, excess Mg is
readily excreted, and there is little risk of causing
hypermagnesemia with recommended doses
 Mg must be given with extreme caution in renal
failure due to the risk of accumulation of Mg and can
cause hypermagnesemia

Monitoring
 Monitor Mg level q 12 – 24 hrs
 Monitor VS
 Knee reflexes
 Check swallow reflex

Hypermagnesemia
 Most common cause is renal failure,
especially if taking large amounts of Mg-
containing antacids or cathartics
 DKA with severe water loss
 Signs and symptoms
 Hypotension, drowsiness, absent DTRs,
respiratory depression, coma, cardiac arrest
 ECG – Bradycardia, cardiac arrest

Treatment
 Withhold Mg-containing products
 Calcium chloride or gluconate IV for acute
symptoms (10% Ca gluconate 10-20ml over
15-30 mins)
 NS IV hydration and diuretics
 Hemodialysis

Evaluation
 Serum magnesium levels WNL
 Improvement of symptoms

Phosphorus Normal 0.8 to 1.6 mmol/l
 The primary anion in the intracellular fluid
 Crucial to cell membrane integrity, muscle
function, neurologic function and metabolism
of carbs, fats and protein
 Functions in ATP formation, phagocytosis,
platelet function and formation of bones and
teeth
 Influenced by parathyroid hormone and has
inverse relationship to Calcium

Hypophosphotemia
 Causes
 Malnutrition
 Hyperparathyroidism
 Certain renal tubular defects
 Metabolic acidosis (esp. DKA)
 Disorders causing hypercalcemia
 Diuretics, glucocorticoids, na bicarbonate
 Rapidly refeeding
 Diabetic ketoacidosis (shift IC)

Sign and Symptoms
 Musculoskeletal
 Muscle weakness
 Respiratory muscle failure
 Osteomalacia
 Pathological fractures
 CNS
 Confusion
 Anxiety
 Seizures
 Coma

Sign and Symptoms
 Cardiac
 hypotension
 decreased cardiac output
 Hematologic
 hemolytic anemia
 easy bruising
 infection risk

Treatment
 Treatment of moderate to severe deficiency
 IV phosphate
 Symptomatic patients should receive 15–30
mmol of phosphorus (Na phosphate or K+
phosphate) administered intravenously over
3–6 hours.
 Oral phosphorus (neutra-Phos) can be used
for asymptomatic patients.(15 mmol/d)
 Monitor levels during treatment

Hyperphosphatemia
 Causes
 Chronic renal failure (most common)
 Hyperthyroidism, hypoparathyroidism
 Severe catabolic states
 Conditions causing hypocalcemia
Net effect of PTH  ↑ serum calcium
↓ serum phosphate
Net effect of calcitriol  ↑ serum calcium
↑ serum phosphate

Role of PTH
 Stimulates renal reabsorption of calcium
 Inhibits renal reabsorption of phosphate
 Stimulates bone resorption
 Inhibits bone formation and mineralization
 Stimulates synthesis of calcitriol
Net effect of PTH  ↑ serum calcium
↓ serum phosphate

Sign and Symptoms
 Cardiac irregularities
 Hyperreflexia
 Eating poorly
 Muscle weakness
 Nausea

Treatment
 Prevention is the goal
 Restrict phosphate-containing foods
 Administer phosphate-binding agents (Ca
carbonate, sevelamar, lanthanum)
 Diuretics
 Cinacalcet –increase the sensitivity of Ca
receptor on PTH gland to Ca conc PTH
 Treatment may need to focus on correcting
calcium levels

Evaluation
 Lab values within normal limits
 Improvement of symptoms

Regulation of blood pH
 The lungs and kidneys play important role in
regulating blood pH.
 The lungs regulate pH through retention
(hypoventilation) or elimination (hyperventilation) of
CO2 by changing the rate and volume of ventilation.
 The kidneys regulate pH by excreting acid, primarily
in the ammonium ion (NH4
+), and by reclaiming
HCO3
- from the glomerular filtrate (and adding it
back to the blood).

Normal Values for Blood Buffer in Arterial
Blood.
 The following values are determined by blood gas
analyzer:
 pH 7.35 – 7.45
 PCO2 35 – 45 mm Hg
 H2CO3 2.4 mmoles/L of plasma
 HCO3
- 24 mmoles/L of plasma
 PO2 80 – 110 mm Hg

Four Basic Types of Imbalance
 Respiratory Acidosis
 Respiratory Alkalosis
 Metabolic Acidosis
 Metabolic Alkalosis

Respiratory Acidosis
Carbonic acid excess
 Exhaling of CO2 inhibited
 Carbonic acid builds up
 pH falls below 7.35
 Cause = Hypoventilation (see chart)
 When CO2 level rises hypoventilation, producing
more H2CO3, the equilibrium produces more H3O+,
which lowers the pH – acidosis.
CO2 + H2O  H2CO3  H3O+ + HCO3
-
H2CO3

Respiratory Acidosis: CO2 ↑ pH ↓
 Symptoms: Failure to ventilate, suppression of
breathing, disorientation, weakness, coma
 Causes: Lung disease blocking gas diffusion (e.g.,
emphysema, pneumonia, bronchitis, and asthma);
depression of respiratory center by drugs,
cardiopulmonary arrest, stroke, poliomyelitis, or
nervous system disorders

