Chapter 70: Palpitations

Palpitations are an unpleasant awareness of the beating of the heart. By definition it does not always imply ‘racing’ of the heart but any sensation in the chest, such as ‘pounding’, ‘flopping’, ‘skipping’, ‘jumping’, ‘thumping’ or ‘fluttering’ of the heart. The problem requires careful attention and reassurance (if appropriate) because heartbeat is regarded as synonymous with life. To the practitioner it may simply represent anxiety or it could be a prelude to a cardiac arrest. In many circumstances prompt referral to a cardiologist is imperative.

A summary of the diagnostic strategy model is presented in TABLE 70.1, which includes significant causes of palpitations.

Probability diagnosis

If the palpitations are not caused by anxiety or fever, the common causes are sinus tachycardia and premature complexes/ectopics (atrial or ventricular). Sinus tachycardia, which by definition is a rate of 100–160/min, may be precipitated by emotion, stress, fever or exercise.

PSVT and atrial fibrillation are also quite common arrhythmias. Some cardiologists claim that the commonest arrhythmia causing a patient to visit the family doctor is the symptomatic ventricular ectopic beat.¹

Sinus tachycardia can be differentiated clinically from PSVT in that it starts and stops more gradually than PSVT (abrupt) and has a lower rate of 100–150 compared with 160–220.

Important causes of tachyarrhythmias are:

• ischaemic heart disease, especially acute coronary syndromes

• hypertension

• heart failure

• mitral disease

• thyrotoxicosis

• atrial septal deficit

Serious disorders not to be missed

It is vital not to overlook acute coronary syndromes as a cause of the arrhythmia manifesting as palpitations. About 25% of infarcts are either silent or unrecognised. Sinister life-threatening arrhythmias are:

• ventricular tachycardia

• atypical ventricular tachycardia (torsade de pointes)

• sick sinus syndrome (SSS)

• complete heart block

It is also important not to miss:

• hypokalaemia

• hypomagnesaemia

Pitfalls

There are many pitfalls in the diagnosis and management of arrhythmias, especially in the elderly, where symptoms of infection may be masked. Palpitations associated with the menopause can be overlooked. Valvular lesions, usually associated with rheumatic heart disease, such as mitral stenosis, and aortic incompetence may cause palpitations. The rare tumour, phaeochromocytoma, presents with palpitations and the interesting characteristic of postural tachycardia (a change of more than 20 beats/ min). The toxin from tick bites in dermatomes T1–5 can cause palpitations.

General pitfalls

• Misdiagnosing PSVT as an anxiety state

• Overlooking a cardiac arrhythmia as a cause of syncope or dizziness

• Overlooking atrial fibrillation (AF) in the presence of a slow heartbeat

• Overlooking mitral valve prolapse in a patient, especially a middle-aged woman presenting with unusual chest pains and palpitations (auscultate in standing position to accentuate click(s) ± murmurs)

Seven masquerades checklist

Surprisingly, all the masquerades have to be considered, either as direct or indirect causes: depression, especially with anxiety and in the postpartum period; diabetes, perhaps as an arrhythmia associated with a silent myocardial infarction or with hypoglycaemia; drugs as a very common cause (see TABLE 70.2); anaemia, causing a haemodynamic effect; hyperthyroidism; spinal dysfunction of the upper thoracic vertebrae T1–5; and urinary tract infection, especially in the elderly.

PSVT has been described as resulting from injury or dysfunction of the upper thoracic spine (especially T4 and T5) in the absence of organic heart disease.² The author has personally encountered several cases of PSVT alleviated by normalising function of the spine.

Psychogenic considerations

Emotional factors can precipitate a tachycardia, which in turn can exaggerate the problem in an anxious person. Some people have a cardiac neurosis, often related to identification with a relative or friend. A family history of cardiac disease can engender this particular anxiety. Evidence of anxiety and depression should be sought in patients presenting with palpitations without clinical evidence of cardiovascular disease.

Careful attention to basic detail in the history and examination can point the way clearly to the clinical diagnosis.

History

Ask the patient to describe the onset and offset of the palpitations, the duration of each episode and any associated features. Then ask the patient to tap out on the desk the rhythm and rate of the heartbeat experienced during the ‘attack’. If the patient is unable to do this, tap out the cadence of the various arrhythmias to find a matching beat.

An irregular tapping ‘all over the place’ suggests atrial fibrillation, while an isolated thump or jump followed by a definite pause on a background of a regular pattern indicates premature beats (ectopics/extrasystoles) usually of ventricular origin. The thump is not the abnormal beat but the huge stroke volume of the beat following the compensatory pause.

