This document provides information on ECG changes seen in ischemic heart disease. It discusses the blood supply of the heart and how different coronary artery occlusions can cause specific ECG changes. These include ST segment elevation or depression, T wave changes, and pathologic Q waves indicating injury, ischemia or necrosis in different heart regions. Examples are provided of ECG tracings demonstrating myocardial infarction patterns involving the inferior, lateral, anterior and posterior walls. It also discusses non-Q wave infarction and pseudoinfarction ECG patterns that can mimic myocardial injury. The effects of conditions like electrolyte abnormalities, drugs, and cardiac syndromes on the ECG are summarized.
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.
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.
Case-1: A 45 years old lady presented with sudden severe chest discomfort with excessive sweating for last 2 hours. She was diabetic and dyslipidemic and hypertensive. She had history of taking oral contraceptive pills (OCP).. She had the following ECG.
Case: A 34 years old lady presented with shortness of breath , chest discomfort, palpitations , cough, fever , joint pain and skin rash. Her CXR showed nodular lesion in lung field and cardiomegaly. Her serum BNP level was raised. Her echocardiography showed dilated cardiomyopathy with low ejection fraction. She had the following ECG.
Case: A 34 years old lady presented with shortness of breath , chest discomfort, palpitations , cough, fever , joint pain and skin rash. Her CXR showed nodular lesion in lung field and cardiomegaly. Her serum BNP level was raised. Her echocardiography showed dilated cardiomyopathy with low ejection fraction. She had the following ECG.
Case: A 51 years old gentleman presented with occasional chest discomfort. He was diabetic and smoker. He had a history of myocardial infarction 6 weeks back. He had the following ECG.
How to read ECG systematically with practice strips Khaled AlKhodari
This lecture simplifies the steps of reading ECG systematically. It starts with a simple heart anatomy and the logical steps that should be followed to perfect ECG reading without missing any abnormality. Finally, there are some practice ECG strips that include but not only MI, STEMI, Wellens syndrome, Pulmonary embolism, LVH, arrhythmias... and others
Case-1: A 45 years old lady presented with sudden severe chest discomfort with excessive sweating for last 2 hours. She was diabetic and dyslipidemic and hypertensive. She had history of taking oral contraceptive pills (OCP).. She had the following ECG.
Case: A 34 years old lady presented with shortness of breath , chest discomfort, palpitations , cough, fever , joint pain and skin rash. Her CXR showed nodular lesion in lung field and cardiomegaly. Her serum BNP level was raised. Her echocardiography showed dilated cardiomyopathy with low ejection fraction. She had the following ECG.
Case: A 34 years old lady presented with shortness of breath , chest discomfort, palpitations , cough, fever , joint pain and skin rash. Her CXR showed nodular lesion in lung field and cardiomegaly. Her serum BNP level was raised. Her echocardiography showed dilated cardiomyopathy with low ejection fraction. She had the following ECG.
Case: A 51 years old gentleman presented with occasional chest discomfort. He was diabetic and smoker. He had a history of myocardial infarction 6 weeks back. He had the following ECG.
How to read ECG systematically with practice strips Khaled AlKhodari
This lecture simplifies the steps of reading ECG systematically. It starts with a simple heart anatomy and the logical steps that should be followed to perfect ECG reading without missing any abnormality. Finally, there are some practice ECG strips that include but not only MI, STEMI, Wellens syndrome, Pulmonary embolism, LVH, arrhythmias... and others
ECG-T wave inversion , Dr. Malala Rajapaksha ,Cardiology unit,General Hospit...malala720
This is a presentation on “What are the deferential Diagnosis a clinician think of when the clinician encounter T inversions in an ECG of a patient”. This will be help full in day today clinical practice and also in academic purposes.
