Electrolyte and Acid-Base

Disorders
LTC John Armstrong, MD
 Learning Objectives
Define the functional fluid
compartments
Describe the causes, symptoms/signs,
and management of disorders in
Concentration
Electrolyte composition
Acid-base balance
 Overview
Common in hospitalized patients and
chronic care settings
Determine disorders from clinical
scenario
Confirm with lab series
 Fluid Compartments
1/3 2/3

I
N
EXTRACELLULAR

T
V E
A R
S S
C T
INTRACELLULAR
U I
L T
A I
R A
L
 Principles
Across compartments
H2O freely permeable
Osmolality equilibrates
Concentrations vary: membrane
permeability and active transport
sustain gradients
Within a compartment
meq cations = meq anions
 Fluid Compartments
Extracellular Intracellular

Na+ K+

Mg2+ Ca 2+
Cl-
Phosphates
HCO 3
-
Proteins
 Fluid and Electrolyte Balance
Volume: total body water
Concentration: Na+
Composition
K+
Ca++, Mg++, Phos
H+, HCO3-
Electrolyte Content of Body Fluids
HCO3
Fluid Na +
Cl -
K+
-
H+ Ca2+

Serum 140 105 4 25 0 9

Gastric 60 90 10 0 90 0
Pancreas 140 70 5 90 0 0
Ileum 130 110 10 30 0 0
Colon 50 40 30 20 0 0
 The Regulators
Kidney
Major volume and
electrolyte regulator
Chronic acid/base regulator
Lung: acute acid/base regulator
 Clinical Case
66 y.o. man with O2-dependent COPD
70-kg weight
Baseline pCO2: 52
Incarcerated umbilical hernia x 3 days
Non-feculent vomiting x 3 days
Minimal urine output
Pulse 135, blood pressure 90/60,
respiratory rate 30, SaO2 88%
What are your predictions?

Volume status?
Na+?
K+?
Cl-?
Acid/base disorders?
Sodium Homeostasis:
135-145 meq/L
The Kidneys Priorities

#1 Conserve sodium
#2 Excrete free water
#3 Conserve free water
 Sodium Homeostasis
Extracellular Intracellular

Na+

free free
H2O H2O
 Sodium Homeostasis
Extracellular Intracellular

Na+

free free
H2O H2O
Sodium Homeostasis
Extracellular Intracellular

Na+

free free
H2O H2O
Hyponatremia: Na+ < 135 meq/L
Symptom severity
Degree of change
Acuteness of change
Severe (< 120 meq/L): neuropsychiatric
Lethargy
Disorientation
Agitation
Seizures/coma
 Hyponatremia Causes
Overhydration: free water
Iatrogenic administration of hypotonic IV
fluids
Congestive heart failure
Liver failure
Dehydration: hypertonic loss
GI and third-space losses
Diuretic renal losses
Euhydration: SIADH
 Hyponatremia Management
Assess volume status
Address underlying cause
(In oliguria) Analyze urine Na+ and
osmolality relative to serum Na+ and
osmolality
urine Na+ and osmolality = renal
conservation of sodium and water
urine Na+ and osmolality = renal
loss of sodium and water
 Hyponatremia Management
Overhydration due to hypotonic fluids:
d/c hypotonic fluids, use NS
Overhydration due to edematous states
Restrict sodium and water intake
Improve underlying condition
Dehydration: NS volume replacement
SIADH
Fluid restriction
Correction of underlying process
 Hyponatremia Management
Severe hyponatremia (acute change or
symptomatic)
Goal: symptoms resolution or 130 meq/L
Correct at 1meq/L/hour with 3% saline
Rapid correction
Central pontine myelinolysis
Flash pulmonary edema
Monitored setting essential
Hypernatremia: Na+ > 145 meq/L

