HEADACHE AND DIZZINESS

 A 75-year-old man is brought to hospital with an episode of dizziness. He still feels unwell when he is seen 30 min after the onset. He was well until the last 6 months, since when he has had some falls, irregularly

On some occasions he lost consciousness and is unsure how long he has been unconscious. On a few occasions he has fallen, grazing his knees, and on others he has felt dizzy and has had to sit down but has not lost consciousness. These episodes usually happened on exertion, but once or twice they have occurred while sitting down. He recovers over 10–15 min after each episode.

He lives alone and most of the episodes have not been witnessed. Once his granddaughter was with him when he blacked out. Worried, she called an ambulance. He looked so pale and still that she thought that he had died. He was taken to hospital, by which time he had recovered completely and was discharged and told that he had a normal electrocardiogram (ECG) and chest X-ray.

There is no history of chest pain or palpitations. He has had gout and some urinary frequency. A diagnosis of benign prostatic hypertrophy has been made for which he is on no treatment. He takes ibuprofen occasionally for the gout. He stopped smoking 5 years ago. He drinks 5–10 units of alcohol weekly. The dizziness and blackouts have not been associated with alcohol. There is no relevant family history. He used to work as an electrician.

Examination

He is pale with a blood pressure of 96/64 mmHg. The pulse rate is 33/min, regular. There are no heart murmurs. The jugular venous pressure is raised 3 cm with occasional rises. There is no leg oedema; the peripheral pulses are palpable except for the left dorsalis pedis. The respiratory system is normal.

 

Questions •

What is the cause of his blackout? 

What does the ECG show?

Explanation : 

The blackouts do not seem to have had any relationship to posture. They have been a mixture of dizziness and loss of consciousness. The one witnessed episode seems to have been associated with loss of colour. This suggests a loss of cardiac output usually associated with an arrhythmia. This may be the case despite the absence of any other cardiac symptoms. There may be an obvious flushing of the skin as cardiac output and blood flow return.

The normal ECG and chest X-ray when he attended hospital after an episode do not rule out an intermittent conduction problem. On this occasion the symptoms have remained in a more minor form. The ECG shows third-degree or complete heart block. There is complete dissociation of the atrial rate and the ventricular rate which is 33/min. The episodes of loss of consciousness are called Stokes–Adams attacks and are caused by self-limited rapid tachyarrhythmias at the onset of heart block or transient asystole. Although these have been intermittent in the past he is now in stable complete heart block and, if this continues, the slow ventricular rate will be associated with reduced cardiac output which may cause fatigue, dizziness on exertion or heart failure. Intermittent failure of the escape rhythm may cause syncope.

On examination, the occasional rises in the jugular venous pressure are intermittent ‘cannon’ a-waves as the right atrium contracts against a closed tricuspid valve. In addition, the intensity of the first heart sound will vary.

The treatment should be insertion of a pacemaker. If the rhythm in complete heart block is stable then a permanent pacemaker should be inserted as soon as this can be arranged. This should be a dual-chamber system pacing the atria then the ventricles (DDD, dual sensing and pacing, triggered by atrial sensing, inhibited by ventricular sensing) or possibly a ventricular pacing system (VVI, pacing the ventricle, inhibited by ventricular sensing). If there is doubt about the ventricular escape rhythm then a temporary pacemaker should be inserted immediately.