Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
Lecture covers the pharmacology of anticholinergic drugs. Includes classification, therapeutic uses, adverse effects of anticholinergics. Atropine has been described as prototype drug.
This presentation deals with the use of various drugs in the treatment of heart failure such as Digoxin, ace inhibitors, beta bloockers, calcium channel blockers
Scope: This subject is intended to impart the fundamental knowledge on various aspects
(classification, mechanism of action, therapeutic effects, clinical uses, side effects and
contraindications) of drugs acting on different systems of body and in addition,emphasis
on the basic concepts of bioassay. Objectives: Upon completion of this course the student should be able to
1. Understand the mechanism of drug action and its relevance in the treatment of
different diseases
2. Demonstrate isolation of different organs/tissues from the laboratory animals by
simulated experiments
3. Demonstrate the various receptor actions using isolated tissue preparation
A Power point presentation on Betalactam antibiotics suitable for undergraduate medical students. This Ppt is already presented in theory class lectures to the students of NEIGRIHMS, Shillong, Meghalaya
A Powerpoint presentation on drugs excretion and elimination suitable for UG medical students. This ppt is already presented to my students in one of the theory classes.
A PowerPoint presentation on "NSAIDS" suitable for reading by UG and PG Medical/Paramedical students of Pharmacology and Pharmacy sciences. This Ppt. is prepared for academic purpose only and already presented to my students in one of the theory classes of mine.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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
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
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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.
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
2. Introduction
• Irregularity in Cardiac Rhythm
• Bradyarrhythmia: Failure of impulse generation
resulting in slow heart rates
• Heart Block: Results from failure of impulse to
propagate normally from atrium to ventricle –
usually defect in AV node or His-Purkinje system
• Tachyarrhythmias: Abnormally rapid heart
rhythms
– Common clinical condition
– Treated by Antiarrhythmic Drugs - Drugs used to
prevent or treat irregularities of Cardiac Rhythm
3. Causes of Arrhythmia
• Root causes: When the normal sequence of impulse
generation and propagation is perturbed
4. Arrhythmias –
pacemaker acticity
• Enhanced Automaticity: Pacemaker cells or
ordinary fibres
– Results due to patholgical increase in phase 4 slope -
accelerated pacemaker rate
– May result from current of Injury
– Physiology: ACh reduces such pacemaker rate – by
decreasing phase 4 and hyperpolarization
– Ventricular wall cells (WMCs) may also show such
pace maker activity – due to ischaemia
5. Triggered
Activity
• A normal AP interrupted/followed by a abnormal
depolarization (a triggering rhythm)
Delayed After Depolarization: Caused by Digoxin
toxicity, Myocardial Ischaemia or Adrenergic stress or
Heart failure – due to Ca++ overload
Early After Depolarization: Due to interruption in
phase 3 repolarization
Causes: Slow heart rate, Hypokalaemia and drugs prolonging
QT interval – quinidine, sotalol, procainamide etc. (block IK
channel)
Torsades de pointes: due to marked prolongation of
APD – polymorphic ventricular tachycardia – long QT
interval and frequent changing of QRS
6. Reentry
• One of the causes of the most arrhythmias
• Normally, impulses propagate in synchronized
manners
• But, here one impulse reenters and re-excites
areas of heart more than once – no need for new
impulse generation
• Re-entering of impulses may be
1. Anatomically defined reentry – Circus movement
type
2. Functionally defined reentry - Microentry circuit
8. Anatomically defined reentry – Accessory
pathway (WPW syndrome)
Wolf-Parkinson-White Syndrome
AV nodal reentry, Atrial flutter and PSVT
9. Fractionation of Impulse
• Increased Vagal activity – Atrial ERP brief and
inhomogenous
• Premature impulses get conducted by fibres
having short ERP – then to the fibres with
longer ERP and so on
• Asynchronous activation of atrial fibres –
inhomogenicity – Atrial fibrilation etc.