Acid-Base Imbalances
 Normal
H2CO3 ……………… HCO3
24 mEq/L
1.2 mEq/L
7.4
1 20

1 13
7.21

 Respiratory acidosis compensates by
metabolic alkalosis
 Compensated by the kidney increasing
production of bicarbonate
Acute Hypercapnia:
HCO3 increases 1 mmol/L for
each 10 mmHg increase in
PaCO2 >40
Chronic Hypercapnia:
For each 10 mmHg increase in
PaCO2 >40 HCO3 incr. 3.5
mmol/L

Acute Respiratory Acidosis:
25 y.o. IV drug user s/p heroin overdose:
pH 7.10 pCO2 80 Bicarbonate 24
80 – 40 = 40. For every 10 CO2 inc 3.5 mmol
HCO3 increases
10---------------- 3.5
40--------------- ? 40/10 = 4 x 3.5 = 14
24 + 14 = 38 HCO3

Chronic Respiratory Acidosis:
65 y.o. patient with stable COPD:
Significant Renal Compensation
But when he arrives in the ED, this is the only ABG you
have:
 7.23/85/pO2/35
 35-24=11. 11/3.5 = 3. 3 x 10 =30. 40 + 30 = 70
 Baseline pCO2 = 70. Pt. has acute resp acidosis.

Respiratory Alkalosis
 Decreasing of CO2 level due to a hyperventilation,
which expels large amounts of CO2, leads to a
lowering in the partial pressure of CO2 below normal
and the shift of the equilibrium from H2CO3 to CO2
and H2O. This shift decreases H3O+ and raises blood
pH – alkalosis.
CO2 + H2O H2CO3 H3O+ + HCO3
-

Respiratory Alkalosis: CO2 ↓ pH ↑
 Symptoms: Increased rate and depth of breathing,
numbness, light-headedness, tetany
 Causes: hyperventilation due to anxiety, hysteria,
fever, exercise; reaction to drugs such as salicylate,
quinine, and antihistamines; conditions causing
hypoxia (e.g., pneumonia, pulmonary edema, and
heart disease)
 Treatment: Elimination of anxiety producing state,
rebreathing into a paper bag

Acid-Base Imbalances
Normal
H2CO3 ……………… HCO3
24 mEq/L
1.2 mEq/L
1 20
7.4

Respiratory Alkalosis
1 40
7.70

 Acute Hypocapnia:
 HCO3 decreases 2 mmol/L for every 10
mmHg decrease in PaCO2 <40
 Chronic Hypocapnia:
 For every 10 mmHg decrease in PaCO2 <40
HCO3 decreases 5 mmol/L

Respiratory Alkalosis:
15 y.o. girl who just who has panic attack
Reality: 7.65/20/pO2/20, because hypocapnia
leads to lower bicarb as well.
40 – 20 = 20. For every 10 CO2 HCO3 dec by 5 mmol
20/10 = 2 x 5 = 10
24 – 10 = 14

3 most important equations so far
 Chronic resp. acidosis: steady-state pCO2 is
increased by 10 for every 3.5 increase in
HCO3
 Acute metabolic acidosis:
 pCO2 = 1.5 x HCO3 + 8 (+/- 2)
 Acute metabolic alkalosis:
 pCO2 = 0.9 x HCO3 + 15

METABOLIC ACIDOSIS
 Metabolic acidosis represents an increase in
acid in body fluids .
 Reflected by a decrease in [HCO3 -] and a
compensatory decrease in pCO2.

Metabolic Acidosis
 Impaired cardiac contractility
 Decreased threshold for v fib
 Decreased Hepatic and Renal perfusion
 Increased Pulm Vasc resistance
 Inability to respond to catecholamines
 Vascular collapse

Test Case
23 year old AIDS patient c/o weakness and
prolonged severe diarrhea. He appears
markedly dehydrated.
pH 7.25 pCO2 25 pO2 110 HCO3 11
151 129 60
2.0 12 2.0
Acute metabolic acidosis:
pCO2 = 1.5 x HCO3 + 8 (+/- 2)
= 1.5 x 11 + 8
= 24.5

Metabolic Acidosis
18 y.o. WF presents in DKA
ABG: pH 7.00 pCO2 25 Bicarbonate 6
If Pure metabolic acidosis, then pCO2=(1.5)(6) + 8= 17
. pCO2=1.5 x HCO3 + 8 +/- 2
= 1.5 x 6 + 8
= 9 + 8
= 17

Respiratory Compensation
Metabolic Acidosis:
 Occurs rapidly
 Hyperventilation
 “Kussmaul Respirations”
 Deep > rapid (high tidal
volume)
Metabolic Alkalosis:
 Calculation not as accurate
 Hypoventilation
 Restricted by hypoxemia
 PCO2 seldom > 50-55
pCO2=1.5 x HCO3 + 8 +/- 2
Winter’s formula pCO2=0.9 x HCO3 + 15

METABOLIC ALKALOSIS:
 Metabolic alkalosis represents an increase in
[HCO3 -] with a compensatory rise in pCO2.

Test Case
An 80 year old man has been confused and c/o
SOB for one week. He also has a hearing
problem and has seen 3 ENT docs in the past
month. Family denies medications.
pH 7.53 pCO2 15 pO2 80 HCO3 12
140 108
3.0 13
120 Diagnosis?
AG = 140 - 121 = 19

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