This document provides information on ECG localization of myocardial infarction. It discusses the branches of the coronary arteries and their blood supply territories. It describes concepts like injury vector, ST elevation and depression cut-offs, and ECG changes seen in different types of MI such as anterior wall MI, inferior wall MI, right ventricular MI, and posterior wall MI. It also discusses ECG patterns that can indicate high-risk coronary artery disease such as left main occlusion. Overall, the document is a guide for using the ECG to localize the site and artery of myocardial infarction.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
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.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
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.
This is a review of features in ECG to diagnose the culprit artery responsible for the infarction.
Localization of the occluded vessel in acute myocardial infarction is important for many reasons:
to know which artery is to dilate and stent; to assess the severity of the lesion; to compare with
the echocardiographic area with hypokinesia or akinesia and to differentiate the recent from
the old occluded vessel. The ST-segment changes in 12-lead ECG form the basis of diagnosis,
management, and prognosis.
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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.
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.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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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
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
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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
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3. BRANCHES:-
Right coronary artery
• Conus branch
• AV Nodal branch
• RV branch
• Acute marginal branch
• Posterior descending artery(PDA)
• Posteriolateral artery(PL)
Left coronary artery/ Left main
coronary artery
• Left anterior descending artery(LAD)
o Septal branches(S1,S2,S3)
o Diagonal branches(D1,D2,D3)
• Left circumflex artery(LCX)
o Atrial branch
o Obtuse marginals(OM1,OM2)
o Posteriolateral branch
6. Dominance of Coronary Artery:-
Supplies circulation to inferior wall and inferior portion of posterior septum
Passes crux and IVS, giving rise to PDA and Posterolateral branches
Also give rise to AV Nodal branch
Non dominant artery- smaller in size, terminates early
CODOMINANT coronary circulation- posterior crux of heart receive twigs from both right and
left system, making this water-shed area have advantage of twin supply
RCA-70%
LCX-10%
Co-dominant-20%
8. The Concept of Injury Vector- Direct and
Reciprocal changes
Injury Vector is oriented towards the injured area and generates ST
Elevation in the leads facing the Vector’s head.
ST Depression in the leads facing the Vector’s tail(opposed leads).
Leads perpendicular to dominant Vector will record an Isoelectrical ST
segment.
ST Elevation in one territory often have ST Depression in other territories.
The additional ST Deviation may represent ischemia due to coronary disease
in non infarct related arteries(ischemia at distance) or may represent pure
“mirror image” reciprocal changes
9. The Concept of Injury Vector- Direct and
Reciprocal changes
10. The Concept of Injury Vector- Direct and
Reciprocal changes
Proximal LAD
Distal LAD
RCA
LCX
13. Q Wave and Non Q Wave Infarction
The presence or absence of Q waves on the surface ECG does
not reliably distinguish between transmural and
nontransmural/subendocardial Infarct.
Q Wave on ECG signify abnormal electrical activity but not
synonymous with irreversible myocardial damage.
Also, absence of Q Wave may simply reflect the insensitivity
of standard 12 lead ECG, especially in zones of LV supplied by
LCX.
19. Left anterior descending
Artery supply..
• Anterior wall (by Diagonal
artery) {1, 7,13}.
• Anterior part of septum
(by Septal artery) {2,8,14}.
• RBB { by 1ST Septal }
• Apex (17)
• Sometimes segment 15.
20. Right coronary artery
supplies..
• Right ventricle.
• Inferior wall {4, 10, 15}.
• Inferior septum{ 3 ,9,
15}.
• Sometimes part of
Lateral wall { 5, 11, 16}.
21. Left circumflex
artery supplies..
• Anterior lateral
wall {6, 12, 16}.
• Inferior lateral
wall { 5, 11}.
• (if Dominant) Part
of Inferior wall {4,
10, 15}.
22. Anterior Wall Myocardial Infarction
Proximal to 1st Septal and 1st Diagonal branch (40%)
Distal to Septal and Diagonal branches (40%)
Proximal to D1 but distal to S1 (5%)
Proximal to S1 but distal to D1(5%)
Selective D1 D2 occlusion
Selective S1 S2 occlusion
AnteroSeptal Zone : occlusion of LAD and its branches
23.
24. Proximal LAD Occlusion
(Dominance of basal area)
INJURY VECTOR- Anterior and Upwards to right or left
ST Elevation in aVR and V1 >= 2.5 mm
ST Depression in inferior leads(II III aVF) and in V5
Abnormal Q wave in aVL
ST Depression in III + aVF >= 2.5 mm
25.
26. Distal LAD Occlusion
(Dominance of InferoApical area)
Absence of ST depression in INFERIOR
LEADS
Distal to S1 – Abnormal Q wave in V4-V6
Distal to D1- ST Depression in aVL
27.
28. Proximal to S1, Distal to D1
(Dominance of Septal area)
Antero septal infarction
ST Elevation in aVR and V1 >= 2.5 mm
ST Elevation in V1-V3/V4 and in II III aVF
ST Depression in V6, I, aVL
ST Elevation in V3R
RBBB/QRBBB
29.
