321 lecture ecg
TRANSCRIPT
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Electrocardiogram: The Basics
BMEN 321
October 31, 2006
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Background Reading
• This lecture summarizes information in Bioelectromagnetism by Malmivuo and Plonsey and can be found on the web at butler.cc.tut.fi/~malmivuo/bem/bembook
• We cover chapters 15 and 19
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The Heart
• The heart consists of four chambers– The right atrium and
right ventricle: responsible for delivery of deoxygenated blood to lungs
– The left atrium and left ventricle: responsible for delivery of oxygenated blood to the body
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The Heart: PhasesThere are two phases of the cardiac cycle
• Systole: The ventricles are full of blood and begin to contract. The mitral and tricucuspid valves close (between atria and ventricles). Blood is ejected through the pulmonic and aortic valves.
• Diastole: Blood flows into the atria and through the open mitral and tricuspid valves into the ventricles.
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ECG
• The ECG records the electrical signal of the heart as the muscle cells depolarize (contract) and repolarize.
• Normally, the SA Node generates the initial electrical impulse and begins the cascade of events that results in a heart beat.
• Recall that cells resting have a negative charge with respect to exterior and depolarization consists of positive ions rushing into the cell
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Cell Depolarization
• Flow of sodium ions into cell during activation
Depol Repol. Restoration ofionic balance
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ECG Leads• In 1908, Willem
Einthoven developed a system capable of recording these small signals and recorded the first ECG.
• The leads were based on the Einthoven triangle associated with the limb leads.
• Leads put heart in the middle of a triangle
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ECG LeadsThe basic values
The lead values
Also note that by KVL: VI + VIII = VII
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ECG: Electric Signal
• Assumptions– Model cardiac source as a dipole producing an
electric heart vector, p.– Model body as an infinite, homogeneous volume
conductor
• The leads will pick up the projection of the electric heart vector, p, along the lead
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Propagating Activation Wavefront
• When the cells are at rest, they have a negative transmembrane voltage – surrounding media is positive
• When the cells depolarize, they switch to a positive transmembrane voltage – surrounding media becomes negative
• This leads to a propagating electric vector (pointing from negative to positive)
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Propagating Activation Wavefront
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Propagating Activation Wavefront
Depol. toward positive electrodePositive Signal
Repol. toward positive electrodeNegative Signal
Depol. away from positive electrodeNegative Signal
Repol. Away from positive electrodePositive Signal
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Propagating Activation Wavefront
• When the activation does not align directly with the lead (or propagate directly toward and electrode), the signal is proportional to component of the activation direction along the lead direction.
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ECG Signal• Heart behaves as a syncytium:
a propagating wave that once initiated continues to propagate uniformly into the region that is still at rest.
• The depolarization wavefront defines a dividing line between activated and resting cells.
• Elsewhere, the signal is zero• Will propagate along conduction
paths – sinus node – AV node – bundle branches – Purkinjie fibers
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ECG Signal• The excitation begins at the
sinus (SA) node and spreads along the atrial walls
• The resultant electric vector is shown in yellow
• Cannot propagate across the boundary between atria and ventricle
• The projections on Leads I, II and III are all positive
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ECG Signal
• Atrioventricular (AV) node located on atria/ventricle boundary and provides conducting path
• Pathway provides a delay to allow ventricles to fill
• Excitation begins with the septum
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ECG Signal
• Depolarization continues to propagate toward the apex of the heart as the signal moves down the bundle branches
• Overall electric vector points toward apex as both left and right ventricles depolarize and begin to contract
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ECG Signal• Depolarization of the right
ventricle reaches the epicardial surface
• Left ventricle wall is thicker and continues to depolarize
• As there is no compensating electric forces on the right, the electric vector reaches maximum size and points left
• Note the atria have repolarized, but signal is not seen
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ECG Signal
