The ECG in patients with palpitations and syncope

Initial assessment

The ECG is of paramount importance for the diagnosis of arrhythmias. Many arrhythmias are not noticed by the patient, but are still of clinical importance (e.g. atrial fibrillation). Symptoms, when they occur, are often transient, and the patient may be completely well at the time he or she consults a doctor. A baseline 12-lead ECG is a critical element of the initial assessment of anyone with suspected arrhythmia, but as always the history and physical examination are also extremely important. The main purpose of the history and examination is to help decide whether a patient’s symptoms could be the result of an arrhythmia, and whether the patient has a cardiac or other disease that may cause an arrhythmia.

The clinical history and physical examination

Palpitations

‘Palpitations’ mean different things to different patients, but a general definition would be ‘an awareness of the heartbeat’. Arrhythmias, fast or slow, can cause poor organ perfusion and so lead to syncope (a word used to describe all sorts of collapse), breathlessness and angina. Some rhythms can be identified from a patient’s description, such as:

• A patient recognizes sinus tachycardia because it feels like the palpitations that he or she associates with anxiety or exercise.
• Extrasystoles are described as the heart ‘jumping’ or ‘missing a beat’. It is not possible to distinguish between supraventricular and ventricular extrasystoles from a patient’s description, although they can be differentiated from an ECG.

• A true pathological tachyarrhythmia such as an atrioventricular (AV) nodal re-entry tachycardia begins suddenly and sometimes stops suddenly. The heart rate is often ‘too fast to count’. Severe attacks are associated with dizziness, breathlessness and chest pain (Table 2.1).

TABLE 2.1

Diagnosis of Sinus Tachycardia or a Pathological Tachycardia From a Patient’s Symptoms
Symptoms	Sinus tachycardia	Pathological tachycardia
Timing of initial attack	Attacks probably began recently	Attacks probably began in teens or early adult life
Associations of attack	Exercise, anxiety	Usually no associations, but occasionally exercise-induced
Rate of start of palpitations	Slow build-up	Sudden onset
Rate of end of palpitations	‘Die away’	Classically sudden, but often ‘die away’
Heart rate	< 140 bpm	> 160 bpm
Associated symptoms	Paraesthesia due to hyperventilation	Chest pain Breathlessness Dizziness Syncope
Ways of terminating attacks	Relaxation	Breath holding } in some arrhythmias Valsalva’s manoeuvre}

Dizziness and syncope

These symptoms may have a cardiovascular or a neurological cause. Remember that cerebral hypoxia, however caused, may lead to a seizure, and that can make the differentiation between cardiac and neurological syncope very difficult. Syncope is defined as ‘a transient loss of consciousness characterized by unresponsiveness and loss of postural tone, with spontaneous recovery and not requiring specific resuscitative intervention’.

Fig. 2.1 shows an EEG that was being recorded in a 46-year-old woman with episodes of limb shaking, suspected of being generalized tonic–clonic seizures. She lost awareness during events, and had violent limb shaking for several seconds as she came round. She felt nauseated, but was rapidly reoriented. By chance, she had one of her ‘attacks’ while her EEG was being recorded, and from the ECG being routinely recorded in parallel, it became clear that the problem was not seizures, but periods of asystole – in this case lasting about 15 s. The numbered arrows in Fig. 2.1 mark significant features. The recording begins with a routine period of hyperventilation, with the EEG showing an eye-blink in the anterior leads and the ECG showing sinus rhythm. There are then (at arrow 1 on the record) one (or possibly two) ventricular extrasystoles, followed by a narrow complex beat (probably sinus) and another ventricular extrasystole, with a different configuration from the previous ones. Asystole follows, and after 7–8 s (at arrow 2) there is global EEG slowing, and the patient became unresponsive. After 4 s (at arrow 3), there is global attenuation (reduction in signals) in the EEG and after another 3 s, there is an escape beat whose morphology suggests a ventricular origin. This is followed by a beat with a narrow QRS complex and possibly an inverted T wave, and then there is gross artefact due to the ECG lead being checked. During that period, sinus rhythm was restored. There was then (at arrow 4) global EEG slowing for 5 s, followed by (at arrow 5) violent limb thrashing for about 12 s as the patient regained consciousness – these movements were not clonic, and were thought to represent anxiety or fear. Normal EEG and ECG activity were then resumed (at arrow 6).

