This document discusses fluid and electrolyte imbalance, focusing on sodium and potassium. It begins by outlining where fluid is distributed in the body. It then discusses daily fluid intake and losses. Key points about sodium include that it maintains extracellular fluid balance, nerve impulse transmission, and is regulated by aldosterone and urine output. Causes, symptoms, and treatment of hyponatremia and hypernatremia are summarized. Regarding potassium, it notes its role in muscle function and that the kidney plays a dominant role in regulation. Causes, symptoms, and ECG changes of hypokalemia are outlined.
fluid and electrolyte imbalance
normal physiology of fluid regulation
FLUID IMBALANCES- fluid volume excess, fluid volume deficit, third spacing,
ELECTROLYTE IMBALANCES- hypo and hypernatremia, hypo and hyperkalemia, hypo and hypercalcemia
fluid and electrolyte imbalance
normal physiology of fluid regulation
FLUID IMBALANCES- fluid volume excess, fluid volume deficit, third spacing,
ELECTROLYTE IMBALANCES- hypo and hypernatremia, hypo and hyperkalemia, hypo and hypercalcemia
In medicine, dialysis is the process of removing excess water, solutes, and toxins from the blood in people whose kidneys can no longer perform these functions naturally. This is referred to as renal replacement therapy.
In medicine, dialysis is the process of removing excess water, solutes, and toxins from the blood in people whose kidneys can no longer perform these functions naturally. This is referred to as renal replacement therapy.
Sodium is necessary for the body to maintain fluid balance and is critical for normal body function. It also helps to regulate nerve function and muscle contraction.
Hyponatremia and Hyponatremia.
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No one is complete so reading and thinking may open the door to the hidden ground.
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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.
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- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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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.
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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.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
3. • A healthy person consumes an average of 2000 mL of
water per day, approximately 75% from oral intake
and the rest extracted from solid foods.
4. Daily water losses include:
• 800 to 1200 mL in urine
• 250 mL in stool
• 600 mL insensible losses
Insensible losses of water occur through
skin (75%)
lungs (25%)
increased by such factors
fever (100-150 ml/day for each degree rise over 37 c)
hyperventilation.
5. Sensible water losses such as sweating or pathologic
loss of gastrointestinal (GI) fluids vary widely, but
these include the loss of electrolytes as well as
water.
6. Signs and symptoms of volume disturbances
SYSTEM VOLUME DEFICIT VOLUME EXCESS
Generalized Weight loss
Decreased skin turgor
Dry mucous membrane
Weight gain
Peripheral edema
Cardiac Tachycardia
Hypotension
Collapsed neck veins
Increased cardiac output
Increased central venous
pressure
Distended neck veins
Murmur
Renal Oliguria
Azotemia
GI Ileus Bowel edema
Pulmonary ------------- Pulmonary edema
10. Sodium Na
• Most abundant cation in extracellular fluid
• Normal range:135 to 145 mEq/L
• Daily requirement 1-2 mmol/kg/day
• 600ml-1000ml of normal saline is sufficient to provide daily requirement
• Maintains balance of extracellular fluid
• Transmission of nerve impulse
• Neuromuscular and myocardial nerve impulse
11. Sodium (Na) regulation
• Aldosterone
• Urine output
• Salt intake
Note : To a large extent, extracellular fluid sodium
concentration and osmolarity are regulated by the amount
of extracellular water. The body water in turn is controlled
by
(1) fluid intake, which is regulated by factors that determine
thirst, and
(2) renal excretion of water.
12. Hyponatremia
• defined as a serum [Na+] <135 mmol/L
• one of the most common electrolyte abnormalities encountered
in hospitalized pts
• Symptoms include nausea, vomiting, confusion, lethargy, and
disorientation
• if severe (<120 mmol/L) and/or abrupt, seizures, central
herniation, coma, or death may result
• Clinical manifestations primarily have a central nervous system
origin and are related to cellular water intoxication and
associated increases in intracranial pressure
13. Causes of hyponatremia with decreased extracellular volume
(hypovolemia)
Extra Renal :
• Vomiting ,Diarrhea ,Hemorrhage, Burns, Pancreatitis
Renal: high urine sodium levels (>20 mEq/L)
• Osmotic diuresis (e.g. hyperglycemia, severe
uremia)
• Diuretics
• Adrenocortical insufficiency
• Tubulo-interstitial renal disease
• Unilateral renal arterystenosis
• Recovery phase of acute tubular necrosis
14. Causes of hyponatremia with normal extracellular volume
(euvolemic)
• Abnormal ADH release
• Vagal neuropathy (failureof inhibition of ADH release)
• Deficiency of adreno corticotrophic hormone (ACTH) or
glucocorticoids (Addison’s disease)
• Hypothyroidism
• Severe potassium depletion
• Syndrome of inappropriate antidiuretic hormone
• Major psychiatric illness ‘Psychogenic polydipsia’