Key questions

• Do the palpitations start suddenly? How long do they last?

• What do you think brings them on?

• Are they related to stress or worry or excitement?

• What symptoms do you notice during an attack?

• Do you have pain in the chest or breathlessness during the attack?

• Do you feel dizzy or faint during the attack?

• What medications do you take?

• How much coffee, tea, Coke do you drink?

• Have you been using nasal decongestants?

• Did you eat Chinese food before the attack?

• Do you smoke cigarettes, and how many?

• Do you take any of the social drugs, such as cocaine or marijuana?

• Have you ever had rheumatic fever?

• Have you lost weight recently or do you sweat a lot?

Chest pain may indicate myocardial ischaemia or aortic stenosis; breathlessness indicates anxiety with hyperventilation, mitral stenosis or cardiac failure; dizziness or syncope suggests severe arrhythmias such as SSS and complete heart block, aortic stenosis and associated cerebrovascular disease.

Examination

The ideal time to examine the patient is while the palpitations are being experienced. Often this is not possible and the physical examination is normal. Measurement of the heart rate may provide a clue to the problem.

As a working guide, a rate estimated to be about 150 beats/minute suggests PSVT, atrial flutter/fibrillation or ventricular tachycardia (see FIG. 70.1). A rate less than 150 beats per minute is more likely to be sinus tachycardia, which may be associated with exercise, fever, drugs or thyrotoxicosis.³

Assess whether the pulse is regular or irregular. If irregular, the possible causes are ectopic beats, atrial fibrillation and atrial flutter with varying degrees of block.

The nature of the pulse, especially the pulse pressure and rhythm, should be carefully evaluated (see FIG. 70.2). Look for evidence of fever and infection and features of an anxiety state or depressive illness.

Have the patient hyperventilate for 3 minutes to determine whether the arrhythmia is induced. Evidence of underlying disease such as anaemia, thyroid disorder, alcohol abuse or cardiac disease including the JVP and pulmonary congestion should be sought. Also look for evidence of a mitral valve prolapse (mid-systolic click; late systolic murmur). Possible signs in the patient presenting with palpitations are shown in FIGURE 70.3.⁴

Investigations

The number and complexity of investigations should be selected according to the problem and test availability. A checklist would include:

• blood tests (for underlying disease):

  • – haemoglobin and film

  • – thyroid function tests

  • – serum electrolytes and magnesium

  • – serum digoxin ? digitalis toxicity

  • – virus antibodies ? myocarditis

• chest X-ray

• cardiac (ischaemia and function):

  • – ECG (12 lead)

  • – ambulatory 24-hour ECG monitoring

  • – echocardiography (to look for valvular heart disease and assess left ventricular function)

  • – electrophysiology studies

  • – exercise stress test (? underlying CAD)

  • – event monitor (can record up to 2 weeks)

  • – implantable monitor (may last 1 year)

Children may complain of palpitations which may be associated with exercise, fever or anxiety. Various arrhythmias can occur with three requiring special consideration—PSVT, heart block and ventricular arrhythmias.⁵

PSVT is characterised by beats at 200–300 per minute, the fastest rates occurring in infants. The cause is often not found but some children have ECG abnormalities compatible with the Wolff–Parkinson–White (WPW) syndrome. The recommended first-line treatment of PSVT is vagal stimulation via the application of ice packs to the upper face (forehead, eyes and nose) of the affected infant. Intravenous adenosine will usually terminate the episode.

A particular concern is these children who have the familial long QT syndrome. They are prone to develop ventricular tachyarrhythmias, which may lead to sudden death. Consider it in children developing syncope on exertion.

The older the patient, the more likely is the onset of palpitations due to cardiac disease such as myocardial infarction/ischaemia, hypertension, arrhythmias and drugs, especially digoxin. Occasional atrial and ventricular arrhythmias, especially premature complexes (ectopics), occur in 40% of old people⁶ and treatment is rarely required. Atrial fibrillation occurs in 5–10% of patients over 65 years of age, 30% of whom have no clinical evidence of cardiovascular disease. A rapid ventricular rate with symptoms is the only indication for digoxin in the elderly but beware of SSS, especially if dizziness or syncope accompanies the fibrillation.

In the elderly, thyrotoxicosis may present as sinus tachycardia or atrial fibrillation with only minimal signs—the so-called ‘masked thyrotoxicosis’—so it is easy to overlook it. The only clue may be bright eyes (‘thyroid glitter’) due to conjunctival oedema (see CHAPTER 23).

Facts and figures

• See FIGURE 70.4 for tracings of important arrhythmias.

