This slide was first presented during the Malaysian 1st Emergency Medicine Annual Scientific Meeting, in conjunction with the Academy of Medicine Malaysia, Academy of Medicine Singapore and the Academy of Medicine Hong Kong Tripartite Meeting in Aug 2016.
Fluid management and Fluid Responsiveness in ICCU / ICU at ASMIHA workshop 2018Isman Firdaus
It is very important for cardiologist or intensivist to determined fluid overload vs loss fluid. Misconception of hypervolemic and hypovolemic state was very important.
Fluid management and Fluid Responsiveness in ICCU / ICU at ASMIHA workshop 2018Isman Firdaus
It is very important for cardiologist or intensivist to determined fluid overload vs loss fluid. Misconception of hypervolemic and hypovolemic state was very important.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/_i1H_i3tOuw
Arabic Language version of this lecture is available at:
https://youtu.be/SYmZ9CmmN5g
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Updated global adult sepsis guidelines, released in October 2021 by the Surviving Sepsis Campaign (SSC), place an increased emphasis on improving the care of sepsis patients after they are discharged from the intensive care unit (ICU) and represent greater geographic and gender diversity than previous versions.
The new guidelines specifically address the challenges of treating patients experiencing the long-term effects of sepsis. Patients often experience lengthy ICU stays and then face a long, complicated road to recovery. In addition to physical rehabilitation challenges, patients and their families are often uncertain how to coordinate care that promotes recovery and matches their goals of care.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Nl2xKEmvRWk
Arabic Language version of this lecture is available at:
https://youtu.be/K14fWBNdEco
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This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/_i1H_i3tOuw
Arabic Language version of this lecture is available at:
https://youtu.be/SYmZ9CmmN5g
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Updated global adult sepsis guidelines, released in October 2021 by the Surviving Sepsis Campaign (SSC), place an increased emphasis on improving the care of sepsis patients after they are discharged from the intensive care unit (ICU) and represent greater geographic and gender diversity than previous versions.
The new guidelines specifically address the challenges of treating patients experiencing the long-term effects of sepsis. Patients often experience lengthy ICU stays and then face a long, complicated road to recovery. In addition to physical rehabilitation challenges, patients and their families are often uncertain how to coordinate care that promotes recovery and matches their goals of care.
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/Nl2xKEmvRWk
Arabic Language version of this lecture is available at:
https://youtu.be/K14fWBNdEco
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
This lecture is based on National guidelines(Sri Lanka) and guidelines by NHS UK. all the materials used to prepare the lecture are trusted and high in quality. also the books referred are internationally recognized. both hyper and hypokalemia management included in the lecture. lecture is free and you can even download. i kept no copy rights. i appreciate your support, comments and suggestions. also i would be grateful if you can make these lectures popular. wishing your success.
A simple presentation on hypokalemia. The most common electrolyte disorder in the Critical Care practice.The presentation is based on a mortality and morbidity case report and discussion. It covers all the basic aspects of understanding the causes of hypokalemia in ICU and its management. Target audience are residents ICU and ER but all health care workers can benefit.
Fluid and electrolyte management in surgical patients.KETAN VAGHOLKAR
Fluid and electrolyte management has to be aggressive. It is pivitol in speedy recovery in GI surgery. Changes should be anticipated and treated promptly. A detailed knowledge of this is essential for optimum management especially in the ICU.
Disaster and Mass Casualty Incidents (updated 7th July 2020)Chew Keng Sheng
A new updated slide on an overview of disaster management in Malaysia, including the formation of NADMA as the dedicated agency to coordinate disaster management in Malaysia.
Predatory publishing is a relatively recent phenomenon that seems to be exploiting some key features of the open access publishing model, sustained by collecting APCs that are far less than those found in legitimate open access journals. This CME aims to introduce to the participants on the phenomenon of predatory journals, why they continue to thrive, characteristics that are suggestive of a predatory journal, and how one can take step to minimize the risk of faling into predatory journal publication
A short sharing on doctor-patient communication to First year medical students in Universiti Malaysia Sarawak, to be supplemented with anecdotal accounts.
Sensitivity, specificity and likelihood ratiosChew Keng Sheng
A short tutorial on sensitivity, specificity and likelihood ratios. In this presentation, I demonstrate why likelihood ratios are better parameters compared to sensitivity and specificity in real world setting.
