Upload
chirantan-chirurgery
View
837
Download
6
Tags:
Embed Size (px)
DESCRIPTION
ECG Proff.Sumit Kr Ghosh Dept of Internal Medicine Medical College 88 College Street Kolkata
Citation preview
ECG
Dr. Sumit Kr. GhoshAsst. Professor
Department of MedicineMedical College & Hospital,
Kolkata
INTRODUCTION
Graphic representation of electrical activities of heart
Resting ECG
Exercise ECG / TMT
24-hr ECG / Holter
READING ECG
• Rate
• Rhythm
• Axis
• Lie & Rotation
• Voltage
• Waves & Intervals
• Abnormalities
ECG PAPER
STANDARDISATION
• 1mv will produce deflection of 10 mm / 1 cm
• Stylus should have an appropriate pressure
WAVES & INTERVALP Q R S T > 5mmq r s < 5mm
PQRSTUJ-pointJδPRQRSSTQTTPPP & RR
LEADSLead = paired electrode
12 leads
Limb leads Precordial leads Frontal or Coronal plane leads Horizontal plane leads Bipolar unipolar (low EP) unipolar I, II, III aVR, aVL, aVF v1, v2, v3, v4, v5, v6 rt side septum lt sideI, avL, v5, v6 : lateral wall II, III Avf : inferior wall
Long leadsV7, v8, v9V1r – v9r3v1 – 3v9Esophageal leads
Resultant vector
• Towards lead : positive / upward deflection
• Away from lead : negative / downward deflection
• Perpendicular to lead : equiphasic deflection
RATE
Ventricular rate vs Atrial rate
Rate = 1500/ no of small square = 300/no of large square
Depends on speed of ECG paper
Usual speed = 90m/hr =1.5m/min
No of QRS complex in 1 min = HR
RHYTHM
• Regular :~ Sinus ~ Nodal~ Idioventricular
• Irregular :~ Regularly irregular~ Irregularly irregular
AXIS• Normal axis : 0 to +90 degree (most cases +40 to +60 degree)• LAD : 0 to -90 degree (slight LAD : 0 to -30 degree
marked LAD : -30 to -90 degree ) • RAD : +90 to ± 180 degree• Inderminate / NW axis : -90 to ± 180 degree
an expression of : - marked RAD - marked LAD - discharge of ectopic ventricular pacemaker
AXIS DETERMINATION• Lead I,II & III• Pairs of perpendicular leads• Perpendicular to the lead where R=S• In degree
I II III
↑ ↑ ↑ Normal
↑ ↑ ↓ ↓ LAD
↓ ↑ ↑ RAD
+
+
_
_ I
aVF
0± 180
- 90
+ 90
NORMAL AXIS RAD LAD INDETERMINATE AXIS
EASY TO REMEMBER
I (left) aVF (right)
↑ ↑ Normal
↑ ↓ LAD
↓ ↑ RAD
↓ ↓ Indeterminate
LAD
• LAHB• LBBB
• Inf wall MI• Pacing from apex of RV/LV• WPWIsolated LVH does not cause
LAD
RAD
• RV dominance - acq. Rt heart disease : pulm embolism chr. Cor pulmonale - cong. heart disease : TOF• Anterolateral MI• LPHB• WPW
LIE & ROTATION• LIE : in frontal plane [ vertical (90 degree) to horizontal (0 degree )
• Rotation : in horizontal plane~ Clockwise – persistent S waves in v5, v6~ Anti-clockwise – R waves in v2
P - WAVE
• Atrial activity (RA earliar than LA)• Best seen in lead II & v1• Normal duration : 0.08 s – 0.1 s (not > 0.11 s)• Normal amplitude : not > 2 mm ( max – 2.5 mm)• Diphasic in v1• Inverted in aVR (normally), wrong electrode placement,
dextrocardia, retrograde atrial activation• Absent : Atrial fibrillation, nodal rhythm, hyperkalemia• P-pulmonale : tall & peaked (amplitude > 2.5 mm) » » RAH• P-mitrale : wide & notched (duration > 0.11 s) » » LAH• P-tricuspidale
QRS COMPLEX
• Ventricular depolarisationQ-wave : initial negative deflection septal depolarisation :: from left to rightR-wave : depolarisation of venticular muscle massS-wave : depolarisation of postero-basal part of left
ventricle, superiormost part of ventricular septum• High amplitude : RVH / LVH• Low amplitude : Low voltage complex
(< 5 mm in limb leads & < 10 mm in precordial leads)
Standardisation is important• Taller in v5 than v6
QRS COMPLEXQRS in precordial leads
T-WAVE
• Ventricular repolarisation
• Blunt apex with 2 asymerical limbs : proximal limb shallower than distal
• Tall –peaked : hyperkalemia
• Tall- wide : hyperacute stage of MI
• Inverted : IHD, Ventricular strain, CVA
• Flat : thick chest wall, emphysema, pericardial effusion, hypokalemia
U-WAVE
• Positive deflection after T & before P of next cycle
• Slow repolarisation of Purkinje’s fibres, septum, papillary muscles but uncertain
• Mid-precordial leads – v2 to v4
• Prominent : hypokalemia
• Inverted / absent : diastolic overload / myocardial dysfunction
P-R INTERVAL
• Beginning of P-wave to beginning of QRS complex
• Intra-atial, AV nodal & His-Purkinje coduction• Normal duration : 0.12 – 0.20 s• Prolonged : Acute rheumatic fever, 1st degree
