Branch Block
163Case 35 Left Bundle Branch Block
Table 35.1: Causes of left bundle branch block
• Myocardial infarction
• Aortic valve stenosis
• Systemic hypertension
• Dilated cardiomyopathy
• Fibrocalcerous degeneration.
CLINICAL DISCUSSION
Left bundle branch block (LBBB) often indicates the presence of organic heart disease. A variety of cardiac conditions can cause LBBB including myocardial infarction, systemic hypertension, aortic valve disease, cardiomyopathy and fibrocalcerous degeneration (Table 35.1). On the other hand, right bundle branch block (RBBB) is sometimes observed in normal individuals. Typical causes of RBBB are atrial septal defect, acute pulmonary embolism and chronic obstructive pulmonary disease.
RBBB does not distort the QRS complex, but only adds a terminal deflection due to delayed right ventricular depolarization. Therefore, changes of myocardial infarction such as appearance of Q waves and loss of R wave height, can be readily diagnosed in the presence of RBBB. However, it is difficult to diagnose myocardial infarction in the presence of LBBB, since the QRS complex is completely distorted.
Figure 35.3: Diagram to represent left anterior hemiblock (LAHB)
Figure 35.4: ECG showing left axis deviation due to left anterior hemiblock
164 Section 11 Typical ECG Abnormalities
Table 35.2: Criteria for diagnosing MI in presence of LBBB
• Presence of q wave in L1, V5 and V6
• Terminal S wave in leads V5 and V6
• S-T segment drift greater than 5mm
• Upright T wave concordant with QRS
The criteria for the diagnosis of myocardial infarction in the presence of LBBB are given in Table 35.2.
In left bundle branch block (LBBB), there is paradoxical splitting of the second heart sound (S2). The A2 component of S2 is delayed due to late depolarization of the left ventricle and follows the P2. During inspiration, when P2 gets delayed due to increased venous return, the splitting of S2 becomes narrow instead of physiological widening. Besides LBBB, another cause of paradoxical splitting of S2 is aortic valve stenosis in which left ventricular ejection time is prolonged. Other reasons for paradoxical splitting of A2 are pre-excitation of the right ventricle through an accessory bypass tract or premature activation of the right ventricle by an external pacemaker. LBBB causes a jerky motion of the interventricular septum on echocardiography. This should not be diagnosed as septal infarction, unless the septum fails to thicken during systole.
MANAGEMENT ISSUES
There is no specific treatment of left bundle branch block. The underlying heart disease is to be managed on its own merit. There is a word of caution regarding the use of drugs which block the A-V node such as verapamil, diltiazem and beta blockers. They may cause complete heart block, particularly if the block is bifascicular or trifascicular to begin with. Bifasicular block includes right bundle branch block and left anterior hemiblock. Trifasicular block is bifasicular block with a prolonged P-R interval.
C A S E
36 Features of
Hypokalemia
CASE PRESENTATION
A 48-year old man sought consultation from a physician for pain and weakness in both arms, since the last 3 days. There was no history of chest pain, breathlessness, palpitation or sweating. The heaviness in the arms was aggravated by lifting a light weight, but not by movement at the neck. The patient also complained of fatigue and pain over his calf muscles while walking. He had systemic hypertension for several years for which he was presently prescribed losartan 50 mg and hydrochlorthiazide 25 mg. The patient also suffered from bronchial asthma, for which he used an inhaler containing a combination of salmeterol and fluticasone. Recently, he had a gastro-intestinal infection with profuse vomiting and diarrhea that lasted 2 days.
Besides age and hypertension, other cardiovascular risk factors in the patient were prediabetes and a modestly elevated serum cholesterol.
On examination, the patient was coherent, comfortable and in no distress. There was no anemia, cyanosis, icterus or ankle edema. The JVP was not raised, thyroid gland was normal and there were no palpable lymph-nodes. The pulse rate was 72 beats/min with a BP of 130/80 mm Hg. The precordium was unremarkable and the apex beat was normally located. The S1 and S2 were normal and no gallop sound was heard. No murmur or pericardial friction rub was audible. The breath sounds were normal without rhonchi or crepts. An ECG was obtained (Fig. 36.1) following which he was asked to immediately see a cardiologist. His blood biochemistry was Glucose 128 mg/dl, Urea 38 mg/dl, Creatinine 1.2 mg/dl, LDL cholesterol 147 mg/dl, Sodium 131 m Eq/L and Potassium 2.9 m Eq/L.
Figure 36.1: ECG showing flat T waves with prominent U waves
166 Section 11 Typical ECG Abnormalities
Table 36.1: ECG features of progressive hypokalemia
• Reduced amplitude of the T wave
• Flat T wave with prominent U wave
• S-T segment sagging; only U wave.
The ECG features of hypokalemia depend upon its severity (Fig. 36.2). In mild hypokalemia, only the T wave amplitude is reduced. In moderate hypokalemia, the U wave becomes more prominent than the T wave. In severe hypokalemia, there is sagging of the S-T segment and only the U wave is visible (Table 36.1).
Figure 36.2: ECG features of progressively increasing hypokalemia
ECG INTERPRETATION
The ECG showed normal sinus rhythm. The P wave and QRS complex were normal in morphology. There were no significant Q waves and the S-T segment was isoelectric. The T wave was reduced in amplitude, while the U wave was prominent. The Q-T interval seemed to be prolonged. These findings are consistent with the diagnosis of hypokalemia. Hypokalemia is an important cause of T wave change. The T wave is either reduced in amplitude, flattened or inverted. This is associated with prominence of the U wave that follows the T wave. The low T wave followed by a prominent U wave produces a ‘camel-hump’ effect.
In hypokalemia, the T wave is flattened and the prominent U wave may be mistaken for the T wave. This may falsely suggest prolongation of the Q-T interval, whereas it is actually the Q-U interval. Hypokalemia therefore causes pseudo-prolongation of the Q-T interval, at the expense of T wave. The U wave that is exaggerated and approximates the size of the T wave is considered to be a prominent U wave. Other causes of prominent U wave are cardiovascular drugs e.g. digitalis, quinidine and psychotropic agents e.g. phenothiazines, tricyclic antidepressants.
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