Brief description of drugs which are used to alter cardiac action potential in arrythmic patients. It focuses on understanding of action potentials in short descriptions as possible.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
Cardiac muscle (The Guyton and Hall Physiology)Maryam Fida
In the heart there is Atrial muscle and Ventricular muscle which are separated from each other by the fibrous AV Rings containing Valves.
ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep sheet. Superficial sheet is common over both atria. Deep sheet is separate for each atrium. Muscle fibers in the deep sheet are at right angle to the muscle fibers in the superficial sheet.
FUNCTIONS OF THE ATRIUM:
1. Receive venous blood from large veins. So atria act as reservoir.
2. Conduct the blood into the ventricles.
3. Atrial contraction is responsible for last 25 % of ventricular filling.
4. In the right atrium there is SA Node(Pace maker) and AV node.
5. In the wall of the atria, there are low pressure stretch receptors and these are involved in various reflexes like brain bridge reflex and left atrial reflex.
6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone. Whenever NaCl increases in ECF, it causes release of ANH which causes natriuresis.
VENTRICULAR MUSCLE:
Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm and thickness of left ventricle is 8 – 12 mm.
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a number of cardiac cells, united at ends in series. Where as in skeletal muscle each muscle fiber is individual cell.
4.Cardiac muscle cells are branching and interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act as separate functional syncytium and impulses from atria are conducted to ventricles through the AV Node and AV Bundle.
7. Sarcoplasmic system is present. In skeletal muscle triad is at the junction of A and I bands. In cardiac muscle T Tubules are much large and thus in cardiac muscle if we take a section it may form a diad or a triad. And these diads and triads are present at the level of Z Disks.
8.Between adjacent cardiac cells there are side to side and end to end connections and these are the intercellular junctions. These junctions are Gap Junctions. Or intercalated discs
9.When one part of myocardium is excited the whole muscle is excited.
10.Whole myocardium obeys all or none law as a whole.
11.No spike potential but action potential with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period is 150 milli sec
Because of long refractory period cardiac muscle cannot be tetanized.
Cardiac cycle refers to a complete heartbeat from its generation to the beginning of the next beat.
Cardiac events that occur from –
beginning of one heart beat to the beginning of the next are called the cardiac cycle.
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
Cardiac cycle refers to a complete heartbeat from its generation to the beginning of the next beat.
Cardiac events that occur from –
beginning of one heart beat to the beginning of the next are called the cardiac cycle.
Cardiac muscle has three types of membrane ion channels that play important roles in causing the voltage changes of the action potential. They are (1) fast sodium channels, (2) slow sodium-calcium channels, and (3) potassium channels
Depolarization: First, the action potential of cardiac muscle is caused almost entirely by sudden opening of large numbers of so-called fast sodium channels that allow tremendous numbers of sodium ions to enter the cardiac muscle fiber from the extracellular fluid. These channels are called “fast” channels because they remain open for only a few thousandths of a second and then abruptly close. After depolarization, there's a brief repolarization that takes place with the efflux of potassium through fast acting potassium channels.
Plateau: Secondly, another entirely different population of slow calcium channels, which are also called calcium-sodium channels. This second population of channels differs from the fast sodium channels in that they are slower to open and, even more important, remain open for several tenths of a second. During this time, a large quantity of both calcium and sodium ions flows through these channels to the interior of the cardiac muscle fiber, and this maintains a prolonged period of depolarization, causing the plateau in the action potential.
Repolarization: When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the influx of calcium and sodium ions ceases, the membrane permeability for potassium ions also increases rapidly; this rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential.
“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
Conductive system of heart by Dr. Pandian M Pandian M
The student will be able to: (MUST KNOW)
Name the parts of conducting system of the heart.
Appreciate the importance of AV nodal delay.
Explain the mechanism of AV nodal delay.
Give the conduction velocity in different cardiac tissues.
Understand the propagation of electrical impulse in conducting system of heart.
