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.
crème de la crème basics to understand electrocardiographic analysis in an easy & simple way with some specifications to its use in Emergency medicine/clinical toxicology practice.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
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.
crème de la crème basics to understand electrocardiographic analysis in an easy & simple way with some specifications to its use in Emergency medicine/clinical toxicology practice.
Non infarction Q waves
Precise guide for Allied Health Science Students especially cardiac specialty students, DGNM, B.Sc Nursing & M.Sc Nursing Students regarding Non Infarction Q waves
Case-1:
A 23 years old medical student presented with occasional palpitation, shortness of breath and chest discomfort. He had the following ECG.
A 53 years old gentleman presented with palpitations for last 5 hours. He is smoker, diabetic, dyslipidemic and hypertensive. He had exertional chest discomfort for last 5 years and did coronary angiogram 3 years back and CAG revealed TVD and advised for revascularization. But he refused and was irregular in medication and reluctant for life style modification. He came to emergency department with this ECG.
Introduction to Electrophysiology - Supraventricular Tachycardias (1/4 lectures)Jose Osorio
What is cardiac Electrophysiology?
This presentation will cover basics of EP. It is Part 1 of 4 lectures about EP.
Part 1 - basics of EP and Supraventricular Tachycardias (SVT)
Part 2 - Ventricular arrhythmias and Cardiac Devices
Part 3 - Afib
Part 4 - EKG
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Case-1:
A 23 years old medical student presented with occasional palpitation, shortness of breath and chest discomfort. He had the following ECG.
A 53 years old gentleman presented with palpitations for last 5 hours. He is smoker, diabetic, dyslipidemic and hypertensive. He had exertional chest discomfort for last 5 years and did coronary angiogram 3 years back and CAG revealed TVD and advised for revascularization. But he refused and was irregular in medication and reluctant for life style modification. He came to emergency department with this ECG.
Introduction to Electrophysiology - Supraventricular Tachycardias (1/4 lectures)Jose Osorio
What is cardiac Electrophysiology?
This presentation will cover basics of EP. It is Part 1 of 4 lectures about EP.
Part 1 - basics of EP and Supraventricular Tachycardias (SVT)
Part 2 - Ventricular arrhythmias and Cardiac Devices
Part 3 - Afib
Part 4 - EKG
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
An electrocardiogram (ECG or EKG) records the electrical signal from your heart to check for different heart conditions. Electrodes are placed on your chest to record your heart's electrical signals, which cause your heart to beat. The signals are shown as waves on an attached computer monitor or printer
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
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
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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2. What is an ECG?
The electrocardiogram (ECG) is a
representation of the electrical events of the
cardiac cycle.
Each event has a distinctive waveform, the
study of which can lead to greater insight into a
patient’s cardiac pathophysiology.
3. What types of pathology can we identify
and study from ECGs?
•
•
•
•
•
Arrhythmias
Myocardial ischemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (i.e. hyperkalemia,
hypokalemia)
• Drug toxicity (i.e. digoxin and drugs which prolong
the QT interval)
4. ECG PAPER
• Light lines small squares- 1 X 1 mm
• Bold lines large squares 5 X 5 mm
• Horizontal axis=time
1. Distance across small square=0.04 sec.
2. Distance across large square=0.2 sec.
• Vertical axis=voltage
1. Distance across small square=0.1 mV
2. Distance across large square=0.5 mV
5.
6. Anatomy of Heart and ECG signal
Normal ECG signal
Conducting System of Heart
7.
8. ECG Leads
Leads are electrodes which measure the
difference in electrical potential between
either:
1. Two different points on the body (bipolar leads)
2. One point on the body and a virtual reference point
with zero electrical potential, located in the center of
the heart (unipolar leads)
9. ECG Leads
The standard ECG has 12 leads:
3 Standard Limb Leads
3 Augmented Limb Leads
6 Precordial Leads
The axis of a particular lead represents the viewpoint from
which it looks at the heart.
33. Regular rhythm
• If H.R. is normal ( normal , atrial flutter)
• If bradycardia
# no P or inverted ( nodal rhythm )
# normal P
@ regular relation with QRS ( complete HB, sinus bradycadia)
@ irregular relation with QRS ( partial HB)
If tachycardia
# Abnormal QRS ( vent . Tachycardia )
# normal QRS
@ Normal P (SVT atrial )
@absent or inverted P ( SVT nodal )
34. Irregular rhythm
• If irregular irregularity ( AF)
• If occasional irregularity
# normal QRS ( Supravent. extrasystole )
# abnormal ORS ( Vent. Extrasystole )
35. Normal Sinus Rhythm – the rules!
•
•
•
•
•
•
P before every QRS
PR interval <0.2 seconds (5 baby squares)
QRS after every P wave
QRS <0.12 seconds (3 baby squares)
Regular and identical
Rate 60-100 bpm
– <60 bpm – sinus bradycardia
– >100 bpm – sinus tachycardia
45. Left Bundle Branch Block
Criteria
•
•
•
•
QRS duration ≥ 120ms
Broad R wave in I and V6
Prominent QS wave in V1
Absence of q waves (including physiologic
q waves) in I and V6
54. P waves
• It is important to remember that the P wave represents the
sequential activation of the right and left atria, and it is common
to see notched or biphasic P waves of right and left atrial
activation.
