This document discusses the pharmacist's role in managing electrolyte abnormalities and provides guidance on replacing and monitoring key electrolytes, including potassium, magnesium, phosphorus, and chloride. It outlines signs and symptoms of electrolyte imbalances, risk factors, recommended replacement doses and rates based on severity, monitoring parameters, and considerations for oral versus intravenous administration. The pharmacist plays an important role in evaluating electrolyte disturbances, verifying physician orders, ensuring safe administration, and monitoring patients receiving electrolyte replacements or maintenance therapy.
Clinical pharmacokinetics and its application--
1)definition
2) APPLICATIONS OF CLINICAL PHARMACOKINETICS
Design of dosage regimens:
a) Nomograms and Tabulations in designing dosage regimen,
b) Conversion from intravenous to oral dosing,
c) Determination of dose and dosing intervals,
d) Drug dosing in the elderly and pediatrics and obese patients.
Pharmacokinetics of Drug Interaction:
a) Pharmacokinetic drug interactions
b) Inhibition and Induction of Drug metabolism
c) Inhibition of Biliary Excretion.
Therapeutic Drug monitoring:
a) Introduction
b) Individualization of drug dosage regimen (Variability – Genetic, Age and Weight, disease, Interacting drugs).
c) Indications for TDM. Protocol for TDM.
d) Pharmacokinetic/Pharmacodynamic Correlation in drug therapy.
e) TDM of drugs used in the following disease conditions: cardiovascular disease, Seizure disorders, Psychiatric conditions, and Organ transplantations
Dosage adjustment in Renal and Hepatic Disease.
a. Renal impairment
b. Pharmacokinetic considerations
c. General approach for dosage adjustment in renal disease.
d. Measurement of Glomerular Filtration rate and creatinine clearance.
e. Dosage adjustment for uremic patients.
f. Extracorporeal removal of drugs.
g. Effect of Hepatic disease on pharmacokinetics.
Population Pharmacokinetics.
a) Introduction to Bayesian Theory.
b) Adaptive method or Dosing with feedback.
c) Analysis of Population pharmacokinetic Data
Clinical pharmacokinetics and its application--
1)definition
2) APPLICATIONS OF CLINICAL PHARMACOKINETICS
Design of dosage regimens:
a) Nomograms and Tabulations in designing dosage regimen,
b) Conversion from intravenous to oral dosing,
c) Determination of dose and dosing intervals,
d) Drug dosing in the elderly and pediatrics and obese patients.
Pharmacokinetics of Drug Interaction:
a) Pharmacokinetic drug interactions
b) Inhibition and Induction of Drug metabolism
c) Inhibition of Biliary Excretion.
Therapeutic Drug monitoring:
a) Introduction
b) Individualization of drug dosage regimen (Variability – Genetic, Age and Weight, disease, Interacting drugs).
c) Indications for TDM. Protocol for TDM.
d) Pharmacokinetic/Pharmacodynamic Correlation in drug therapy.
e) TDM of drugs used in the following disease conditions: cardiovascular disease, Seizure disorders, Psychiatric conditions, and Organ transplantations
Dosage adjustment in Renal and Hepatic Disease.
a. Renal impairment
b. Pharmacokinetic considerations
c. General approach for dosage adjustment in renal disease.
d. Measurement of Glomerular Filtration rate and creatinine clearance.
e. Dosage adjustment for uremic patients.
f. Extracorporeal removal of drugs.
g. Effect of Hepatic disease on pharmacokinetics.
