ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course (2022)

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ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-xiii
Table of Contents
TABLE OF CONTENTS (Volume 1)
Fluids, Electrolytes, and Nutrition 1-1
Fluid Management; Osmolality; Hypertonic Saline; Hypotonic Intravenous Fluids; Hyponatremia
and Hypo-osmolality States; Hypernatremia and Hyperosmolar States; Disorders of K+
; Disorders
of Magnesium Homeostasis; Disorders of Phosphorus Homeostasis; Disorders of Calcium Homeostasis;
Enteral Nutrition; Parenteral Nutrition
Endocrine and Metabolic Disorders 1-55
Thyroid Disorders; Pituitary Gland Disorders; Adrenal Gland Disorders; Obesity; Polycystic Ovary
Syndrome; Diabetes Mellitus; Treatment of Diabetes Mellitus Complications; Diabetes Insipidus
Pulmonary Disorders and Adult Immunizations 1-113
Asthma; Chronic Obstructive Pulmonary Disease; Adult Immunizations
Geriatrics 1-169
Optimizing Pharmacotherapy in Older Adults; Dementia; Behavioral and Psychological
Symptoms of Dementia; Urinary Incontinence; Benign Prostatic Hypertrophy; Osteoarthritis
(OA); Rheumatoid Arthritis (RA); Gout
Biostatistics: A Refresher 1-217
Introduction to Statistics; Types of Variables and Data; Types of Statistics; Population Distributions;
Confidence Intervals; Hypothesis Testing; Decision Errors, Statistical Tests and Choosing a
Statistical Test; Correlation and Regression; Survival Analysis; Summary of Selecting Statistical Tests
Study Designs: Fundamentals and Interpretation 1-241
Introduction: Why Do Pharmacists Need to Know About Study Design and Interpretation;
Various Concepts in Study Design; Case Reports/Case Series; Observational Study Designs;
Incidence, Prevalence, Relative Risks/Risk Ratios, Odds Ratios, and Hazard Ratios; Randomized
Controlled Trial Design; Other Issues to Consider in Controlled Trials; Controlled Clinical Trials:
Analysis; Common Approaches to Analyzing Clinical Trials; Systematic Review/Meta-analysis;
Summary Measures of Effect; Reporting Guidelines for Clinical Studies; Pharmacoeconomic
Studies; Sensitivity/Specificity/Predictive Values; Professional Writing: The Publication Process
Anticoagulation 1-273
Stroke Prevention in Nonvalvular Atrial Fibrillation; Anticoagulation in Valvular Disease;
Prevention of Venous Thromboembolism; Treatment of Venous Thromboembolism; Reversal
of Anticoagulation
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ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-xiv
Table of Contents
Critical Care 1-329
Interpretation of Hemodynamic Parameters; Treatment of Shock; Interpretation of Acid-Base
Disturbances; Cardiac Arrest; Acute Respiratory Failure; Pain, Agitation, Delirium, and
Neuromuscular Blockade; Glucose Control; Preventing Stress Ulcers; Pharmacologic Therapy
for Preventing Venous Thromboembolism; Preventing Ventilator-Associated Pneumonia;
Nutrition Support in Critically Ill Patients; Intracranial Hemorrhage
Chronic Care in Cardiology 1-389
Heart Failure; Atrial Fibrillation; Hypertension; Dyslipidemia; Chronic Coronary Heart Disease
and Chronic Stable Angina
Acute Care in Cardiology 1-451
Acute Coronary Syndrome; Acute Decompensated Heart Failure; Acute Life-Threatening
Arrhythmias; Hypertensive Crises
Neurology 1-513
Epilepsy; Ischemic Stroke; Parkinson Disease; Headache; Multiple Sclerosis; Peripheral Neuropathy

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ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course2-xiii
Table of Contents
TABLE OF CONTENTS (Volume 2)
General Psychiatry 2-1
Schizophrenia; Major Depressive Disorder (MDD); Bipolar Disorder; Anxiety and Related Disorders
(OCD, PTSD); Insomnia; Substance Use Disorders
Infectious Diseases I 2-71
Respiratory Tract Infections; Urinary Tract Infections; Skin and Structure Infections; Diabetic
Foot Infections; Osteomyelitis; Central Nervous System Infections; Endocarditis; Peritonitis and
Intra-abdominal Infections; Clostridioides difficile Infection; Surgical Prophylaxis
Infectious Diseases II 2-125
Human Immunodeficiency Virus; Opportunistic Infections: Patients with HIV; Tuberculosis; Fungal
Pharmacotherapy; Antifungal Agents
Men’s and Women’s Health 2-173
Hormone Therapy and Menopause; Osteoporosis; Drugs in Pregnancy; Drugs in Lactation;
Complications in Pregnancy; Overview of Contraception; Combined Hormonal Contraceptives,
Containing Both an Estrogen and a Progestin Hormone; Progestin-only Contraceptives, Containing
Only a Progestin Agent with No Estrogen; Intrauterine Devices (IUDs) and Systems (IUSs);
Implant (Nexplanon); Lactic Acid, Citric Acid, and Potassium Bitartrate Vaginal Gel (Phexxi);
Emergency Contraception; Menstrual Disorders (Independent Study); Infertility; Sexually
Transmitted Infections Including Pelvic Inflammatory Disease, Gynecologic Infections;
Prostatic Infections; Male Sexual Dysfunction
Pharmacokinetics: A Refresher 2-259
Basic Pharmacokinetic Relationships; Absorption; Distribution; Clearance; Nonlinear
Pharmacokinetics; Noncompartmental Pharmacokinetics; Data Collection and Analysis;
Pharmacokinetics in Renal Disease; Pharmacokinetics in Hepatic Disease; Pharmacodynamics;
Therapeutic Drug Monitoring
Nephrology 2-297
Acute Kidney Injury or Acute Renal Failure; Drug-Induced Kidney Damage; Chronic Kidney
Disease; Renal Replacement Therapy; Managing the Complications of Chronic Kidney Disease;
Dosage Adjustments in Kidney Disease
Oncology Supportive Care 2-345
Antiemetics; Pain Management; Treatment of Febrile Neutropenia; Use of Colon-Stimulating
Factors for Prevention of Febrile Neutropenia; Thrombocytopenia; Anemia and Fatigue;
Chemoprotectants; Oncologic Emergencies; Miscellaneous Antineoplastic Pharmacotherapy
Gastrointestinal Disorders 2-391
Gastroesophageal Reflux Disease (GERD); Peptic Ulcer Disease; Upper GI Bleeding; Inflammatory
Bowel Disease; Complications of Liver Disease; Viral Hepatitis; Nausea and Vomiting; Pancreatitis;
Diarrhea; Constipation; Irritable Bowel Syndrome
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ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course2-xiv
Table of Contents
Pediatrics 2-479
Sepsis and Meningitis; Respiratory Syncytial Virus Infection; Otitis Media; Immunizations;
Pediatric Seizure Disorders; Attention-Deficit/Hyperactivity Disorder
Healthcare Systems and Population Health 2-523
Introduction; Quality Improvement (QI); Technology Supports Initially Focused on Production
and Productivity with Dispensing; Quality Medication Use in Healthcare Systems; Population
Health; Communication and Education for Providers and Staff; Barriers in Communication
with Patients and Caregivers; Conclusion
Drug Information and Communication Strategies in Pharmacy 2-545
Retrieving Drug Information; Communicating Drug Information

