The electric axis (see below) is normal The electrical bus Clinical electro cardiographists traditiooally assume that for some specific

ds the R wave gradually becomes taller and taller from V7 lo V5 and S becomes smaller and smaller from VI 10 V5 . 0 is present in VS and V6 but absent in V1 4. In all leads P wave, PR intervals, QRS complex have normal values and ST segment is isoelectric 5. The electric axis (see below) is normal The electrical bus Clinical electro cardiographists traditiooally assume that for some specific purposes, the electircal events of the ventricle can be represented by a single resultant dipole (and I he moment to momenl change of the direction of me resultant dipole need not be considered). The assumption rather, has no sound theoretical basis, vet surprisingly, it is a very good working rule. This single resultant dipole is called the etectrical axis [fig 6.11 7 a) Fig 571,7 Upper- normal heart, middle - left ventricular hypertrophy (boot shaped enlargement of heart) left axis deviation; lower - right ventricular hypertrophy (right am deviation) Normal hearts have a normal axis (fig.5 11 7a) If The axis rotates (deviates) anticlockwise it is called left axis deviation (5 11.7b). Left axjs deviation is due is such conditions like left ventricular hypertrophy (which causes a boot shaped enlargement of the heart) and others Conversely if there is a clockwise rotation there is right axis deviation (5 11 7c) which may be due to right ventricular hypertrophy. Axis determinations, are made by finding the amplitudes of the R waves in the bipolar limb leads. For example, if the P is tallest in the lead II, the electrical axis is parallel to the lead II {normal) (fig 5 11 7a), if R is tallest m lead I the axis is parallel! to the lead I (Left axis deviation) (5 11 7b), where as when the R is tallest in lead III the axis is parallel to the lead III and there is right axis deviation (fig.5.11.7c) APPLIED PHYSIOLOGY Myocardiaf infarction. Common findings (fig 5.11.8) are - (i) elevation (in acute stage) or depression (in sub acute or chronic stage) of the ST segment, (mi) presence of Q wave where it should be normally absent or big O wave where Ft should be normally present, and (iii) inversion of T wave (iv) normally the height of R wave progresses from V1 to VS but in myocardial infarction this progressive increase jn height does not occur (see also fig. 5 21 6) Fig. 5 11 8 An etevated ST segment in acute infarction of heart muscle Myocardial ischemia Common finding is depression of ST segment which may or may not be associated with other signs. Presence of a normal ECG, however, does not rule out cardiac ischemia. 3 Hypertrophy Left ventricular hypertrophy is usually associated with larger R in V5, V6, deeper S in V1 V2 and ft anix deviation These changes may or may not be associated with inversion of T wave and depression of ST A Heart Block In AV block the PR interval is more than 0.2 sec In bundle branch block the duration of QRS is more than 0.11 sec. Presence of RSR' (in V1) pattern denotes right bundle branch block (fig 5.11.9 a) whereas a sluired and broad ORS to V5 andV6 denote left bundle branch block (fig.5.11.9 b) Wolf-Parkinson-While (WPW) Syndrome This syndrome (-=disease] is raie but academically important In WPW syndrome, there is an additional connecting (in addition, to the normal AV jurrctional tissue connection) path between the atria and ventricle. and this additional path is called "bundle of Kent.'As a result of the presence of bundle of Kent, conduction between hyper and the ventncle is abnormally rapid, the characlenstic ECG features are (i) short PR interval, value around 0.1 sec (ii) broader ORS camplex 6. Hyparkalemia and hypokalemia The causes of hyper and hypokalemia wilh their pathophysiology have been described elsewhere in this book (chap 3 sec VIII) Here only ECG signs will be described It is to ba remembered, hyperkatemia (excess concentration of K+ ions in the ECF) can be rapidly fatal In early stages of hyperkalemia, T wave becomes Latter As the hyperkalemia progresses, AV block acid atnal paralysis develop, so that prolonged PR interval and absence of P are found in ECG record QRS becomes prolonged due to delayed conductivity in the ventricular conducting system 7. Arrhythmias (alnal and ventricular) In today's clinical practice, for the diagnosis of the arrhythmias, ECG's help is of supreme value, because accurate diagnosis is usually nol possible otherwise. However the issue is complex and mis author thinks that they should be better learnt from bigger Letfs HOW TO READ ECG Finally, some Lips are given below, about how to read ECG records of a given subject 1.Count [he heart rate (see above, for the techmc) 2 See whether the rhythm is sinus or not Sinus rhythm means where the pace maker is SAN. In sinus rhythm, the normal sequence of P, Q, R, S.T are maintained and P waves are upright where they should be upnght. Now-a-days, the condition, 'sick sinus rhythm', is increasingly diagnosed In this condition, there is damage of Ihe SAN (= sick sinus) rasullmg in severe bratiycardia and even syncopal attacks ECG however may show only bradycardis and nothing else It should be remembered, that Ihe rhythm may be 'normal sinus rhythm' (NSR) but there may be other signs of cardiac damage 9n the ECG For example, in a case of NSR there can be marked depression of ST segmenl (ischemia). In a normal ECG record., the heart rate (HR) fluctuates For example ai the beginning of a given ECG record Ihe HR may be 7Q/min, but wilhm a few seconds, as me ECG recording continues, Ihe HR may be 75/min This is normal and is due to (usually) respirahon and is called 'normal sinus arr