10. Arrhythmia Conditions - Clinically
• Extrasystole: premature beats due to abnormal automaticity/after
depolarization – AES, VES or AV nodal ES
• Paroxysmal Supraventricular Tachycardia (PSVT): Sudden onset of
atrial tachycardia 150-200/minute (1:1), reentry phenomenon (AV
node)
• Atrial Flutter: 200-350/minute (2:1 to 4:1 AV block), reentrant
circuit in right atrium
• Atrial Fibrillation: Asynchronous activation of atrial fibres 350-
550/min with irregular 100 to 160 ventricular beats – due to
electrophysiological inhomogenicity of atrial muscles (bag of
worms)
• Ventricular tachycardia: 4 or more consecutive extrasystole of
ventricles – monomorphic or polymorphic
• Ventricular Fibrillation: rapid irregular contractions – fatal (MI,
electrocution)
• Torsades de pointes: polymorphic ventricular tachycardia, rapid
asynchronous complexes, rise and fall in baseline of ECG
• Atrio-ventricular Block (A-V Block): vagal influence or ischaemia -
1st, 2nd and 3rd degree – slowed conduction, drop beat and no
14. Class I - antiarrhythmics
Class I antiarrhythmics: are further classified to
Ia, Ib and Ic – based on repolarization and potency of Na+
blockade – state dependant manner
Lidocaine
Phenytoin
Flecainide
Propafenone
Na+ blockade: Ic>1a>1b ERP: 1a>2c>1b
15. Subclass – I A - quinidine,
procainamide, disopyramide
• Binds to Na+ channels in open state and prevent conduction of
ions (Refractory – Rest – Open – Refractory) - Moderate sodium
channel blockade in open state
• Prolong refractoriness by blocking several types of potassium
channel
• Delayed Na channel recovery
• Delayed AV conduction
• Useful in conditions where Na+ channels open frequently –
ectopic beats - atrial tachycardia and atrial fibrillation and
ventricular arrhythmias
• Abolish reentry – unidirectional block to bidirectional block
• Electrophysiology changes: Lengthen action potential, slow rate
of rise of phase 0, Prolong repolarization ---------------- also prolong
AV node ERP - ECG changes: Prolong PR, QRS, QT
16. Subclass - IB
• Lowest potency for Na+ channel blocker -
inactivated state
• Do not delay channel recovery
• EP changes: Shorten action potential, Limited
effect on rate of rise of phase 0, Shorten
repolarization ------------- no ERP effect on AV
node (shorten)
• ECG: Shorten QT
• Used in Treatment and prevention of ventricular
tachycardia and fibrillation after Myocardial
Infarction – lignocaine IV , e.g, lignocaine,
mexilitine, phenytoin, propafenone
17. Subclass IC
• Propafenone, Flecainide, Encainide, Moricizine
• Marked Na+ channel blockade in open state – with longest recovery
time
• Refractory period of AV node is increased – marked delay in
conduction
• Electrophysiology changes: No effect on length of action potential,
Markedly reduces rate of rise of phase 0 and ---------- marked delay
in AV conduction with little effect on repolarization
• ECG: markedly prolong PR and QRS complex
• Prolong refractoriness by blocking outward-rectifying potassium
channels
• General reduction in excitability
• Used in life threatening ventricular fibrillation since they have
highest affinity to Na+ channels involving AV node - WPW syndrome
and Paroxysmal atrial fibrillation
19. Antiarrhythmic -
Quinidine
• Dextroisomer of Quinine: N+ channel blocking and antivagal
action
• Actions:
Inhibition of Na channel – slanted O phase and Decreases phase 4
Prolongation of APD – due to K+ channel block
Increase in ERP – due to delay in Na+ and K+ channel recovery
Net result is delay in conductivity and increase in refractoriness
Fall in BP – direct cardiac depression
Other actions include – alpha blockade, decreased skeletal muscle contractility,
uterine contractions, vomiting and diarrhoea etc.
Kinetics: well absorbed orally, half life – 10 Hrs
Uses:
Broad spectrum antiarrhythmic
Atrial fibrillation and flutter, prevention of PSVT and prevention of ventricular
tachycardia
Adverse effects: Not used now for adverse effects like
Proarrhythmia (torsades de pointes), sudden cardiac arrest or VF,
cinchonism, angioedema, vascular collapse etc.
Available as 200, 300 mg tabs. And 300 mg/ml Injections
20. Procainamide
• Procaine derivative (amide)
• Identical action with quinidine except:
– Minimal antivagal action
– Lesser suppression of ectopic automaticity
– Lesser depression of contractility and AV conduction
– No alpha blocking action
• Kinetics:
– Absorbed orally and bioavailability is 80%
– Metabolized in liver to N-acetyl-procainamide (NAPA) – blocks K
channel and prolongs repolarization
• Dosage – 250 mg tabs and 1gm/ml injections
– Antiarrhythmic – 0.5 to 1 gm oral followed by 0.25-0.50 mg
every 2 Hrs
• Uses: Mainly for monomorphic VTs and to prevent
recurrences
• ADRs: Hypersensitivity, flushing, hypertension, torsedes de
pointes and CNS symptoms – mental confusion,
hallucinations and weakness
21. Antiarrhythmic – Lidocaine
(Lignocaine)
• Popular antiarrhythmic and also local anaesthetic (membrane
stabilizing action)
• Lowest potency for Na+ channel inactivated state – ECTOPIC Foci
– Enhance phase – 4 depolarization in partially depolarized or stretched PF –
After depolarization antagonized – no effect on SAN
– Practically no action on Atrial fibres
– Rate of 0 phase in AVN and ventricles – not affected
– Reduction in APD in PF and ventricular myocardium
• Actions:
– Selective action on partially depolarized and cells with long APD – normal
ventricular and conducting fibres – not affected
– Suppression of automaticity in ectopic foci (reentry) – one way or two way
block
– Enhanced phase-4 depolarization in partially depolarized or stretched PF
(APD long)
– Little effects on cardiac contractility and arterial BP
22. Lidocaine – contd.
• Kinetics: Ineffective orally, given IV lasts for 10-20 minutes.