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-4
Learning Objectives
1. Recommend an appropriate intravenous fluid reg-
imen and monitoring parameters given a patient
clinical scenario.
2. Discuss the appropriate roles and risks of hyper-
tonic and hypotonic saline, recommend treatment
regimens, and discuss appropriate monitoring
parameters to ensure safe and effective use of these
intravenous fluids.
3. Assess electrolyte abnormalities and recommend
an appropriate pharmacologic treatment plan based
on individual patient signs and symptoms.
4. Recommend a patient-specific enteral nutrition
(EN) or parenteral nutrition (PN) formula, infusion
rate, and monitoring parameters based on nutri-
tional needs, comorbidities, and clinical condition.
Abbreviations in This Chapter
AA amino acid
ADH antidiuretic hormone
ASPEN American Society for Parenteral and Enteral
Nutrition
BEE basal energy expenditure
BUN blood urea nitrogen
D5W 5% dextrose
EC extracellular
ECG electrocardiogram
EN enteral nutrition
GI gastrointestinal
IBW ideal body weight
IC intracellular
ICU intensive care unit
IS interstitial
LBW lean body weight
MW molecular weight
NG nasogastric
PN parenteral nutrition
SCr serum creatinine
SIADH syndrome of inappropriate secretion of
antidiuretic hormone
TBF total body fluid
WBC white blood cell count
Self-Assessment Questions
Answers and explanations to these questions can be
found at the end of this chapter.
1. A 74-year-old woman (weight 72 kg) arrives in
the emergency department with a 3-day history
of cough, body temperature of 102°F (38.9°C),
and lethargy. She has the following vital signs and
laboratory values: blood pressure 72/40 mm Hg,
heart rate 115 beats/minute, urine output 10 mL/
hour, white blood cell count (WBC) 18 × 103 cells/
mm 3, hemoglobin 12.5 g/dL, and blood urea nitro-
gen (BUN)/serum creatinine (SCr) ratio of 28:1.7
mg/dL (baseline SCr 1.2 mg/dL), and blood glu-
cose 82 mg/dL. After a 500-mL fluid bolus of 0.9%
sodium chloride, her blood pressure is 80/46 mm
Hg and her heart rate is 113 beats/minute. Her chest
radiograph is consistent with pneumonia. Her med-
ical history includes coronary artery disease and
arthritis. Which is the most appropriate treatment
at this time?
A. Furosemide 40 mg intravenously.
B. 5% albumin 500 mL infused over 4 hours plus
norepinephrine titrated to maintain a systolic
blood pressure of 90 mm Hg or higher.
C. 1000-mL fluid bolus with 5% dextrose (D5 W)
and 0.9% sodium chloride.
D. 1000-mL fluid bolus with 0.9% sodium chloride.
2. An order has been received for 2% sodium chlo-
ride. Assume no commercially available product is
available. Using 0.9% sodium chloride and 23.4%
sodium chloride, first determine how much of each
is necessary to prepare 1 L of 2% sodium chloride.
Second, calculate the osmolarity of 2% sodium
chloride. Finally, determine whether the resultant
solution should be administered through a cen-
tral or peripheral intravenous infusion (molecular
weight [MW] of sodium chloride is 58.5, osmotic
coefficient is 0.93).
A. Mix 951 mL of 0.9% sodium chloride plus
49 mL of 23.4% sodium chloride; osmolarity =
635 mOsm/L; peripheral intravenous infusion.
B. Mix 951 mL of 0.9% sodium chloride plus
49 mL of 23.4% sodium chloride; osmolarity
= 954 mOsm/L; central intravenous infusion.
C. Mix 850 mL of 0.9% sodium chloride plus
150 mL of 23.4% sodium chloride; osmolarity
= 954 mOsm/L; central intravenous infusion.

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Fluids, Electrolytes, and Nutrition
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D. Mix 850 mL of 0.9% sodium chloride plus
150 mL of 23.4% sodium chloride; osmolarity
= 513 mOsm/L; peripheral intravenous infusion.
3. A 68-year-old man is admitted to the hospital for
worsening shortness of breath during the past 2
weeks caused by heart failure. His serum sodium
concentration on admission was 123 mEq/L. Other
abnormal laboratory values include brain natri-
uretic peptide of 850 pg/mL and SCr of 1.7 mg/
dL. Chest radiography is consistent with pulmo-
nary edema. The patient weighs 85 kg on admis-
sion, which is up 3 kg from his baseline weight.
The patient is not experiencing nausea, headache,
or mental status changes. The physician orders 3%
sodium chloride to treat the hyponatremia. Which
recommendation is best?
A. 3% sodium chloride is an appropriate choice
because the hyponatremia is probably acute.
B. A 250-mL bolus of 3% sodium chloride is
appropriate if used in combination with furo-
semide to prevent volume overload.
C. 3% sodium chloride is appropriate if the serum
sodium does not increase more than 10 mEq/L
in 24 hours.
D. The risks of 3% sodium chloride outweigh the
potential benefit for this patient.
4. A 55-year-old man with diabetes and kidney dis-
ease has hyperkalemia. His laboratory values
include potassium (K+
) 7.2 mEq/L, calcium (Ca 2+
)
9 mg/dL, albumin 3.5 g/dL, and blood glucose 302
mg/dL. His electrocardiogram (ECG) is abnormal,
with peaked T waves. What is the best recommen-
dation for initial treatment?
A. Regular insulin 10 units intravenously plus
50 g of dextrose intravenously.
B. 10% calcium gluconate 10 mL intravenously.
C. Sodium polystyrene sulfonate (Kayexalate)
15 g orally.
D. Sodium bicarbonate 50 mEq intravenously
over 5 minutes.
5. A 68-year-old woman (weight 60 kg) is admitted
to the hospital after a cardioembolic stroke. Her
medical history is significant for atrial fibrillation,
acute myocardial infarction, and diabetes. She has
been unconscious for 48 hours. The medical team
decides to start providing nutrition. All of her lab-
oratory values, including glucose concentrations,
are normal. Although she currently has no enteral
access, she does have a peripheral intravenous
catheter. Which nutritional regimen is best for this
patient?
A. Insert a central intravenous catheter and initi-
ate parenteral nutrition (PN) containing 60 g
of amino acids (AAs), 250 mL of 20% lipid
emulsion, 300 g of dextrose, standard elec-
trolytes, multivitamins, and trace elements
in a volume of 2000 mL administered over
24 hours.
B. Insert a central intravenous catheter and ini-
tiate PN containing 40 g of AAs, 250 mL of
20% lipid emulsion, 200 g of dextrose, stan-
dard electrolytes, multivitamins, and trace
elements in a total volume of 2000 mL admin-
istered over 24 hours.
C. Insert a nasogastric (NG) or nasoduodenal
feeding tube and infuse an isotonic formula
(1 kcal/mL) starting at 25 mL/hour and
advance to a goal rate of 65 mL/hour.
D. Insert a percutaneous endoscopic gastrostomy
feeding tube and infuse an isotonic formula
(1 kcal/mL) starting at 25 mL/hour and
advance to a goal rate of 100 mL/hour.
6. A 70-year-old man is admitted to the hospital with
peritonitis caused by severe inflammatory bowel
disease. The patient has received adequate fluid
resuscitation, and he is prescribed appropriate
antibiotics. After several days of the patient being
unable to tolerate oral or enteral nutrition, the phy-
sician consults the pharmacist to recommend a PN
formula to be administered through a central line.
The patient is hemodynamically stable, with nor-
mal electrolyte concentrations. Weight is 55 kg,
BUN/SCr is 20/1.1 mg/dL, and WBC is 17 × 103
cells/mm 3. Assuming that appropriate electrolytes,
multivitamins, and trace elements are included,
which PN formula, when administered over 24
hours, will best provide this patient adequate calo-
ries, AAs, and lipids?
A. AAs 10% 700 mL, dextrose 30% 325 mL,
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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-6
lipid 20% 500 mL.
B. AAs 10% 450 mL, dextrose 70% 400 mL,
lipid 20% 250 mL.
C. AAs 10% 800 mL, dextrose 70% 350 mL,
lipid 20% 250 mL.
D. AAs 15% 900 mL, dextrose 50% 500 mL,
lipid 20% 250 mL.
7. A 59-year-old man has been admitted to the hos-
pital after several days of vomiting and diarrhea.
In the emergency department, he had several
runs of nonsustained ventricular tachycardia. His
plasma potassium on admission is 2.8 mEq/L.
After 100 mEq of potassium chloride is infused
over 24 hours, his repeated K+ is 3.2 mEq/L, and he
continues to have runs of ventricular tachycardia.
Other laboratory values include Na+ 143 mEq/L,
magnesium 1.4 mg/dL, phosphorus 3 mg/dL, Ca2+
9 mg/dL, and ionized Ca2+ 1.1 mmol/L. Which
treatment would be best to give next?
A. Administer potassium chloride 20 mEq intra-
venously over 1 hour each for 4 doses and
recheck K+
.
B. Administer magnesium sulfate as a 2 g slow
intravenous infusion over 2 hours.
C. Administer potassium phosphate 15 mmol
intravenously over 4 hours.
D. Administer calcium gluconate 2 g intrave-
nously over 5 minutes.
8. Which nutritional strategy can best prevent
gut mucosal atrophy and subsequent bacterial
translocation?
A. PN enriched with glutamine.
B. PN enriched with branched-chain AAs.
C. Enteral nutrition (EN).
D. Zinc supplementation.
9. A female patient (weight 80 kg) in the intensive care
unit has developed acute kidney injury caused by
sepsis, and she requires intermittent hemodialysis
daily to maintain her BUN/SCr ratio at 49:2.5 mg/
dL. Currently, she is receiving appropriate antibi-
otics and is hemodynamically stable. She has also
been receiving PN providing 72 g of AAs per day.
What is the best recommendation for this patient’s
protein intake?
A. Reduce AAs to 40 g/day.
B. Reduce AAs to 64 g/day.
C. Increase AAs to 96 g/day.
D. Increase AAs to 160 g/day.