ACLS 2015 Updates - The Malaysian PerspectiveChew Keng Sheng
This set of slide was presented during the Kelantan Resuscitation Update 22 Nov 2015 in accordance to the latest ACLS/ILCOR 2015 Guidelines. However, I have emphasized on certain important aspects relevant within the Malaysian context. Nonetheless, in general, there are no major changes for this year 2015
My talk in April 2015 in Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
My talk in April 2015 Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
New or Presumed New LBBB To Be Treated As a STEMI Equivalent? A Contra Argume...Chew Keng Sheng
My 6-page notes to go along with the "debate" of whether new or presumed new LBBB per se (without any other qualification) should be treated as STEMI equivalent
An introduction to the rationale and the two types (Write-in and Select-Menu) of Key Feature Questions. This presentation is based on an original article by Page and Bordage (1995).
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. Objectives
1. Hyperkalemia
a. Basic science - potassium adaptation (feedforward control)
b. Pseudohyperkalemia
c. Clinical features
d. Treatment
2. Hypokalemia
3. Hyponatremia
a. Adjusting serum sodium according to glucose level
b. Formula for calculating sodium deficits - the caveat
c. Goal and rate of correction
2
4. The role of Aldosterone
revisited
Aldosterone stimulates renal K+ excretion
only at supraphysiological levels, with
little effect within the physiological range of
K+
A kaliuretic reflex arising from receptors in
the gut, portal vein or liver (?).
Rabinowitz, L. Aldosterone and potassium homeostasis.
Kidney Int 49.6 (1996): 1738-1742.
4
5. Youn, J.H. and McDonough, A.A. "Recent advances in understanding integrative control of potassium
homeostasis." Annual review of physiology 71 (2009): 381-401. 5
6. The ‘gut feeling’ is literally telling us that it is not easy to
get hyperkalemia in a normal healthy individual!
Image source: pixabay.com
6
7. Potassium Adaptation
Potassium Adaptation: enhanced
efficiency of potassium excretion when
potassium intake is increased
Hyperkalemia is a rare occurrence in
normal individuals because of
potassium adaptation
Youn, J.H. and McDonough, A.A. "Recent advances
in understanding integrative control of potassium
homeostasis." Annual review of physiology 71
(2009): 381-401.
7
8. What do we know
1. Increasing potassium intake alone is not a common cause of hyperkalemia
unless it occurs acutely
2. Persistent hyperkalemia means impaired urinary potassium excretion (e.g.
reduction in aldosterone secretion or responsiveness, acute or chronic kidney
disease, etc)
3. Large release of potassium from the cells (increased tissue breakdown)
causing a transient elevation
8
10. Pseudohyperkalemia
Traumatic hemolysis from venipuncture (can be
up to 20% of samples). Lab reports as “slightly
hemolyzed”
Release from muscle cells distal to a tourniquet
with fist clenching
Common in cases of leucocytosis (TWC > 50,000
- 100,000/mm3
) or thrombocytosis (>500,000 - 1
million/mm3
)
10
11. Effects of fist clenching
Don BR et al (1990): Both repeated fist clenching
and isometric handgrip increased the plasma
potassium level by as much as 1.6 mmol/l from the
contracting arm.
Don, Burl R et al. "Pseudohyperkalemia caused by fist
clenching during phlebotomy." New England Journal of
Medicine 322.18 (1990): 1290-1292.
Solid circles represent patients,
open circles represent controls
11
12. Thrombocytosis
Potassium moves out of platelets after clotting has occurred. Therefore, serum
potassium is normally higher than plasma potassium by 0.1 - 0.5 mmol/l
Graber et al (1988): N = 283 controls and 161 patients with reactive
thrombocytosis.
Hyperkalemia noted in 34% of patients with a platelet count >500,000/mm3
vs 9%
of patients with a platelet count less than 250,000/mm3
An increase of K+ level of 0.15 mmol/l for every increase of 100,000/mm3
in the
platelet count.
Graber, Mark et al. "Thrombocytosis elevates serum potassium." American Journal of Kidney Diseases 12.2
(1988): 116-120.12
13. Leucocytosis
High white blood cell counts (>120,000/mm3
) (e.g., due to chronic lymphocytic
leukemia) causes pseudohyperkalemia due to cell fragility.
May be more prominent when blood is sampled in heparinized tubes
Centrifugation of a heparinized tube causes in vitro cell destruction and release of
potassium
Lee, Hong-Kee et al. "Pseudohyperkalemia—is serum or whole blood a better specimen type than
plasma?." Clinica Chimica Acta 396.1 (2008): 95-96.
13
14. Exclude pseudohyperkalemia
Suspect when there no apparent cause for
hyperkalemia in an asymptomatic patient
Look for wide variability in repeated
measurements of K+ level
Attempt venipuncture without a tourniquet,
repetitive fist clenching. If a tourniquet is required,
release tourniquet after needle insertion. Then
waiting for about one minute (or 2) before drawing
the blood sample.