Symptoms dependent on rate of

change, level, and volume status
Neuropsychiatric
Restlessness
Hyperreflexia
Weakness
Delirium
 Hypernatremia Causes
free water relative to Na+
Skin: burns
GI: hypotonic diarrhea
Renal: central/nephrogenic DI
Na+ relative to free water
Iatrogenic
Hyperaldosteronism
 Hypernatremia Management
Assess volume status
Determine cause
Correct free water deficit with D5W
Maximum rate of Na+ correction: 1
meq/L/hr
Monitored setting
Rapid correction: cerebral edema to
herniation
 Hypernatremia Management
Additional management considerations
Central DI: add DDAVP
Nephrogenic DI: sodium restriction
Excess sodium
Stop administration
Remove with loop diuretic (e.g.,
Lasix)
 A Few Words about Chloride
Maintains tonicity
Promotes renal reabsorption of Na+
Helps regulation of acid via reciprocal
relationship with HCO3-
Renal acid excretion depends
bicarbonate reabsorption with
chloride excretion
 A Few Words about Chloride
Normal range: 95-110 meq/L
Hypochloremia
Common cause: loss of gastric juice
Management: in context, NS
Hyperchloremia
Common cause: NS hyper-
resuscitation
Management: hypotonic fluid
Potassium Homeostasis:
3.5-4.5 meq/L

20 meq intravascular

K +

4200 meq
Intracellular
Hypokalemia: K+ < 3.5 meq/L
Cardiac
Flattened T waves
Prominent U waves
P-R interval
QRS widening
Neuromuscular:
weakness and lethargy
GI: ileus
 Hypokalemia Causes
Potassium loss
Diuresis
Gastrointestinal loss
Intracellular displacement
Alkalosis
Inadequate intake
 Hypokalemia Management
Assess
Acid-base status
Glycemic state
Renal function
Review
Current medications (e.g., diuretics)
Nutrition status (potassium intake)
Obtain ECG
 Hypokalemia Treatment
Replete K+
> 3 meq/L: oral (avoids renal
secretion)
< 3 meq/L or ECG changes: IV
Maximum safe rate: 20 meq/L/hr
through a central line in monitored
setting
Hyperkalemia: K+ > 5.0 meq/L
Cardiac
Peaked T waves
Shortening of QT interval
QRS widening/ST segment
depression
Sine wave/cardiac arrest
Neuromuscular: lethargy and
weakness
GI: vomiting and diarrhea
 Hyperkalemia Causes
Poor renal excretion H
E
Renal failure
M
K+-sparing diuretics O
L
Cell death Y
Burns S
I
Crush injury/tissue necrosis S
Acidosis
Hyperkalemia Management
Verify the value
Stop any K+ administration
Obtain ECG
Assess
Renal function
Ischemic tissue
 Hyperkalemia Management
Protect the heart: calcium gluconate
Drive K+ intracellularly
Insulin and glucose
Bicarbonate
Remove excess K+
If kidneys work: diuretics
If kidneys do not work
Resins
Hemodialysis
Calcium Homeostasis: 8-10.5 mg/dL
Mg 2+
Parathormone

Vitamin D

Calcium Calcium Calcium

Phosphate Phosphate Phosphate
 Hypocalcemia: Ca2+ < 8 mg/dl
Neuromuscular
Perioral numbness
Tingling of fingertips and toes
Hyperactive tendon reflexes
Carpopedal spasm
Muscle cramps
Cardiac: Q-T interval
 Hypocalcemia Causes
Poor absorption
Renal failure
Fat malabsorption
Tissue binding: acute pancreatitis
Hypoparathyroidism
Iatrogenic
Hypomagnesemia
 Hypocalcemia Management
Assess serum Phos and Mg 2+
Review history
Renal failure
Neck surgery
Nutrition status
 Hypocalcemia Management
Replete Mg 2+
Acute: intravenous calcium gluconate
or calcium chloride
Chronic: oral calcium and Vitamin D
Hypercalcemia: Ca 2+ > 10.5 mg/dL

Neuromuscular
Weakness and fatigue
Headaches
Back pain
Renal: polyuria
Gastrointestinal: vomiting
 Hypercalcemia Causes
Increased release of Ca 2+ from bone
Metastatic cancer
Breast
Lung
Renal
Hyperparathyroidism
 Hypercalcemia Management
Rehydrate with normal saline
Promote diuresis (nonthiazide
diuretics)
Monitor K+ and Mg 2+
 Hypercalcemia Management
Metastatic cancer
Calcitonin: bone resorption, renal
excretion
Bisphosphonates: bone
resorption
Steroids
Hyperparathyoidism:
parathyroidectomy
Magnesium Homeostasis: 1.5-2.5 meq/L