• Cardiac arrhythmias account for about 25% of management decisions in cardiology (see TABLE 70.3)

• Commonest are premature (ectopic) ventricular beats and atrial fibrillation.

• PSVT is next most common—6 per 1000 of population.

• The commonest mechanism of paroxysmal tachycardias is re-entry (see FIG. 70.5).

• Electrophysiological studies are the gold standard investigation for tachycardias but are rarely needed for diagnosing most arrhythmias.

• Almost all antiarrhythmic drugs have a proarrhythmic potential (i.e. they may worsen existing arrhythmias or provoke new arrhythmias in some patients) (see TABLE 70.4). Always consider the no-treatment option.

• Sinus tachycardia is usually physiological. If no obvious cause, but the symptoms are troublesome, treat with a beta blocker or verapamil.¹⁰

• Avoid digoxin in cases with an accessory pathway.

• If ‘quinidine syncope’ occurs, consider torsade de pointes as the cause.

• Any patient commencing antiarrhythmic therapy should have a 12-lead ECG 1–2 weeks later to check the QT interval. If prolonged, treatment should usually be ceased.

• The two main indications for permanent pacemaking are SSS (only if symptomatic) and complete heart block.

Management strategies

• Treat the underlying cause.

• Give appropriate reassurance.

• Provide clear patient education.

• Explain about the problems of fatigue, stress and emotion.

• Advise moderation in consumption of tea, coffee, caffeine-containing soft drinks and alcohol.

• Advise about cessation of smoking and other drugs.

Sinus bradycardia

Look for causation (e.g. hypothyroidism and drugs). Correct the cause. Treatment is required only if symptomatic, which is uncommon at rates >40–45 beats/min. Use IV atropine if acute treatment is required. However, mild or transient bradyarrhythmias may be asymptomatic or even physiological, such as in a healthy athlete. Palpitations are not a feature but they can cause dizziness, fatigue or syncope (e.g. Stokes–Adams attack—transient bradycardia due to complete heart block).

Stokes–Adams attack

• Sudden onset without warning

• Patient falls to ground

• Collapse with loss of consciousness

• Pallor and still as if dead with slow or absent pulse

• Recovery—in seconds back to normal

• Patient flushes as pulse increases

• Refer for management as attacks may be recurrent

Premature (ectopic) atrial complexes

• These are usually asymptomatic.

• Management is based on reassurance.

• Check lifestyle factors such as excess alcohol, caffeine, stress and smoking; avoid precipitating factors.

• Treatment is rarely required and should be avoided if possible.

• At present there is no ideal anti-ectopic agent.

• They may be a forerunner of other arrhythmias (e.g. PSVT, atrial fibrillation).

• For intolerable symptoms give:⁶

  • atenolol or metoprolol 25–100 mg (o) daily

  • or

  • verapamil SR 160–480 mg (o) daily

Premature (ectopic) ventricular complexes

• These are also usually asymptomatic (90%).

• They occur in 20% of people with ‘normal’ hearts.

• Symptoms are usually noticed at rest in bed at night.

• Check lifestyle factors as for atrial premature beats.

• Drugs that can cause both types of premature beats include digoxin and sympathomimetics.

• Look for evidence of ischaemic heart disease, mitral valve prolapse (especially women), thyrotoxicosis and left ventricular failure.

• Ventricular premature complexes may be a forerunner of other arrhythmias (e.g. ventricular tachycardia).

• If symptomatic but otherwise well with a normal chest X-ray and ECG, reassure the patient.

• Drug therapy: never commence drug therapy without performing an echocardiograph. This will help to guide the choice of agent. Class 1 agents can make the arrhythmia worse or even life-threatening if there is reduced ventricular function. If this is the case, the patient should be referred to a cardiologist.

• For troublesome symptoms, the beta blockers atenolol or metoprolol can be used e.g. atenolol 25–100 mg (o) daily.

• SVT can be paroxysmal or sustained.

• Rate is 160–220/min.

• There are at least eight different types of SVT with differing risks and responses to treatment.

• PSVT commonly presents with a sudden onset in otherwise healthy young people.

• Passing copious urine after an attack is characteristic of PSVT.

• Look for predisposing factors such as an accessory pathway and thyrotoxicosis.

• Approximately 60% are due to atrioventricular (AV) node re-entry and 35% due to accessory pathway tachycardia (e.g. WPW).⁸

• Look for evidence of accessory pathways after reversion because accessory pathways can lead to sudden death (avoid digoxin in WPW).

• Consider SSS in a patient with SVT and dizziness.