Fig. 2.1 EEG recorded during a syncopal attack

Note

• EEG and ECG lead I (lower trace)

• Paper speed five times normal ECG speed

• (a) Sinus rhythm at about 70 bpm, ventricular extrasystoles interrupted by one narrow complex beat, then asystole

• (b) Asystole followed by an escape beat, a narrow complex beat and gross artefact

• (c) Sinus rhythm restored, with a period of limb thrashing before resumption of a normal record
Courtesy of Dr A. Michell, Addenbrooke’s Hospital, Cambridge

Some causes of syncope are summarized in Box 2.1.

Box 2.1

Cardiovascular Causes of Syncope

Obstructed blood flow in heart or lungs

• Aortic stenosis
• Pulmonary embolus
• Pulmonary hypertension
• Hypertrophic cardiomyopathy
• Pericardial tamponade
• Atrial myxoma

Arrhythmias

• Tachycardias: patient is usually aware of a fast heartbeat before becoming dizzy
• Bradycardias: slow heart rates are often not appreciated. A classical cause of syncope is a Stokes–Adams attack, due to a very slow ventricular rate in patients with complete heart block. A Stokes–Adams attack can be recognized because the patient is initially pale but flushes red on recovery

Postural hypotension, occurring immediately on standing

Seen with:

• Loss of blood volume
• Autonomic nervous system disease (e.g. diabetes, Shy–Drager syndrome, amyloid neuropathy)
• Patients being treated with antihypertensive drugs

Neurally mediated reflex syncopal syndromes

• Vasovagal (neurocardiogenic) (simple faints)
• Situational (e.g. after coughing, sneezing, gastrointestinal stimulation of various sorts, post-micturition)
• Carotid sinus hypersensitivity

Table 2.2 shows some clinical features of syncope, and possible causes.

TABLE 2.2

Diagnosis of Causes of Syncope
Symptoms and signs	Possible diagnosis
Family history of sudden death	Long QT syndrome, Brugada syndrome, hypertrophic cardiomyopathy
Caused by unpleasant stimuli, prolonged standing, hot places (situational syncope)	Vasovagal syncope
Occurs within seconds or minutes of standing	Orthostatic hypotension
Temporal relation to medication	Orthostatic hypotension
Occurs during exertion	Obstruction to blood flow (e.g. aortic stenosis, pulmonary hypertension)
Occurs with head rotation or pressure on neck	Carotid sinus hypersensitivity
Confusion for more than 5 min afterwards	Seizure
Tonic–clonic movements, automatism	Seizure
Frequent attacks, usually unobserved, with somatic symptoms	Psychiatric illness
Symptoms or signs suggesting cardiac disease	Cardiac disease

Physical examination

If the patient has no symptoms at the time of the examination, look for:

• evidence of any heart disease that might cause an arrhythmia
• evidence of non-cardiac disease that might cause an arrhythmia
• evidence of cardiovascular disease that might cause syncope without an arrhythmia
• evidence (from the history or examination) of neurological disease.

It is only possible to make a confident diagnosis that an arrhythmia is the cause of palpitations or syncope if an ECG recording of the arrhythmia can be obtained at the time of the patient’s symptoms. If the patient is asymptomatic at the time of examination, it may be worth arranging for an ECG to be recorded during an attack of palpitations, or for a period of continuous ‘ambulatory’ ECG monitoring (see Ch. 3), in the hope that an episode of the arrhythmia will be detected.

The ECG

Even when the patient is asymptomatic, the resting 12-lead ECG can be very helpful, as summarized in Table 2.3.

TABLE 2.3

ECG Features Between Attacks of Palpitations or Syncope
ECG appearance	Possible cause of symptoms
ECG completely normal	Symptoms may not be due to a primary arrhythmia – consider anxiety, epilepsy, atrial myxoma or carotid sinus hypersensitivity
ECGs that suggest cardiac disease	Left ventricular hypertrophy or left bundle branch block – aortic stenosis Right ventricular hypertrophy – pulmonary hypertension Anterior T wave inversion – hypertrophic cardiomyopathy
ECGs that suggest intermittent tachyarrhythmia	Left atrial hypertrophy – mitral stenosis, so possibly atrial fibrillation Pre-excitation syndromes Long QT syndrome Flat T waves suggest hypokalaemia Digoxin effect – ?digoxin toxicity
ECGs that suggest intermittent bradyarrhythmia	Second degree block First degree block plus bundle branch block Digoxin effect

Syncope due to cardiac disease other than arrhythmias

The ECG may indicate that syncopal attacks have a cardiovascular cause other than an arrhythmia.

ECG evidence of left ventricular hypertrophy or of left bundle branch block may suggest that syncope is due to aortic stenosis. The ECGs in Figs 2.2 and 2.3 were recorded from patients who had syncopal attacks on exercise due to severe aortic stenosis.