• Anti-depressant therapy
• Increased sensitivity to ADH : Chlorpropamide ,Tolbutamide
• ADH-like substances : Oxytocin , Desmopressin
15. Causes of hyponatremia with normal extracellular volume (euvolemic) contd.
• Unmeasured osmotically active substances stimulating osmotic ADH
release
• Glucose
When hyponatremia in the presence of hyperglycemia is being evaluated, the corrected sodium
concentration should be calculated as follows:
For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should
decrease by 1.6 mEq/L
• Chronic alcohol abuse
• Mannitol
• Sick-cell syndrome (leakage of intracellular ions)
17. High
• Increased intake
• Postoperative ADH
secretion
• Drugs
Normal
• Hyperglycemia
• ↑Plasma Lipids/proteins
• SIADH
• Water intoxication
• Diuretics
Low
• Decreased sodium intake
• GI losses
• Renal losses
• Diuretics
• Primary renal disease
HYPONATREMIA
VOLUME STATUS
18. Treatment
• This is directed at the primary cause whenever
possible.
In a healthy patient:
• give oral electrolyte–glucose mixtures; ORS
• increase salt intake ; 60–80 mmol/day.
• In a patient with vomiting or severe volume depletion:
■ give intravenous fluid with potassium supplements, i.e. 1.5–2
L 5% Dextrose (with 20 mmol K+) and 1 L 0.9%
saline over 24 hours PLUS measurable losses
■ correction of acid–base abnormalities is usually not
required
Euvolemic hyponatremia is managed by restriction of water
intake (to 1000 or even 500mL per day) with review of
diuretic therapy. Magnesium and potassium deficiency must
be corrected. In mild sodium deficiency, 0.9% saline given
slowly (1 L over 12 hours) is sufficient.
19. The aim of treatment should be to correct the serum sodium
concentration at a rate no faster than 1mmol/L/hour or
25mmol/L/day.
In asymptomatic patient 0.5mmol/L/hr is acceptable.
• Those who have profound hyponatremia ; <120mEq/L and/or
neurological symptoms
Hypertonic saline 3%: 100 to 200 ml over 30 min.
20. HYPERNATRAEMIA
• This is much rarer than hyponatremia and nearly alwaysindicates a
water deficit.
• impaired thirst or impaired conscious state
• pituitary diabetes insipidus (failure of ADH
secretion)
• nephrogenic diabetes insipidus (failure of response to
ADH)
• osmotic diuresis, e.g. hyperglycemic, hyperosmolar
state
• excessive loss of water through the skin or lungs.
• Excessive administration of sodium may also contribute,
for example: excessive reliance on 0.9% (150 mmol/L)
saline for volume replacement
• administration of drugs with a high sodium content
(e.g. piperacillin)
• use of 8.4% sodium bicarbonate after cardiac arrest
21. note that…..
• Hypernatremia is always associated with increased plasma
osmolality, which is a potent stimulus to thirst. None
of the above cause hypernatremia unlessthirst sensation
is abnormal or access to water limited. For
instance, a patient with diabetes insipidus will
maintain a normal serum sodium concentrationby
maintaining a high water intake until an intercurrent
illness prevents this. Thirst is frequently deficient in
elderlypeople, making them more prone to water
depletion. Hypernatremia may occur in the presence
of normal, reduced or expanded extracellular
volume, and does not necessarily imply that total body
sodium is increased.
22. High
• Iatrogenic sodium
administration
• Mineralocorticoid
excess
• Aldosteronism
• Cushing’s disease
• Congenital adrenal
hyperplasia
Normal
• Nonrenal water loss
• Skin
• GI
• Renal water loss
• Renal disease
• Diuretics
• Diabetes insipidus
Low
• Nonrenal water loss
• Skin
• GI
• Renal water loss
• Renal (tubular)
disease
• Osmotic diuretics
• Diabetes insipidus
• Adrenal failure
Hypernatremia
Volume status
23. Clinical features of Hypernatremia
• Symptoms of hypernatraemia are non-specific.
• Nausea, vomiting,
• fever
• confusion
• A history of longstanding polyuria, polydipsia
and thirst suggests diabetes insipidus.
24. Treatment
The aim of treatment should be to correct the serum sodium concentration at a rate no faster
than 1mmol/L/hour or 25mmol/L/day.
