1. The document discusses various cardiac arrhythmias including supraventricular tachycardias, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
2. It provides details on characteristics, causes, diagnosis, and treatment of these arrhythmias based on American and European cardiology guidelines.
3. The treatment discussed includes electrical cardioversion, antiarrhythmic medications, catheter ablation, and implantable cardioverter defibrillators.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrioventricular reciprocating tachycardia.The incidence of WPW is between 0.1% and 0.3% in the general population.Sudden cardiac death in people with WPW is rare (incidence of less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the abnormal accessory pathway.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
Tachy Arrhythmias - Approach to ManagementArun Vasireddy
Tachyarrhythmias are disorders of heart rhythm which may present with a tachycardia i.e. a heart rate >100 bpm.
This article provides an overview of tachyarrhythmias in general and goes on to cover the most common tachyarrhythmias in more detail. The acute management of tachyarrhythmias, in an emergency setting, will be covered in the 'Acute' section of the fastbleep website.
Tachyarrhythmias are clinically important as they can precipitate cardiac arrest, cardiac failure, thromboembolic disease and syncopal events. As such, they crop up time and time again in exam papers and on the wards.
Tachyarrhythmias are classified based on whether they have broad or narrow QRS complexes on the ECG. Broad is defined as >0.12s (or more than 3 small squares on the standard ECG). Narrow is equal to or less than 0.12s. Broad QRS complexes are slower ventricular depolarisations that arise from the ventricles. Narrow complexes are ventricular depolarisations initiated from above the ventricles (known as supraventricular). One important exception is when there is a supraventricular depolarisation conducted through a diseased AV node. This will produce wide QRS complexes despite the rhythm being supraventricular in origin.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Cardiac arrhythmias occur frequently in ICU patients.
12% incidence of ventricular plus supra ventricular arrhythmias for a general icu population.
The most common arrhythmia is sinus tachycardia. Atrial arrhythmias also occur with some frequency , where as ventricular arrhythmias are less common but usually more ominous.
Not all arrhythmias seen in the ICU are of new onset , some patients have preexisting arrhythmias that can be exacerbated by their critical illness
Critical Care Summit Egypt 2015 Common Arrhythmias in the ICUDr.Mahmoud Abbas
Lecture presented by Dr Khaled Farouk at Egyptian Critical Care Summit 2015, the leading ICU event and medical exhibition in Egypt. www.criticalcareegypt.com
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
download notes of the presentation and study with its print out
surviving sepsis guidelines - Notes are made from surviving sepsis guidelines 2016 article to assist medical students and residents to grasp subject in a easy to read format in a step wise manner. Resources: surviving sepsis guidelines 2016 (free access article)
Pulmonary embolism - Notes are made from textbook of Internal medicine to assist medical students and residents to grasp subject in totality. Resources: Harrison's 20thEd, ESC 2019 guidelines on PE
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.
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
- 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
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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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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
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2 Case Reports of Gastric Ultrasound
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.
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.