10 meq intravascular

Mg 2+

2000 meq
Intracellular
Hypomagnesemia: Mg 2+<1.5 meq/L

Symptoms the same as hypocalcemia

Cardiac ventricular dysrhythmias
 Hypomagnesemia Causes
Inadequate intake
Chronic alcoholism
Absence of magnesium in nutrition
Starvation
Extreme loss
GI: chronic diarrhea, fistulas
Renal: diuresis
 Hypomagnesemia Management
Check K + and Ca 2+
Repletion
Magnesium gluconate PO
Severe: magnesium sulfate IV
Monitored setting
20 meq/hour, to total dose of
2 meq/kg/day
Monitor deep tendon reflexes
 Hypermagnesemia: Mg 2+ > 2.5
meq/L
Neuromuscular
Progressive loss of deep tendon
reflexes
Lethargy and weakness
Cardiac: similar to hyperkalemia
 Hypermagnesemia Causes
Intake > output
Renal failure
Magnesium-containing antacids
Iatrogenic
Acidosis: similar to potassium
Hypermagnesemia Management
Protect the heart: calcium gluconate
Volume resuscitate
Eliminate excess magnesium
Stop magnesium administration
Correct acidosis
Normal kidneys: loop diuretics
Abnormal kidneys: hemodialysis
Phosphate Homeostasis:
2.5-4.5 mg/dL

ATP

Phos 2- 1 / Ca 2+
Hypophosphatemia:
Ph < 2.5 mg/dL
Neuromuscular
Weakness and fatigue
Hyporeflexia
Numbness
Cardiorespiratory
Diaphragmatic failure
cardiac contractility
 Hypophosphatemia Causes
intake: nutritional support without
phosphate
loss
Hyperparathyroidism
GI
Diarrhea
Phosphate-binding antacids
Hypophosphatemia Management
Check Ca 2+ ; if elevated, beware
phosphate replacement
Stop phosphate-binding antacids
Replete
> 1 mg/dL: enteral or IV
< 1 mg/dL: IV in a monitored setting
Confirm underlying cause
Hyperphosphatemia:
Ph > 4.5 mg/dL
Symptoms: same as hypocalcemia
Ectopic calcification in muscles and
organs
 Hyperphosphatemia Causes
renal excretion
Renal failure
Hypoparathyroidism
intake
Phosphate-containing laxatives/enemas
Iatrogenic: mmol vs. meq
Release of intracellular phosphate
Tumor lysis
Tissue necrosis
 Hyperphosphatemia
Management
Eliminate excess phosphate
Eliminate intake
Normal renal function: diuresis with
normal saline and diuretics
Abnormal renal function
Phosphate-binding antacids
Hemodialysis
Find underlying cause
 Acid-Base Homeostasis
Respiratory path: acute

Eliminates CO2 through lungs

Buffers carbonic acid with Hgb

Metabolic path: chronic

Eliminates H+ through the kidney

Buffers acid with HCO3-, plasma
proteins, and phosphates
 Acid-Base Homeostasis

Central Relationship
H2O + CO2 H2CO3 H+ + HCO3-

Normal Values
pH = 7.40
pCO2 = 40
HCO3- = 25
Acid-Base Disorders

Metabolic
Acidosis: HCO3-
Alkalosis: HCO3-
Respiratory
Acidosis: pCO2
Alkalosis: pCO2
Acid-Base Analysis

Step 1: pH
< 7.35:
acidemic
> 7.45: alkalotic
 Acid-Base Analysis
Step 2: primary process
Relate pH and pCO2
pH & pCO2 change in same direction:
metabolic process
pH & pCO2 change in opposite
direction: respiratory process
Review HCO3- to confirm primary process
and define compensatory response
 Compensatory Acid-Base
Response
Metabolic acidosis: respiratory
alkalosis
Metabolic alkalosis: respiratory
acidosis
Respiratory acidosis: metabolic
alkalosis
Respiratory alkalosis: metabolic
acidosis
 Acid-Base Analysis
Step 3: calculate anion gap
Anion Gap = Na+ - Cl- - HCO3-
Normal = 10
Difference due to hidden anions
like albumin
Abnormal: elevated with hidden
acids
 Metabolic Processes

H
+
HCO3 -
Metabolic Acidosis:
HCO3- < 22 meq/L
Addition of acid Loss of HCO3-
( anion gap) (normal anion gap)
Lactic acid GI loss: diarrhea,
Ketoacids fistula
Renal failure Renal
Intoxicants Tubular
Salicylates acidosis
Hyperchloremia
 Metabolic Acidosis: Management

