This document provides an overview of how to interpret an electrocardiogram (ECG). It describes the basic components of an ECG including patient data, paper speed, calibration, lead placement, and waveform intervals. It then examines each waveform in more detail, covering the P wave, QRS complex, T wave, ST segment, and cardiac rhythm and axis. Key signs and abnormalities are outlined for each component to guide ECG interpretation.
Image result for ecgen.wikipedia.org
An electrocardiogram (ECG) is a test which measures the electrical activity of your heart to show whether or not it is working normally. An ECG records the heart's rhythm and activity on a moving strip of paper or a line on a screen.
There is no difference between an ECG and an EKG. Both refer to the same procedure, however one is in English (electrocardiogram – ECG) and the other is based on the German spelling (elektrokardiogramm – EKG). ... The most common EKG is called the 12-lead EKG.
Image result for ecgen.wikipedia.org
An electrocardiogram (ECG) is a test which measures the electrical activity of your heart to show whether or not it is working normally. An ECG records the heart's rhythm and activity on a moving strip of paper or a line on a screen.
There is no difference between an ECG and an EKG. Both refer to the same procedure, however one is in English (electrocardiogram – ECG) and the other is based on the German spelling (elektrokardiogramm – EKG). ... The most common EKG is called the 12-lead EKG.
Basic EKG and Rhythm Interpretation Symposia - The CRUDEM FoundationThe CRUDEM Foundation
Basic EKG and Rhythm Interpretation Symposia presented in Milot, Haiti at Hôpital Sacré Coeur.
CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
ECG localization of accessory pathways slideshareCardiology
This presentation is simplified view of accessory pathways in heart and their localization with help of algorithms and ECG examples. Try to read this PPT in power point to see full effects and animations.
Basic EKG and Rhythm Interpretation Symposia - The CRUDEM FoundationThe CRUDEM Foundation
Basic EKG and Rhythm Interpretation Symposia presented in Milot, Haiti at Hôpital Sacré Coeur.
CRUDEM’s Education Committee (a subcommittee of the Board of Directors) sponsors one-week medical symposia on specific medical topics, i.e. diabetes, infectious disease. The classes are held at Hôpital Sacré Coeur and doctors and nurses come from all over Haiti to attend.
ECG localization of accessory pathways slideshareCardiology
This presentation is simplified view of accessory pathways in heart and their localization with help of algorithms and ECG examples. Try to read this PPT in power point to see full effects and animations.
Review of the anatomy and physiology
Review of the conduction system
ECG:basics term,
ECG RECORDING: leads, electrodes, waveforms and intervals
Determining heart rate
ECG Analysis/Interpretation
-Normal ECG & Abnormal ECG
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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.
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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
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.
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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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4. Basic Components
1. Patient Data
2. Paper Speed
3. Calibration
4. Check correct lead placement
5. Waveform and Intervals
6. Heart Rate
7. Rhythm
8. Axis
5. Patient Data
• Confirm the name and date of birth of the patient matches the
details on the ECG.
• Confirm the date and time the ECG was performed.
6. Paper Speed
• The standard paper speed is 25mm/sec:
• 1mm (small square) = 0.04 sec (40ms)
• 5mm (large square) = 0.2 sec (200ms)
7. Calibration
• Standard calibration of the ECG is 10mm/mV .
• At this calibration, 1 miliVolt calibration signal is expected to produce a
rectangle of 10 mm height and 5 mm width.
8. Check correct lead placement
• If leads are reversed,
• 1. polarity in lead I will be predominantly negative or downwards.
While this can be an expected finding in some patients (i.e., severe
pulmonary disease, acute PE, etc) a negative deflection in lead I should
still catch your attention, no matter the cause. To confirm lead
misplacement you will also notice:
• 2. Leads III and II will be the reverse of one another.
• 3. aVR and aVL are reversed.
• 4. aVF is unchanged.
9. P wave
• Represents atrial depolarization
Next we look at the P-waves and answer the following questions:
• Are P-waves present?
• If so, is each P-wave followed by a QRS complex?
• Do the P-waves look normal? (check duration, direction and shape)
• If not present, is there any atrial activity e.g. sawtooth baseline → flutter waves /
chaotic baseline → fibrillation waves / flat line → no atrial activity at all?
• Hint – If P-waves are absent and there is an irregular rhythm it may suggest
atrial fibrillation
10.
11. • Diphasic P wave: often seen in lead V1 and V2, has positive negative configuration.
• When amplitude is low P wave appears entirely positove or negative in lead V1, but
is rarely negative in V2.
• In remaining precordial leads, P wave is always upright due to right to left spread of
atrial activation impulse.
• Amplitude of P-wave: Seldom exceeds 25% of R wave, but normal range is affected
by factors such as:
1. Position of heart
2. Proximity to recording electrodes
3. Degree of atrial filling
4. Extent of atrial fibrosis
12. QRS complex
• Represent ventricular depolarization
• There are several aspects of the QRS complex you need to
assess:
• Width
• Height
• Morphology
13.
14. • Width
• Width can be described as NARROW (< 0.12 seconds) or BROAD (> 0.12 seconds)
• A narrow QRS complex occurs when the impulse is conducted down the bundle of
His and the Purkinje fibre to the ventricles. This results in well organised
synchronised ventricular depolarisation.