Population Pharmacokinetics.
a) Introduction to Bayesian Theory.
b) Adaptive method or Dosing with feedback.
c) Analysis of Population pharmacokinetic Data
hospital formulary is developed under the guidance of pharmacy and therapeutic commitee of the hospital.pharmacist working in a hospital should play an important role in the preparation of the hospital formulary
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
Non compartmental pharmacokinetics & physiologic pharmacokinetic models by aktDr Ajay Kumar Tiwari
Non Compartmental Analysis
-Assumptions to be made
-Statistical Moment Theory
-Mean Residence Time
-Mean Transit Time (MTT), Mean Absorption Time (MAT), and Mean Dissolution Time (MDT)
-Other Pharmacokinetic Parameters
-Advantages and Disadvantages of Noncompartmental Versus Compartmental Population Analyses
Physiologic Pharmacokinetic Models
-Physiologically based pharmacokinetic (PBPK) modeling
-Assumption to be made
-advantages & disadvantage
Pharmaceutical care concepts - clinical pharmacy ShaistaSumayya
The pharmaceutical care is defined as “the direct, responsible provision of medication-related care for the purpose of achieving definite outcomes that improve a patient’s quality of life.”
Pharmaceutical care involves the process through which a pharmacist cooperates with a patient and other professional in designing , implementation, and monitoring a therapeutic plan that will produce specific therapeutic outcomes for the patient
Introduction to daily activities of clinical pharmacist.
Drug therapy monitoring,
Medication chart review
Clinical Progress
Pharmacist intervention
Detection and management of ADRs
hospital formulary is developed under the guidance of pharmacy and therapeutic commitee of the hospital.pharmacist working in a hospital should play an important role in the preparation of the hospital formulary
DRUG INTERACTIONS (MECHANISMS OF DRUG-DRUG INTERACTIONS)N Anusha
A Drug interaction is an interaction between a drug and some other substance, such as another drug or a certain type of food, which leads to interaction that could manifest as an increase or decrease in the effectiveness or an adverse reaction or a totally new side effect that is not seen with either drug alone that can be severe enough to alter the clinical outcome.
Every time a drug is administered with any other prescription medicine, OTC products, herbs or even food we expose ourselves to the risk of a potentially dangerous interaction.
Non compartmental pharmacokinetics & physiologic pharmacokinetic models by aktDr Ajay Kumar Tiwari
Non Compartmental Analysis
-Assumptions to be made
-Statistical Moment Theory
-Mean Residence Time
-Mean Transit Time (MTT), Mean Absorption Time (MAT), and Mean Dissolution Time (MDT)
-Other Pharmacokinetic Parameters
-Advantages and Disadvantages of Noncompartmental Versus Compartmental Population Analyses
Physiologic Pharmacokinetic Models
-Physiologically based pharmacokinetic (PBPK) modeling
-Assumption to be made
-advantages & disadvantage
Pharmaceutical care concepts - clinical pharmacy ShaistaSumayya
The pharmaceutical care is defined as “the direct, responsible provision of medication-related care for the purpose of achieving definite outcomes that improve a patient’s quality of life.”
Pharmaceutical care involves the process through which a pharmacist cooperates with a patient and other professional in designing , implementation, and monitoring a therapeutic plan that will produce specific therapeutic outcomes for the patient
Introduction to daily activities of clinical pharmacist.
Drug therapy monitoring,
Medication chart review
Clinical Progress
Pharmacist intervention
Detection and management of ADRs
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
7. HYPOMAGNESEMIA
• Irritability, confusion, arrhythmias, weakness,
nystagmus,seizures, coma, and death
• concomitant hypokalemia and hypocalcemia
Hypocalcemia
• Tetany, muscle spasms, lethargy, seizures
Chloride
• Tonicity Disturbence
8. • Working with physicians, pharmacists play an important role in
the determination of underlying causes of these disorders,
particularly when disorders are medication-related, and in
providing knowledge of the potential implications of individual
medications.
• Pharmacists also often evaluate and recommend treatment of
electrolyte disturbances.
• What are the standards for safe and effective administration in
Peripheral Vs Central line ?
the Recommended maximum concentrations and maximum
rates of infusion?
• Available Intravenous and oral forms?
9. • How to replace and maintain the electrolytes?
- REPLACEMENT DOSE, central venous catheter.
- MAINTANCE DOSE.
• Physician orders verification and calculations
millmoles (mmol) , milliequivalnts (mEq) or grams or
percentage.
• Proper Labeling .
• High risk Electrolytes? auxiliary labeling
Concentrated electrolytes shall not be part of routine floor stock.
• Administration :
- Do not give IV PUSH (except for magnesium and calcium).
