Normal Ecg Flashcards
The electrocardiogram (ECG) is
graphical record of potential differences generated during cardiac electrical activity.
The electrical potentials are produced in the heart as the sum of
of the potentials generated by the heart muscle cells during depolarization and repolarization.
Depolarisation =
change of the transmembrane potential determinated by the movement of electrical charges (electrons or ions)
Repolarisation=
restoration of the resting transmembrane potential, induced by the movement of the electric charges in the opposite direction, which compensates for depolarization
Where are the V1, V2 electrodes placed?
4th intercostal space
What is the most common error in performing an ECG?
L to R reversal
V1 and V2 are often misplaced. Such misplacement usually involves placing these leads too high on the chest. The resulting ECG may generate erroneous ECG patterns:
incomplete right bundle branch block, anterior T wave inversion, septal Q waves, ST-segment elevation. These features may falsely suggest acute or old cardiac ischemia, pulmonary embolism, or a type-2 Brugada pattern. On rare occasion, conversely, high placement of V1 and V2 may reveal a true type-1 Brugada pattern. The emergency clinician needs to be aware of the possibility of lead misplacement, and should know how to suspect it based on unusual P wave morphology in V1 and V2.
What physiological / pathological situation mimics the L to R reversal?
Dextrocardia
The 6 chest electrodes
V1- 4th intercostal space ,right sternal border
V2 - 4th intercostal space , left sternal border
V3 - Midway b/w V2 + V4 , left anterior axillary line
V4 - 5th intercostal space , Left midclavicular line
V5 - level with V4 , left anterior axillary line
V6 - level with V4 , left mid axillary line
ECG lead =
the spatial ratio between two points where the electrodes are placed in the electric field of the heart.
Bipolar (standard) limb leads (I, II and III)
They form an equilateral triangle, with the heart located in the center
were introduced by Einthoven.
Unipolar (augmented) limb leads (aVR, aVL, aVF)
were introduced by Wilson.
Precordial leads (V1-V6)
are unipolar leads, in which the (positive) exploratory electrode is placed on the chest, near the heart
Limb leads – Eithoven’s triangle
The heart walls “seen” from the different ecg limb leads :
Lateral wall of the LV : DI, aVL
Inferior wall : DII,DIII, aVF
Endocavitary wall/layer of the heart: aVR
Precordial leads
The heart walls “seen” from the precordial leads:
Anterior wall of the heart : V1,V2
Interventricular septum: V3
Apex : V4
Lateral wall of the LV : V5,V6
Ecg graph paper: - Small boxes of - Large boxes of Paper speed : Voltage calibration:
1) 1mm
2) 5mm
3) 25 mm/sec
4) 10 mm /mV
ECG Recommended steps
Heart rate Axis Morphology of the waves Segments and intervals analysis Chamber enlargements Specific changes
The cardiac cycle normally begins with initiation of the impulse at the
sinoatrial, or SA node.
After the SA node fires, the resulting depolarization wave passes through
the right and left atria, stimulating atrial contraction and producing the P-wave on the surface ECG.
Following activation of the atria, the impulse proceeds to the
trioventricular (AV) node, which is the only normal conduction pathway between the atria and the ventricles.
The AV node slows impulse conduction, allowing time for the atria to contract and blood to be pumped from the atria to the ventricles prior to ventricular contraction. Conduction time through the AV node accounts for most of the duration of the PR interval.
Just below the AV node, the impulse passes through the bundle of His.
After the impulse passes through the bundle of His
it proceeds through the left and right bundle branches.
After leaving the left and right bundle branches,
the impulse passes through the Purkinje fibers, which are interlacing fibers of modified cardiac muscle. On the ECG this is represented as the Q wave.
The impulse passes quickly through the bundle of His, the left and right bundle branches, and the Purkinje fibers, leading to
depolarization and contraction of the ventricles.
