This document discusses pediatric fluid therapy and body fluid compartments. It begins by describing the different fluid compartments in the body, including total body water, extracellular fluid, and intracellular fluid. It then focuses on neonatal fluid management, noting that extracellular fluid is initially greater than intracellular fluid at birth, and describing appropriate intravenous fluid volumes for neonates. The document also discusses fluid requirements in children, evaluation of intravascular volume, choice of fluid types including crystalloids, colloids, and blood products, and provides guidelines for fluid resuscitation in dehydrated children.
Information about how cell get injured from different stimuli. Mechanism of cellular injury. Different types of cellular injury. Different examples of cellular injury with images which makes it easy to understand.
Information about how cell get injured from different stimuli. Mechanism of cellular injury. Different types of cellular injury. Different examples of cellular injury with images which makes it easy to understand.
Water and Electrolyte balance in surgical patientsDaniroxx
To help understand the need for Iv fluid therapy and electrolyte imbalances and their correction in surgical patients. It aims to keep the patient well hydrated with good urine output and avoid vital sign derangements and to avoid complications of wrongly advised fluids.
Fluid and electrolyte balance in oral surgeryPunam Nagargoje
• ELECTROLYTE BALANCE
• Def: - concentration of individual electrolytes in the body fluid compartments is normal and remains relatively constant.
• Electrolytes are dissolved in body fluids
• Sodium predominant extracellular cation, and chloride is predominant extracellular anion. Bicarbonate also in extracellular spaces
• Electrolyte balance
• Na + (Sodium)
– 90 % of total ECF cations
– 136 -145 mEq / L
– Pairs with Cl- , HCO3- to neutralize charge
– Low in ICF
– Most important ion in regulating water balance
– Important in nerve and muscle function
• Electrolyte imbalances: Sodium
• Hypernatremia (high levels of sodium)
– Plasma Na+ > 145 mEq / L
– Due to ↑ Na + or ↓ water
– Water moves from ICF → ECF
– Cells dehydrate
• HYPERATREMIA
• Hypernatremia Due to:
– Hypertonic IV soln.
– Oversecretion of aldosterone
– Loss of pure water
• Long term sweating with chronic fever
• Respiratory infection → water vapor loss
• Diabetes – polyuria
– Insufficient intake of water .
• Clinical manifestations
of Hypernatremia
• Thirst
• Lethargy
• Neurological dysfunction due to dehydration of brain cells
• Decreased vascular volume
• TREATMENT OF HYPERNATREMIA:
• Lower serum Na+
– Isotonic salt-free IV fluid [5% dextrose]
– Oral solutions preferable
• Hyponatremia
• Overall decrease in Na+ in ECF
• Two types: depletional and dilutional
• Depletional Hyponatremia
Na+ loss:
– diuretics, chronic vomiting
– Chronic diarrhea
– Decreased aldosterone
– Decreased Na+ intake
• Clinical manifestations of Hyponatremia
• Neurological symptoms
– Lethargy, headache, confusion, apprehension, depressed reflexes, seizures and coma
• Muscle symptoms
– Cramps, weakness, fatigue
• Gastrointestinal symptoms
– Nausea, vomiting, abdominal cramps, and diarrhea
• Tx – limit water intake or
• discontinue medicines such as diuretics
• TREATMENT OF HYPONATREMIA
• Hyponatremia which develops quickly should be treated quickly & vice-versa
• Patients with severe hypoNa (<115) are at risk of neurological damage
• Too rapid correction causes CENTRAL PONTINE MYELINOLYSIS.
• Targeted rate of correction: 0.5-1.0 mEq/L/hour
• Raise plasma Na by <10-12 mEq/L on first day
• Correction @ rate >25mEq/L places at high risk for central pontine myelinolysis
• Hypokalemia
• Normal serum k+ conc is 3.5 to 5.0 mEq/l
• Serum K+ < 3.5 mEq /L
• Beware if diabetic
– Insulin gets K+ into cell
– Ketoacidosis – H+ replaces K+, which is lost in urine
• β – adrenergic drugs or epinephrine
• Causes of Hypokalemia
• Decreased intake of K+
• Increased K+ loss
– Chronic diuretics
– Acid/base imbalance
– Trauma and stress
– Increased aldosterone
– Redistribution between ICF and ECF
• Treatment of hypokalamia
• Metabolic acidosis increases serum K+ levels & vice versa
• Post-op patients on fluid therapy should receive approx 60mEq/day to prevent hypokalemia
• 1mEq/L fall in serum K+= 200-400 mEq total body K+ deficit
• Failure to ↑ Sr. K+ even after sufficient correction should
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.