1. Col Bharat Malhotra
Senior Advisor (Medicine)
REFERENCE
Harrison’s Principles of internal medicine Harrisons 21th Ed
Davidson’s Principles and practice of Medicine (2018)
European and American Cardiology guidelines
2. Inappropriate Sinus tachycardia
Atrial Tachycardia
AVNRT
AVRT & Accessory pathways SUPRA
VENTRICULA
R
VENTRICULA
R
Atrial Flutter
Atrial Fibrillation
Ventricular Tachycardia
Ventricular Fibrillation
SOMETIMES SVT WITH BROAD COMPLEX
QRS OCCURS IN
SVT with BBB
SVT with PREEXCITATION
ANTIDROMIC AVRT
HYPERKALEMIA
ALWAYS HAS A BROAD COMPLEX QRS
VENTRICULAR TACHYCARDIA
3. • > 3 CONSEQUETIVE COMPLEX ORIGINATING IN
VENTRICLES AT RATE > 100 BEATS/MIN
• GRAVE CARDIAC ARRHYTHMIA
• ALWAYS ASSOCIATED WITH SERIOUS HEART DISEASE
• MAY DEGENERATE INTO VENTRICULAR FIBRILLATION
Life
Threatenin
g
5. American Heart Association Cardiology Guidelines
• > 3 BEATS
• TERMINATES SPONTANEOUSLY
NONSUSTAINED
VT
• > 30 SECONDS
• REQUIRE TERMINATION IN < 30 SEC
SUSTAINED
VT
• STABLE SINGLE QRS MORPHOLOGY
MONOMORPHIC
VT
POLYMORPHIC
VT
• MULTIFORM QRS MORPHOLOGY
TORSADES DE POINTES
• POLYMORPHIC VT
• IN SETTING OF LONG QT INTERVAL
• WAXING AND WAINING QRS AMPLITUDE
6. • SYMPTOM RELATED TO ARRHYTHMIA
• PALPITATION, LIGHTHEADEDNESS
• SYMPTOM RELATED TO UNDERLYING HEART DISEASE
• CHEST PAIN, DYSNOEA
• ORTHOPNEA, PND, EDEMA
• PRECEPITATING FACTORS – EXERSIZE, STRESS, OTHERS
• PAST HISTORY: KNOWN CARDIAC ILLNESS ( ESP IHD) /
THYROID ILLNESS/ CARDIAC RISK FACTORS/
• NON CARDIAC ILLNESS
• MEDICATIONS, FAMILY HISTORY
• PULSE, BLOOD PRESSURE, CVS
• Pulse / Heart Rate and regularity
• Blood pressure
Hemodynamically
unstable
Hemodynamically
stable
7. Prior documentation of cardiac assessment
• Assess prior ECG in sinus rhythm to look for
evidence of heart disease
• Prior ECHO report if any
ECG during tachycardia
On Recovery
• ECHO
• Coronary angiography – assess for IHD
• Electrophysiological study
8. History of myocardial infarction
Broad QRS complex tachycardia
Atrioventricular dissociation (pathognomonic)
Capture/Fusion beat (pathognomonic)
Extreme left axis deviation
No response to carotid sinus massage or IV adenosine
Intracardiac ECG for
AV dissociation
Capture/ Fusion beat
9. SVT HAS NARROW COMPLEX QRS.
SOMETIMES SVT HAS BROAD COMPLEX
QRS
BBB
PREEXCITATION
ANTIDROMIC AVRT
HYPERKALEMIA
VENTRICULAR TACHYCARDIA
ALWAYS HAS A BROAD
COMPLEX QRS
AV DISSOCIATION
CAPTURE/FUSION BEAT
D/D
11. Prompt action to restore sinus rhythm then prophylactic Therapy
• Synchronized DC
Cardioversion
• IV Amiodarone bolus
Followed by infusion
or IV B Blocker
• Correct
Hypokalemia, Mg
Acidosis, Hypoxia
Acute Coronary syndrome
Hemodynamically
unstable
Hemodynamically
stable
Evaluate for IHD
Assess for structural
abnormality of heart
Oral B Blocker,
Oral Amiodarone (can be added)
Recurrent VT + structural heart
disease Implantable
cardioverter defibrillator (ICD)
EP Study + Catheter ablation
Ongoing Treatment
14. Start CPR
O2, Attach Defib
IV Access
Call for help
Epinephrine 1mg 3-5min
Advance Airway
Amiodarone 300mg
Rx Reversable causes
shock
shock
shock
CPR
QUALITY
15.
