ECG EXAMINATION Seminary of pathophysiology Pavel Maruna.
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Transcript of ECG EXAMINATION Seminary of pathophysiology Pavel Maruna.
![Page 1: ECG EXAMINATION Seminary of pathophysiology Pavel Maruna.](https://reader036.fdocuments.in/reader036/viewer/2022081506/56649d9d5503460f94a863f9/html5/thumbnails/1.jpg)
ECG EXAMINATION
Seminary of pathophysiology
Pavel Maruna
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SA node(= pacemaker)
AV node
Bundle of His
Right and left bundle branches
Purkynje fibres
Electrical conduction in heart
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Cellular depolarization
• What do we measure?
• What is positive and negative vector?
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12-lead ECG examination
Limb leads
aVR
aVF
aVL
Bipolar leadsI, II, III
Pseudounipolar leadsaVR, aVL, aVF
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Chest leads
12-lead ECG examination
Unipolar leads
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12-lead ECG examination
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QRS axis(Axis of QRS complex depolarization)
- 30° to + 105°
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initiation of impulse in the SA node
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atrial depolarization
initiation of impulse in the SA node
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initiation of impulse in the SA node
atrial depolarization
depolarization of AV nodus and bundle of His
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septal depolarization
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septal depolarization
early ventricular depolarization
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septal depolarization
early ventricular depolarization
late ventricular depolarization
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ventricular systole
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ventricular systole
ventricular repolarization
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ventricular systole
ventricular repolarization
repolarization of bundle of His
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PR (PQ) interval
(0,12 - 0,20 s)
QRS complex
(0,06 - 0,10 s)
QTc interval
(to 0,44 s)
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What to see on the curve?
• Rhythm?
• P wave
• Intervals
• QRS complex
• ST segment
• T wave (U wave)
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P wave
Physiology:• positive orientation (possible biphasic in I lead)• duration < 0,11 s, amplitude < 2,5 mm
Pathology:• hypertrophy of left or right atrium• abnormal conduction (SVES)
Electrical impulse originates in the SA nodeImpulse triggers atrial depolarization
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P wave
P mitrale
High P amplitude due to left atrial hypertrophy
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depolarization of AV node and bundle of His
It represents the physiological delay in conduction from atrial depolarization to the beginning of ventricular depolarization. It is electrically neutral.
Limits: 0,12 - 0,20 s
Physiological importance:
1. synchronization of both atrial and ventric. systoles2. protection against the transmission of supraventricular tachyarrhythmia to vetricular tachycardia
PR (PQ) interval
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PR (PQ) intervalAV blockade
1st = prolongation of PR interval
2nd = partial blockade (transmission of selected impulses)
- Wenckenbach
- Mobitz
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PR (PQ) intervalAV blockade
3rd = complete blockade
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QRS complex
Depolarization of the ventricles
Physiology:
• duration 0,06 - 0,10 s
• Q < 0,04 s, < 25 % of R wave
• Sokolow index (S in V2 + R in V5) < 35 mm (< 45 mm for young)
• axis of ventricular depolarization -30 to +105 °
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Physiology:
• duration 0,06 - 0,10 s
• Q < 0,04 s, < 25 % of R wave
• Sokolow index (SV2 + RV5) < 35 mm (< 45 mm for young)
• axis of ventricular depolarization -30 to +105 °
• VAT (ventricular activation time) of LV < 0,04 s, RV < 0,03 s
QRS complex
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QRS complex
Both QRS complex duration and shape is depend on:
1. Physiology of His-Purkine´s system or aberrant signal passing
VES
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QRS complex
Both QRS complex duration and shape is depend on:
1. Physiology of His-Purkine´s system or aberrant signal passing
RBBB ......................(QRS prolongation, rSR´ in V1, negative T wave)
V1
Intraventricular blockades
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RBBB
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QRS complex
Both QRS complex duration and shape depend on:
2. Myocardial mass
cardiomyopathy
RV hypertrophy
LV hypertrophy
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QRS complex
Both QRS complex duration and shape is depend on:
3. Factors affecting signal velocity - metabolic, endocrine, and pharmacological
high sharp T wave
wide QRS complex
hyperkalemia
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QRS complex
digitalis
Both QRS complex duration and shape is depend on:
3. Factors affecting signal velocity - metabolic, endocrine, and pharmacological
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LV, RV hypertrophyLV, RV hypertrophy
Prolongation Shortening
QRS complex
hyperkalemia, digoxinhyperkalemia, digoxin
intraventricular blockadeVES
intraventricular blockadeVES
diffuse alteration(amyloid, fibrosis)diffuse alteration(amyloid, fibrosis)
artificial factors(obesity, pericard. effusion)
artificial factors(obesity, pericard. effusion)
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QRS complex
Pathological Q wave
Q wave prolongation (> 0,04 s) and depression (> 25 % R)
Manifestation of transmural myocardial necrosis
„Cavity potential“
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Patological Q
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ST segment
• From „J point“ on the end of QRS complex, to inclination of T wave
• Normally, all cells have the same potential = ST segment is electrically neutral (on isolectric line)
The length between the end of the S wave (end of ventricular depolarization) and the beginning of repolarization
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ST segment
Physiological changes
sympathicus ... ST depression, „anchor-like“ curveparasympathicus (vagus) ... ST elevationsyndrome of an early repolarization
Artificial changes
depend on lead localization, chest malformation etc.