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
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
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
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
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Body Fluid Compartments
TOTAL BODY WATER (60%)
EXTRACELLULAR FLUID
(1/3 TBW)
INTRACELLULAR FLUID
(2/3 TBW)
INTERSTITIAL FLUID
(3/4 ECF)
PLASMA
(1/4 ECF)
TRANSCELLULAR
FLUID
Accurate for children 6 months of age and older
3. Body Fluid Compartments
90
80
70
60
50
40
30
20
10
0
Preterm Term 6
months
1 year Adult
Total Body Water
Muscle Mass
Fat
B
o
d
y
C
o
m
p
o
s
i
t
i
o
n
(%)
4. Body Fluid Compartments
• ICF – 2/3 TBW
• The proportion of ECF is much greater to that
of the ICF in the preterm infants.
• Upon birth, there is gradual shift from the ECF
to the ICF
5. Neonatal Fluid Management
• At birth: ECF is greater than ICF
• A few days after birth:
ECF contraction and wt loss due to ANP induced diuresis 2°
to ↑ pulmonary blood flow & stretch of left atrial receptors
• This is followed by ↑ water and Na requirements to match
those of the growing infant
Implication: Fluids should be restricted until the postnatal weight
loss has occurred.
6. Neonatal Fluid Management
• If a baby requires IV fluids from birth, they shld be given 10%
dextrose in the following volumes
Day 1 60 ml/kg/day Day 4 110
Day 2 80 Day 5 120
Day 3 100
• Na+ 3 mmol/kg/day & K+ 2 mmol/kg/day shld be added after
the postnatal diuresis or if Na+ drops
• A premature neonate may require an additional 30 ml/kg/day
and additional Na+
7. Neonatal Fluid Management
• Fluid requirements are titrated to the:
patient’s changing weight
urine output
serum sodium
9. Clinical and laboratory assessment of the severity of
dehydration in children
Signs and
Symptoms
Mild
Dehydration
Moderate
Dehydration
Severe
Dehydration
Wt loss (%) 5 10 15
Fluid deficit
(ml/kg)
50 100 150
Vital Signs
Pulse Normal ↑, weak greatly ↑, feeble
BP Normal Normal to low ↓, orthostatic
Respiration Normal Deep Deep & rapid
10. Clinical and laboratory assessment of the
severity of dehydration in children
Signs and
Symptoms
Mild
Dehydration
Moderate
Dehydration
Severe
Dehydration
Behavior Normal Irritable Hyperirritable
to lethargic
Thirst Slight Moderate Intense
Skin turgor Normal Decreased Greatly ↓
Ant. fontanelle Normal Sunken Markedly
depressed
Urine flow
(ml/kg/hr)
<2 <1 <0.5
Urine SG 1.020 1.020 – 1.030 >1.030
12. Crystalloids
• sterile aqueous solutions which may contain
glucose, various electrolytes, organic salts and
nonionic compounds
• rapidly equilibrates with ECF
15. Types
• Saline e.g. 0.9% saline, Hartmann’s solution
0.18% saline in 4% glucose.
• Glucose : e.g. 5% glucose, 10% glucose, 20%
glucose.
• Postassium chloride
• Sodium bicarbonate : e.g. 1.26%, 8.4%.
16. Crystalloid Solutions: Based on Use
• Maintenance-type solutions
– water loss
– hypotonic solutions
• Replacement-type solutions
– water and electrolyte losses
– isotonic electrolyte solutions
17. Type of IV solution
based on tonicity
Type of IV solution
Isotonic Hypotonic Hypertonic
18. Isotonic solution
A solution that has the same salt
concentration as the normal cells of the body
and the blood.
Ex:
1- 0.9% NaCl .
2- Ringer Lactate .
3- Blood Component .
4- D5W.
19. Hypertonic solution:
A solution with a higher salts concentration
than in normal cells of the body and the blood.
Ex:
1- D5W in normal
Saline solution .
2-D5W in half normal
Saline .
3- D10W.
20. Hypotonic solution
A solution with a lower salts concentration
than in normal cells of the body and the
blood.
EX:
1-0.45% NaCl .
2- 0.33% NaCl .