- Mechanical infusion pump for all replacement electrolytes.
10.
11. • Renal function
• Salt form
• acid/base status
• Time of lab draw
• Route of administration
• Absorption issues
• Diarrhea, nausea/vomiting
13. Hypokalemia
Severity Serum K
concentration
(mEq/L)
Initial I.V. K
replacement dose
Mild/Moderate
2.5-3.4 20-40 mEq
Severe >2.5 40-80 mEq
• Every 1 mEq/L below 3.5 represents a 100-200 mEq deficit.
• One time dose of 40 mEq is not adequate replacement.
• Magnesium levels should be monitored and replacement given if necessary
since potassium repletion is ineffective in the presence of hypomagnesemia.
• Oral replacement if asymptomatic and K is < 3.8 mEq/L.
• Oral = IV K at same doses. Potassium chloride slow release tablet contains 8
mmol potassium per tablet. (Tablets should not be crushed or chewed).
• Liquid has unpleasant taste.
14. .
• Adult doses from 40-100 mEq/day may be required for potassium repletion given in 2
- 4 divided doses per day.
• In adults, start with 20-40 mEq/day and titrate to desired level. A 40 mEq dose may be
given every 2 hours for a maximum dose of 120 mEq within a 6 hour period.
• Oral potassium can be prescribed in conjunction with IV potassium.
• When oral potassium therapy is combined with parenteral supplementation for adults, a
maximum total dose (IV + PO) is 120 mEq within a 6 hour period.
• Do not use sustained release potassium products, when an immediate response is
desired. potassium chloride solution, should be used for a quicker response.
• Avoid dextrose vehicles - may stimulate insulin release and decrease K specially in
Initial replacement therapy.
• Potassium salts MUST NEVER be given IM or as an IV push.
15. • Potassium levels must be checked after each replacement dose. If
using immediate release preparations, a level should be checked no
sooner than 60 minutes.
If using a sustained release product, a level should be checked no
sooner than 3 hours.
Patients receiving maintenance doses of oral potassium do not require
levels after each dose.
16. • All IV maintenance infusions with KCl at a concentration greater than 40 mEq/L
must be administered via an infusion pump.
• Peripheral administration.
• Central administration.
• Cardiac Monitoring:
greater than 10 mmol/hour
SERUM less than or equal to 2.5 mmol/L.
DOSE exceeds 80 mmols
- Rapid infusion of KCl may cause cardiac arrest.
17. - Risk Factors for developing hypokalemia:
• Severe vomiting/diarrhea
• amphotericin B
• Chronic diuretics
• metabolic alkalosis
• insulin
• beta2 agonists (e.g., terbutaline)
• Decreased intake of K+
• Acid/base imbalance
• Trauma and stress
• Increased aldosterone
• Beware if diabetic
– Insulin pushes K+
into cells
– Ketoacidosis – H+
replaces K+
, which is lost in urine
• β – adrenergic drugs or epinephrine
18. • A single salbutamol nebulizer treatment may lower serum K by
0.2-0.4 mmol/L.
• A single dose of succinylcholine will increase serum K by 0.5-
1.0 mmol/L.
• Hyperkalaemia may occur with TMP/SMX (trimethoprim-
sulfamethoxazole) therapy and with the use of hypertonic
agents (e.g. D50, mannitol).
• A serum K of 3-4 mmol/L correlates with a 100-200 mmol K
deficit. At a serum K of 2-3 mmol/L, the deficit is 200-400 mmol.
• Serum potassium may be expected to increase by ˜ 0.25
mmol/L for each 20 mmol IV KCL infused.
• Hypokalemia :
• intracellular shift, including albuterol, insulin, theophylline, and
caffeine.
19. Hyperkalaemia:
- Risk Factors for developing hyperkalemia:
• Serum K+ > 5.5 mEq / L
• Check for renal disease
• Massive cellular trauma
• Insulin deficiency
• Addison’s disease
• Potassium sparing diuretics (spironolactone, amiloride, etc.)