• Does not exceed 2.5 mm (height) in lead II
• Less than 0.12 seconds (width) in lead II
• Abnormal P:
–
–
–
–
–
–
RAE ( P Pulmonale )
LAE ( P mitrale )
Atrial flutter
Nodal rhythm ( absent with regular rhythm )
AF( absent with irregular rhythm )
Dextrocardia
65. PR interval
• measured from beginning of P to beginning
of QRS
• 0.12-0.20 s ( 3-5 small squares).
• Best seen in lead II .
66. PR interval
Short PR: < 0.12s
.
1- Preexcitation syndromes:
*WPW (Wolff-Parkinson-White) Syndrome: An accessory pathway
connects the right atrium to the right ventricle or the left atrium to
the left ventricle, and this permits early activation of the ventricles
(delta wave) and a short PR interval.
69. PR interval
2- AV Junctional Rhythms with retrograde atrial activation (inverted
.
P waves in II, III, aVF): Retrograde P waves may occur before the
QRS complex (usually with a short PR interval), in the QRS
complex (i.e., hidden from view), or after the QRS complex (i.e., in
the ST segment).
3- Ectopic atrial rhythms originating near the AV node (the PR
interval is short because atrial activation originates close to the AV
node; the P wave morphology is different from the sinus P)
4- Normal variant
5- tachycardia
70. PR interval
Prolonged PR: >0.20s
1-First degree AV block (PR interval usually constant)
2-Second degree AV block (PR interval may be normal or
.
prolonged; some P waves do not conduct)
Type I (Wenckebach): Increasing PR until nonconducted P wave
occurs
Type II (Mobitz): Fixed PR intervals plus nonconducted P waves
3-AV dissociation: Some PR's may appear prolonged, but the P
waves and QRS complexes are dissociated .
4- Rheumatic fever
5- Digitalis
78. The QRS Axis
The QRS axis represents the net overall
direction of the heart’s electrical activity.
Abnormalities of axis can hint at:
Ventricular enlargement
Conduction blocks (i.e. hemiblocks)
79. The QRS Axis
By near-consensus, the
normal QRS axis is defined
as ranging from -30° to +90°.
-30° to -90° is referred to as a
left axis deviation (LAD)
+90° to +180° is referred to as
a right axis deviation (RAD)
82. The Quadrant Approach
1. Examine the QRS complex in leads I and aVF to determine if
they are predominantly positive or predominantly negative. The
combination should place the axis into one of the 4 quadrants
below.
83. The Quadrant Approach
2. In the event that LAD is present, examine lead II to determine if
this deviation is pathologic. If the QRS in II is predominantly
positive, the LAD is non-pathologic (in other words, the axis is
normal). If it is predominantly negative, it is pathologic.
85. Quadrant Approach: Example 2
Positive in I, negative in aVF
Predominantly positive in II
Normal Axis (non-pathologic LAD)
86. The Equiphasic Approach
1. Determine which lead contains the most equiphasic QRS
complex. The fact that the QRS complex in this lead is
equally positive and negative indicates that the net
electrical vector (i.e. overall QRS axis) is perpendicular to
the axis of this particular lead.
2. Examine the QRS complex in whichever lead lies 90° away
from the lead identified in step 1. If the QRS complex in
this second lead is predominantly positive, than the axis of
this lead is approximately the same as the net QRS axis. If
the QRS complex is predominantly negative, than the net
QRS axis lies 180° from the axis of this lead.
89. QRS complex
• Normal: 0.06 - 0.10s
Prolonged QRS Duration (>0.10s):
A-QRS duration 0.10 - 0.12s
1- Incomplete right or left bundle branch block
2-Nonspecific intraventricular conduction delay (IVCD)
3-Some cases of left anterior or posterior fascicular block
B-QRS duration > 0.12s
1-Complete RBBB or LBBB
2-Nonspecific IVCD
3-Ectopic rhythms originating in the ventricles (e.g., ventricular
tachycardia, pacemaker rhythm)
90. Left Bundle Branch Block
Criteria
•
•
•
•
QRS duration ≥ 120ms
Broad R wave in I and V6
Prominent QS wave in V1
Absence of q waves (including physiologic
q waves) in I and V6
101. Right Ventricular Hypertrophy
Although there is no widely accepted criteria for
detecting the presence of RVH, any combination of
the following ECG features is suggestive of its
presence:
• Right axis deviation
• Right atrial enlargement
• Down sloping ST depressions in V1-V3 (RV strain
pattern)
• Tall R wave in V1
103. Q Wave
• Normal (physiologic) or due to pathology
(pathologic).
