P-Waves
Changes in P-wave morphology have been well described in resting tracings and are very useful in identifying right and left sided hemodynamic alterations due to both volume and pressure load.Careful study has revealed that it is P-wave deviation i.e. altered during ischaemia. As left ventricular end diastolic pressure increases with a loss of ventricular compliance, the left atrial wall distended by increasing pressure, which apparently slows conduction through the atrium and this prolongs the depolarization wave. The low amplitude of the P-waves however, makes the measurements difficult, which probably accounts for the low sensitivity of these findings. When the other signs of ischaemia are absent, the deviation of P-wave from rest to exercise should be measured (best in lead 2). An increased duration of greater than 20 milliseconds provides a specificity of 64 per cent.
U-Waves
The U-wave is usually upright if the T is also upright and is highest at low rates. When the heart rate increases to more than 90, the U-wave is rarely visible because it merges with the end of the T-wave and the ascending limb of the P-wave. Most of the workers believe that it represents after potentials of the T-wave. The U-wave is accentuated by a larger diastolic volume, hypokalemia and increased digitalis or calcium. Occasionally in patients with very low potassium, the U-wave can become so tall that it is mistaken for a tall T-wave. Patients with inverted U-waves may have an overload of central volume and the tall U-waves may represent a distended papillary muscle.
In patients with CAD incidence of inverted or diphasic U-waves is about 30 per cent at rest and 62 per cent after exercise. If one makes an analysis of inverted U-waves, LVH is the most common cause; angina is responsible for about 20 per cent.
Localisation of Ischaemia by Electrocardiographic Patterns
Exercise induced ischaemia is usually primarily a subendocardial affair, resulting in what is believed to be a generalized process, it has long been believed that exercise testing cannot localized the culprit artery. There are several exceptions to this statement.
ST Elevation due to Transmural Ischaemia
When ST elevation occurs with exercise it usually identifies the LAD as the culprit artery. ST elevation in leads II, III, and aVF which is much less common, identifies right coronary disease and in V2, V3 identifies LAD disease.
ST Elevation in aVR
Lead aVR often develops ST elevation as a reciprocal of ST depression in lead V2 to V6 or leads 2 and 3. It may occasionally show ST elevation in the absence of significant changes in the other leads. aVR is positioned so that it reflects the left ventricular cavity and when the right and left coronary beds are ischaemic and cancel out, changes in the apex can be manifested. It has been suggested that ST elevation in aVR of a 0.5 mm is significant for ischaemia. It has been reported that this finding has a sensitivity of 89 per cent but a specificity of only 44 per cent for LAD disease.
Changes in P-wave morphology have been well described in resting tracings and are very useful in identifying right and left sided hemodynamic alterations due to both volume and pressure load.Careful study has revealed that it is P-wave deviation i.e. altered during ischaemia. As left ventricular end diastolic pressure increases with a loss of ventricular compliance, the left atrial wall distended by increasing pressure, which apparently slows conduction through the atrium and this prolongs the depolarization wave. The low amplitude of the P-waves however, makes the measurements difficult, which probably accounts for the low sensitivity of these findings. When the other signs of ischaemia are absent, the deviation of P-wave from rest to exercise should be measured (best in lead 2). An increased duration of greater than 20 milliseconds provides a specificity of 64 per cent.
U-Waves
The U-wave is usually upright if the T is also upright and is highest at low rates. When the heart rate increases to more than 90, the U-wave is rarely visible because it merges with the end of the T-wave and the ascending limb of the P-wave. Most of the workers believe that it represents after potentials of the T-wave. The U-wave is accentuated by a larger diastolic volume, hypokalemia and increased digitalis or calcium. Occasionally in patients with very low potassium, the U-wave can become so tall that it is mistaken for a tall T-wave. Patients with inverted U-waves may have an overload of central volume and the tall U-waves may represent a distended papillary muscle.
In patients with CAD incidence of inverted or diphasic U-waves is about 30 per cent at rest and 62 per cent after exercise. If one makes an analysis of inverted U-waves, LVH is the most common cause; angina is responsible for about 20 per cent.
Localisation of Ischaemia by Electrocardiographic Patterns
Exercise induced ischaemia is usually primarily a subendocardial affair, resulting in what is believed to be a generalized process, it has long been believed that exercise testing cannot localized the culprit artery. There are several exceptions to this statement.
ST Elevation due to Transmural Ischaemia
When ST elevation occurs with exercise it usually identifies the LAD as the culprit artery. ST elevation in leads II, III, and aVF which is much less common, identifies right coronary disease and in V2, V3 identifies LAD disease.
ST Elevation in aVR
Lead aVR often develops ST elevation as a reciprocal of ST depression in lead V2 to V6 or leads 2 and 3. It may occasionally show ST elevation in the absence of significant changes in the other leads. aVR is positioned so that it reflects the left ventricular cavity and when the right and left coronary beds are ischaemic and cancel out, changes in the apex can be manifested. It has been suggested that ST elevation in aVR of a 0.5 mm is significant for ischaemia. It has been reported that this finding has a sensitivity of 89 per cent but a specificity of only 44 per cent for LAD disease.
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