16. * MANY ARE BENIGN (NO RX)
* CORRECT PRECIPITATING FACTORS
Alcohol excess, Myocardial ischemia, Hyperthyroidism, Metabolic Acidosis,
electrolyte disturbance
HEMODYNAMIC UNSTABLE/ LIFE-THREATENING ARRHYTHMIAS
Synchronized DC cardioversion
HEMODYNAMIC STABLE
Acute management by drugs long term management by drugs
Use as few drugs as possible (use carefully)
Reviewed regularly attempts made to withdraw therapy if possible
RADIOFREQUENCY ABLATION in recurrent supraventricular tachycardia, atrial
futter, AF
ELECTROPHYSIOLOGICAL STUDY (EP STUDY) may help to identify the optimum
therapy
19. I (a) Block Na+ channel and prolong action potential
Quinidine, Procainamide, Disopyramide
I (b) Block Na+ channel and shorten action potential
Lidocaine, Mexiletine
I (c) Block Na+ channel with no effect on action potential
Flecainide, Propafenone
Class II: β-adrenoceptor antagonists (β-blockers)
Atenolol, Bisoprolol, Metoprolol
Class III: Potassium Channel Blocker
Amiodarone, Ibutilide, Dofetilide, Dronedarone, sotalol
Class IV: slow calcium channel blockers
Verapamil, Diltiazem
Others : Digoxin and Adenosine
20. Class Drugs Route USES
Ia Quinidine, Procainamide,
disopyramide
-- V Arrhythmia (hardly used)
Ib Lidocaine,
Phenytoin
Mexiletine
IV
IV
--
V Arrhythmia in ACS (less used)
V Arrhythmia of Digitalis toxicity
V Arrhythmia of Digitalis toxicity
--
Ic Flecainide,
Propafenone
IV,O Rhythm control AF ( in Normal heart)
Contraindicated in Atrial Flutter
II Atenolol,
Bisoprolol, Metoprolol
IV,O Rate Control PSVT, A flutter, AF
III Amiodarone
Dronedarone
Ibutilide, Dofetilide,
Sotalol
IV,O Rhythm control AF
Broad complex tachycardia
VT, VF
IV Verapamil, Diltiazem IV,O Rate Control PSVT, A flutter, AF
Other Adenosine
Digoxin
IV
O
Acute management PSVT
Rate control as add on for AF
21. AMIODARONE
USE Rhythm control AF
Broad complex tachycardia
Ventricular Tachycardia, Ventricular Fibrillation
MECHANISM
VERY LONG
HALF LINE
Class III ( K+ blocking drug) prolongs the action potential duration
Also has effect on class 1 (Na+ blocking) Class 2 & Class 4 (weak
adrenergic and calcium channel-blocking action hence slow it AV node
conduction)
DOSE 150 MG iv STAT OVER 10 MINS THEN 1MG/MIN OVER 6 H THEN 0.5
MG/MIN OVER 18 HOURS
300 MG IV BOLUS (IN VENTRICULAR FIBRILLATION)
CARDIAC
Side Effects
CAUSES PERIPHERAL VASODILATION
SYMPTOMATIC BRADYCARDIA, AV BLOCK
TORSADES DE POINTES
NONCARDIAC
Side Effects
HEPATITIS, PHOTODERMATITIS, PULMONARY FIBROSIS
CORNEAL MICRODEPOSITS, OPTIC NEURITIS
HYPERTHYROIDISM, HYPOTHYROIDISM
22.
23. A 44-year-old man
Past history NAD
Presents with palpitations - 3 hours.
BP is 134/80 mmHg, Pulse is regular at 168 beats/min, and SpO2 is 98% RR
20/min. Chest Clear. CVS – no murmur
24. A 79-year-old man
Past history of - coronary artery with a left ventricular ejection fraction of 30%,
and hypertension. At his last clinic visit 1 months ago his heart rate was
regular and electrocardiogram (ECG) showed no rhythm abnormalities.
Presents to your office with palpitations. BP is 108/56 mmHg, Pulse is regular
at 88 beats/min, and SpO2 is 98% Respiratory Rate 20/min. Chest Clear. CVS
– no murmur
Based on this ECG, the patient now has a definite (class I) indication for which
of the following therapies:
25. A 62-year-old man
Has severe retrosternal chest pain of 2 hours with palpitations. Smoker,
Diabetes and hypertension since 11 years. BP 108/76 mmHg Pulse 134/min
RR 21/Min
Chest Clear, CVS no murmur.
26. A 68-year-old lady
Past history of – CAD, Hypertension on regular medication 6 years
Presented with Palpitations, Lightheadedness and dyspnea – 1 hour
BP 102/ 60 mmHg Pulse 154/Min Chest- Basal crackles, CVS – No murmur