14
16. Clinical Features
Vague symptoms, may be overshadowed by primary illnesses that precipitate the
hyperkalemia
Most serious manifestations - muscle weakness or paralysis, cardiac conduction
abnormalities, and cardiac arrhythmias
Usually occur when the serum potassium concentration is ≥7.0 mmol/l
Absence of symptoms do not rule out hyperkalemia
16
17. Muscle Weakness
Muscle weakness may mimic Guillain-Barré syndrome - ascending muscle
weakness that begins with the legs and progresses to the trunk and arms
Sphincter tone and cranial nerve function are typically intact
Symptoms resolve with correction of the hyperkalemia.
17
18. ECG Manifestations
ECG manifestations depends on:
● the absolute se K+ level
● the rate of increase
Alfonzo, Annette VM et al. "Potassium disorders—clinical
spectrum and emergency management." Resuscitation 70.1
(2006): 10-25.
Note:
progression and severity of ECG changes do
not correlate well with the serum potassium
concentration 18
19. ECG Manifestations
In a retrospective review of 90 hypokalemic patients by Montague et al (2008),
although the probability of ECG abnormalities increased with increasing serum
potassium, but the ECG was insensitive for the diagnosis of hyperkalemia.
Szerlip et al (1986) reported 2 cases of severe hyperkalemia >9.0 mmol/l with no
expected ECG manifestations
Szerlip, Harold M, James Weiss, and Irwin Singer. "Profound hyperkalemia without electrocardiographic
manifestations." American Journal of Kidney Diseases 7.6 (1986): 461-465.
Montague, Brian T, Jason R Ouellette, and Gregory K Buller. "Retrospective review of the frequency of
ECG changes in hyperkalemia." Clinical Journal of the American Society of Nephrology 3.2 (2008):
324-330.
19
20. ECG Manifestations
Seen commonly when se K+ >5.5
mmol/l
Earliest ECG manifestation is
narrow-based, peaked T waves
(vs broad-based T waves in
myocardial infarction or
intracranial lesions)
Best seen leads II, III, V2 - V4
Only 22% of patients Parham, Walter A et al. "Hyperkalemia revisited." Texas Heart Institute
Journal 33.1 (2006).
Image Graphic 80441 Version 5.0 from UptoDate
20
21. As the hyperkalemia gets more severe, there is progressive lengthening of the PR
interval and QRS duration
When se K+ level reaches 8 - 9 mmol/l, SA node may stimulate the ventricles
directly without evidence of atrial activity. This is because the SA node is less
susceptible to the effects of hyperkalemia; the absence of P wave and widened
QRS mimics ventricular tachycardia
When se K+ reaches 10 mmol/l, the progressively widened QRS merges with T
wave producing sine wave
Parham, Walter A et al. "Hyperkalemia revisited." Texas Heart Institute
Journal 33.1 (2006).
ECG Manifestations
21
23. Calcium
Hyperkalemia-induced depolarization of the
resting membrane potential leads to
inactivation of sodium channels and
decreased membrane excitability
Calcium restores the gap between resting
membrane potential to the threshold potential
Effect seen within 1 min, last 30 - 60 minutes
Calcium gluconate vs calcium chloride
Solid line - normal action
potential
Dotted line- hyperkalemic effect
Parham, Walter A et al. "Hyperkalemia revisited." Texas Heart Institute Journal 33.1 (2006).23
24. Insulin
Insulin works by stimulating Na-K-ATPase pump to drive potassium into the cells
Independent of its effect on glucose.
Glucose administration is to prevent hypoglycemia (not always necessary if se
glucose >13 mmol/l)
Glucose without insulin may cause paradoxical effect by increasing plasma
osmolality, drawing water and K+ out of cells
Alfonzo, Annette VM et al. "Potassium disorders—clinical spectrum and emergency management."
Resuscitation 70.1 (2006): 10-25.
24
25. Insulin
Effect begins in 10 to 20 min, peaks at 30 to 60 minutes, and lasts for 4 - 6 hours
Reduce potassium by 0.6 - 1.0 mmol/l
Renal failure patients maybe resistant to the glucose-lowering effect of insulin, but
the hypokalemic effect of insulin is still intact because Na-K-ATPase activity can
still be enhanced
Alvestrand, A et al. "Insulin-mediated potassium uptake is normal in uremic and healthy subjects."
American Journal of Physiology-Endocrinology and Metabolism 246.2 (1984): E174-E180.
