This document provides information on normal cardiac cell properties and the heart's pacemaker cells. It discusses impulse conduction through the heart and the components of the electrocardiogram (ECG). Criteria for a normal heart rhythm are outlined. Mechanisms of arrhythmias including abnormal impulse initiation and conduction are explained. Various types of arrhythmias originating from the sinoatrial node or atria are described, including their causes, ECG characteristics, signs/symptoms, and management.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
Heart arrhythmia, also known as irregular heartbeat or cardiac dysrhythmia, is a group of conditions where the heartbeat is irregular, too slow, or too fast. Arrhythmias are broken down into: Slow heartbeat: bradycardia. Fast heartbeat: tachycardia. Irregular heartbeat: flutter or fibrillation.
ECG Lecture: Sinus arrest, sinoatrial exit block, AV block and escape rhythmsMichael-Joseph Agbayani
Simple ECG lecture about sinus arrest, sinoatrial exit block, AV block and escape rhythms. Slideshow was made with an audience of medical professionals in mind.
Heart arrhythmia, also known as irregular heartbeat or cardiac dysrhythmia, is a group of conditions where the heartbeat is irregular, too slow, or too fast. Arrhythmias are broken down into: Slow heartbeat: bradycardia. Fast heartbeat: tachycardia. Irregular heartbeat: flutter or fibrillation.
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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.
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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.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
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.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
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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.
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
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
4. Properties of cardiac cells
Automaticity
• Ability to initiate an impulse spontaneously and
continuously.
Excitability.
• Ability to be electrically stimulated.
Conductivity
• Ability to transmit an impulse along a membrane in
an orderly manner.
Contractility
• Ability to respond mechanically to an impulse.
5. Pacemakers of the Heart
• SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
• AV Node - Back-up pacemaker with an
intrinsic rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker with
an intrinsic rate of 20 - 45 bpm.
6. Impulse Conduction & the ECG
Sinoatrial node
AV node
Bundle of His
Bundle Branches
Purkinje fibers
7. The “PQRST”
• P wave - Atrial
depolarization
• T wave - Ventricular
repolarization
• QRS - Ventricular
depolarization
8. The PR Interval
Atrial depolarization
+
delay in AV junction
(AV node/Bundle of His)
(delay allows time for
the atria to contract
before the ventricles
contract)
9. The ECG Paper
• Horizontally
– One small box - 0.04 s
– One large box - 0.20 s
• Vertically
– One large box - 0.5 mV
10.
11. ECG Composed of Waves And Complexes
P- WAVE QT- INTERVAL
QRS- COMPLEX PR- INTERVAL
T- WAVE ST- SEGMENT
12. Criteria's of a normal heart rhythm
1. Presence of one upright and consistent-
appearing P wave before each QRS
complex.
2. P-R interval between 0.12-0.20 seconds
3. A consistent appearing QRS complex of
less than 0.12 seconds.
4. Consistent R-R interval
5. A heart rate between 60-100 beats/minute
6. The ST segment should be isoelectrical
13. Arrhythmias
• It is a disturbance in the
rhythmic patterns of the heart.
Results from abnormal
impulse initiation, abnormal
conduction or both mechanism
together.
14. Four Steps to Identify Arrhythmias
1- Begin by labeling the P wave, QRS
complex, T wave, PR interval, and QT
interval.
2- Calculate the atrial and ventricular heart
rates.
3- Determine if the rhythm is regular or
irregular.
4- Evaluate the waveform of the ECG in
detail for additional clues:
17. Mechanisms Of Arrhythmias
The major mechanisms of arrhythmias are
ABNORMAL IMPULSE INITIATION
Enhanced normal automaticity
Abnormal automaticity
Triggered activity due to afterdepolarization
ABNORMAL IMPULSE CONDUCTION
Conduction blocks
Reentry
1
2
18. Enhanced normal automaticity
• Automaticity is defined as the ability of a cell
to independently initiate an action potential.
21. II. Disorder of impulse conduction
• S.A. Block
• First degree AV Block
• Second Degree A.V.Block
» Mobitz type I
» Mobitz type II
• Third Degree or Complete A.V Block
23. Mechanism responsible for phase 4
depolarization
1. Decreased outward permeability to
potassium
2. Increased inward permeability to sodium
3. Reduced sodium pump activity
4. Increased inward permeability to calcium
24. Rhythms Originating in SA Node
SINUS BRADYCARDIA
• It is characterized by atrial and ventricular rates
of less than 60 beats/minutes.