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-7
BPS Pharmacotherapy Specialty Examination Content.
This chapter covers the following sections of the Pharmacotherapy Specialty Examination Content Outline
1. Domain 1: Patient-Centered Pharmacotherapy
a. Task 1, Knowledge statements a-c, e, f, h, j-m, p, q
b. Task 2, Knowledge statements a, b, d
c. Task 3, Knowledge statements a-e
d. Task 4, Knowledge statements a
2. Domain 2: Application of Evidence to Practice and Education. Task 1, Knowledge statements g
3. Domain 3: Healthcare Systems and Population Health
a. Task 1, Knowledge statements e
b. Task 2, Knowledge statements a
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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-8
I. FLUID MANAGEMENT
A. Distribution of total body fluid (TBF) (Figure 1)
75% of extracellular fluid is interstitial
(this fluid “bathes the cells” and is
separated from intravascular space by the
semipermeable capillary membrane)
25% of extracellular fluid is intravascular
(about 5 L of blood volume)
60% of TBF
is intracellular
(enclosed by the
cell membrane)
40% of TBF is
extracellular
Figure 1. Distribution of total body fluid.
TBF = total body fluid.
1. Estimated as 60% of lean body weight (LBW) in men and 50% in women; a healthy adult (weight 70
kg) has about 42 L of fluid
2. Total body water is further divided into intracellular (IC) space and extracellular (EC) space.
a. About 60% of TBF is IC, and 40% is EC; the IC and EC fluid compartments are separated by cell
membranes, which are highly permeable to water.
b. The EC compartment is also divided into the interstitial (IS) space and the intravascular space; the
IS and intravascular fluid compartments are separated by the capillary membrane, which is perme-
able to almost all solutes except proteins.
i. 75% of the EC fluid is in the IS space.
ii. 25% of the EC fluid is in the intravascular space; the EC fluid in the intravascular space is
known as plasma, and it measures about 3 L; if you also consider about 2 L of fluid found in
red blood cells (thus, IC fluid), the total blood volume is about 5 L.
3. The approximate distribution of TBF into the IC and EC compartments with further distribution of
the EC fluid into the IS and intravascular compartments is important to remember for determining the
distribution of intravenous fluid.
B. Distribution of intravenous fluid (Table 1)
Table 1. Distribution of Intravenous Fluid
Intravenous Fluid Infused Volume (mL) Equivalent Intravascular Volume Expansion (mL)
Normal saline 1000 250
Lactated Ringer solution 1000 250
Normosol-R and Plasma-Lyte 1000 250
5% Dextrose 1000 100
Albumin 5% 500 500
Albumin 25% 100 500
Hydroxyethyl starch 6% 500 500

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-9
1. Crystalloids are intravenous fluids that can contain water, sodium (Na+
), chloride (Cl –
), and other elec-
trolytes. Lactated Ringer solution is a crystalloid that contains mostly Na+ and Cl – , but also lactate,
potassium (K+
), and calcium (Ca 2+
). Normosol-R and Plasma-Lyte are crystalloids that contain mostly
Na+ and Cl – but also acetate, K+, and magnesium (Mg2+
). D5 W is also a crystalloid, but it should not
be used for fluid resuscitation because of the smaller amount of fluid that remains in the intravascular
compartment.
a. Na and Cl – do not freely cross into cells, but they will distribute evenly in the EC space.
b. For 0.9% sodium chloride or lactated Ringer solution, only 25% remains in the intravascular space,
and 75% distributes in the IS space; therefore, when 1 L of 0.9% sodium chloride or lactated Ringer
solution is administered, about 250 mL of fluid remains in the intravascular compartment.
2. D5W is isosmotic and, because of rapid metabolism, it has the net effect of administering “free” water.
a. D5W is metabolized to water and carbon dioxide.
b. Water can cross any membrane in the body; therefore, it is evenly distributed in TBF (“free”
because it is free to cross any membrane).
i. Many experts avoid administering D5W whenever possible in patients with neurologic injury
and elevated intracranial pressure (ICP) because it can cross into cerebral cells, causing fur-
ther elevation in ICP.
ii. Some practitioners avoid the use of D5W because of the risk of hyperglycemia, although D5 W
contains only 5 g of dextrose/100 mL, which is equivalent to 17 kcal/100 mL.
c. For D5W, 60% distributes to the IC space and 40% distributes to the EC space. Of the 40% distrib-
uted to the EC space, 25% remains in the intravascular space, and 75% distributes to the IS space.
Therefore, when 1 L of D5W is administered intravenously, about 100 mL of fluid remains in the
intravascular compartment.
3. Colloids include packed red blood cells, pooled human plasma (5% albumin, 25% albumin, and 5%
plasma protein fraction), semisynthetic glucose polymers (dextran), and semisynthetic hydroxyethyl
starch (hetastarch).
a. Colloids are too large to cross the capillary membrane; therefore, they remain primarily in the
intravascular space (although a small portion “leaks” into the IS space).
b. Except for 25% albumin, administering 500 mL of colloid results in a 500-mL intravascular vol-
ume expansion.
c. Because 25% albumin has an oncotic pressure about 5-fold that of normal plasma, it causes a
fluid shift from the IS space into the intravascular space. For this reason, 100 mL of 25% albumin
results in around 500 mL of intravascular volume expansion. This hyperoncotic solution should
generally be avoided in patients requiring fluid resuscitation, because although the intravascular
space expands, fluid shifts out of the IS space, potentially causing dehydration. It may be useful in
patients who do not require fluid resuscitation but who could benefit from a redistribution of fluid
(e.g., ascites, pleural effusions).
d. Hydroxyethyl starch and dextran products have been associated with coagulopathy and kidney
impairment. In addition to acute kidney injury, hydroxyethyl starch is associated with increased
mortality in critically ill patients (JAMA 2013;309:678-88; N Engl J Med 2012;367:124-34).
C. Fluid Resuscitation
1. Intravascular fluid depletion can occur because of shock (hypovolemic or septic shock), and it is asso-
ciated with reduced cardiac function and organ hypoperfusion.
2. Signs or symptoms (Box 1) usually occur when about 15% (750 mL) of blood volume is lost (e.g., hem-
orrhage) or shifts out of the intravascular space (e.g., septic shock).
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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-10
Box 1. Signs and Symptoms of Intravascular Volume Depletion
Tachycardia (HR > 100 beats/minute)
Hypotension (SBP < 80 mm Hg)
Orthostatic changes in HR or BP
Increased BUN/SCr ratio > 20:1
Dry mucous membranes
Decreased skin turgor
Reduced urine output
Dizziness
Improvement in HR and BP after a 500- to 1000-mL fluid bolus
BP = blood pressure; BUN = blood urea nitrogen; HR = heart rate; SBP = systolic blood pressure; SCr = serum creatinine.
3. Fluid resuscitation is indicated for patients with signs or symptoms of intravascular volume depletion.
4. The goal of fluid resuscitation is to restore intravascular volume and to prevent organ hypoperfusion.
5. Because intravascular volume depletion can cause organ dysfunction and death, prompt resuscitation
is necessary.
a. Intravenous fluids are infused rapidly, preferably through a large-bore catheter.
b. Intravenous fluids are administered as a 500- to 1000-mL bolus, (~30 mL/kg in septic patients)
after which the patient is reevaluated; this process is continued as long as signs and symptoms of
intravascular volume depletion are improving (Box 1).
Table 2. Content of Common Crystalloid Solutions
Contents (mEq/L) Osmolarity (mOsmol/L)
Sodium chloride 0.9% (NS) Na 154
Cl 154
308
Lactated Ringer (LR) Na 130
Cl 109
K 4
Ca 3
Lactate 28
273
Normosol-R Na 140
Cl 98
K 5
Mg 3
Acetate 27/Gluconate 23
295
Ca = calcium; Cl = chloride; K = potassium; Mg = magnesium; Na = sodium.
6. Crystalloids (0.9% sodium chloride or lactated Ringer solution) are recommended for fluid resuscitation
in hypovolemia (Table 2).
a. Lactated Ringer solution is historically preferred in surgery and trauma patients, but no evidence
suggests superiority over normal saline for fluid resuscitation in these settings.
b. The lactate in lactated Ringer solution is metabolized to bicarbonate, and it can theoretically be
useful for metabolic acidosis; however, lactate metabolism is impaired during shock. Thus, lactated
Ringer solution may be an ineffective source of bicarbonate.