• Depolarization front continues to propagate to the back of the left ventricular wall
• Electric vector decreases in size as there is less tissue depolarizing
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ECG Signal
• Depolarization of the ventricles is complete and the electric vector has returned to zero
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ECG Signal• Ventricular repolarization
begins from the outer side of the ventricles with the left being slightly dominant
• Note that this produces an electric vector that is in the same direction as the depolarization traveling in the opposite direction
• Repolarization is diffuse and generates a smaller and longer signal than depolarization
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ECG Signal
• Upon complete repolarization, the heart is ready to go again and we have recorded an ECG trace
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Normal ECG Signal
• P – atrial depolarization
• QRS complex – ventricular depolarization
• T – ventricular repolarization
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Cardiac Cycle
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Augmented Leads• Three additional limb leads are also used:
aVR, aVL, and aVF
• These are unipolar leads
• Each lead uses the average of the average of the other two leads as reference– VR = ΦR – (ΦL + ΦF)/2
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Precordial Leads
• Measure potentials close to the heart, V1- V6
• Unipolar leads
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ECG Information
• The 12 leads allow tracing of electric vector in all three planes of interest
• Not all the leads are independent, but are recorded for redundant information
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ECG Diagnosis
• The trajectory of the electric vector resulting from the propagating activation wavefront can be traced by the ECG and used to diagnose cardiac problems
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Electric Axis of the Heart• This axis changes during cardiac cycle as shown
earlier – generally lies between +30º and -110º in the frontal plane and +30º and -30º in the transverse plane
• Clinically, it is generally taken where the QRS complex has the largest positive deflection
• Note: Often use –aVR
• Deviation to R: increased activity in R vent. – obstruction in lung, pulmonary emboli, some heart disease
• Deviation to L: increased activity in L vent. – hypertension, aortic stenosis, ischemic heart disease
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Cardiac Rhythm: SupraventricularNORMAL SINUS RHYTHMImpuses originate at S-A node at normal rate
SINUS TACHYCARDIAImpuses originate at S-A node at rapid rate
All complexes normal, evenly spacedRate > 100/min
SINUS TACHYCARDIAImpuses originate at S-A node at rapid rate
All complexes normal, rhythm is irregularLongest R-R interval exceeds shirtest > 0.16 s
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Cardiac Rhythm: Supraventricular
ATRIAL FLUTTERImpulses travel in circular course in atria – No interval between T and P
Rapid flutter waves, ventricular response irregular
ATRIAL FIBRILLATIONImpuses have chaotic, random pathways in atria
Baseline irregular, ventricular response irregular
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Cardiac Rhythm: VentricularPREMATURE VENTRICULAR CONTRACTIONA single impulse originates at right ventricle
Time interval between normal R peaks is a multiple of R-R intervals
VENTRICULAR TACHYCARDIAImpulse originate at ventricular pacemaker – odd/wide QRS complex - often due to myocardial infarction
Wide ventricular complexesRate> 120/min
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Cardiac Rhythm: Ventricular
VENTRICULAR FIBRILLATIONChaotic ventricular depolarization – ineffective at pumping blood – death within minutes
Rapid, wide, irregular ventricular complexes
PACER RHYTHMImpulses originate at transvenous pacemaker
Wide ventricular complexes preceded by pacemaker spikeRate is the pacer rhythm
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Activation Sequence DisordersA-V BLOCK, FIRST DEGREEAtrio-ventricular conduction lengthened
P-wave precedes each QRS-complex but PR-interval is > 0.2 s
A-V BLOCK, SECOND DEGREESudden dropped QRS-complex
Intermittently skipped ventricular beat
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Bundle-branch BlockRIGHT BUNDLE-BRANCH BLOCKQRS duration greater than 0.12 sWide S wave in leads I, V5 and V6
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Atrial Hypertropy: Enlarged AtriaRIGHT ATRIAL HYPERTROPHYTall, peaked P wave in leads I and II
LEFT ATRIAL HYPERTROPHYWide, notched P wave in lead IIDiphasic P wave in V1
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Ventricular Hypertropy: Enlarged VentricleLEFT VENTRICULAR HYPERTROPHYLarge S wave in leads V1 and V2
Large R wave in leads V6 and V6
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Myocardial Ischemia and Infarction
• Oxygen depletion to heart can cause an oxygen debt in the muscle (ischemia)
• If oxygen supply stops, the heart muscle dies (infarction)
• The infarct area is electrically silent and represents an inward facing electric vector…can locate with ECG