Bipolar leads (I, II, III) electrically form an equilateral triangle named after Willem Einthoven, the scientist who developed the ECG. These leads, combined with unipolar augmented leads (aVL, aVR, aVF) examine the heart in the frontal plane. Rearranging these six limb leads, allowing an intersection representing the heart, forms the hexaxial reference system. The arrows represent the normal path of electrical current for each lead. This graphical representation of cardiac electrical activity aids interpretation of ventricular axis in the frontal plane.
Frontal ventricular axis determination
Normal cardiac electrical activity progresses systematically from the SA node, via internodal fibres to the AV node. Conduction continues via the bundle of His, through right and left bundle branches to Purkinje fibres, resulting in ventricular contraction. Depolarization towards a positive electrode produces a positive deflection on the ECG. When viewing the heart in the frontal plane, mean ventricular depolarization (as denoted by the QRS complex) lies between −30° and +90°. Ventricular axis may be determined using the limb leads. The simplest approach is the quadrant method, examining leads I and aVF. These perpendicular limb leads outline the majority of the normal axis.
Normal axis – positive QRS complex in both leads.
Extreme right axis deviation – negative QRS complex in both leads.
Right axis deviation – negative complex in lead I, positive complex in aVF.
Left axis deviation – positive complex in lead I, negative complex in aVF. However, as the normal axis ranges from −30° to +90°, this average vector may represent a normal axis. Examination of lead II is also required; if QRS complex is positive the axis is normal (ranging from 0° to −30°).
An alternative equiphasic approach exists, founded on the principle that depolarization travelling perpendicular to a lead produces an equiphasic QRS complex.
1.1.9
Ejection fraction equation
EF = SVEDV ×100
SV = EDV – ESV
EF = ejection fraction
EDV = end-diastolic volume
ESV = end-systolic volume
SV = stroke volume
The ejection fraction simply describes the amount of blood that is ejected from the ventricle during systolic contraction (stroke volume) as a proportion of the amount of blood that is present in the ventricle at the end of diastole (end-diastolic volume). A 70 kg individual would normally have a stroke volume of about 70 ml and an end-diastolic volume of about 120 ml.
The ejection fraction equation is used to calculate the stroke volume as a percentage of the end-diastolic volume. It gives an indication of the percentage of the ventricular volume that is ejected during each systolic contraction. It can be applied to the left or the right ventricles, with normal values being 50–65%. Right and left ventricular volumes are roughly equal and therefore ejection fractions are broadly similar.
In clinical practice, it can be calculated using echocardiography, pulmonary artery catheterization, nuclear cardiology or by contrast angiography.
In aortic stenosis, the ventricle will compensate for the increased obstruction to outflow by hypertrophy. This will initially maintain the ejection fraction and the pressure gradient across the valve. As the disease progresses and the valve area narrows, the hypertrophied ventricle becomes stiff and less compliant and will no longer be able to compensate. A reduction in the stroke volume (and ejection fraction) is seen, resulting in a fixed reduced cardiac output. The myocardium will eventually fail as compliance continues to worsen.
1.1.10
Electrocardiogram
An electrocardiogram (ECG) is a non-invasive, transthoracic interpretation of cardiac electrical activity over time. Thorough assessment requires a systematic approach including rate, rhythm, axis (normal axis is −30° to +90°), and wave morphology/interval.
Morphology and intervals
P wave – represents atrial depolarization. A positive deflection should be present in all leads except aVR.
PR interval – from the start of the P wave to the end of the PR segment. Normal value 0.12–0.2 s (3–5 small squares). This interval is rate dependent; as heart rate increases, the PR interval decreases.
QRS wave – represents ventricular depolarization. The normal duration is ≤0.12 s. A Q wave in leads V1–V3 is abnormal.
ST segment – from the junction of the QRS complex and the ST segment to the beginning of the T wave. A normal ST segment is isoelectric.
T wave – represents repolarization of the ventricles.
QT interval – from the start of the QRS complex to the end of the T wave. This interval represents the time for ventricular activation and recovery. Heart rate variability occurs and therefore a corrected QT interval (QTc) can be calculated (normal value is <0.44 s).
ECG changes associated with acute coronary syndromes and myocardial infarction
Acute coronary syndromes – include non-ST-elevation myocardial infarction and unstable angina. The primary ECG changes observed are ST segment depression and T wave flattening or inversion.
Myocardial infarction – early evidence of transmural ischaemia and myocardial infarction includes hyperacute T waves followed by ST elevation. Q wave formation may begin within 1 hour of infarction. Inverted T waves are a later sign within 72 hours of cell death. Stabilization of the ST segment usually occurs within 12 hours, although ST elevation may persist for more than 2 weeks.
1.1.11
Electrocardiogram – cardiac axis and QTc
Division of the hexaxial reference system into four quadrants allows further interpretation of the cardiac ventricular axis (for calculation see Section 1.1.8 – Einthoven triangle).
The normal QRS axis ranges from −30° of left axis deviation (LAD) to +90°.
LAD is defined as an axis between −30° and −90°. This may be an isolated finding or can be associated with pathology. Causes include: left ventricular hypertrophy, left bundle branch block (LBBB), left anterior fascicular block, myocardial infarction, and mechanical shifts of the heart (i.e. pneumothorax).
Right axis deviation (RAD) is defined as an axis between +90° and +180°. Causes include: physiological variant in infants and children, right ventricular hypertrophy, myocardial infarction, left posterior fascicular block, chronic lung disease, dextrocardia, and ventricular arrhythmias.
Extreme right axis deviation (ERAD) is defined as an axis of −90° to +180°. This is a rare finding associated with dextrocardia, ventricular arrhythmias or a paced rhythm.
Precordial axis
Assessment of the precordial leads, V1–V6, enables determination of the precordial axis as described by R wave progression. Normal R wave progression is characterized by a primarily negative QRS complex in V1 and a primarily positive QRS complex in V6. Transition between negative and positive complexes occurs between the V2 and V4 leads.
Early R wave progression is characterized by much more positive QRS complexes in leads V1 and V2. This observation is always pathological and may be due to posterior myocardial infarction (with the positive QRS complexes representing reciprocal Q waves), right ventricular hypertrophy, RBBB, or Wolff–Parkinson–White syndrome.
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