• It occur gradually or suddenly for a brief period.
• It is usually a benign dysrhythmias and is
common among general population
• It is commonly seen in athletes and also be
associated with sleep
25. Sinus Bradycardia
CAUSES Stimulation
Carotid Sinus Massage
Increased vagal tone
vomiting
suctioning
severe pain
extreme emotions
Decreased sympathetic tone
Intra Occular Pressure
Valsalva maneuver
27. • Right and left Vagus nerve fibers of the
parasympathetic nerve system plays an
important role in the rate of impulse formation,
the speed of conduction and the strength of
cardiac contraction.
• Stimulation of the Vagus nerve causes a
decrease rate of firing of the SA node, slowed
impulse conduction of the AV node, and
decreased force of cardiac muscle contraction.
28. • Stimulation of the sympathetic nerve
system that supply the heart has essentially
the opposite effect on the heart.
29. Valsalva maneuver
• The Valsalva maneuver or Valsalva
manoeuvre is performed by moderately forceful
attempted exhalation against a closed airway,
usually done by closing one's mouth and
pinching one's nose shut.
30.
31.
32. • Variations of the maneuver can be used either in
medical examination as a test of cardiac function
and autonomic nervous control of the heart, or to
"clear" the ears and sinuses (that is, to equalize
pressure between them) when ambient pressure
changes, as in diving, hyperbaric oxygen therapy,
or aviation.
• The technique is named after Antonio Maria
Valsalva
33. The normal physiological response
consists of 4 phases
• Initial pressure rise: On application of
expiratory force, pressure rises inside the chest
forcing blood out of the pulmonary circulation
into the left atrium. This causes a mild rise in
stroke volume.
34. • Reduced venous return and compensation:
Return of systemic blood to the heart is impeded
by the pressure inside the chest. The output of the
heart is reduced and stroke volume falls. This
occurs from 5 to about 14 seconds in the
illustration. The fall in stroke volume reflexively
causes blood vessels to constrict with some rise in
pressure (15 to 20 seconds).
35. • This compensation can be quite marked
with pressure returning to near or even
above normal, but the cardiac output and
blood flow to the body remains low. During
this time the pulse rate increases.
36. • Pressure release: The pressure on the chest is
released, allowing the pulmonary vessels and
the aorta to re-expand causing a further initial
slight fall in stroke volume (20 to 23 seconds)
due to decreased left ventricular return and
increased aortic volume, respectively. Venous
blood can once more enter the chest and the
heart, cardiac output begins to increase.
37. • Return of cardiac output: Blood return to
the heart is enhanced by the effect of entry
of blood which had been dammed back,
causing a rapid increase in cardiac output
(24 seconds on). The stroke volume usually
rises above normal before returning to a
normal level. With return of blood pressure,
the pulse rate returns towards normal.
44. Sinus Bradycardia
• Etiology: SA node is depolarizing slower
than normal, impulse is conducted normally
(i.e. normal PR and QRS interval).
45. Management
Inj Atropine Sulphate is administered if
presented with hypotension, restless, chest
pain, other signs of hemodynamic changes
Decrease the Vagal stimulation
Avoid drugs which causes Bradycardia
Transcutaneous pacing
Dopamine
Epinephrine
Isoproterenol
46. Sinus Tachycardia
• It is characterized by an atrial and ventricular
rate of 100 beats/minute or more.
• Generally the upper limit of sinus tachycardia
is 160 beats/ minute.
47. Sinus Tachycardia
Causes
• Increased Sympathetic Stimulation
Exercise
Emotions/ excitement
Fever
Fear
Acute pain
Any condition that require a higher
basal metabolism
48. Causes……..
• Hyper metabolic States
• Blood Loss
• Consumption of alcohol, caffeine and tobacco.
• Drugs like
Atropine
Dopamine
Dobutamine
Nor epinephrine
amphetamines
49. • It can be a short term compensatory response
to heart failure, anemia, hypovolemia, and
hypotension.
• Hyperthyroidism
Causes……..
54. Sinus Tachycardia
• Etiology: SA node is depolarizing faster
than normal, impulse is conducted
normally.