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Fluids, Electrolytes, and Nutrition
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c. Lactated Ringer solution has been considered to provide a more physiologic amount of Cl
(109 mmol/L) than 0.9% sodium chloride (154 mmol/L). A balanced fluid regimen (e.g., lactated
Ringer solution, Plasma-Lyte 148) was associated with a reduction in the incidence of acute kid-
ney injury compared with a standard regimen (e.g., 0.9% sodium chloride, colloids containing
Cl 120–130 mmol/L) (JAMA 2012;308:1566). In a multicenter, retrospective cohort study, a bal-
anced solution (lactated Ringer) was compared with isotonic fluid (0.9% sodium chloride) in
patients with sepsis. In these patients with vasopressor-dependent sepsis, those receiving balanced
fluid had a lower risk of in-hospital mortality (Crit Care Med 2014;42:1585-91). More recent studies
have shown that, compared with 0.9% sodium chloride, balanced crystalloids result in a lower rate
of a composite outcome of any cause of death, new renal replacement therapy, and persistent renal
dysfunction in intensive care unit (ICU) patients. There was no difference found in hospital-free
days in non-ICU patients (N Engl J Med 2018; 378:819-39).
7. There is no difference between crystalloids and colloids in the time to achieve fluid resuscitation or in
patient outcomes. Colloids have not been shown to be superior to crystalloids, and they are associated
with higher cost and some adverse effects. The following are examples of other, although controversial,
uses of colloids:
a. Colloids can be considered after fluid resuscitation with crystalloid (usually 4–6 L) has failed to
achieve hemodynamic goals or after clinically significant edema limits the further administration
of crystalloid.
b. Albumin can be considered in patients with a low albumin concentration who have required a large
volume of resuscitation fluids.
c. Albumin (theoretically, 25% is preferred) can be considered in conjunction with diuretics for
patients with clinically significant edema (e.g., pulmonary edema causing respiratory failure) and
a low albumin concentration, when appropriately dosed diuretics are ineffective.
D. Maintenance intravenous fluids
1. Maintenance intravenous fluids are indicated in patients who are unable to tolerate oral fluids.
2. The goal of maintenance intravenous fluids is to prevent dehydration and to maintain a normal fluid and
electrolyte balance.
3. Maintenance intravenous fluids are typically administered as a continuous infusion through a periph-
eral or central intravenous catheter.
4. Common methods of estimating the daily volume in children and adults:
a. Administer 100 mL/kg for first 10 kg, followed by 50 mL/kg for the next 10–20 kg (i.e., 1500 mL
for the first 20 kg) plus 20 mL/kg for every kilogram greater than 20 kg or
b. Administer 20–40 mL/kg/day (for adults only).
c. Adjust fluids according to the individual patient’s input, output, and estimated insensible loss.
5. A typical maintenance intravenous fluid is D5W with 0.45% sodium chloride plus 20–40 mEq of potas-
sium chloride per liter. The potassium chloride content can be adjusted for the individual patient.
6. If 150 mEq of sodium bicarbonate is added to 850 mL of 0.9% sodium chloride, the resultant solution is
equivalent to about 1.6% sodium chloride. When an infusion of 150 mEq of sodium bicarbonate per liter
is indicated, it is recommended to add sodium bicarbonate to D5 W or sterile water for injection instead
of 0.9% sodium chloride.
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Patient Case
Questions 1 and 2 pertain to the following case.
A 65-year-old man (weight 80 kg) with a 3-day history of a body temperature of 102°F (38.9°C), lethargy, and
productive cough is hospitalized for community-acquired pneumonia. His medical history includes uncontrolled
hypertension and coronary artery disease. His vital signs include heart rate 104 beats/minute, blood pressure
112/68 mm Hg, and body temperature 101.4°F (38.6°C). His urine output is 10 mL/hour, K 4 mEq/L, BUN is 46
mg/dL, SCr is 1.7 mg/dL, and WBC is 10.4 × 103 cells/mm3. Other laboratory values are normal.
1. Which is most appropriate at this time?
A. Furosemide 40 mg intravenously.
B. Albumin 25% 100 mL intravenously over 60 minutes.
C. Lactated Ringer solution 1000 mL intravenously over 60 minutes.
D. D5W/0.45% sodium chloride plus potassium chloride 20 mEq/L to infuse at 110 mL/hour.
2. After 2 days of appropriate antibiotic treatment, the patient has a WBC of 9 × 103 cells/mm3
, and he is afebrile.
His blood pressure is 135/85 mm Hg, and his urine output is 45 mL/hour. His albumin is 3.2 g/dL, BUN is
14 mg/dL, and SCr is 1.4 mg/dL. All other laboratory values are normal. His appetite is still poor, and he is
not taking adequate fluids. He has peripheral intravenous access. Which option is most appropriate to initiate?
A. Peripheral PN to infuse at 110 mL/hour.
B. Albumin 5% 500 mL intravenously over 60 minutes.
C. D5W/0.45% sodium chloride plus potassium chloride 20 mEq/L to infuse at 110 mL/hour.
D. Lactated Ringer solution to infuse at 75 mL/hour.
II. OSMOLALITY
A. Plasma osmolality is normally 275–290 mOsm/kg.
1.Terminology
a. Osmolality is a measure of the osmoles of solute per kilogram of solvent (Osm/kg), whereas osmo-
larity is a measure of osmoles of solute per liter of solution (Osm/L).
b. Plasma osmolarity (mOsm/L) can be calculated as osmolality × 0.995, showing that there is no clin-
ically significant difference between them (i.e., plasma osmolarity is about 1% lower than plasma
osmolality).
2. Plasma osmolality is maintained within a normal range by thirst and secretion of arginine vasopressin
(i.e., antidiuretic hormone [ADH]) from the posterior pituitary.
3. Sodium salts are the primary determinant of plasma osmolality, and they regulate fluid shifts between
the IC and EC fluid compartments.
4. Plasma osmolality (mOsm/kg) can be estimated: (2 × Na+ mEq/L) + (glucose mg/dL/18) + [(BUN mg/
dL) ÷ 2.8].
5. Increases in plasma osmolality cause an osmotic shift of fluid into the plasma, resulting in cellular
dehydration and shrinkage.
6. Decreases in plasma osmolality cause an osmotic shift of fluid into cells, resulting in cellular over-
hydration and swelling.

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B. Intravenous fluids can be classified by their osmolarity relative to plasma.
1. Isotonic fluid does not result in a fluid shift between fluid compartments because the osmolarity is
similar to plasma.
2. Hypertonic fluid, such as NaCl 3%, can cause fluid to shift from the IC to the EC compartment, with
subsequent cellular dehydration and shrinkage.
3. Hypotonic fluid, such as NaCl 0.225%, with an osmolarity less than 150 mOsm/L can cause fluid to
shift from the EC to the IC compartment, with subsequent cellular overhydration and swelling.
a. Red blood cell swelling can cause cell rupture (i.e., hemolysis).
b. Brain cells can swell, causing cerebral edema and herniation; this is most likely to occur with acute
hyponatremia (occurring in less than 2 days).
C. Definitions
1. Equivalent weight = Molecular weight (MW) divided by valence.
a. A milliequivalent (mEq) = 1/1000 of an equivalent.
b. Examples of equivalent weight are shown in Table 3.
c. 1 mol = equivalent weight
Table 3. Electrolyte MW, Valence, and Equivalent Weight
Electrolyte MW Valence Equivalent Weight (g)
Sodium 23 1 23
Potassium 39 1 39
Chloride 35.5 1 35.5
Magnesium 24 2 12
MW = molecular weight.
2. Osmoles = number of particles in a solution (assuming complete dissociation).
a. A milliosmole = 1/1000 of an osmole.
b. Examples of osmoles are shown in Table 4.
Table 4. Osmoles
Salt Osmoles
NaCl 2
KCl 2
CaCl 2 3
CaCl 2 = calcium chloride; KCl = potassium chloride; NaCl = sodium chloride.
3. Converting MW to milliequivalents (Box 2)
Box 2. Converting MW to Milliequivalents
Convert 23.4% NaCl (concentrated NaCl) to mEq/mL
MW of NaCl = 23 + 35.5 = 58.5 (add MW of Na + Cl)
23.4 g 1 equiv 1000 mEq
––––––– × –––––––– × –––––––––– = 4 mEq/mL
100 mL 58.5 g 1 equiv
MW = molecular weight; NaCl = sodium chloride.