• A broad QRS complex occurs if there is an abnormal depolarisation sequence – for
example, a ventricular ectopic where the impulse spreads slowly across the
myocardium from the focus in the ventricle. In contrast, an atrial ectopic would
result in a narrow QRS complex because it would conduct down the normal
conduction system of the heart. Similarly, a bundle branch block results in a broad
QRS because the impulse gets to one ventricle rapidly down the intrinsic
conduction system then has to spread slowly across the myocardium to the other
ventricle.
15. • Height
• Describe this as SMALL or TALL:
• Small complexes are defined as < 5mm in the limb leads or <10 mm in
chest leads.
• Tall complexes imply ventricular hypertrophy (although can be due to body
habitus e.g. tall slim people). There are numerous algorithms for measuring
LVH, such as the Sokolow-Lyon index or the Cornell index.
16. • Morphology
• You need to assess the individual waves of the QRS complex.
• Delta wave
• The mythical ‘delta wave’ is a sign that the ventricles are being activated
earlier than normal from a point distant to the AV node. The early
activation then spreads slowly across the myocardium causing the slurred
upstroke of the QRS complex. Note – the presence of a delta wave does
NOT diagnose Wolff-Parkinson-White syndrome. This requires evidence
of tachyarrhythmias AND a delta wave.
17.
18. • Q-waves
• Isolated Q waves can be normal. A pathological Q wave is > 25% the size of
the R wave that follows it or > 2mm in height and > 40ms in width. A single Q
wave is not a cause for concern – look for Q waves in an entire territory
(anterior / inferior) for evidence of previous MI.
19. • R and S waves
• Look for R wave progression across the chest leads (from small in V1 to
large in V6). The transition from S > R wave to R > S waveshould occur in
V3 or V4. Poor progression (i.e. S > R through to leads V5 and V6) can be
a sign of previous MI but can also occur in very large people due to lead
position.
•
20. T waves
• The T waves represent repolarisation of the ventricles
• Tall T waves
• T waves are tall if they are:
• > 5mm in the limb leads AND
• > 10mm in the chest leads (the same criteria as ‘small’ QRS complexes)
• Tall T waves can be associated with:
• Hyperkalaemia (“Tall tented T waves”)
• Hyperacute STEMI
21. • Inverted T waves
• T waves are normally inverted in V1 and inversion in lead III is a normal variant.
• Inverted T waves in other leads are nonspecific sign of wide variety of conditions:
• Ischaemia
• Bundle branch blocks (V4 – 6 in LBBB and V1 – V3 in RBBB)
• Pulmonary embolism
• Left ventricular hypertrophy (in the lateral leads)
• Hypertrophic cardiomyopathy (widespread)
• General illness
22. • Biphasic T waves
• Biphasic T waves have two peaks and can be
indicative of ischaemia and hypokalaemia
• Flattened T waves:
• Another non-specific sign, this may
represent ischaemia or electrolyte imbalance.
23. P-R interval
• P-R interval
• The P-R interval should be between 120-200 ms (3-5 small
squares)
• Prolonged PR interval (>0.2 seconds)
• A prolonged PR interval suggests there is atrioventricular
delay (AV block)
24. ST segment
• The ST segment is the part of the ECG
between the end of the S wave and start of
the T wave.
• In a healthy individual it should be an
isoelectric line.
25. • ST elevation
• ST elevation is significant when it is greater than 1 mm (1 small
square) in 2 or more contiguous limb leads or >2mm in 2 or more chest
leads.
• It is most commonly caused by acute full thickness myocardial
infarction.
26. • ST depression
• ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial
ischaemia.
27. • Heart rate can be calculated using the following method (if regular):
• Count the number of large squares present within one R-R interval. Divide 300 by this number to
calculate the heart rate e.g. 4 large squares in an R-R interval: 300/4 = 75 beats per minute
• If the rhythm is irregular:
• The first method of calculating the heart rate doesn’t work when the R-R interval differs
significantly throughout the ECG and therefore another method is required
• Count the number of complexes on the rhythm strip (each rhythm strip is 10 seconds long)
• Multiply the number of complexes by 6 (giving you the average number of complexes in 1
minute)
• e.g. 10 complexes on a rhythm strip X 6 = 60 beats per minute
Heart Rate
28.
29. Rhythm
• The heart rhythm can be regular or irregular.
• Irregular rhythms can be either:
• Regularly irregular (i.e. a recurrent pattern of irregularity)
• Irregularly irregular (i.e. completely disorganised)
• Mark out several consecutive R-R intervalson a piece of paper, then
move them along the rhythm strip to check if the subsequent
intervals are the same.
If you are suspicious that there is some AV block, map out atrial rate &
ventricular rhythm separately (i.e. mark P waves & R waves). As you move
along the rhythm strip, you can then see if PR interval changes, if QRS
complexes are missing or if there is complete dissociation between two.
30.
31. Cardiac Axis
• Cardiac axis describes the overall direction of electrical spread within
the heart.
• To determine the cardiac axis you need to look at leads I,II and III.
• Normal cardiac axis
• In normal cardiac axis:
• Lead II has the most positive deflection compared to Leads I and III
32. • Right axis deviation:
• Lead III has the most positive deflection and
Lead I should be negative. This is commonly
seen in individuals with RVH.
• Left axis deviation:
• Lead I has the most positive deflection
• Leads II and III are negative
• Left axis deviation is seen in individuals with
heart conduction defects