• Remember: sinus tachycardia is a response
to physical or psychological stress, not a
primary arrhythmia.
55. Management
• Treatment is directed at the cause
• Digitalis
• Beta-blockers
• Diltiazem
• Carotid Sinus Massage
56. Sinus Arrest/Sinus Pause
• Sinus node automaticity is depressed
• Impulses are not formed when expected
• No P wave or no QRS complex is generated
• Patient may feel palpitation from the
increased stroke volume that accompanies
the next beet after the pause.
57. Etiology
• Vagal Stimulation
• Hypoxia
• Myocardial ischemia
• Injury to SA node
• Carotid sinus sensitivity
• MI
• Drugs:- Digitalis, Beta-Blocker and Ca-
Channel Blockers
58. ECG Characteristics
• Rate- Normal unless sinus node fails to
form impulse
• Rhythm-Irregular
• P_waves- present when SA Node Initiates
• PR interval –normal if P waves present
• QRS –present, absent when arrest
59.
60. Management
• Treatment is directed to the Cause
• Discontinue/withheld offending drugs
• Minimize Vagal Stimulation
• Inj Atropine sulphate
• Insertion of a permanent pacemaker
61. Sick Sinus Syndrome
• The term sick sinus syndrome is used to
describe the rhythm in which there is
marked sinus bradycardia, sinus pause or
periods of sinus arrest alternating with
paroxysms of rapid atrial arrhythmias.
• The term brady- tachy syndrome is
commonly used to describe the same
arrhythmias.
62. Causes
• Inflammatory cardiac disease.
• Cardiomyopathy
• Sclerodegenerative process involving both
the SA and AV node
• Drugs
beta-blockers
calcium-channel blockers
digitalis, amiodarone, and adenosine.
63. Etiologies of Sick Sinus Syndrome
More Common
Sinus node fibrosis
Atherosclerosis of the
SA artery
Congenital heart
disease
Excessive vagal tone
Drugs
Less Common
Familial SSS (due to
mutations in SCN5A)
Infiltrative diseases
Pericarditis
Lyme disease
Hypothyroidism
Rheumatic fever
64. ECG characteristics
• Rate :varies from bradycardiac to tachycardiac
rates depending on sinus node function and
presence of atrial tachy dysrhythmias
• Rhythm: irregular
• P waves : normal during sinus rhythm
• PR interval : may be normal depend upon the
state of AV conduction
• QRS complex: usually normal
66. Abrupt termination of atrial flutter with variable AV block,
followed by sinus arrest with a junctional escape beat.
67. Clinical manifestations
• Patients are usually elderly and present with
lightheadedness and/or syncope,
• but it can also manifest as
• angina,
• dyspnea,
• and palpitations.
68. Treatment
• Ing.Atropine sulphate for brady arrhythmias
• Atntiarrhyhmics like quinidine or
procainamide
• Permanent pacemaker insertion
70. Atrial Tachycardia
It is rapid atrial rhythm at a rate of 120 to 250
b/min. It is due to rapid firing of an ectopic
foci present in the atria
Atrial tachycardia frequently occurs in
paroxysms.
71. Possible mechanisms of atrial Tachy
arrhythmias.
• Two groups of fundamentally different
mechanisms are responsible for producing
Tachy arrhythmias
• 1- those mechanisms based on some form of
abnormal impulse formation
• 2- based on a disorder of impulse conduction,
leading to circulating excitation or reentry.
72. Pathophysiology
• The spontaneous depolarization in the fibers
in the center of the sinus node is normally
the fastest, and therefore this depolarization
brings these fibers to a discharge before
others. Thus under normal conditions,
automaticity of the dominant pacemaker in
the center of the sinus node suppress the
subsidiary pacemakers in the atria.
73. • Abnormal impulse formation may be
defined as the generation of impulses by
fibers other than the dominant pacemaker
fibers in the centre of the sinus node
regardless of whether the abnormal
impulse is generated spontaneously or
induced by foregoing normal or abnormal
activities.
74. • Normal impulse formation is the occurrence
of a spontaneous depolarization before the
onset of an action potential, the so- called
diastolic depolarization.
• If depolarization occurs either during
repolarization or under special conditions
directly after repolarization the term
abnormal impulse formation may be used.
75. • There are some muscle fibers in the right
atrium close to the crista terminalis that have a
some characteristics of purkinje fibers (ie.