In asymptomatic patient 0.5mmol/L/hr is acceptable
• Treatment is that of the underlying cause for
example:
in ADH deficiency, replace ADH in the form of
desmopressin, a stablenon-pressor analogue of
ADH.
• remember to withdraw nephrogenicdrugs wherepossible
and replace watereitherorally or, if necessary,
intravenously.
25. Treatment contd.
In severe (> 170 mmol/L) hypernatraemia:
• 0.9% saline (150 mmol/L) should be used initially.
• Avoid too rapid drop in serumsodium concentration;
• the aim is correction over 48 hours
• as over-rapid correction may lead to cerebral edema.
In less severe (e.g. > 150 mmol/L) hypernatraemia :
• the treatment is 5% dextrose or 0.45%saline; the
latter is obviously preferable in hyperosmolar diabetic
coma.Very large volumes –upto 5 L a day or
more – may need to be given in diabetes insipidus.
27. Potassium
• Main intracellular cation
• Normal conc. : 3.5-5.0 mEq/L
• Daily requirement 0.5-1 mEq/L
• The average dietary intake of potassium is approximately 50 to
100 mEq/day
• Regulates neuromuscular excitability and muscle contraction
• Role in glycogen formation and protein synthesis
• Role in acid base balance
28. Potassium regulation
• The kidney plays a dominant role in K+ regulation.
• aldosterone
• Insulin, β2-adrenergic agonists, and alkalosis tend to promote
K+ uptake by cells
• acidosis, insulinopenia, major surgery or acute
hyperosmolality (e.g., after treatment with mannitol)
promote the efflux or reduced uptake of K+.
29. HYPOKALEMIA
much more common than hyperkalemia in the surgical patient.
Clinical features
• usually asymptomatic
• severe hypokalemia (< 2.5 mmol)
causes muscle weakness.
• Paralytic ileus, constipation
• symptomatic hyponatremia
• increased frequency of atrial and
ventricular ectopic beats ,cardiac arrest.
• diminished tendon reflexes, paralysis.
30. ECG changes suggestive of hypokalemia
• U waves
• T-wave flattening
• ST-segment changes
• arrhythmias
31. Causes of HYPOKALEMIA
Vomiting
Severe diarrhea
Purgative abuse
Villous adenoma
Ileostomy
Fistulae
high nasogastric output
34. Causes of hypokalemia contd.
• Reduced intake of K+
Intravenousfluids without K+
Dietary deficiency
• Redistribution into cells
β-Adrenergic stimulation
Acute myocardial infarction
Beta-agonists: e.g. fenoterol, salbutamol
Insulin treatment, e.g. treatment of diabetic ketoacidosis
Alkalosis
35. Management of Hypokalemia
• correction of the underlying disease process (e.g., diarrhea)
• or withdrawal of an offending medication (e.g., loop or thiazide diuretic),
• oral KCl supplementation
• Correction of Mg deficiency
• If hypokalemia is severe (<2.5 mmol/L) and/or if oral supplementation is not
feasible or tolerated, IV KCl can be administered through a central vein with
cardiac monitoring, at rates that should not exceed 10 mmol/ h.
• KCl should always be administered in saline solutions, rather than dextrose; the
dextrose-induced increase in insulin can acutely exacerbate hypokalemia.
36. HYPERKALEMIA
Clinical features
• Serum potassium greaterthan 7.0 mmol/L is an
emergency
• ECG changes ; high peaked T waves (early), widened QRS complex,
flattened P wave, prolonged PR interval (first-degree block), sine wave formation,
and ventricular fibrillation.
• Severe hyperkalemia may predispose to suddendeath from
arrhythmias , asystole & cardiac arrest.
• GI symptoms include nausea, vomiting, intestinal colic, and diarrhea
• Neuromuscular symptoms range from weakness to ascending paralysis to
respiratory failure.
39. Correction of severe Hyperkalemia
• IMMEDIATE
ECG monitor
i.v. access
Protect myocardium
10 mL of 10% calcium gluconate i.v. over 5 min
,
Effect is temporary but dose can be repeated after
15 min
40. • Drive K+ into cells
• Insulin regular 20 units + 100 mL of 25%
glucose i.v. over 10–15min
• Nebs with salbutamol
• followed by regular checks of blood glucose
and plasma K+
• Repeat as necessary
• correction of severe acidosis (pH < 6.9)
– infuseNaHCO3 (1.26%) and/or salbutamol 0.5
mg in 100 mL of 5% glucose over 15
min (rarely used)
41. To be continued.
In next presentation
• Calcium
• Bicarbonate with (acid base balance)
• Magnesium