AV block• Progressive prolongation : Mobitz type-I (2nd
degree AV block) » » Wenckebach phenomenon• Shortened : WPW syndrome, AV nodal rhythm
QRS INTERVAL• Total ventricular depolarisation• Beginning of Q-wave ( beginning of P-wave,
if no Q-wave present) to termination of S-wave
• Normal duration : usually not > 0.09 sec (range 0.05-0.11 s)
• Prolonged : Intaventricular conduction defect or BBB ≥ 0.12 sec » » complete BBB
• Intrinsicoid deflection / ventricular activation time : time taken for an impulse to traverse myocardiumVAT normally not > 0.02 s in v1, v2 & not > 0.04 s in v5, v6
ST SEGMENT
• End of QRS complex to beginning of T• Normal ST segment merges smoothly & imperceptibly with
proximal limb of T : difficult to separate• Time interval between ventricular depolarisation &
repolarisation• Isoelectric to TP segment• Elevated :
~ with upward convexity : AMI, coronary spasm, LV Aneurysm~ with upward concavity : acute pericarditis
• Depressed :~ oblique/plane/sagging : CAD~ mirror image of correction mark : digitalis effect~ upward convexity : strain pattern
• End of QRS complex & beginning of ST segment : J point
QT INTERVAL
• Beginning of Q to end of T• Ventricular depolarisation + repolarisation• Corrected QT or QTc : as QT changes with heart rate• Bazett’s formula : QT interval √RR intervalIt should be ≤ 0.44 sProlonged : acute rheumatic carditis, hypokalemia,
hypocalcemia, drugsShortened : hypercalcemia, digitalis, hyperthermia
QTc =
PP & RR INTERVAL• PP interval : distance between 2 successive P waves
- reflects atrial rate
• RR interval : distance between 2 successive R waves - reflects ventricular rate
• Normally PP = RR
Atrial hypertrophy :LAH : P-mitrale RAH : P- pulmonaleBi-atrial hypertrophy
Ventricular hypertrophy :LVHRVHBi-ventricular hypertrophy
LVH• Voltage criteria :
~ Sv1 + Rv6 > 35~ Sv1 / Rv6 ≥ 20~ Rv6 ≥ Rv5~ RI ≥ 15~ RaVL ≥ 11~ Rall(12) > 175
• Horizontal heart • VAT in v5/v6 > 0.04 s• Strain pattern in I, aVL, v5, v6
LAD is not a criteria for isolated LVH
• Pressure overload LVH • Volume overload LVH
RVH• Voltage criteria :
~ R > S~ Rv1 > 5 mm~ persistent Sv5 / Sv6
• Usually RAD (most common & at times only manifestation); but axis may be normal
• Vertical heart• VAT in v1 > 0.02 s• Strain pattern in v1, Avr• Associated P-pulmonale may be there
BIVENTRICULAR HYPERTROPHY
• LVH + RAD• LVH + Clockwise rotation • Tall Rv6 + tall Rv1 ( R > S)
CORONARY INSUFFICIENCY
• Impaired coronary blood flow : present all the time : absolute
• Increased demand : present time to time : relative• ST depression : horizontality, upward sloping, plane,
downward sloping• ST elevation : coronary vasospasm
more severe than ST depression • T wave :
~ symmetrical limbs with sharp vertex : coronary insufficiency~ asymmetrical limbs with blunt vertex : strain, digitalis effect
• Inverted U
MYOCARDIAL INFARCTION
ECG CHANGES• Hyperacute phase
~ increased amplitude of R wave~ increased VAT~ slope elevation of ST segment~ tall & wide T
• Fully evolved phase
~ pathological Q~ ST elevation with upward convexity~ symmetrical T inversion
• Chronic stabilized phase
~ pathological Q~ ST segment & T may be normal or point towards coronary insuffiency
Indicative & reciprocal changes
AMI
LV RVv1 & v4R
Anterior wall
Extensive anterior wallI, aVL, v1 to v6
Anterolateral wallI, aVL, v4 to v6
Anteroseptal walv1 to v4
Apical wallV5,V6
Inferior wallII, III, aVF
Posterior wallmirror-image change
in v1 to v3, esp v2
PATHOLOGICAL Q• Present in indicative leads• 0.04s in duration• >4 mm deep• >1/4th of R wave magnitude
Physiological Q• Septal depolarisation from left to right• Present in lateral leads I, aVL, v5,v6
Loss of Q : early feature of LBBB
Deep Q with giant negative T : HOCM
• Sinus rhythm : 60-100 beats/min• Sinus arrythmia (sinus node rate can change with
inspiration/expiration, especially in younger people variation of the P-P interval from one beat to the next by at least 0.12 seconds
• Sinus tachycardia : regular sinus rhythm with sinus node rate > 100/min
• Sinus bradycardia : regular sinus rhythm with sinus node rate < 60 / min
Similarities :Premature
EctopicEtiology
Dissimilarities :
SVPB VPB
Focus in Atrium ( other than SA node)
Ventricle