Relatively low resting potential and develops
spontaneous depolarization under certain
conditions)
77. ECG Characteristics
• Rate- 140-250/min,
• Rhythm- regular unless there is block
• P-wave- differ in configuration
• PR interval- may be shorter and difficult to
measure
• QRS- Usually normal
80. Management
• Sedation to terminate the rate
• Carotid sinus massage
• Cardioversion if severe symptoms occurs
• Beta-blockers
• Radiofrequency catheter ablation of the
ectopic focus
81. Atrial Flutter
A rapid well-organized contraction of the atrium
at a rate of 200-350 contractions per minute
which is fired by ectopic foci present in the
atria.
Atrial flutter can be classified in to two types
type-1 which is the commonest one has an
atrial rate of 240-340 beats/ minute
84. ECG Characteristics
• Rate- Atrial 250 to 350b/min
Ventricular 150 to 200b/min
• Rhythm- Atrial Rhythm is regular
Ventricular may be irregular
• P waves- saw tooth appearance
• QRS- usually normal
• PR Interval not measurable
88. Management
• Carotid Sinus Massage
• Digitalis
• Ca Channel Blockers
• Beta Blockers
• Synchronized Cardioversion if 1:1
89. ATRIAL FIBRILLATION
• Atrial fibrillation is an extremely
rapid and disorganized pattern of
depolarization in the atria where the
rate is 400 to 600b/min.
92. ECG Characteristics
• Rate- atrial- 400 to 600b/min
ventricular- 110 to160b/min
• Rhythm- irregular
• P wave- not present. Atrial
activity is chaotic.
• PR Interval- not measurable
• QRS- Usually normal
97. Premature Ventricular Contraction
• Premature contraction that is
generated by the ectopic foci
present in the ventricles. Which
fires independently.
99. Etiology
• Ischemia or MI
• Hypoxia
• Hypokalemia
• Digitalis toxicity
• Acidosis
• Hyper metabolic states
100. P V C s
• UNIFOCAL
• MULTIFOCAL
• BIGEMINY
• TRIGEMINY
• COUPLETS
• TRIPLETS
101. • After each normal QRS complex there is one
Ectopic appear
102. • After two QRS complex which
are from normal sinus rhythm
then the ectopic foci fires called
Trigeminy
103.
104. • When 2 ectopic appears
sequentially in a row or pairs
called Couplets
105. • When 3 ectopic occurs
sequentially in one row is
called Triplets
106. ECG Characteristics
• Rate- 60-100b/min
• Rhythm- Irregular
• P-waves usually present in sinus
rhythm not related to PVC
• QRS- wide and bizarre, greater
than 0.12sec
107. Management
• Treatment is directed to the cause
• If PVCs are associated with heart
disease can be treated
• Inj lidocaine bolus followed by
titrated drip
108. Ventricular Tachycardia
• It is repetitive firing of the
ventricular ectopic foci at a rate
more than 100 to 200b/min, which
may cause the heart to beat
inefficiently.
109. Etiology
• Ischemia
• Acute MI
• Hypoxia
• Hypokalemia
• Digitalis toxicity
• Acidosis
• Hypermetabolic states
110. ECG Characteristics
• Rate- ventricular rate 100 to
200b/min
• Rhythm- usually regular
• P-waves present if S.A.Node fires
may be buried in QRS or T
• PR Interval- not measurable
• QRS- wide, bizarre and greater
than 0.12sec
113. Management
• Cardioversion
• Defibrillation can be done when the
patient is pulseless
• Inj Lidocaine bolus and drip as
maintenance dose
• Antiarrhythmic like inj Amidarone
or inj MgSo4
• Resuscitative measures to kept
ready
116. ECG Characteristics
• Rate- rapid, uncoordinated, ineffective
• Rhythm- Chaotic, irregular
• P waves- not seen
• PR interval- none
• QRS – no formed QRS complex
117.
118. Management
• Defibrillation
• CPR must be performed
• Anti-arrhythmic like
inj Lidocaine
inj Procainmide
inj MgSo4 most commonly
used
• Beta-Blockers
119. Disorders of impulse Conduction
• S.A. Block
• First degree AV Block
• Second Degree A.V.Block
» Mobitz type I
» Mobitz type II
• Third Degree or Complete A.V Block
• Bundle Branch Block
» RBBB
» LBBB
120. First Degree A.V.Block
• It is defined as prolonged AV
conduction time of supraventricular
impulses into the ventricles.