30. Proximal to D1, Distal to S1
(Dominance of Lateral area)
ST Elevation in aVL and lead I
Q waves in lateral leads
ST Depression in lead III >lead II
ST Depression in lead III + aVF >= 2.5 mm
31.
32. Selective Occlusion of D1 branch
INJURY VECTOR- Upwards Forwards and to Left
Area affected- Mid Low Anterior wall and Mid Low
lateral wall
ST Elevation in I, aVL and precordial leads V2-
V6(variable)
ST Depression in II, III, aVF (lead III > lead II)
33.
34. Selective Occlusion of S1 branch
INJURY VECTOR- Anteriorly Upward and to Right
Area affected- Septal wall with occasionally certain
extension to Anterior wall
ST Elevation in V1,V2, aVR
ST Depression in II, III, aVF (lead II > lead III) and V6
No ST Elevation in aVL
38. Occlusion of RCA
ST Elevation in lead III > lead II
ST Depression in lead I and aVL
ST Depression in Right precordial leads < Inferior leads
PROXIMAL OCCLUSION:-
STE in V1 >V3 V4
STD in V3: STE in III < 0.5
DISTAL OCCLUSION:-
STD in V3: STE in III = 0.5 to 1.2
39.
40. Occlusion of LCX
ST Elevation in lead II > lead III
ST Elevation (isoelectric) in lead I and aVL
STE in Inferior leads < right precordial leads
If LCX is dominant Then… .. ST Depression in aVL, ST
Elevation in lead I and V5 V6
45. Right ventricular Myocardial Infarction
14 to 36%
ST Elevation in lead III > II
ST Elevation in V3R and V4R
ST Elevation in V1 to V3, V1>V2
ST Elevation in V1 , ST Depression in V2 (discordant)
ST Depression in V2 >= 50% of ST Elevation in aVF
46. Posterior Wall Myocardial Infarction
ST Depression in Precordial Leads with R waves and upright
T waves
Generally V1 to V4, may extent to V6 in case of large MI
Maximal ST depression in V4-V6, is seen in TVD and low
LVEF
Can occur in both RCA or LCX artery involvement
51. Other ECG Changes in patient of MI with
LBBB:-
LBBB is associated with 7% of all infarcts
Presence of abnormal Q wave
Notching of S waves (CABRERA SIGN)
Regression of R wave in precordial leads(V1 to V6)
Notching of R waves (CHAPMAN SIGN)
LEFT axis deviation
52.
53. OCCLUSION
Multivessal
LCX
LAD
RCA
Inf. MI with ST
dep. In V4-V6.
INFERIOR WALL
MI +
a) with ST elev. In
II >III.
b) with ST dep in
aVL and in V1-
V3.
c) with ST elev. In
V5-V6.
d) V3 ST dep: III
ST elev. > 1.2.
INFERIO
R MI
with ST
elev. In
III> II.
Proximal
Distal
a) ST elev. In V2.
b) V3 ST dep: III
ST elev.< 0.5.
V3 ST
dep: III ST
elev 0.5-
1.2.
ANT. MI
with ST
dep. >=1
in inf.
leads
ANT. MI
with NO
ST dep. in
inf. Leads.
Distal
Proxim
al
Proximal to S1
•ST elev. In
V1>2.5mm
•ST elev in
aVR.
•ST dep. in V5.
Proximal to
D1
•Abn. Q in
aVL.
Distal to S1
•Abn. Q in
V4-V6.
Distal to
D1
• ST dep.
54. PROGNOSTIC VALUE of ECG in MI:-
Q wave V/S Non Q wave infarction
Site of Infarction
Anterior wall
Inferior wall- reciprocal ST depression in V1-V4
Complete AV Block
Extensive RV infarction
Abnormal T waves
Higher T wave amplitude- better
Q wave MI with STE>2mm and positive T waves- large infarct, less chance of reoccurance
Inverted T waves in QMI indicates Transmural infarct
55. Associated BBB
LBBB- 34% increase risk of in hospital mortality
BBB – associated with 53% higher risk of 30 day mortality (GUSTO-1 Trial)
AV block – 20% mortality then 4% in non AV block (TAMI trial)
QT dispersion- risk of Arrythmia
60. Left main occlusion or Triple Vessal
Disease:
Marked downsloping ST depressions in I, II, V4-V6 and ST Elevation
in aVR.
aVR STE more in LMCA than LAD
V1 STE less in LMCA then LAD
Higher mortality rate for those with higher STE in aVR
Acute LMCA occlusion causes serious hemodynamic deterioration,
but more commonly seen is subtotal occlusion with collaterals from
RCA.
63. CONCLUSION:-
Sensitivity of ECG for Autopsy proven MI is 55 to 61%
ECG provides important information about culprit artery and
site of occlusion
ST Elevation equivalents should not be missed
Important prognostic value