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D. Calculating the osmolarity of intravenous fluids in milliosmoles per liter
1. The osmotic coefficient can be used to calculate the osmolarity of intravenous fluids because salt forms
do not completely dissociate in solution. However, commercially available products often have different
reported osmolarities than if if the osmolarity is calculated using the osmotic coefficient.
a. With sodium chloride, for example, there is some ionic attraction between Na+ and Cl, and they
do not completely dissociate; rather, they are about 93% dissociated in solution (thus, the osmotic
coefficient is 0.93).
b. In clinical practice and in commercially available products, most do not consider the osmotic coef-
ficient when calculating the osmolarity of sodium chloride or other electrolytes. In reality, the
osmotic coefficient is probably not clinically relevant (but it is used in the following examples for
completeness).
2. Normal saline (0.9% sodium chloride) (Table 5)
Table 5. Calculation for Normal Saline Using the Osmotic Coefficient
Molecular Weight Osmoles Osmotic Coefficient
58.5 g/mol 2 0.93
0.9 g 1 mol 2 Osm 1000 mOsm 1000 mL––––––– × –––––– × –––––– × –––––––––– × –––––––– × 0.93 = 287 mOsm/L
100 mL 58.5 g 1 mol 1 Osm 1 L
3. D5W (MW 198 g/mol) (Box 3)
Box 3. Calculation for D5 W
5 g × 1 mol 1000 mOsm 1000 mL––––––– × –––––– × –––––––––––– × –––––––– = 252.5 mOsm/L
100 mL 198 g 1 mol 1 L
4. Osmolarity of D5W/normal saline using the osmotic coefficient = 252.5 mOsm/L + 287 mOsm/L =
539.5 mOsm/L.
5. Osmolarity of normal saline + potassium chloride 20 mEq/L (Box 4)
Box 4. Calculation for NS plus KCl Using the Osmotic Coefficient
Step 1: Convert mEq to weight (g)
1 equiv 74.5 g
20 mEq × –––––––––– × –––––––– = 1.49 g of KCl
1000 mEq 1 equiv
Step 2: Calculate mOsm/L
1.49 g 1 mol 2 Osm 1000 mOsm
––––––– × –––––––– × –––––––– × –––––––––––– = 40 mOsm/L
L 74.5 g 1 mol 1 Osm
Step 3: Add osmolarity of NS + KCl = 287 mOsm/L + 40 mOsm/L = 327 mOsm/L
NS = normal saline; KCl = potassium chloride.

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III. HYPERTONIC SALINE
A. Concentration: Typically use 3% (954 mOsm/L), 7.5% (2393 mOsm/L), or 23.4% (7462 mOsm/L). Sodium
chloride 3% and 23.4% are available commercially, whereas other concentrations must be extemporane-
ously prepared.
B. Common uses of hypertonic saline
1. Hypertonic saline is used in traumatic brain injury to reduce an elevated ICP and thereby increase
cerebral perfusion pressure. It is typically used if sustained ICP is greater than 20 mm Hg as measured
with an ICP monitor.
2. Hypertonic saline is used for symptomatic hyponatremia (symptoms described later in the Hyponatremia
section).
a. Symptoms generally do not occur unless serum sodium is 120 mEq/L or less, and they increase in
severity as Na+ decreases.
b. Symptoms of severe hyponatremia include coma and seizures.
c. In an effort to prevent severe symptoms from occurring, some practitioners treat asymptomatic
or moderately symptomatic (e.g., lethargy, confusion) hyponatremia before serum sodium con-
centrations reach 120 mEq/L or less because of the increased risk of severe symptoms below this
concentration.
C. Inappropriate use of hypertonic saline
1. Chronic asymptomatic hyponatremia
a. Asymptomatic syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is usually
treated with fluid restriction of less than 1000 mL of fluid per day.
b. Hyponatremia is generally a water problem (i.e., an excess of free water) rather than a deficiency
of Na; thus, hypertonic saline makes little sense in the absence of symptoms (see Hyponatremia
section).
2. Hyponatremia associated with severe hyperglycemia (pseudohyponatremia; i.e., diabetic ketoacidosis)
a. Typically, serum sodium decreases in a nonlinear fashion in response to hyperglycemia (i.e.,
Na + decreases by about 1.6 mEq/L for every 100-mg/dL elevation in glucose of 100–400 mg/dL;
however, another version of the formula shows that Na + decreases by about 2.4 mEq/L for every
100-mg/dL elevation in glucose above 100 mg/dL). Corrected Na+ = serum Na+ + [1.6 (glucose
– 100)/100]
b. As hyperglycemia is corrected with insulin, the serum sodium will normalize.
3. Hyponatremia associated with hypervolemia (i.e., heart failure leads to tissue hypoperfusion, which
triggers ADH secretion, causing reabsorption of water from the kidneys and leading to hyponatremia)
a. In general, this situation is treated with fluid restriction or diuresis.
b. Symptomatic hyponatremia is uncommon in patients with heart failure.
c. Hypertonic saline could be considered in symptomatic patients; however, they may also need
diuresis to prevent worsening volume overload.
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D. Preparation of hypertonic saline (Commercially available products should be used whenever possible to
minimize the risk of error) (Figure 2)
Choose base solutions
Set up alligation
Add and subtract
Divide
Steps Example
For this example, use concentrated NaCl available as 23.4% vials
and sterile water to make 1000 mL of 7.5% HS
7.5 parts/23.4 parts = x/1000 mL; x = 320.5 mL of 23.4% NaCl
15.9 parts/23.4 parts = x/1000 mL; x = 679.5 mL of sterile water
7.5 parts (from 23.4% NaCl)
15.9 parts (from sterile water)
23.4 parts total
23.4%
0
7.5%
23.4%
0
7.5%
Figure 2. Calculations to prepare hypertonic saline.
HS = hypertonic saline; NaCl = sodium chloride.
E. Hypertonic saline dose
1. Dose options for traumatic brain injury and other neurological injuries
a. 3% hypertonic saline 250 mL or 2–4 mL/kg intravenously over 1–15 minutes administered for
elevated ICP
b. 23.4% hypertonic saline 30 mL over 20–30 minutes administered for elevated ICP
i. Standing orders such as 30 mL every 4–6 hours are sometimes used or may be used as needed
for a sustained ICP greater than 20 mm Hg.
ii. If hypertonic saline is needed for prolonged reduction in ICP, a 3% hypertonic saline continu-
ous infusion may be recommended.
2. Dose options for patients with symptomatic hyponatremia
a. Treatment of patients with symptomatic hyponatremia involves a small but quick increase in serum
sodium by 0.75–1 mEq/L/hour to a concentration of 120 mEq/L, though not more than 10–12 mEq
in 24 hours. Next, the infusion can be reduced so that Na+ increases by 0.5 mEq/L/hour. For severe
symptoms, it is reasonable to increase serum sodium by up to 2 mEq/L/hour for a short time, as
long as the maximum change of 10–12 mEq in 24 hours is not exceeded. If hypertonic saline is
used for mild symptoms, a slower change in serum sodium of 0.5 mEq/L/hour would be appropri-
ate, although some would avoid hypertonic saline altogether. Some protocols are more conserva-
tive, recommending a maximum change of 8 mEq in 24 hours. If the maximum rate is exceeded in
24 hours or the rate in sodium rise is increasing too rapidly, some practitioners recommend coun-
teracting the quick rise with desmopressin or dextrose 5% in water (more info in hypernatremia
section).
b. Estimate an infusion rate of 3% hypertonic saline by multiplying ideal body weight (IBW) by
desired rate of serum sodium increase per hour. (Note: IBW is used to avoid overdosing patients
with obesity.)
i. For example, 70 kg × 1 mEq/L/hour = 70 mL/hour to increase serum sodium by 1 mEq/L in
1 hour. The infusion can be adjusted to achieve goal changes in serum sodium.
ii. Infusion rate of 3% hypertonic saline is generally 1–2 mL/kg/hour.
iii. In general, 3% hypertonic saline is not recommended in asymptomatic patients; if used in an
asymptomatic patient, the administration rate should generally not exceed 0.5–1 mL/kg/hour.