QRS complex Morphology similar
Narrow
Morphology dissimilar
Wide
ST-T No significant change Usually displaced in opposite direction of QRS
Compensatory pause Incomplete Complete
APC / SVPB vs. VPC / VPB
SUPRAVENTRICULAR TACHYARRYTHMIA
SVTs from a sinoatrial source:• Inappropriate sinus tachycardia • Sinoatrial node reentrant tachycardia (SANRT) SVTs from an atrial source:• Ectopic (unifocal) atrial tachycardia (EAT) • Multifocal atrial tachycardia (MAT) • Atrial fibrillation with a rapid ventricular response • Atrial flutter with a rapid ventricular response
SVTs from an atrioventricular source (junctional tachycardia):• AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating
tachycardia (JRT) • AV reentrant tachycardia (AVRT) - visible or concealed (including
Wolff-Parkinson-White syndrome) • Junctional ectopic tachycardia
PAT / PSVT / AVNRT• A run of rapidly repeated SVPBs ( usually ≥ 3 )• Narrow QRS• Rate around 160-220/ min • Usually 1:1 conduction; sometimes AV block associated
(PAT with block)• Prolonged PR
• Management : carotid sinus massage, adenosine,
verapamil, DC cardioversion
Atrial fibrillation
• Chaotic atrial excitation & contraction• Atrial rate 350-600 / min• No definite P; replaced by ‘f’ wave• Irregularly irregular ventricular rhythm• Narrow QRS• Etiology : • Management :
Atrial flutter• Regular atrial contraction• Atrial rate 220-350 / min• Ventricular rate ½ - ¼ th of atrial rate; may be
irregular; QRS complex : normal morphology • “Saw-toothed” appearance; flutter wave
VENTRICULAR TACHYARRYTHMIA
VT
VFl
VFVPC
Bigeminy : alternate sinus beat & VPC
Trigeminy : 2 sinus beat followed by VPC
Couplets / pairs : 2 successive VPCs
VT : ≥ 3 consecutive VPCs with rate >100
VT
Sustained VT : >30s in duration & symptomatic : generally requires termination by anti-tachycardia pacing techniques
Non-sustained VT : episodes are short (≥3 beats) and terminate spontaneously
Monomorphic VT : regular rate and rhythm and fixed shape or morphology of the ECG trace
Polymorphic VT : irregular in rate and rhythm and has varying shapes or morphologies on the ECG
Monomorphic VT may deteriorate into polymorphic VT to VF
VFl
• High frequency (250- 350/min) beats• The ECG signal looks like sinusoidal or ‘sine-
like wave’ form • High rate of contraction of heart chambers : time
of blood flow into the chamber becomes very small : very little blood flows to body
• The person who is experiencing VFl is close to unconsciousness
VF
• Most dangerous arrythmia• Ventricular rate 350-450/min• Totally uncoordinated : no discriminate waves :
totally irregular, bizarre & deformed deflections of varying width, height & shape
• No audible heart sounds, no palpable pulse• Treatment : immediate electrical defibrillation• If lucky to survive from VT, chance of VF in near
future
ATRIOVENTRICULAR CONDUCTION DEFECTS
• 1st degree
• 2nd degree~ Mobitz type I~ Mobitz type II~ Constant / fixed AV block
• 3rd degree / Complete block
1st degreeProlonged PR interval (>0.2 s)
2nd degreeMobitz type IMobitz type IIConstant / fixed AV block
3rd degree / Complete blockNo SA impulse pass through AV
nodeIdioventricular rhythmNo synchrony between atrial rhythm
& ventricular rhythm
Mobitz type I Mobitz type II
More common Less common
Benign Serious
Inf wall MI Ant wall MI
Proximal to bundle of His
Distal to bundle of His
Prognosis better Prognosis worse
INTERVENTRICULAR CONDUCTION DEFECTS
• Unilateral bundle branch block ( LBBB, RBBB)
• Peripheral block ( LAHB, LPHB, Septal block)
• Bifascicular block
• Trifascicular block
BBB
LBBB• M pattern or M-shaped complexes in lead I, aVL, v5, v6• Absent Q• ST depression with T inversion• QRS interval more or less 0.12s• Usually LAD• Usually VAT prolonged
Most cases have organic heart diseaseRecent onset LBBB : think of AMIPresence of Q in lateral leads : never LBBB
RBBB
• RSR’ pattern in v1, v2, aVR, v3R• ST depression with T inversion • Wide & slurred S in I, aVL, v5, v6• QRS interval more or less 0.12 s• Usually VAT prolonged
Commoner than LBBB, often without any cardiac diseases
LAHB• LAD• qR in I, aVL & rS in II, III, aVF
LPHB• RAD• qR in II, III, aVF
Bifascicular block• RBBB + LAHB
• RBBB + LPHB
• LAHB + LPHB
Trifascicular block• LAD + RBBB + Prolonged PR