Chemotherapy induced Nausea and Vomiting
Professional and patient data
ارشادات للقئ والغثيان مع العلاج الكيمائي
Dr Salah Mabrouk Khallaf
د. صلاح مبروك خلاف
استشاري علاج الاورام
Last update of thyroid cancer management from diagnosis till follow up
You can request other lectures by emailing me at salahmab76@yahoo.com or calling me 0020 100 408 1234
Dr Salah Mabrouk Khallaf
الفوائد العظيمة وراء الكشف المبكر لسرطان الثدي
جراحة بسيطة
يمكن الاستغناء عن العلاج الكيمائي في المراحل المبكرة
يمكن ايضا الاستغناء عن العلاج الاشعاعي في المراحل المبكرة
العودة الي الحياة الطبيعية بسرعة
فائدة للفرد والاسرة والمجتمع والدخل القومي
معهد حنوب مصر للاورام
Chemotherapy classes
for more lectures please contact
Dr. Salah Mabrouk Khallaf
MD Medical Oncology & BMT
South Egypt Cancer Institute
Email: salahmab76@yahoo.com
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.
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.
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.
- 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
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!
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
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
3. Lefteft anterioranterior descending arterydescending artery usually supplies
1.the anterior and anterolateral walls of the left ventricle
2.the anterior two-thirds of the septum.
Left circumflexLeft circumflex coronarycoronary artery usually supplies
the posterolateral wall of the left ventricle.
RightRight coronary arterycoronary artery (RCA) supplies
the right ventricle,
the inferior (diaphragmatic) and
true posterior walls of the left ventricle,
the posterior third of the septum.
1.The RCA also supplies SA Node (60%)and the AV nodal
coronary artery in 85-90% of individuals; the remaining is
supplied by a branch of the LCX.
4. J-Point
Junction between end of QRS and beginning of ST
segment; Where QRS stops & makes a sudden
sharp change of direction
5. ST Segment
Segment between J-point and beginning of T wave
Need reference point
Compare to TP segment
DO NOT use PR segment as reference!
6. – ST segment elevation or depression
• More than one millimeter (one small box)
• Present in two anatomically contiguous leads
7. • Infarction – always requires previous ECG for
comparison
• Identifying Injury
(1) Ischemia – inverted T waves (earliest sign) –
symmetrical down- and upslope, opposite direction of
QRS
(2) Acute injury – ST elevation
• Can occur without Q waves: "non Q-wave MI"
• ST depression may indicate "subendocardial
infarction"
(3) Necrosis (non-conductive tissue) – Q-waves
• Significant if more than one small square wide or
greater than 1/3 the amplitude of the QRS
• Remain even after acute infarction is over
8. Q-wave MI
Evolution of typical transmural
MI
A. Normal ECG prior to MI
B. Hyperacute T ± ST elevation
C. Marked ST elevation +
hyperacute T (transmural injury)
D. Pathologic Q waves, less ST
elevation, terminal T wave
inversion (necrosis)
E. Pathologic Q waves, T wave
inversion (necrosis and fibrosis)
F. Pathologic Q waves, upright T
waves (fibrosis)
9. Lateral Wall
• I, aVL, V5, V6
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6
10. Anterior Wall
• V3, V4
– Left anterior chest
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6
11. Septal Wall
• V1, V2
– Along sternal borders
– Look through right
ventricle & see septal
wall
I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
V1 V2
V3
V4
V5
V6
12. I AVR V1 V4
II AVL V2 V5
III AVF V3 V6
Inferior Wall lateral Wall anterior Wall
Septal Wall Posterior Wall
13. Inferior MI Family of Q-wave MI's
includes
1. inferior
2. true posterior
3. right ventricular MI's
14. Inferior MI
• Pathologic Q waves and evolving ST-T changes
in leads II, III, aVF