122. ECG Characteristics
• Rate- 60 to 100b/min
• Rhythm- Regular
• P waves- normal, precede every QRS
• PR Interval- Greater than 0.20 sec
• QRS complex- usually normal
125. Second Degree A.V.Block
• It occurs when one atrial impulse
at a time fails to be conducted to
the ventricles.
It is classified into two
• Mobitz type I
• Mobitz type II
126. Type I Second degree A.V.Block
• It is a progressive increase in
conduction times of consecutive atrial
impulses into the ventricles until one
impulse fail to conduct or is ‘dropped’
128. ECG Characteristics
• Rate- usually normal
• Rhythm- irregular unless 2:1
conduction present
• P waves- normal. Some p waves are
not conducted to the ventricle, but
only one at time fails.
• PR Interval- gradually lengthens in
consecutive beats.
• QRS- normal unless BBB
130. Management
• Treatment depends on the
conduction ratio, ventricular rate
• If the ventricular rate slow give
inj Atropine Sulphate
• Removal of precipitating factor
• Temporary pacing can be done.
131. Type II Second degree A.V.Block
• It is sudden failure of conduction of
an atrial impulse to the ventricles
without progressive increase in
conduction time.
132. ECG Characteristics
• Rate- normal
• Rhythm- irregular
• P waves- usually regular and
precede QRS.
Periodically a P
wave is not followed by a
QRS
• PR interval- constant unless there
is block
• QRS- usually normal
138. ECG Characteristics
• Rate- atrial normal, Ventricular
rate is less that 45/min
• Rhythm- Regular
• P waves- independent
• PR Interval- no consistent PR
interval
• QRS- Normal If ventricles
controlled by Junctional
pacemaker, may be wide
139.
140. Management
• Onset is sudden or associated with
MI pacing can be done without delay
• CPR should performed if the cardiac
out put severly diminished
141.
142.
143.
144.
145.
146.
147. Ventricular Asystole
• It refers to the absence of any
ventricular rhythm; there is no QRS
complex, no pulse and no cardiac
output.
148.
149. Management
• Cardio Pulmonary Resuscitation
• Endotracheal Intubation immediately
• Obtain IV Access
• Confirm Asystole in more than one lead
• Consider immediate Transcutaneous
Pacing
• Epinephrine 1 mg IV push q3-5 minutes
– Consider Vasopressin as alternative
• Atropine 1 mg IV q3-5 minutes
150. The P wave is caused by atrial
depolarization. The P wave duration is
normally less than 0.12 sec. The P wave is
usually smooth and positive.
The QRS complex represents ventricular
depolarization. The normal QRS interval
range is from 0.04 sec - 0.12 sec, measured
from the first deflection to the end of the
QRS complex
The T wave due to ventricular
repolarization The wave is normally
rounded and positive.
151. • The PR interval is the beginning of the P wave to
beginning of QRS complex. It is normally 0.12 -
0.20 seconds. (onset of atrial depolarization to onset of
ventricular depolarization)
• The QT interval begins at the onset of the QRS
complex and to the end of the T wave.
• The ST Segment represents the period of
ventricular muscle contraction before
repolarization.
152. • The ECG below illustrates primary ST-T wave abnormalities (leads
I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave
abnormalities such as these may be related to ischemia, infarction,
electrolyte abnormalities, medications, CNS disease, etc.
153. • In the above ECG the ST-T waves are "normal" for
LBBB; i.e., they are secondary to the change in the
ventricular depolarization sequence.
154.
155. Wolff-Parkinson-White Preexcitation
• Early ventricular activation in region of the accessory AV pathway
• Short PR interval (<0.12s)
• Initial slurring of QRS complex (delta wave) representing early ventricular
activation through normal ventricular muscle in region of the accessory
pathway
• Prolonged QRS duration (usually >0.10s)
• Secondary ST-T changes due to the altered ventricular activation sequence
156.
157.
158.
159. The ectopic atrial rate is 150 bpm. Some of the ectopic P waves are easily seen and indicated by the
arrows. Other P waves are burried in the T waves and not so easily identified. Atrial tachycardia with AV
block is often a sign of digitalis intoxication. 3:2 and 2:1 AV block is seen in this example.