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c. Alternatively, some practitioners recommend a 250-mL bolus of 2%–3% hypertonic saline over
30 minutes or 50 mL of 3% hypertonic saline administered as a bolus every 30 minutes for
two doses.
F. Administration of hypertonic saline
1. Use central intravenous access because the osmolarity is greater than 900 mOsm/L.
2. If no central line is available, consider using 2% hypertonic saline.
3. Some practitioners use 3% hypertonic saline through a peripheral intravenous access site in an emer-
gency, because the osmolarity is close to the cutoff range for peripheral administration. Recent litera-
ture suggests that 3% sodium chloride can safely be administered through a peripheral line (J Neurosci
Nurs 2017;49:191-5). If a peripheral site is used, use a large vein and monitor for phlebitis.
G. Clinical goals and monitoring for administering hypertonic saline in patients with symptomatic hyponatremia
1. Goals
a. Decrease symptoms (described later).
b. Safe serum sodium achieved usually in the range of 120–125 mEq/L to avoid adverse neurologic
outcomes. Note that the immediate goal for patients with symptomatic hyponatremia is not neces-
sarily a normal serum sodium.
c. Reached maximum safe amount of change in serum sodium
i. Maximum safe amount of change is generally regarded as 10–12 mEq/L in 24 hours.
ii. Some practitioners suggest a maximum change of 8 mEq/L in 24 hours.
2. Monitoring of serum sodium every 1–4 hours depending on severity of symptoms
H. Complications of hypertonic saline
1. Osmotic demyelination syndrome (includes central pontine and extrapontine myelinolysis) can occur
with rapid correction of hyponatremia.
a. It is characterized initially by lethargy and affect changes, followed by permanent neurologic dam-
age, including paraparesis, quadriparesis, dysarthria, dysphagia, and coma.
b. It is more likely to occur with rapid correction of chronic hyponatremia than with acute hypona-
tremia. This partly explains why it is advisable not to administer hypertonic saline in patients with
chronic asymptomatic hyponatremia.
c. Prevent this complication by avoiding changes in serum sodium of more than 10–12 mEq/L in
24 hours or more than 18 mEq/L in 48 hours.
2. Hypokalemia can occur with large volumes of hypertonic saline.
3. Hyperchloremic acidosis can result from the administration of chloride salts (i.e., sodium chloride).
It can be prevented by administering hypertonic saline in a 1:1 or 2:1 ratio of sodium chloride and
sodium acetate or using fluid with less chloride content.
4. Hypernatremia
5. Phlebitis if administered in a peripheral vein
6. Heart failure
a. Fluid overload can result from initial volume expansion.
b. Over time, hypertonic saline can have a diuretic effect, leading to intravascular volume depletion.
7. Coagulopathy caused by platelet dysfunction
8. Hypotension if hypertonic saline is administered rapidly
I. Other considerations when using hypertonic saline.
a. Because hypokalemia can cause hyponatremia, remember to correct K+ depletion if present. As K+
is replaced, serum sodium will increase.
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IV. HYPOTONIC INTRAVENOUS FLUIDS
A. Hypotonic fluids administered intravenously can cause cell hemolysis and patient death.
1. Albumin 25% diluted with sterile water to make albumin 5% has an osmolarity of about 60 mOsm/L,
which can cause hemolysis.
2. “Quarter normal saline,” or 0.225% sodium chloride, has an osmolarity of 77 mOsm/L and can cause
hemolysis.
B. Avoid using intravenous fluid with an osmolarity less than 150 mOsm/L.
1. Sterile water alone should never be administered intravenously.
2. Some prescribers use hypotonic saline for a patient with hypernatremia.
a. In reality, a patient with mild hypernatremia generally needs water, not additional Na+
.
b. Therefore, for patients with hypernatremia, enteral administration of water is preferable.
c. If the enteral route is unavailable, recommend D5 W administered intravenously.
C. Prevent a potentially fatal error by recommending one of the following alternatives to 0.225% sodium
chloride:
1. Recommend changing 0.225% sodium chloride to D5 W alone or a combination of D5W and 0.225%
sodium chloride.
2. Alternatively, if there are concerns related to hyperglycemia with using D5W (50 g of dextrose or
170 kcal/L), recommend using 2.5% dextrose and 0.225% sodium chloride.
3. Alternatively, potassium chloride can be added to increase osmolarity.
4. Recommend administering water enterally (by mouth or feeding tube).
5. If 0.225% sodium chloride is used, recommend use by central venous line.
V. HYPONATREMIA AND HYPO-OSMOLALITY STATES
A. Sodium salts are the primary determinants of plasma osmolality (and subsequent fluid shifts between the
IC and EC compartments).
1. A reduction in serum sodium to less than 136 mEq/L usually correlates with a reduction in plasma
osmolality.
2. Hyponatremia with subsequent hypo-osmolality causes fluid to shift into cells (cellular overhydration).
Hypotonic hyponatremia can be divided into three types according to volume status (Table 6).

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Table 6. Classification of Hyponatremia
Hypovolemic Hyponatremia Euvolemic Hyponatremia Hypervolemic Hyponatremia
Description Deficit of both Na+ and fluid,
but total Na+ is decreased more
than total body water
Normal total body Na+
with excess fluid volume
(i.e., dilutional)
Excess Na+ and fluid, but fluid
excess predominates
Example Fluid loss (e.g., emesis,
diarrhea, fever), third spacing,
renal loss (diuretics), cerebral
salt wasting
SIADH, medications Heart failure, cirrhosis,
nephrotic syndrome
Diagnosis Urine Na+ < 25 mEq/L
indicates nonrenal loss of Na+
(e.g., emesis, diarrhea); urine
Na+ > 40 mEq/L indicates
renal loss of Na+a
Urine osmolality > 100
mOsm/kg (indicates impaired
water excretion in presence
of plasma osmolality
< 275 mOsm/kg); urine
sodium > 40 mEq/La
Urine Na+ < 25 mEq/L
indicates edematous disorders
(i.e., heart failure, cirrhosis,
nephrotic syndrome); urine Na+
> 25 mEq/L indicates acute or
chronic renal failure a
Treatment Fluid resuscitation (see above);
in patients with cerebral salt
wasting because of a neuro-
logic injury, hyponatremia
can be prevented in patients
with neurologic injuries with
sodium chloride tablets or
fludrocortisone
If drug-induced SIADH,
remove offending agent; fluid
restriction; demeclocycline;
vasopressin receptor
antagonists (e.g., conivaptan,
tolvaptan), some institutions
use urea
Sodium and water restriction;
treat underlying cause;
vasopressin receptor
antagonists (e.g., conivaptan,
tolvaptan), diuretics
Na + = sodium; SIADH = syndrome of inappropriate secretion of antidiuretic hormone.
aUrine Na+ measurement may be inaccurate if a patient is receiving diuresis.
3. In select cases, hyponatremia is associated with either a normal or an elevated plasma osmolality.
a. This is known as pseudohyponatremia because Na+ content in the body is not actually reduced.
Instead, Na+ shifts from the EC compartment into the cells in an attempt to maintain plasma osmo-
lality in a normal range. Another adaptation to increased plasma osmolality is the shift of water
from inside cells to the EC compartment, which further dilutes the Na+ concentration.
i. Severe hyperlipidemia can be associated with a normal or elevated plasma osmolality.
ii. Severe hyperglycemia (i.e., during diabetic ketoacidosis) is associated with an elevated plasma
osmolality.
b. Once the underlying condition is corrected, Na+ will shift out of the cells, and hyponatremia will
resolve.
B. Causes of hyponatremia
1. Replacement of lost solute with water
a. Loss of solute (e.g., vomiting, diarrhea) usually involves the loss of isotonic fluid; therefore, alone,
it will not cause hyponatremia.
b. After the loss of isotonic fluid, hyponatremia can develop when the lost fluid is replaced with water.
c. A common cause of hyponatremia in hospitals is the postoperative administration of hypotonic
fluid.
2. Volume depletion and organ hypoperfusion stimulate ADH secretion to increase water reabsorption in
the collecting tubules, potentially causing hyponatremia.
3. SIADH and cortisol deficiency are both related to the excessive release of ADH.