Therefore given as IV bolus 50-100 mg followed by 20-40 mg
every 10-20 minutes. Half-life prolonged in CHF (coz. Vd
decreases) and 70-80% metabolized by liver
• Adverse effects: Neurological – drowsiness, paresthesia,
blurred vision, nystagmus and fits etc.
– No proarrhythmic effects – no cardiotoxicity
• Uses: 50-100 mg bolus and 10-20 mg every 20 minutes
– 1st line of drug in Arrhythmia following acute MI and cardiac
surgery
– Prevention of ventricular tachycardia
– Digitalis toxicity – no AV block
• LA lignocaine Vs Antiarrhythmic lignocaine ?
23. Beta blockers
• Drugs used are beta-blockers: Propranolol, Sotalol, Esmolol
and Acebutlol
• Suppression of adrenergically mediated activity
• Propranolol - Membrane stabilizing effect like quinidine on
heart – high doses – clinical dose: cardiac adrenergic
blockade
• Clinical doses (antiarrhythmic effect) - Block beta-1
receptor in heart and decreases heart rate
1. Decrease in phase 4 depolarization and automaticity in SA
node, AVN, PF and other ectopic foci (Adrenaline causes
ventricular ES and fibrilation by increasing the phase 4
depolarization !!!)
2. Prolongation of ERP of AVN – impede AV conduction
24. Uses of Propranolol
• Arrhythmias associated with increased sympathetic
activity – sinus tachycardia, atrial extrasystoles
provoked by emotion and exercise
• Less effective in PSVT than adenosine and verapamil
• Propranolol is used to treat sympathetically mediated
arrhythmias - phaeochromocytoma and halothane
anaesthesia
– Sinus tachycardia, atrial and nodal extrasystole and nodal
extrasystole provoked by exercise
Does not abolish AF or Afl but decreases ventriculsar rate
• Reduce mortality after MI – anti-ischaemic action
• Esmolol IV – quickly terminates AF and fluttter and
used in emergency control of arrhythmia due to
anaesthetics
25. Class-III
Antiarrhythmics
• Class III drugs K channel blockers prolong
repolarization (increase refractoriness) by blocking
outward potassium conductance
– Prolongation of Cardiac action potential
– Increased ERP
• Drugs – Amiodarone Ibutilide, dofetilide,
sotalol (II + III action) and bretylium
• Bretylium is used only in life threatening
arrhythmias
26. Amiodarone
Long acting and highly lipophillic and Iodine containing
compound
MOA: - multiple actions
1. Blocking of delayed rectifier K+ channel – prolongs APD
2. Weak class I (lidocaine like) – depresses conducton in
partially depolarized and long APD
3. II (beta- blocker) – NC alpha and beta; and class IV actions
4. Also direct coronaray and peripheral vasodilator
• Overall – Slowed conduction and supressed automaticity
Kinetics: Incompletely and slowly absorbed – daily oral dose is
given for several days for actions to develop, t1/2 = 3-8
weeks
Dose: 400-600 mg/day p.o for many days followed by 100-200
mg/day as maintenance (100-300 mg slow IV)
27. Amiodarone
Uses:
• Most tachyarrhythmic conditions – ventricular and supraventricular
• Recurrent VT and VF
• WPW syndrome
Adverse effects:
• Photosensitization – skin pigmentation
• Peripheral neuropathy – weak shoulder and pelvic muscles
• Myocardial depression – bradycardia
• Pulmonary alveolitis and fibrosis – kept below 200 mg
• Corneal micro deposits – on long term use
• Hypothyroidism, goitre – inhibition of T4 to T3
Drug Interactions: Digoxin and warfarin (reduced renal clearance)
28. Class IV -
Antiarrhythmics
• Three important classes:
– Phenylalkylamines – hydrophillic Verapamil
– Dihydropyridines – lipophilic Nifedepine
– Benzothiazepines – hydrophilic Diltiazem
• Verapamil and diltiazem: are useful in
Arrhythmia
• Relatively selective AV nodal L-type calcium
channel blockers – depression of Ca++ mediated
depolarization and delay recovery
– Slows SA node automaticity
– reduced phase 4 depolarization in SAN and PF –
extinction of latent pacemakers and DAD
– Prolongation of AVN ERP – reentry terminated
– Negative ionotropic action
29. Class IV – contd.
• Uses: Verapamil
1. PSVT:
• For termination of attack – 5 mg IV over 2-3 minutes
(reflex bradycardia)
• For prevention of attack 60-120 mg orally tds
2. Reduce ventricular rate in Atrial fibrillation (AF)
and Atrial flutter – with digitalis
30. Miscellaneous Agents
Adenosine:
• Endogenously produced important chemical mediator used in
PSVT
• MOA:
– Activation of ACh sensitive K+ channel - membrane hyperpolarization
of SA node (G-protein coupled adenosine receptor A1)
– depression of SA node and also slowing of AV conduction
– shortening of action potential in atrium and reduced excitability
– Also indirectly reduces Ca++ current in AV node – depression of
reentry in PSVT
31. Adenosine – contd.
• Very short half life – 20-30 sec. - Uptake by RBCs
and endothelial cells (5-AMP and inosine)
• Administered intravenously – available as free
base or ATP
– 6 - 12 mg/ATP 10 - 20 mg given as a rapid intravenous
bolus (administered over a 1-2 second period)
– If the first dose does not result in elimination of the
supraventricular tachycardia within 1-2 minutes - 12
mg should be given as a rapid intravenous bolus
• ADR: chest tightness, dyspnoea, fall in BP and
flushing etc.
32. When Antiarrhythmics ?
• Asymptomatic and those which do not interfere
haemodynamics – AES, VES, 1st degree block and
bundle branch block – no need of treatment
• Therapy needed:
– Life threatening VT, TdP and VF
– Causing breathlessness, hypotension and cardiac
failure
– Marked palpitation – PSVT, VT, AF and TdP
– Myocardial infarction
34. The Pacemaker
• Surgical implantation of electrical
leads attached to a pulse generator
1) Leads via subclavian vein and
advanced to the chambers on the
vena cava (right) side of the heart
2) 2 leads - right atrium, and right
ventricle
3) Pulse generator containing
microcircuitry and battery are
attached to leads and placed into a
“pocket” under the skin near the
clavicle
4) Pulse generator sends signal - to
contract atria, then ventricles
• Pulse generator - sense electrical
activity - only deliver electrical
impulses when needed.
• Pacemakers : can only speed up a
heart experiencing bradycardia,
cannot alter a condition of
tachycardia
35. Expected Questions ??
• Classification of anttiarrhythmic drugs
• Lidocaine as antiarrhythmic agent
• Amiodarone as antiarrhythmic agent
• Role of Beta blockers (Propranolol) and Ca++
channel blockers (Verapamil) in Arrhythmia
• Short Note: Adenosine
Editor's Notes
The gross electrical activities that can be observed in ecg are due to the action potentials generated in different cardiac tissues.
The fast sodium channel can be modeled as being controlled by a number of gates . Each gate (or gating variable) can attain a value between 1 (fully open) and 0 (fully closed). The product of all the gates denotes the percentage of channels available to conduct Na + . Following the model of Hodgkin and Huxley , the sodium channel contains three gates: m , h , and j . In the resting state, the m gate is closed (zero) and the h and j gates are open (one). Hence, the product denoting the percentage of conducting channels is also zero. Upon electrical stimulation of the cell, the m gate opens quickly while simultaneously the h and j gates close more slowly. For a brief period of time, all gates are open ( i.e. non-zero) and Na + can enter the cell following its electrochemical gradient . If, as above, the resting membrane potential is too positive, the h or j gates may be considerably less than one, such that the product of m , h and j becomes too small upon depolarization.
Electrical activities in different part of the cardiac tissues can be recorded externally over the skin by placing electrodes on both side of the heart – called ECG or EKG
Abnormal pacemaker activity can occur if myocardial cells are damaged eg ischaemic heart disease also via catecholamine overactivity
Ventricles can be excited with each sinus node depolarization. The will generally travel via AV node and accessory pathway if present. However accessory pathways have fast action tissues and AV node has slow action tissues. Thus in patients with WPW syndrome has premature atrial impulses and cannot excite accessory pathway as not enough threshold can be generated there but can excite AV node slowly and conducts the impulse. The impulse will pass down the ventricular wall and somewhere meets the accessory pathway which is by now may be no longer refractory and the impulse traverse back to the atrium and again reach the AV node and reenter ventricle.
Atrial fibrillation - Atria remains dilated and quiver like bag of worms Torsades de pointes – polymorphic ventricular tachycardia
Pharmacologically, minimum interval between the two propagating action potentials. It is closely related to AP duration (APD). An AP can be evoked in fast channel fibres before complete repolarization. Because Na+ channel recover in a voltage-dependent manner, above the threshold potential. In contrast, the Ca++ channels recover in time dependent manner.