• Decreased blood pH
• Exercise pushes K+ out of cells
• use of high dose TMP/SMX for PCP in HIV infected patients
- Hemodialysis
20. Management :
• 10% Calcium Gluconate or Calcium Chlorideas calcium will antagonize
the effects of potassium to rapidly stabilize cardiac muscle function
• Insulin (0.1U/kg/hr) and IV Glucose
• albuterol
• Metabolic alkalosis (if the patient is acidemic)
– 1 L H20 with 150meq of NaHCO3
• Lasix 1mg/kg (if renal function is normal)
• Sodium polystyrene sulfonate acts as a cation exchange resin,
binding to potassium in the gastrointestinal tract to facilitate
elimination.
• Renal replacement therapy
22. HYPOMAGNESEMIA
• thiazide and loop diuretics, amphotericin, cisplatin, cyclosporine, and digoxin.
• 1 g IV Mg = 8 mEq= 4 mmol
• Normal serum levels needed for potassium and calcium replacement (If
the magnesium concentration is low, it should be corrected, otherwise it will
be difficult to normalize potassium and calcium).
• Approximately 50% of the dose given is renally eliminated.
• Replace P.O. if patient can tolerate (diarrhea -rate limiting side effect ,may be
reduced by dividing daily doses).
Serum Mg
concentration
(mEq/L)
Oral Intravenous
1.0-1.5 (mild/moderate) Magnesium oxide
400 mg 1-2 tablets TID
8-32 mEq
<1.0 (severe) N/A 32-64 mEq
23. • An additional consideration is that magnesium levels drawn after
infusion may be falsely elevated due to magnesium’s slow
distribution into body tissues
• Takes 3 to 5 days for total repletion.
• Max IV rate = 1 g per hour.
• < 20% (200 mg/ml) concentration before administration.
• MAX. CONC. : 1 gm in 5 ml D5W or NS
• MAX. INFUSION RATE: 1 gm over 7 minutes
24. • For Mg levels > 1.2 mg/dl AND asymptomatic, oral* therapy may be
used:
• *Oral absorption is variable with 15-50 % of a dose being absorbed.
1-2 tablets daily
• Magnesium sulfate may be given IM, however it can be very painful.
Doses greater than 1 gm must be given in different injection sites.
• For symptomatic patients, bolus doses of IV magnesium are
required.
• For asymptomatic patients, adding magnesium to the patient's
maintenance IV fluids will allow for better retention of magnesium
• HYPERMAGNESEMIA
• ntravenous calcium (chloride or gluconate) to stabilize cardiac and
neuromuscular function.
• loop diuretics or renal replacement therapy
26. HYPOPHOSPHATEMIA
• Role in several important body functions
• Potassium Phosphate.
• Sodium Phosphate.
• Sodium Phosphate and Normal Saline.
• Recommended Total dose infused over 4-6 hrs to reduce risk of
(hypocalcemia and soft tissue calcification, hypotension, renal
failure)
• Oral Phosphateshould be used if asymptomatic/mild hypophosphatemia (can
cause diarrhea) (will decrease Mg absorption)
• Magnesium, calcium and aluminum containing antacids may bind phosphorus
and prevent its absorption.
PO4 Concentration (mg/dL) IV replacement dose
2.3-3.7 0.08-0.16 mmol/kg
1.5-2.2 0.16-0.32 mmol/kg
<1.5 0.32-0.64 mmol/kg
27. • Millimoles
• Maximum rate= 10 mmol/hr
- KPhos 15 mmol / 100 ml NS or D5W over 3 hours centrally.*
- NaPhos 15 mmol / 100 ml NS or D5W over 3 hours centrally.
Unless total calcium is < 7.5 mg/dL or > 11 mg/dL (corrected)
phosphorus is > 2 mg/dL OR significant renal dysfunction
(Clcr < 10 ml/min)
• IDEAL body weight (IBW) or adjusted weighs for obese patient.
• 4 hours after replacement completed.