• Q waves usually largest in lead III, next largest
in lead aVF, and smallest in lead II
• Example #1: frontal plane leads with fully
evolved inferior MI (note Q-waves, residual ST
elevation, and T inversion in II, III, aVF)
15. • Example #2: Old inferior MI (note largest
Q in lead III, next largest in aVF, and
smallest in lead II)
16. True posterior MI
• ECG changes are seen in anterior precordial
leads V1-3, but are the mirror image of an
anteroseptal MI:
1. Increased R wave amplitude and duration (i.e., a
"pathologic R wave" is a mirror image of a
pathologic Q)
2. R/S ratio in V1 or V2 >1 (i.e., prominent anterior
forces)
3. Hyperacute ST-T wave changes: i.e., ST
depression and large, inverted T waves in V1-3
4. Late normalization of ST-T with symmetrical
upright T waves in V1-3
5. Often seen with inferior MI (i.e., "inferoposterior
17. • Example #1: Acute inferoposterior MI (note tall R
waves V1-3, marked ST depression V1-3, ST
elevation in II, III, aVF)
18. • Example #2: Old inferoposterior MI (note
tall R in V1-3, upright T waves and inferior
Q waves)
19. • Example #3: Old posterolateral MI (precordial
leads): note tall R waves and upright T's in V1-3,
and loss of R in V6
20. Right Ventricular MI
• (only seen with proximal right coronary occlusion; i.e., with inferior
family MI's)
• ECG findings usually require additional leads on right chest (V1R to
V6R, analogous to the left chest leads)
• ST elevation, >1mm, in right chest leads, especially V4R (see
below)
21. Anterior Family of Q-wave MI's
• Anteroseptal MI
• Q, QS, or qrS complexes in leads V1-V3 (V4)
• Evolving ST-T changes
• Example: Fully evolved anteroseptal MI (note QS waves
in V1-2, qrS complex in V3, plus ST-T wave changes)
22. • Anterolateral MI
• similar changes, but usually V1 is spared; V4-6
involved
• Example: Acute anterior or anterolateral MI (note
Q's V2-6 plus hyperacute ST-T changes)
23. High Lateral MI
Typical MI features seen in leads I and/or aVL
Example: note Q-wave, slight ST elevation, and T inversion in lead
aVL
(Note also the slight U-wave inversion in leads II, III, aVF, V4-6, a
strong marker for coronary disease)
27. • Notching of the downstroke of the S wave in precordial
leads to the right of the transition zone (i.e., before QRS
changes from a predominate S wave complex to a
predominate R wave complex); this may be a Q-wave
equivalent.
Notching of the upstroke of the S wave in precordial
leads to the right of the transition zone (another Q-wave
equivalent).
rSR' complex in leads I, V5 or V6 (the S is a Q-wave
equivalent occurring in the middle of the QRS complex)
RS complex in V5-6 rather than the usual monophasic R
waves seen in uncomplicated LBBB; (the S is a Q-wave
equivalent).
"Primary" ST-T wave changes (i.e., ST-T changes in the
same direction as the QRS complex rather than the
usual "secondary" ST-T changes seen in uncomplicated
28. • Non-Q Wave MI
• Recognized by evolving ST-T changes over
time without the formation of pathologic Q
waves (in a patient with typical chest pain
symptoms and/or elevation in myocardial-
specific enzymes)
Although it is tempting to localize the non-Q
MI by the particular leads showing ST-T
changes, this is probably only valid for the ST
segment elevation pattern
29. • Evolving ST-T changes may include any of the following
patterns:
• Convex downward ST segment depression only (common)
Convex upwards or straight ST segment elevation only
(uncommon)
Symmetrical T wave inversion only (common)
Combinations of above changes
Example: Anterolateral ST-T wave changes
30. • The Pseudoinfarcts
• These are ECG conditions that mimic myocardial infarction either by
simulating pathologic Q or QS waves or mimicking the typical ST-T
changes of acute MI.