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4. Medications, including thiazide diuretics, antiepileptic drugs (e.g., carbamazepine, oxcarbazepine), and
antidepressants (especially selective serotonin reuptake inhibitors, but also tricyclic antidepressants),
can cause hyponatremia. Drug-induced hyponatremia is more likely to occur in older adults and in
those who drink large volumes of water.
5. Renal failure impairs the ability to excrete dilute urine, predisposing to hyponatremia.
C. Symptoms of hyponatremia (Table 7)
Table 7. Symptoms of Hyponatremia
Serum Sodium (mEq/L) Clinical Manifestations
120–125 Nausea, malaise
115–120 Headache, lethargy, obtundation, unsteadiness, confusion
< 115 Delirium, seizure, coma, respiratory arrest, death
1. Symptoms are generally attributable to hypo-osmolality, with subsequent water movement into brain
cells causing cerebral edema.
2. If hyponatremia occurs chronically, cerebral cell swelling is prevented by osmotic adaptation.
a. Solutes move out of brain cells to prevent the osmotic shift of water into brain cells.
b. For this reason, patients with chronic hyponatremia may show less severe or no symptoms.
3. Neurologic symptoms are related to the rate of change in the serum sodium and to the degree of change
in serum sodium.
4. Acute hyponatremia occurs over 1–3 days.
D. Treatment of hyponatremia
1. Treat underlying cause.
2. Raise serum sodium at a safe rate, defined as a change no greater than 10–12 mEq/L in 24 hours.
3. Treatment depends on volume status, the presence and severity of symptoms, and the onset of
hyponatremia.
a. If the patient is euvolemic or edematous, there are typically two treatment options:
i. Fluid restriction (to less than 1000 mL/day) is the typical first-line recommendation for asymp-
tomatic patients. Note that sodium administration is not recommended for asymptomatic
patients because it can worsen edema.
ii. Vasopressin antagonists (e.g., intravenous conivaptan, oral tolvaptan) can be used in euvole-
mic (i.e., SIADH) or hypervolemic (i.e., heart failure) patients to promote aquaresis, increase
serum sodium, alleviate symptoms, and reduce weight; however, this approach is costly and
has not been shown to improve clinical outcomes (i.e., fall prevention, hospitalization, hos-
pital length of stay, quality of life, mortality) in prospective randomized controlled trials.
Vasopressin antagonists are substrates and inhibitors of cytochrome P450 3A4 isoenzymes.
Monitor for drug interactions with other 3A4 inhibitors that could increase effect and lead to a
rapid increase in serum sodium. Fluid restriction in combination with a vasopressin antagonist
during the first 24 hours can also increase the risk of overly rapid correction of serum sodium.
If needed, fluid restriction can be used after 24 hours. Tolvaptan should not be administered
for more than 30 days to minimize risk of liver injury. Monitor for recurrence of hyponatremia
once treatment is discontinued. In hypervolemic hyponatremia, diuretics can also be used
cautiously.

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b. If the patient has intravascular volume depletion, volume must be replaced first with intravenous
crystalloids (e.g., 0.9% sodium chloride).
i. Until intravascular volume is restored, the patient will continue to secrete ADH, causing water
reabsorption and subsequent hyponatremia.
ii. Once intravascular volume is restored, ADH secretion will decrease, causing water to be
excreted. This can lead to a rapid correction of serum sodium; careful monitoring is necessary
to prevent overly rapid correction.
iii. Volume status can be assessed by skin turgor, jugular venous pressure, and urine sodium.
c. Once intravascular volume is restored, patients who experienced volume depletion, diuretic-in-
duced hyponatremia, or adrenal insufficiency may still need Na+
.
i. The amount of Na+ (in milliequivalents) needed to raise the serum sodium to a safe concen-
tration of about 120 mEq/L (if the serum sodium is less than this) is estimated using LBW as
follows: 0.5 (LBW) × (120 − Na+) for women (multiply LBW by 0.6 for men). LBW has been
estimated using weight in kilograms and height in centimeters for men as LBW = [(0.3)(kg) +
(0.3)(cm) − 29] or for women as LBW= [(0.3)(kg) + (0.4)(cm) − 43]; formula published in 1966
(J Clin Pathol 1966;19:389).
ii. Alternatively, this equation can be modified to estimate the Na+ deficit in the following
manner: 0.5 (LBW) × (140 − Na+) for women (multiply LBW by 0.6 for men). If calculating the
Na+ deficit, it is recommended to administer 25%–50% of the deficit during the first 24 hours
to prevent the overly rapid correction of serum sodium.
iii. Regardless of the method used to estimate Na+ replacement, the amount of Na+ administered
should be guided by serial serum sodium concentrations (e.g., every 4 hours).
d. Patients with symptomatic hyponatremia should be treated with hypertonic saline (see Hypertonic
Saline section).
4. Correct hypokalemia, if present, with hyponatremia.
a. Hypokalemia will cause a reduction in serum sodium because Na+ enters cells to account for the
reduction in IC K+ to maintain cellular electroneutrality.
b. Administration of K+ will help correct hyponatremia.
c. Use caution when giving K+ to prevent overly rapid correction of serum sodium.
Patient Case
Questions 3–5 pertain to the following case.
A 72-year-old woman (weight 60 kg) with a history of hypertension has developed hyponatremia after starting
hydrochlorothiazide 3 weeks earlier. She experiences dizziness, fatigue, and nausea. Her serum sodium is 116 mEq/L.
Her blood pressure is 86/50 mm Hg, and heart rate is 122 beats/minute.
3. In addition to discontinuing hydrochlorothiazide, which initial treatment regimen is best?
A. Administer 0.9% sodium chloride infused at 100 mL/hour.
B. Administer 0.9% sodium chloride 500-mL bolus.
C. Administer 3% sodium chloride infused at 60 mL/hour.
D. Administer 23.4% sodium chloride 30-mL bolus as needed.

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Patient Case (Cont’d)
4. Which is the best treatment goal for the first 24 hours in correcting the patient’s serum sodium from her initial
value of 116 mEq/L?
A. Increase Na+ concentration to 140 mEq/L.
B. Increase Na+ concentration to 132 mEq/L.
C. Increase Na+ concentration to 126 mEq/L.
D. Maintain serum sodium of 116–120 mEq/L.
5. One day later, the patient has somewhat improved. Her blood pressure is 122/80 mm Hg, and heart rate is
80 beats/minute. Her serum sodium is 120 mEq/L, and K+ is 3.2 mEq/L; she still feels tired. She is eating a
regular diet. Her ECG is normal. Which is the best recommendation?
A. D5W/0.9% sodium chloride plus potassium chloride 40 mEq/L to infuse at 100 mL/hour.
B. 0.9% sodium chloride infused at 100 mL/hour.
C. 3% sodium chloride infused at 60 mL/hour.
D. Potassium chloride 20 mEq by mouth every 6 hours for 4 doses.
VI. HYPERNATREMIA AND HYPEROSMOLAL STATES
A. Hyperosmolality with serum sodium greater than 145 mEq/L
1. The osmotic gradient associated with hypernatremia causes water movement out of cells and into the
EC space.
2. Symptoms are related primarily to the dehydration of brain cells.
B. Causes of hypernatremia
1. Loss of water because of fever, burns, infection, renal loss (e.g., diabetes insipidus), gastrointestinal
(GI) loss
2. Retention of Na+ because of the administration of hypertonic saline or any form of Na+
3. Certain neurologic injuries receive hypertonic saline to target a higher sodium goal
C. Prevention of hypernatremia through osmoregulation
1. Plasma osmolality is maintained at 275–290 mOsm/kg, despite changes in water and Na+ intake.
2. Hypernatremia is prevented first by the release of ADH, causing water reabsorption.
3. Hypernatremia is also prevented by thirst.
a. Hypernatremia occurs primarily in adults with altered mental status who have an impaired thirst
response or do not have access to or the ability to ask for water.
b. Hypernatremia can also occur in infants.
D. Cerebral osmotic adaptation
1. Similar to patients with hyponatremia, patients with chronic hypernatremia can have cerebral osmotic
adaptation.
a. Brain cells take up solutes, Na+
, and K+, thus limiting the osmotic gradient between the IC and
EC fluid compartments.
b. This prevents cellular dehydration, and it will increase the brain volume toward a normal value,
despite hypernatremia.
2. Because of osmotic adaptation, patients with chronic hypernatremia may be asymptomatic.