P wave
atrial depolarisation
can be positive , equidiphasic or negative
QRS complex
ventricular depolarisation
Q wave : the first negative deflection before the R wave
R wave: positive deflection
S wave: the first negative wave after the R wave
T wave
ventricular repolarization
can be positive , equidiphasic or negative
Abnormalities of axis can hint at:
Ventricular enlargement Conduction blocks (i.e. hemiblocks)
By near-consensus, the normal QRS axis is defined as ranging from :
-30° to -90° is referred to as :
+90° to +180° is referred to as :
1) -30° to +90
2) left axis deviation (LAD)
3) right axis deviation (RAD)
Key Principles
If the QRS is POSITIVE in any given lead, the axis points in roughly the same direction as this lead.
If the QRS is NEGATIVE in any given lead, the axis points in roughly the opposite direction to this lead.
If the QRS is ISOELECTRIC (equiphasic) in any given lead (positive deflection = negative deflection), the axis is at 90° to this lead.
Common causes of LAD
May be normal in the elderly and very obese Due to high diaphragm during pregnancy, ascites, or ABD tumors Inferior wall MI Left Anterior Hemiblock Left Bundle Branch Block WPW Syndrome Congenital Lesions RV Pacer or RV ectopic rhythms Emphysema
Common causes of RAD
Normal variant Right Ventricular Hypertrophy Anterior MI Right Bundle Branch Block Left Posterior Hemiblock Left Ventricular ectopic rhythms or pacing WPW Syndrome
Normal Sinus Rhythm
Originates in the sinus node Rate between 60 and 100 beats per min P wave axis of +45 to +65 degrees, ie. Tallest p waves in Lead II Monomorphic P waves Normal PR interval of 120 to 200 msec Normal relationship between P and QRS Some sinus arrhythmia is normal
p wave upright in leads
I and II
The P wave
< 3 small squares in duration
< 2.5 mm in amplitude
Junctional escape
Depolarization initiated in AV junction when 1 or more impulses from the sinus node are ineffective or nonexistent.
Rate : 40- 60 bpm
Rhythm : Irregular in single junctional escape complex ; regular in junctional escape rhythm
P waves : depends on the site of the ectopic focus.They will be inverted , and may appear before or after the QRS complex , or they might be absent , hidden by the QRS .
QRS is usually normal
Junctional escape
Depolarization initiated in AV junction when 1 or more impulses from the sinus node are ineffective or nonexistent.
Rate : 40- 60 bpm
Rhythm : Irregular in single junctional escape complex ; regular in junctional escape rhythm
P waves : depends on the site of the ectopic focus.They will be inverted , and may appear before or after the QRS complex , or they might be absent , hidden by the QRS .
QRS is usually normal
( No relation b/w P wave and QRS complex??)
PR interval
AV node conduction
From the beginning of P wave to the beginning of q wave
120-200 ms
Short PR interval
WPW Syndrome delta wave short PR ( 0.08s) long QRS 0.12 sec
Accessory pathway ( Bundle of Kent ) allows early activation of the ventricle ( delta wave and short PR interval)
Normal QRS complex
Completely negative in lead aVR , maximum positivity in lead II
rS in right oriented leads and qR in left oriented leads (septal vector)
Transition zone commonly in V3-V4
RV5 > RV6 normally
Normal duration 50-110 msec, not more than 120 msec
Physiological q wave not > 0.03 sec
Amplitude of QRS
Depends on the following factors
- electrical force generated by the ventricular myocardium
- distance of the sensing electrode from the ventricles
- Body build;a thin individual has larger complexes when compared to obese individuals
Left ventricular hypertrophy
Sokolow & Lyon criteria
Cornel criteria
others
S&L : S (V1) + R(V5 or V6)>35mm
Cornel criteria : S(V3) + R(avL)> 28 mm ( men ) or > 20 mm ( women)
others : R (avL) > 13mm
Premature ventricular Complexes (PVCs)
is a relatively common event where the heartbeat is initiated by the heart ventricles ( arrow ) rather than by the SA node.Rate depends on underlying rhythm and number of PVCs. - Ocassionally ireegular rhythm .