CVS physiology, all details with explanation easy to recall physiology of cardiovascular system. based on Ganong's Review of Medical Physiology. all the high-yield facts are there.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
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.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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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
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
Drugs affecting cardiac action potential
1. Drugs and Their Effects on
Cardiac Action Potential in
Arrythmic Patients
Presented by
Sabarni Sarker
Student, M. Pharm.
Rajshahi University
28 May 2014
2. What is Action Potential?
• Action potential is a short-lasting
event in which the
electrical membrane potential of
a cell rapidly rises and falls
• Action potentials are generated by
special types of voltage-gated ion
channels embedded in a cell's plasma
membrane.
5. Terminology
• Cardiac arrhythmia or irregular heartbeat is any
of a group of conditions in which the electrical
activity of the heart is irregular or is faster or
slower than normal.
• A heartbeat that is too fast is called tachycardia,
a heartbeat that is too slow is called bradycardia.
• After an action potential initiates, the cardiac cell
is unable to initiate another action potential for
some duration of time (which is slightly shorter
than the "true" action potential duration). This
period of time is referred to as the refractory
period.
7. Class IA
These drugs binds to
open and inactivated
sodium channels and
prevents sodium influx,
thus slowing the rapid
upstroke during Phase 0.
It also decreases the
slope of Phase 4
spontaneous
depolarization.
Examples: 1) Quinidine – 1st
antiarrhythmic used, treat
both atrial and ventricular
arrhythmias, increases
refractory period
2)Procainamide
3)Disopyramide
8. Class IB
The IB agents rapidly
associate and
dissociate from
sodium channels. Thus
the actions of Class IB
agents are manifested
when the cardiac cell
is depolarized or firing
rapidly. Class IB drugs
are parlicularly useful
in treating ventricular
arrhythmias.
Examples: Lidocaine,
Mexiletine, Tocainide
9. Class IC
These drugs slowly dissociate from
resting sodium channels and show
prominent effects, even at normal
heart rates. These drugs are
approved only for refractory
ventricular arrhythmias. However,
recent data have cast serious
doubts on the safety of the Class IC
drugs.
Propafenone slows conduction,
weak β – blocker, also some Ca2+
channel blockade
Flecainide (initially developed as a
local anesthetic) Also inhibits
abnormal automaticity
10. Class II
• The Class II agents include the ß-adrenergic
antagonists.
• These drugs diminish Phase 4 depolarization, thus
depressing automaticity, prolonging AV conduction,
and decreasing heart rate andb contractility.
• Includes
Propranolol
Metoprolol
Nadolol
Pindolol
Sotalol
Timolol
Esmolol
11. Class III
Class Ill agents block
potassium channels and
thus diminish the outward
potassium current during
repolarization of cardiac
cells. These agents prolong
the duration of the action
potential without altering
Phase 0 of depolarization or
the resting membrane
potential. Instead, they
prolong the effective
refractory period. All Class III
drugs have the potential to
induce arrhythmias.
It includes Sotalol, bretylim
and amiodarone.
12. Class IV
Class IV drugs are calcium-
channel blockers. They
decrease the inward current
carried by calcium, resulting
in a decreased rate of Phase 4
spontaneous depolarization.
They also slow conduction in
tissues that are dependent on
calcium currents, such as the
AV node. Although voltage
sensitive calcium channels
occur in many different
tissues, the major effect of
calcium-channel blockers is on
vascular smooth muscle and
the heart.
Example: Verapamil,
Diltiazem, Nifedipine
13. Other Drugs
• Digoxin shortens the refractory period in atrial and
ventricular myocardial cells while prolonging the effective
refractory period and diminishing conduction velocity in the
AV node.
• Adenosine is a naturally occurring nucleoside, but at high
doses, the drug decreases conduction velocity, prolongs the
refractory period, and decreases automaticity in the AV
node.
• Implantable cardioverter-defibrillator (ICD) is a
small battery powered electrical impulse generator that is
implanted in patients who are at risk of sudden cardiac
death due to ventricular fibrillation and ventricular
tachycardia.