Patological changes
electric potential of destroyed myocardial area
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ST segment
Ischemic focus has a different electric potential = electric vector leads to this area
1. subendocardial ischemia
(non-Q MI, AP paroxysm)
... ST depresssion
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ST segment
Ischemic focus has a different electric potential = electric vector leads to this area
2. subepicardial ischemia
(Q-MI, spastic form of AP, aneurysma)
... elevation of ST segment
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T wave
Ventricular repolarization
Normally: a repolarization directs from epicardium to endocardium = T wave is concordant with QRS complex
Ischemic area: a repolarization is delayed, an action potential is extended
Vector of repolarization is directed from ischemic area:- subendocardial ischemia ... to epicardium ... T wave elevation- subepicardial ischemia ... to endocardium ... T wave inversion
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T wave
•LV overload
•neurocirculatory asthenia
•sympathetic system
•hypokalemie
•hyperglycemia
•myxoedema
•pancreatitis
•pneumotorax
Diffuse T changes,T wave
asymmetricor biphasic
Nonspecific changes
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T wave
Diffuse T changes,T wave
asymmetricor biphasic
Localized T changesT wave - symmetric
negativity
Ischemia Nonspecific changes
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K+ influence on cardiac conductivity
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Refractory period1. Absolute = Absolutely no stimulation can cause another action potential
2. Relative = It is possible to cause another action potential, but the intensity of the premature contraction will be relative to the time in this period.
„R on T“ phenomena
„Malignant VES“: R wave of the next beat falls in certain portions of the previous T-wave... Serious and life-threatening arrhythmia
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Holter monitoring
Indications:
1. syncope or palpitation of unclear origin2. an unveiling of latent ischemia 3. an antiarrythmic therapy control4. a pacemaker control
24-h ECG recording
Ambulatory ECG device
Analysis of mean, maximal, and minimal HR, occurrence and frequency of major arrhythmia
Confrontation of record and subjective difficulties (patient activity log)
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Patient No. 1
Finding of atrial fibrillation.Pauses > 2 sRare ventricular ES
Holter monitoring
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Patient No. 2
Ventricular fibrillation
Holter monitoring
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Patient No. 3
Ventriculartachycardia
Holter monitoring
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Ergometry, exercise ECG
Indications:
1. specification of ischem. disease prognosis2. suspicion on ischemic disease 3. examination of functional capacity
Gradual load increase in 4-min. intervals, basic level 25 - 75 W
Stopping - submaximal load or complications (accelerated hypertension, polytopic VES, blockades, ST elevation ST, ST depression > 2 mm, T inversion
Coincidence of chest pain + ST changes= confirmation of ischemia
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Q myocardial infarction
ECG changes
Martin Vokurka
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Acute anterior myocardial infarction
ST elevation in the anterior leads V1 - 6, I and aVL
reciprocal ST depression in the inferior leads
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Acute inferior myocardial infarction
ST elevation in the inferior leads II, III and aVF
reciprocal ST depression in the anterior leads
RBBB and bradycardia are also present
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Old inferior myocardial infarction
Q wave in lead III wider than 1 mm (1 small square) and
Q wave in lead aVF wider than 0.5 mm and
Q wave of any size in lead II
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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: frontal plane leads with fully evolved inferior MI (note Q-waves, residual ST elevation, and T inversion in II, III, aVF)
Old inferior MI (note largest Q in lead III, next largest in aVF, and smallest in lead II)
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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)
Acute anterior or anterolateral MI (note Q's V2-6 plus hyperacute ST-T changes)
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| | |
dg.: disperze QT intervalualternans T vlny
dg.: pozdní potenciálydg.: senz. baroreflexu, variabilita fr.
|
náhlá smrtčastější u mužů, etiol. kardiální 30% (ve stáří 80-90%), z kardiálních příčin: 80% tachyarytmie
Nové metody predikce kardiální náhlé smrti (predikce arytmogeneze):
disperze QT intervalu
alternans T vlny spontánní variabilita voltáže T vlny
pozdní potenciály v závěru QRS a během ST
senzibilita baroreflexu index f/ TK po farmakol.stimulaci nebo spontánně
variabilita frekvence periodicita respirační, baroreflexní, termoregulační atd.,
oplošťuje se s věkem, sympatikotomií
(její snížení tedy odráží vyšší riziko maligních dysrytmií)
chronické organ. změny srdce
arytmogenní substrát
nehomogenní repolarizacenehomogennídepolarizace
prodloužení vedení zpomalení vzruchu
maligní arytmie
(nejčastěji komor. re-entry)
vegetativnídysbalance
reverzibilníischemie
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Atrial extrasystole Compensatory pauses
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Ventricular extrasystole
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Atrial fibrillationAtrial flutter
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SV tachycardia
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Ventricular tachycardia
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Ventricular fibrilation (or flutter)Acute situation, hemodynamic arrest – 0 cardiac output, 0 pulsation, coma, resuscitation
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AV block 2rd degree
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AV block 3rd degree
Preexcitation, WPW syndrome
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Bundle branch blocks
LBBB RBBB
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Left anterior fascicular block