- no p wave associated with PVCs
- May produce bizarre looking T wave
Artificial pacemaker
Sharp , thin spike
Rate depends on pacemaker , p wave may be absent or present
Ventricular paced rhythm show wide ventricular pacemaker spikes
localizing MI
Look at ST changes
Q wave in all leads
Location of MI
Anterior
Septum
Left lateral
Lead with ST change : Affected coronary artery :
1) V1,V2,V3,V4 , LAD
2) V1,V2 LAD
3) I ,avL ,V5,V6 Left circumflex artery
Location of MI Inferior Right atrium Posterior Right ventricle
Lead with ST change : Affected coronary artery : 1)II,III,avF RCA 2) aVR ,V1 RCA 3) Posterior chest leads RCA 4) Right sided leads RCA
T wave
Reflects ventricular repolarization ( epicard -> endocard)
Aspect : rounded , assymetric, with steeper downward slope
Consostent with QRS complex
positive in most derivatives
negative :avR +/- in LIII,avF,V1
Amplitude < 1/3 QRS ( <6 mm)
Duration : 0.13 - 0.30 s
Modified by factors:
Physiological : SNVP -> T high asymmetric ( precordial)
Humoral factors :
Decreased PO2 ,Ca++,K+
U wave
corresponds to papillary muscle repolarization or post-depolarization in Purkinje fibers
Aspect : small , rounded
Same direction with T waves from the same derivation
Amplitude < 1/4 from the same derivation :
more obvious decreased FC , [K+]
Better expressed in chest precrodial leads ( V1 ,V2)
QT interval
Normally corrected for HR
Bazett’s formula
Normal 350 to 430 msec
With a normal HR (60-100), the QT interval should not exceed half of the RR interval roughly
Measurement of QT interval
The beginning of the QRS complex is best determined in a lead with an initial q wave -> LI,II,avL,V5 or V6
QT interval shortens with tachycardia and lenghthenswith bradycardia
QTc
Normal QTc Men < 0.43 - borderline 0.43 - 0.45 - prolonged >0.45 Women <0.43 - borderline 0.43 - 0.47 - prolonged >0.47
Causes of Long QTc
Congenital - Romano Ward - Jervell and Lange Nielson Drugs - Antiarrhythmics - Class Ia and III - Antibacterials - Erythromycin Other drugs - Terfanidine, cisapride, TCA
Electrolyte disturbances - Low K and Mg Other causes - IHD - SAH - Bradycardia due to SSS or AV block - Hypothyroidism
Shortened QT
Digitalis effect
Hypercalcemia
Hyperthermia
Vagal stimulation
Normal variants in ECG
Sinus arrhythmia
Persistent juvenile pattern
Early repolarisation syndrome
Non specific T wave changes
Features of ERPS
Vagotonia / athletes’ heart Prominent J point Concave upwards, minimally elevated ST segments Tall symmetrical T waves Prominent q waves in left leads Tall R waves in left oriented leads Prominent u waves Rapid precordial transition Sinus bradycardia
Early Recognition Prevents Streptokinase infusion !
ECG Motion Artifacts Overview
Motion artefact due to tremor or shivering can obscure the waveforms of the ECG or stimulate pathology , making ECG interpretation difficult
In certain circumstances ( e.g hypothermia ) the presence of shivering artefact may actually aid diagnosis
Causes of Tremor
Benign Essential Tremor (physiological tremor ) Parkinsons Disease (resting tremor ) Cerebellar disease (intention tremor) Alcohol /Benzodiazepine withdrawal Anxiety Thyrotoxicosis Multiple sclerosis Drugs : Amphetamines , cocaine , β- agonists (adrenaline , salbutamol) theophylline,caffeine , lithium
Other types of motion artefacts
Fever ( rigors)
Hypothermia (shivering)
Cardiopulmonary resuscitation ( chest compressions)
A non-compliant , mobile ,talkative patient ( = the most common cause)
The role of ECG
HR determination;
Assessment of cardiac conduction function;
Determination of the electrical axis of the heart;
Determination of: cardiac arrhythmias and conduction disorders;
Determination of ischemic changes
It does NOT provide information about the pump function of the heart.