25
26. Salbutamol
A beta-2 agonist drives potassium into the cells by increasing the activity of the
Na-K-ATPase pump
Lowers se K+ level by 0.6 - 1.0 mmol/l
Nebulized form requires much higher dose than dose for asthma (10 - 20 mg vs
2.5 - 5 mg for asthma)
Effect begins in 10 to 20 min, peaks at 30 to 60 minutes, and lasts for 4 - 6 hours
Alfonzo, Annette VM et al. "Potassium disorders—clinical spectrum and emergency management."
Resuscitation 70.1 (2006): 10-25.
26
27. Combined salbutamol + insulin-glucose?
Allon & Copkney (1990):
● insulin with glucose alone: reduced 0.65 +/- 0.09 mmol/l
● salbutamol alone: reduced 0.66 +/- 0.12 mmol/liter
● combined regimen: reduced 1.21 +/- 0.19 mmol/l;
● (p < 0.02)
Alfonzo, Annette VM et al. Potassium disorders—clinical spectrum and emergency management.
Resuscitation 70.1 (2006): 10-25.
Allon, Michael, and Charles Copkney. Albuterol and insulin for treatment of hyperkalemia in hemodialysis
patients. Kidney international 38.5 (1990): 869-872.
27
28. Sodium bicarbonate
More of historical interest
For persistent metabolic acidosis.
In a study by Blumberg et al (1992) on 12 dialysis patients (se K+ of 5.25 - 8.15
mmol/l) received IV bicarbonate over a 6-hour period. No change of potassium
level noted during first 4 hours. Only at four and six hours did a moderate decline
to 5.44 mmol/l (p<0.05) and to 5.30 mmol/l (p<0.01) noted respectively. In 3
patients, no or minimal change noted even after 6 hours
Blumberg, Alfred, Peter Weidmann, and Paolo Ferrari. Effect of prolonged bicarbonate administration on
plasma potassium in terminal renal failure." Kidney international 41.2 (1992): 369-374.
28
30. Introduction
Generally, se K+ decreases by 0.3 mmol/l for every 100 mmol reduction in total
body potassium
Muscle weakness usually does not occur at se K+ level >2.5 mmol/l unless it
develops acutely.
Many hypokalemic patients are also deficient in magnesium. Magnesium is
important for potassium update and for maintenance of intracellular K+ level,
particularly in the myocardium
Alfonzo, Annette VM et al. Potassium disorders—clinical spectrum and emergency management.
Resuscitation 70.1 (2006): 10-25.
30
31. A note on hypomagnesemia
● Can be subtle, commoner than expected - 12% in hospitalized patients (Agus
1999), 65% in ICU patients (Tong & Rude, 2005)
● Neuromuscular - tremor, tetany, convulsions, weakness, delirium, and coma,
etc
● Cardiovascular - widened QRS and peak, tall T waves, then widened PR
interval and ventricular arrhythmias with severe cases
● Accompanying hypocalcemia, hypoparathyroidism, hypokalemia
31
Tong, G.M, and Rude, R.K.. Magnesium deficiency in critical illness. Journal of Int Care Med 20.1 (2005): 3-17.
Agus, Zalman S. Hypomagnesemia.Journal of the American Society of Nephrology 10.7 (1999): 1616-1622.
32. Treatment of hypokalemia
2 g KCl in 200 ml over 2 hours or 1 g KCl in 100 ml over 1 hour
[1 g KCl = 13 mmol/l of potassium]
Rates as high as 40 mmol/hour may be required for life-threatening patients
Advising patient just to increase intake of potassium-rich foods,
such as oranges and bananas may not be effective enough
because dietary potassium is predominantly in the form of
potassium phosphate or potassium citrate which results in the
retention of only 40% as much potassium as KCl.
Image source: https://www.flickr.com/photos/codex41/9725166177 32
34. Classification
1. Hypertonic hyponatremia
a. Hyperglycemia
i. osmotic shift of water from ICF to ECF
ii. Need to do correction
2. Isotonic hyponatremia
a. Hyperlipidemia - Pseudohyponatremia
i. Relatively larger relative proportion of
plasma volume occupied by excess lipids
3. Hypotonic hyponatremia
a. Hypervolemic
b. Euvolemic
c. Hypovolemic
Verbalis JG et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am
J Med. 2013;126(10 Suppl 1):S1-42.34
35. Adjusting se sodium level due to glucose level
High glucose load causes osmotic shift - pulls water out of the cells
Se sodium fall by about 1.6 mmol/l for each 5.5 mmol/L increase in se glucose
concentration (Katz 1973)
Se sodium fall by about 2.4 mmol/l for each 5.5 mmol/L increase in se glucose
concentration (Hillier et al, 1999)
Katz MA. Hyperglycemia-induced hyponatremia--calculation of expected serum sodium depression. N
Engl J Med. 1973;289(16):843-4.
Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J
Med. 1999;106(4):399-403.
35
36. 36
Assuming se sodium falls 2.0* mmol/l for every 5.5 mmol/l
(equivalent of 100 mg/dl)
Corrected serum sodium =
Measured serum sodium + [se glucose - 5.5 mmol/l] * (2.0/5.5)
*1.6 mmol/l (Katz 1973), 2.4 mmol/l (Hillier et al, 1999)
37. 37
Formula for predicting sodium deficits
Sodium deficit
= (Desired se sodium - measured se sodium) * Total body water
= (Desired se sodium - measured se sodium) * 0.5ϕ
* body weight
Note:ϕ
some would take 0.6
In 3% NaCl, sodium concentration is approx 500 mmol/l or 1 ml = 0.5 mmol/l [1 g NaCl = 17 mmol/l]
Therefore, every 1 ml per kg body weight of 3% NACl increases se sodium by 1 mmol/l
38. Caveat:
38
Formulas may not accurately predict the magnitude of change in serum sodium.
In a series of 62 patients with a baseline se sodium of 112 mmol/l given hypertonic
saline (Mohmand et al, 2007), 74% had an increase in se sodium higher than what
was expected.
Reasons:
Correction of hyponatremia using hypertonic saline removes the hypovolemic
stimulus of ADH release (unless it is in SIADH)
Mohmand, Hashim K et al. Hypertonic saline for hyponatremia: risk of inadvertent overcorrection. Clinical
Journal of the American Society of Nephrology 2.6 (2007): 1110-1117.
39. Goal of therapy
● A 4- to 6-mmol/L increase in serum is sufficient to reverse the most serious
manifestations of acute hyponatremia (Sterns et al, 2010)
● In emergency therapy, the goal is to rapidly increase the serum sodium by 4
to 6 mmol/L over a period of 6 hours (Sterns et al, 2010)
Sterns RH, Nigwekar SU, Hix JK. The treatment of hyponatremia. Semin Nephrol. 2009;29(3):282-99.
Sterns RH, Hix JK, Silver S. Treating profound hyponatremia: a strategy for controlled correction. Am J Kidney
Dis. 2010;56(4):774-9.
39
40. Indications for emergency therapy
● Patients with severe symptoms due to hyponatremia, such as seizures or
obtundation.
● Patients with symptomatic acute hyponatremia, even if symptoms are mild.
● Patients with hyperacute hyponatremia due to self-induced water intoxication,
even if asymptomatic during initial evaluation (risk of cerebral edema due to
osmotically driven water across blood-brain barrier).
● Symptomatic patients who have either acute postoperative hyponatremia or
hyponatremia associated with intracranial pathology.
Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH, et al. Diagnosis, evaluation,
and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42.
40
41. Rate of correction
● Risk of osmotic demyelination syndrome (ODS) in severe hyponatremia -
when serum sodium concentration was increased > 10 to 12 mmol/L within 24
hours or more than 18 mmol/l within 48 hours (Sterns 1987; Karp & Laureno,
1993)
● Keep the rate of increase below 8 mmol/l over 24 hours (Sterns et al, 2009;
Sterns et al, 2010)
Sterns RH. Severe symptomatic hyponatremia: treatment and outcome. A study of 64 cases. Ann Intern
Med. 1987;107(5):656-64.
Karp BI, Laureno R. Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction
of hyponatremia. Medicine (Baltimore). 1993;72(6):359-73.
Sterns RH, Hix JK, Silver S. Treatment of hyponatremia. Curr Opin Nephrol Hypertens. 2010;19(5):493-8.41
42. “six a day makes sense for safety; so six
in six hours for severe sx’s and stop”
42
43. 43
Conclusion
1. Hyperkalemia - calcium, insulin, salbutamol are useful (insulin + salbutamol
has synergistic effect)
2. If nebulized salbutamol is used, it is 3 times the normal dose used in asthma.
3. Cranial nerve involvement is not common in hyperkalemia
4. Hyponatremia - remember that it may be higher than expected in the
presence of hyperglycemia
5. formula may be used as a guide, but beware that the rise in sodium may be
higher than expected due to diuresis
6. More important is to know the goal: six a day makes sense, so six in six in
severe sxs and stop