• WPW preexcitation (negative delta wave may mimic pathologic Q
waves)
IHSS (septal hypertrophy may make normal septal Q waves "fatter"
thereby mimicking pathologic Q waves)
LVH (may have QS pattern or poor R wave progression in leads V1-3)
RVH (tall R waves in V1 or V2 may mimic true posterior MI)
Complete or incomplete LBBB (QS waves or poor R wave progression
in leads V1-3)
31. • Pneumothorax (loss of right precordial R waves)
Pulmonary emphysema and cor pulmonale (loss of
R waves V1-3 and/or inferior Q waves with right axis
deviation)
Left anterior fascicular block (may see small q-waves
in anterior chest leads)
Acute pericarditis (the ST segment elevation may
mimic acute transmural injury)
Central nervous system disease (may mimic non-Q
wave MI by causing diffuse ST-T wave changes)
32. • Miscellaneous Abnormalities of the QRS Complex:
• The differential diagnosis of these QRS abnormalities depend on other ECG findings as well as
clinical patient information
Poor R Wave Progression - defined as loss of, or no R waves in leads V1-3 (R £2mm):
• Normal variant (if the rest of the ECG is normal)
LVH (look for voltage criteria and ST-T changes of LV "strain")
Complete or incomplete LBBB (increased QRS duration)
Left anterior fascicular block (should see LAD in frontal plane)
Anterior or anteroseptal MI
Emphysema and COPD (look for R/S ratio in V5-6 <1)
Diffuse infiltrative or myopathic processes
WPW preexcitation (look for delta waves, short PR)
•
33. • Prominent Anterior Forces - defined as R/S ration >1
in V1 or V2
• Normal variant (if rest of the ECG is normal)
True posterior MI (look for evidence of inferior MI)
RVH (should see RAD in frontal plane and/or P-
pulmonale)
Complete or incomplete RBBB (look for rSR' in V1)
WPW preexcitation (look for delta waves, short PR)
34. • Effects of Other Medical Conditions
on EKG
• Pulmonary Embolism
– prominent S wave in I
– Q wave in III
– inverted T waves in III and V1 through
V4
– ST depression in II
– acute incomplete RBBB
– RAD with rightward rotation
35. • Electrolyte Disturbances
• hyperkalemia
– wide flat P – P disappears entirely with severe
hyperkalemia
– wide QRS
– peaked T wave
• hypokalemia
– flat T wave
– U wave (after T wave; represents Purkinje cell
repolarization) – prominent with severe hypokalemia
– can cause torsades des pointes if extreme
• hypercalcemia – shortened QT interval
• hypocalcemia – prolonged QT interval
36. • Drugs
• Digitalis
– therapeutic – ST slopes below baseline, inverted T
waves, shortened QT
– excessive – blocks: SA block, paroxysmal atrial
tachycardia (PAT) with block, AV block (can be 3rd
degree)
– toxic – atrial fibrillation, junctional or ventricular
tachycardia, frequent PVC's, ventricular fibrillation
• Quinidine (blocks potassium channels)
– wide notched P wave
– wide QRS
– very deep ST
– U wave
– long QT interval
37. • Pericarditis
• flat or concave downward ST segment
elevation in leads where QRS is mainly
negative (right chest leads – V1 to V3)
• elevated ST segment with T wave off
baseline in leads where QRS is mainly
positive (lateral/inferior limb leads – aVL, I,
II, aVF, III)
• COPD
• all waves of minimal amplitude; often
leads to RVH with RAD; MAT in some
38. • Effect of Cardiac Syndromes on EKG
• Wolff-Parkinson-White Syndrome – caused by accessory
bundle of Kent that bypasses the AV node to allow
ventricular pre-excitation
– delta wave with apparently shortened PR interval
– can cause tachycardia through three mechanisms:
• (1) rapid conduction of rapid atrial beats (PSVT, atrial flutter, or
atrial fibrillation)
• (2) automaticity foci within the bundle
• (3) re-entry of ventricular depolarization
• Lown-Ganong-Levine Syndrome – caused by James bundle
(extention of the anterior internodal tract) that bypasses the
AV node directly to the bundle of His
– no PR delay (so PR interval is minimal)
– QRS immediately responds to any atrial tachyarrythmias, so
(for example) atrial flutter produces a rapid QRS response
39. • Brugada Syndrome – familial dysfunction of Na+
channels
• characterized by RBBB with ST elevation
(downsloping) in V1 through V3
• can cause deadly arrythmias leading to sudden
cardiac death with no apparent structural heart
disease (responsible for half of all cases)
• Wellen's Syndrome – stenosis of LAD
• causes marked T-wave inversion in V2 and V3
• Long QT Syndrome – QT interval more than 1/2
the cardiac cycle
• predisposed to ventricular arrythmias