• Renal insufficiency (CLcr <20ml/min): reduce dose by 50%
• Maximum is 15 mM of sodium phosphate in 100 ml dextrose 5%
in water
• As a guideline, the phosphorus level will increase by an average
of 1.2 mg/dl with a dose of 0.25mmol/kg
28. • Hyperphosphatemia
• phosphate binders such as calcium carbonate, calcium acetate,
and sevelamer orally with meals to reduce phosphorus
absorption from the gastrointestinal tract.
• renal replacement therapy
30. HYPOCALCEMIA
• NORMAL LEVELS: Total Calcium: 8.4-10.2 mg/dl (2.1-2.6 mmol/L)
• Highly protein bound so always calculate corrected calcium.
Corrected calcium = [(4-albumin) x 0.8] + serum calcium.
• Ionized calcium remains normal in low albumin states.
• Calcium chloride and Calcium gluconate
• Calcium chloride only used in severe situations typically codes
• Gram , mmol
Total Ca (mg/dL) Dosing Continuous IV dose
Mild/moderate
And asymptomatic
0.08-0.16 mmol/kg 4.56-9.12 mEq Ca
over 30-60 minutes
<7.5 (Severe)
Or symptomatic
3 g calcium gluconate
over 10 minutes
repeat PRN
13.6 mEq Ca over 10 min.
repeat PRN
31. – If the magnesium concentration is low, it should be corrected, otherwise it will
be difficult to normalize potassium and calcium
– MAXIMUM RECOMMENDED CONCENTRATIONS:
• Calcium gluconate: 1 gm in 50 ml D5W or NS.
• Calcium chloride*: 1 gm in 100 ml D5W or NS
– INFUSION RATE: Infuse over 30-60 minutes.
Rapid administration may cause bradycardia, hypotension and vasodilation.
– Administration via a central or deep vein is preferred. IM or SC?
– Phosphate and Calcium replacements, Determine Ca x PO4 product in mg/dl
before administering calcium.
If product is greater than 60 mg/dl, there is an increased risk of calcium
phosphate precipitation in the cornea, lung, kidney, cardiac conduction
system, and blood vessels.
32. • Usual maximum total daily dose is 15 g calcium gluconate.
• As a guideline, the total calcium will increase by 0.5 mg/dl for
every gram of calcium gluconate given intravenously.
• ORAL CALCIUM Absorption is variable and depends on
PTH, Vitamin D, and gastric pH.
• USUAL DOSE: 500- 2000 mg elemental calcium a day, in
divided doses (BID-QID)
– ADVERSE EFFECT: Constipation
• For each 5 units of packed RBCs transfused, administer 1-2
grams (1-2 amps) of calcium gluconate.
33. Sodium
• May reflect increased, decreased or normal total body sodium
• Sodium is the major cation that determines serum osmolality,
• Must assess osmolality to treat Various causes (SIADH, CHF, Ascites)
• Normal serum sodium levels are 136 -145 mEq / L.
• Max rate of increase in serum sodium is 8-12 mEq/L in 24 hrs
• Assess underlying cause and treat first.
• acute onset hyponatremia is more likely to be symptomatic and
• can be more rapidly corrected compared to chronic hyponatremia,
which is usually not associated with as severe of symptoms and should
be corrected slowly.
** All replacement doses reflect dosing for patients with
Normal renal function**
34. 34
Treatment of
Hyponatremia
• Correct serum Na by 1mEq/L/hr
• Check serum Na q4hr
• Use 3% saline in severe hyponatremia
• Central venous catheter, venous irritation and pain at the
injection site.
• Administer osmotic diuretic (Mannitol) to excrete the water
rather than the sodium
• Goal is serum Na 130
• Avoid too rapid correction
35. • Hypernatremia: Plasma Na+ > 145 mEq / L
– Excess Na intake (hypertonic IV solution)
– Excess Na retention (oversecretion of aldosterone)
– Loss of pure water
• Long term sweating with chronic fever
• Respiratory infection → water vapor loss
• Diabetes (mellitus or insipidus) – polyuria
– Insufficient intake of water (hypodipsia)
Management:
• 45% NSS. If caused by both Na and fluid loss, will administer
NaCL. If inadequate renal excretion of sodium, will administer
diuretics.