Various Investigation process & procedures involved in treating myocardial infarction

Investigation

The Electrocardiogram

A Q Wave is board (>1mm) and deep (>2mm or more the 25% of the amplitude of the following R wave) negative deflection that starts the QRS complex .

It may occur normally in leads AVR and V(and some times in lead III ) but, in other leads, it is abnormal. Abnormal Q waves are produced by several abnormalities such as left bundle branch block, ventricular tachycardia and the Wolff – Parkinson –white syndrome.

The gradual development of Q waves over minutes or hours suggests the occurrence of a full thickness MI. They develop because the electrical silence of infracted cardiac tissues results in a so called “window”.

Through which the normal endocrinal to epicardial activation of the opposite non infracted ventricular wall is “seen”, resulting in an unopposed depolarization front moving away from an electrode situated over the epicardial surface of the infract, Q waves are usually permanent electrocardiograpic features following full thickness MI.

T waves and ST segment changes result from ischaemia and injury. They are therefore often transient, occurring only during the acute attack.

The progressive changes or evolution of the ECG during the courses of a full thickness with subendocardial infarction only the endocrinal surface is infracted and Q waves do not develop ST segment and T waves changes are therefore the only ECG features of a subendocardial infarction.

Because the injury is endocrinal rather than predominantly epicardial, ST segment depression rather than elevation is usual . ECG changes are usually confined to the ECG leads that “face” he infarction. There fore an inferior wall MI is diagnosed when the ECG findings are seen in leads II, III, and AVF.

Lateral infarction produces changes in leads I, AVL and V. In anterior infarction leads V2 – V5 may be affected. Because there are no posterior leads, a true posterior wall infract is usually diagnosed by the appearance of a mirror image or reciprocal changes in leads V1 and V2. R wave, ST segment depression and tall, upright T waves.

These reciprocal changes can also be seen in association with other infractions . For Example in an inferior wall myocardial infarction, anterior ST segment depression may seen. In right ventricular infarction the ST segment is raised in lead VR4.

Cardiac Markers

• Creatine Kinase (CK):

This peaks with in 24 hours and is usually back to normal by 48 hours. It is also produced by damaged skeletal muscle and brain. Cardiac specific isoforms can be measured (CK – MK) allowing greater diagnostic accuracy. The size of the enzyme rise is broadly proportional to the infract size.

• Cardiac specific troponins:

Troponins T and troponins I are regulatory proteins with a very high specific for cardiac injury. Hey are released early and can persist for up to 7 days.

Immunoassays specific for these proteins can be performed in the laboratory and at the bedside in as little as 15 minutes using modern automated equipment. They are more sensitive and cardiac specific than CK – MB.

• Serial Cardiac Markers:

These should be measured in all patients presenting with suspected MI. Levels greater than twice the upper limits of normal are confirmatory in patients with good history and ECG changes. With successful reperfusion, the enzyme rise should be curtailed.

 

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