21. Crystalloid Solutions: Based on Tonicity
• Balanced salt solutions
– electrolyte composition similar to ECF
– Hypotonic with respect to Na
Fluid Osm pH Na K Other
LR 273 6.5 130 4 Lactate = 28
Normosol 295 7.4 140 5 Mg =3, acetate = 27,
gluconate = 23
Plasmalyte 298.5 5.5 140 5 HCO3 = 50
22. Crystalloid Solutions: Based on Tonicity
• Normal Saline
– isotonic (6.0) and isoosmotic (308)
– contains no buffers or electrolytes
– large volume:
dilutional hyperchloremic acidosis
23. Crystalloid Solutions: Based on Tonicity
• Hypertonic Salt Solutions
– Na concn range from 250 – 1200 meq/L
– Rapid volume expansion after infusion of small
amounts (e.g. 250 mL)
– t½: similar to isotonic saline
– may cause hemolysis at point of injection
24. Glucose containing solutions
• Glucose—given intravenously—is rapidly
metabolized, leaving free water behind
• distributes across all compartments rapidly
25. Sodium Bicarbonate
Type
• Isotonic sodium bicarbonate 1.26%
• Hypertonic sodium bicarbonate (1mmol/ml) 8.4%
Uses
• Correction of metabolic acidosis
• Alkalinisation of urine
Routes
• IV
25
27. Crystalloids
• Advantages
– Inexpensive
– Very low incidence of adverse reactions
• Disadvantages
– Short lived hemodynamic improvement
(intravascular t½: 20 – 30 mins.)
– Peripheral/pulmonary edema
28. Crystalloids
• Best crystalloid
Isotonic crystalloids are preferred over
hypotonic crystalloids
29. Do we have to routinely give glucose containing
solutions?
• Routine dextrose administration is no longer advised.
• There is a growing consensus to selectively administer
intraoperative dextrose only in pts at greatest risk for
hypoglycemia and in such situations to consider the
use of fluids with dextrose concentrations
31. Colloids
Types
• Albumin: e.g. 5%, 20 % , human albumin solution
31
• Dextran: e.g. 6% Dextran
• Gelatin: e.g. 3.5% polygeline (Haemaccel), 4%
succinylated gelatin (Gelofusion)
• Hydroxyethyl starch: e.g. 6% hetastarch
32. Colloids: Classification
• Natural Protein Colloid
– Albumin or Plasma Protein fraction
• Synthetic Protein Colloids
– Hetastarch
– Dextrans
– Gelatins
33. Albumin
• Colloid “gold standard”
• Derived from human pool plasma → heated to 60 C for 10 hrs
→ ultrafiltration
• MW: 69 kDa
• Available as: 5% and 20%
• Albumin 5% osmotically equivalent to an equal volume of
plasma
34. Albumin
• Use with caution in patients with
increased intravascular permeability
(e.g. critically ill, sepsis, trauma, burn)
35. Albumin: Side Effect
• Rare
• Might still have weak anticoagulation effects through
platelet aggregation inhibition or heparin-like effects
on antithrombin III
• These effects are thought to be clinically insignificant
if volume replacement with albumin is kept below
25% of the patient’s blood volume.
39. Hetastarch: average mean MW
1. Low - <70 kDa
2. Medium - 130 – 270 kDa
3. High - >450 kDa
higher MW ⇒ longer volume effect
⇒ greater side effect
40. Hetastarch: Molar Substitution
Definition: CH3CH2OH : glucose units
• Low (0.4 – 0.5)
• High (0.62 – 0.7)
higher MS ⇒ longer volume effect
⇒ greater side effect
41. Hetastarch: C2:C6 ratio
• Hydroxyethyl group attached at C2 hinder
breakdown
• Higher ratio of C2:C6 ⇒ in slower enzymatic
degradation and prolonged action without
increasing side effects.
42. HES Solutions Properties and Availability
HES HES HES
Trade Name Hespan Hextend Voluven
Concn 6 g 6 g 6 g
Volume effect (h) 5 – 6 5 – 6 2 – 3
MW 450 670 130
C2:C6 ratio 4:1 4:1 9:1
43. HES: Unwanted Side Effects
• Hypocoagulable effect
- seems to interfere with the function of vWF, factor VIII
and platelets
• Renal toxicity
- induce renal tubular cell swelling & create hyperviscous
urine
• Pruritus
- accumulation on HES molecules under the skin
44. Gelatins
• polypeptides produced by degradation of
bovine collagen
• ave MW: 30,000 – 35,000 kDa
• requires repeated infusions
• no dose limitation
49. Transfusion: pRBC
Indications:
As replacement fluid in acute blood loss.
As replacement in chronic anemia with a
hemoglobin level between 6 – 10 gm % considering
the following factors:
- The patient symptoms and signs (Tachycardia,
Tchypnea)
- Anemia.
50. Transfusion: FFP
• Indication:
replacement factor deficiencies,
replacement of factor in bleeding induced by warfarin
therapy,
coagulopathy asociated with liver disese
• Initial therapeutic dose: 10–15 mL/kg
• Goal: 30% of the normal coagulation factor
concentration
51. Transfusion: Platelets
• Indication:
pts with thrombocytopenia or dysfunctional
platelets in the presence of bleeding