Acid gain: identify and correct the

underlying cause
Lactic acidosis: restore adequate
tissue perfusion
Ketoacidosis: resuscitate and
control glucose
Renal failure: hemodialysis
 Metabolic Acidosis:
Management
Acid gain
pH < 7.20: NaHCO3 for cardiac
protection
NOT primary treatment
Generates CO2, which must be
excreted by lungs
Significant sodium load
 Metabolic Acidosis:
Management
Bicarbonate loss
Resuscitate with fluids similar in
volume and composition to those
lost
May require bicarbonate
replacement
Address source of bicarbonate loss
Correct hyperchloremia
Metabolic Alkalosis:
HCO3- > 27meq/L
Chloride-responsive
Loss of acid: vomiting
Loss of chloride: vomiting,
diarrhea, diuretics
Loss of potassium
Volume contraction
Chloride-resistent:
hyperaldosteronism
Metabolic Alkalosis: Causes

Kidney: retain Na+

ne
ro
st e
Take Cl-

ldo
a
Take HCO3-/

e:
secrete H+

m
olu
v
Secrete K+
 Metabolic Alkalosis:
Management
Vast majority: chloride-responsive
Evaluation: urine electrolytes
Low Na+
Low Cl-
Higher K+
Solution: replenish chloride with NS
pH > 7.6 with dysrhythmia (very rare):
IV HCl to manage cardiac dysfunction
Respiratory Processes:
pCO2 40
Primary problem with ventilation
(movement of tidal volume to remove
CO2)
Hypoventilation: pCO2
Hyperventilation: pCO2
Respiratory Acidosis:
pCO2 > 45
Disorders affecting gas exchange
Acute or chronic obstructive
pulmonary disease
Pulmonary edema
Acute upper airway obstruction
Respiratory muscle disorders
medullary respiratory center activity
 Respiratory Acidosis:
Management
Improve alveolar ventilation
May require intubation and
mechanical ventilation
Address underlying causes
Caution: use of O2 in COPD

Bicarbonate : creates CO2

Respiratory Alkalosis:
pCO2 < 36
Acute
Hypoxemia
Errors in mechanical ventilation
Fever
Salicylate overdose
Chronic
Central nervous system causes
Chronic hypoxemia (i.e, high altitude)
 Respiratory Alkalosis:
Management

Address underlying cause

Correct hypoxia
Adjust mechanical ventilator
Address fever
 Disorders and Oxygenation

CO2
SaO2 Right shift
2,3 DPG better tissue
oxygenation
pH
CO2
Left shift
worse tissue 2,3 DPG
oxygenation
pH

pO2
 Clinical Case Deja Vu
66 y.o. man with O2-dependent COPD
70-kg weight
Baseline pCO2: 52
Incarcerated umbilical hernia x 3 days
Non-feculent vomiting x 3 days
Minimal urine output
Pulse 135, blood pressure 90/60,
respiratory rate 30, SaO2 88%
 Clinical Predictions
Volume status: hypovolemic
Na+: hyponatremia/low normal
K+: hypokalemia
Cl-: hypochloremia
Acid-base
Respiratory acidosis (chronic--COPD)
Metabolic alkalosis (acute--vomiting)
Respiratory alkalosis (acute--hypoxia)
 The Laboratories

Na+ 128 Cl- 62 BUN 45

K+ 2.5 HCO3- 45 Cr 1.5

ABG: pH 7.65 pCO2 48

 Acid/Base
pH: alkalemic
pH relative to pCO2: metabolic (both )
HCO3-: confirms primary alkalosis
pCO2: lower than baseline, confirms
acute respiratory alkalosis on top of
chronic respiratory acidosis
Anion gap: 21an otherwise hidden
metabolic acidosis!
 Points to Remember

Readily predicted by clinical

presentation
Confirmed (or disconfirmed) by labs
Associated with volume abnormalities
requiring resuscitation
Cross-linked through the regulators
(kidneys and lungs) and across
compartments
 Points to Remember

Asymptomatic Symptomatic
Address cause Prevent harm
Place in context Replete
Replete Place in context
Prevent harm Address cause
 Summary

The functional fluid compartments

The causes, symptoms/signs, and
management of disorders in
Concentration
Electrolyte composition
Acid-base balance