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-23
E. Symptoms of hypernatremia are primarily neurologic.
1. Similar to hyponatremia, the symptoms of hypernatremia are related to the rate of increase in plasma
osmolality and the degree of increase in plasma osmolality.
2. Earlier symptoms include lethargy, weakness, and irritability.
3. Symptoms can progress to twitching, seizures, coma, and death if serum sodium is greater than
158 mEq/L. However, some neurologic injuries may have higher serum sodium targets.
4. Cerebral dehydration can cause cerebral vein rupture with subsequent intracerebral or subarachnoid
hemorrhage.
F. Treatment of hypernatremia
1. Rapid correction of chronic hypernatremia can result in cerebral edema, seizure, permanent neurologic
damage, and death.
a. With osmotic adaptation, the brain volume is raised toward normal despite an elevated serum
osmolality.
b. Osmotic adaptation combined with a rapid reduction in plasma osmolality can cause an osmotic
gradient, causing water to move into brain cells with subsequent cerebral edema.
2. In patients with symptomatic hypernatremia, serum sodium should be reduced slowly by no more than
0.5 mEq/L/hour or 12 mEq/L/day.
3. Treat hypernatremia by replacing water deficit slowly over several days to prevent overly rapid correc-
tion of serum sodium.
a. Using LBW, the estimated water deficit (in liters) is (0.4 × LBW) × [(Serum sodium/140) − 1]
in women (multiply LBW by 0.5 in men).
b. Note that in women and men, total body water is typically about 50% and 60%, respectively, of
LBW. Thus, some sources recommend a variation on the earlier equation as follows: Water deficit
= (0.5 × LBW) × [(Serum sodium/140) − 1] in women (multiply LBW by 0.6 in men). However,
patients with hypernatremia are generally water depleted; thus, the equation using the lower values
above (i.e., 40% or 0.4 and 50% or 0.5) is reasonable.
4. Administer free water orally or intravenously as D5 W.
5. If concurrent Na+ and water depletion occur (e.g., vomiting, diarrhea, diuretic-induced depletion), use
a combination of D5W and 0.225% sodium chloride.
6. If the patient is hypotensive because of volume depletion, first restore intravascular volume with
0.9% sodium chloride to restore tissue perfusion. Normal saline is the preferred crystalloid for fluid
resuscitation, and it is still relatively hypotonic in the patient with hypernatremia.
7. Patients with severe central diabetes insipidus may require desmopressin (DDAVP) (a synthetic analog
of ADH) to replace insufficient or absent endogenous ADH. Diabetes insipidus is marked by increased
urine output and decreased urine specific gravity.
Patient Case
6. A 74-year-old woman (weight 50 kg) has been receiving isotonic tube feedings at 60 mL/hour for the past
8 days through her gastrostomy feeding tube. She recently had an ischemic stroke; she is responsive but is not
able to communicate. Her serum sodium was 142 mg/dL on the day the isotonic formula was initiated, and it
has risen steadily to 149, 156, and 159 mg/dL on days 3, 4, and 8, respectively, after the start of the tube feed-
ings. What is the best treatment for her hypernatremia?
A. Administer sterile water intravenously at 80 mL/hour.
B. Administer D5W intravenously at 80 mL/hour.
C. Administer D5W/0.225% sodium chloride intravenously at 80 mL/hour.
D. Administer water by enteral feeding tube 200 mL every 6 hours.

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-24
VII. DISORDERS OF K+
A. Normal plasma potassium concentrations are 3.5–5 mEq/L.
B. K+ is the primary IC cation (maintains electroneutrality with Na, the primary EC cation).
C. K+ balance is maintained between the IC and EC compartments by several factors, including the following:
1.β 2-Adrenergic stimulation (caused by epinephrine) promotes cellular uptake of K+
.
2. Insulin promotes cellular uptake of K+
.
3. Plasma potassium concentration directly correlates with movement of K+ in and out of cells because
of passive shifts based on the concentration gradient across the cell membrane. (A normal response to
diarrhea-induced hypokalemia is for K+ to shift out of the cells passively, minimizing the reduction in
plasma potassium concentration.)
D. Normal plasma concentrations of K+ are maintained by renal excretion.
E. Hypokalemia (K+ concentration less than 3.5 mEq/L)
1. Causes of hypokalemia
a. Reduced intake seldom causes hypokalemia because renal excretion is minimized because of
increased renal tubular absorption.
b. Increased shift of K+ into cells can occur with the following:
i. Alkalosis
ii. Insulin or a carbohydrate load
iii. β2 -Receptor stimulation caused by stress-induced epinephrine release or administration of a
β-agonist (e.g., albuterol, dobutamine)
iv. Hypothermia
c. Increased GI losses of K+ can occur with vomiting, diarrhea, intestinal fistula, or enteral tube drain-
age, and chronic laxative abuse.
d. Increased urinary losses can occur with mineralocorticoid excess (e.g., aldosterone) and diuretic
use (e.g., loops and thiazides).
e. Hypomagnesemia is commonly associated with hypokalemia caused by increased renal loss of K+;
correction of plasma potassium requires simultaneous correction of serum magnesium.
2. Symptoms of hypokalemia generally occur when plasma potassium is less than 3 mEq/L and can
include the following:
a. Muscle weakness occurs most commonly in the lower extremities, but it can progress to the trunk,
upper extremities, and respiratory muscles. Muscle weakness in the GI tract can manifest as para-
lytic ileus, abdominal distention, nausea, vomiting, and constipation.
b. ECG changes (flattened T waves or elevated U wave) occur.
c. Cardiac arrhythmias (bradycardia, heart block, ventricular tachycardia, ventricular fibrillation)
occur.
d. Digoxin toxicity can occur despite normal serum digoxin concentrations in the presence of
hypokalemia.
e. Rhabdomyolysis can occur because hypokalemia can cause reduced blood flow to skeletal muscle.
3. Treatment of hypokalemia
a. K+ deficit can be estimated as 200–400 mEq of K+ for every 1 mEq/L reduction in plasma potas-
sium (assuming a normal distribution of K+ between EC and IC compartments).
b. Although the K+ deficit can be estimated, K+ replacement is guided by K+ concentrations; recheck
every 2–4 hours if K+ is less than 3 mEq/L.

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Fluids, Electrolytes, and Nutrition
ACCP Updates in Therapeutics® 2022: Pharmacotherapy Preparatory Review and Recertification Course1-25
c. Potassium chloride is the preferred salt in patients with concurrent metabolic alkalosis because
these patients typically lose Cl – through diuretics or GI loss. This is the most common presentation
of hypokalemia.
d. Potassium acetate can be administered intravenously, or potassium bicarbonate can be adminis-
tered orally for patients with a metabolic acidosis that requires frequent K+ supplementation.
e. Guidelines for administering K+ (Table 8)
Table 8. K+ Replacement
Plasma K+
(mEq/L) Treatment a Comments
3–3.5 Oral KCl 40–80 mEq/day if no signs or symptoms
(doses > 60 mEq should be divided to avoid GI adverse effects)
Recheck K+ daily
2.5–3 Oral KCl 120 mEq/day (in divided doses) or IV 60–80 mEq
administered at 10–20 mEq/hr if signs or symptoms
Monitor K+ closely
(i.e., 2 hr after infusion)
2–2.5 IV KCl 10–20 mEq/hr until normalized Consider continuous ECG
monitoring
< 2 IV KCl 20–40 mEq/hr until normalized Requires continuous ECG
monitoring
a
Treatment doses are for patients with normal kidney function and should be reduced for patients with kidney dysfunction or older adults.
ECG = electrocardiogram; GI = gastrointestinal; IV = intravenous; KCl = potassium chloride; K+ = potassium.
i. Patients without ECG changes or symptoms of hypokalemia can be treated with oral
supplementation.
ii.Avoid mixing K+ in dextrose, which can cause insulin release with a subsequent IC shift of K+
.
iii. To avoid irritation, no more than about 60–80 mEq/L should be administered through a periph-
eral vein.
iv. Recommended infusion rate is 10–20 mEq/hour to a maximum of 40 mEq/hour.
v. Patients who receive K+ at rates faster than 10–20 mEq/hour should be monitored using a
continuous ECG.
F. Hyperkalemia
1. Causes of hyperkalemia
a. Increased intake
b. Shift of K+ from the IC to the EC compartment causes hyperkalemia and can occur with the
following:
i. Acidosis
ii.Insulin deficiency
iii. β-Adrenergic blockade
iv.Digoxin overdose
v. Rewarming after hypothermia (e.g., after cardiac surgery)
vi. Succinylcholine
c. Reduced urinary excretion can occur with:
i. Kidney dysfunction
ii. Intravascular volume depletion
iii. Hypoaldosteronism
iv. K+-sparing diuretics
v. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
vi. Trimethoprim

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