• Depth and width are determining criteria
– Q wave >0.04 (40 ms) wide is considered a
significant finding (pathologic)
115. ST segment
From the end of QRS ( J point ) to beginning
of T wave .
isoelectric
116. ST Segment
• The ST segment is normally level with the
T-P segment rather than the PR segment
• Examine every lead for ST segment
elevation of 1 mm or more.
117.
118. Differential Diagnosis of ST
Segment Elevation
1-Normal Variant "Early Repolarization" (usually concave upwards,
ending with symmetrical, large, upright T waves)
2- Ischemic Heart Disease (usually convex upwards, or
straightened) Acute transmural injury - as in this acute
anterior MI
3- Persistent ST elevation after acute MI suggests ventricular
aneurysm
4-ST elevation may also be seen as a manifestation of
Prinzmetal's (variant) angina (coronary artery spasm)
5-ST elevation during exercise testing suggests extremely tight
coronary artery stenosis or spasm (transmural ischemia)
•
119. Differential Diagnosis of ST
Segment Elevation
6-Acute Pericarditis
#Concave upwards ST elevation in most leads
except aVR
# No reciprocal ST segment depression (except in
aVR)
#Unlike "early repolarization", T waves are usually
low amplitude, and heart rate is usually increased.
#May see PR segment depression, a manifestation
of atrial injury
123. ST depression
• >2mm usually indicates ischemia
• Common in normal ECG, especially in
pregnancy
• But:
– Non specific not more than 2mm below
baseline
– It is convex downward or slopes upwards from
the S wave
124. Differential Diagnosis of ST
Segment Depression
1-Normal variants or artifacts: Pseudo-STdepression (wandering baseline due to poor
skin-electrode contact)
2-Physiologic J-junctional depression with
sinus tachycardia (most likely due to atrial
repolarization)
3-Hyperventilation-induced ST segment
depression
125. Differential Diagnosis of ST
Segment Depression
4-Ischemic heart disease
Subendocardial ischemia (exercise induced or during
angina attack )
ST segment depression is often characterized as
"horizontal", "upsloping", or "downsloping"
5-Non Q-wave MI
6- Reciprocal changes in acute Q-wave MI (e.g., ST
depression in leads I & aVL with acute inferior MI)
126. Differential Diagnosis of ST
Segment Depression
7-Nonischemic causes of ST depression
#RVH (right precordial leads) or LVH (left precordial
leads, I, aVL)
# Digoxin effect on ECG
# Hypokalemia
#Mitral valve prolapse (some cases)
#Secondary ST segment changes with IV conduction
abnormalities (e.g., RBBB, LBBB, WPW, etc)
129. The ECG signs of Infarct!
• Abnormal Q waves
• ST segment elevation (Greater than 1mm in 2 or more
adjacent leads)
• Inverted T waves
130. ST Elevation - Myocardial Infarction
• ST elevation in two or more leads
– Must be at least 1mm in limb leads
– Must be at least 2mm in chest leads
144. QT interval
•
•
measured from beginning of QRS to end of T wave
QT Interval (QTc < 0.40 sec) upper limit for QTc =
0.44 sec
1-Bazett's Formula: QTc = (QT)/SqRoot RR (in
seconds)
2-Poor Man's Guide to upper limits of QT: For HR =
70 bpm, QT<0.40 sec; for every 10 bpm increase
above 70 subtract 0.02 sec, and for every 10 bpm
decrease below 70 add 0.02 sec. For example: QT
< 0.38 @ 80 bpm
QT < 0.42 @ 60 bpm
145.
146. QT interval
•
Prolonged QT :
A. Familial long QT
Syndrome (LQTS)
B. Congestive Heart Failure
C. Myocardial Infarction
D. Hypocalcemia &
Hypokalaemia
E. Hypomagnesemia
F. Type I Antiarrhythmic
drugs & Cispride
G. Rheumatic Fever
H. Myocarditis
I. Congenital Heart Disease
•
Short QT :
A. Digoxin (Digitalis)
B. Hypercalcemia
C. Hyperkalemia
147.
148. The U wave is the only remaining enigma of the ECG, and probably
not for long. The origin of the U wave is still in question, although
most authorities correlate the U wave with electrophysiologic events
called "afterdepolarizations" in the ventricles.. The normal U wave
has the same polarity as the T wave and is usually less than one-third
the amplitude of the T wave. U waves are usually best seen in the
right precordial leads especially V2 and V3. The normal U wave is
asymmetric with the ascending limb moving more rapidly than the
descending limb (just the opposite of the normal T wave).
149. Prominent upright U waves
1-Sinus bradycardia accentuates the U wave
2-Hypokalemia (remember the triad of ST segment depression, low
amplitude T waves, and prominent U waves)
3- Quinidine and other type 1A antiarrhythmics
150. Negative or "inverted" U waves
1- Ischemic heart disease (often indicating left main or LAD
disease) Myocardial infarction (in leads with pathologic Q waves)
2-During episode of acute ischemia (angina or exercise-induced
ischemia)
3- During coronary artery spasm (Prinzmetal's angina)
4- Nonischemic causes Some cases of LVH or RVH (usually in
leads with prominent R waves)