Wolff–Parkinson–White syndrome

The structural basis for the arrhythmia of SVT in WPW syndrome is an accessory pathway that bypasses the AV node. A typical ECG shows a short PR interval and slurred upstroke of the QRS complex (delta wave). Patients are prone to sudden attacks of SVT. Up to 30% of patients will develop atrial fibrillation or flutter. Even one episode of PSVT requires consideration for radiofrequency ablation.⁹

Management of PSVT

1. Vagal stimulation can be attempted. Carotid sinus massage was the treatment of choice, but it has fallen out of favour because of the potential for stroke. A popular method is to blow hard into the end of an empty 20 mL plastic syringe to move the plunger. Other methods of vagal stimulation include:

   • Valsalva manoeuvre (easiest for patient)

   • self-induced vomiting

   • ocular pressure (avoid)

   • cold (ice) water to face or swallowing ice

   • immersion of the face in water

2. If vagal stimulation fails

   give adenosine IV (try 6 mg first over 5–10 seconds, then 12 mg in 2 minutes if unsuccessful, then 18 mg in 2 minutes if necessary and well tolerated). Second-line treatment is verapamil IV 1 mg/min up to 10–15 mg (provided patient is not taking a beta blocker).⁸

   Precautions

   • Adenosine causes less hypotension than verapamil but may cause bronchospasm in asthmatics

   • Use only if narrow QRS and BP >80 mm Hg

   • Carefully monitor blood pressure

   • AVOID verapamil if taking beta blockers

   and

   persistent tachycardia with QRS complexes >0.14 s (suggests ventricular tachycardia)

3. In the rare event of failure of medical treatment, consider DC cardioversion or overdrive pacing.

Prevention and maintenance

To prevent recurrences (frequent episodes) use at first atenolol or metoprolol, flecainide (only if no structural heart damage) or sotalol (second line). If these agents fail, consider amiodarone. Do an echocardiograph first to exclude structural heart disease. Radiofrequency catheter ablation, which is usually curative, is indicated for frequent attacks not responding to medical therapy.

Carotid sinus massage¹

Carotid sinus massage causes vagal stimulation and its effect on SVT is all or nothing. It has no effect on ventricular tachycardia. It slows the sinus rate and breaks the SVT by blocking AV nodal conduction.

In general, right carotid pressure tends to slow the sinus rate and left carotid pressure tends to impair AV nodal conduction. Never massage both sides simultaneously. As a rule, avoid this method and use one of the simpler alternatives.

Precautions

Avoid in the elderly (risk of embolism or bradycardia).

Ventricular tachycardia

Management requires special supervision.^9,10 It may be non-sustained, where drug treatment such as beta blockers and amiodarone may be used for symptomatic cases, or sustained, which may result in cardiac arrest. An implantable cardioverter defibrillator or radiofrequency catheter ablation may be used.

Torsades de pointes

This uncommon condition is potentially lethal as it may occasionally be prolonged or jump into ventricular fibrillation with sudden death. It is associated with disorders that prolong the QT interval. Treatment involves cessation of drugs that may prolong the QT interval, correcting electrolyte imbalance (especially potassium), cardiac pacing and IV magnesium sulphate.¹⁰

Atrial fibrillation

Facts and figures

• A common problem (9% incidence in the over-70 age group).

• It usually presents with an irregular ventricular rate of about 160–180 beats/minute in untreated patients with a normal AV node.

• Apart from acute AF (new onset <48 hrs), it tends to fall into one of the ‘three Ps’ patterns:

  • – paroxysmal AF: abrupt onset, spontaneous return to normal rhythm (lasts <48 hrs)

  • – persistent AF: abrupt onset, lasts >7 days

  • – permanent (chronic) AF: cannot be converted to normal rhythm

All types appear to have a similar risk for thromboembolism.

• Remember to look for the underlying cause: myocardial ischaemia (15% of cases), mitral valve disease, thyrotoxicosis, hypertension, pericarditis, cardiomyopathy including chronic alcohol dependence, alcohol binge.

• No cause is found in 12%—isolated^9,10 atrial fibrillation.

• All patients should have thyroid function tests and an echocardiograph to help find a cause.

• With sustained atrial fibrillation there is a 5% chance per annum of embolic episodes. There is a fivefold risk of CVA overall.

• The risk of CVA is greater in those with previous CVA, valvular heart disease, prosthetic mitral valve and cardiac failure.

• For reversion anticoagulate with warfarin for 4 weeks beforehand and maintain for 4 weeks afterwards.

• Digoxin controls the ventricular rate but does not terminate or prevent attacks.

• Sotalol, flecainide and amiodarone are used for conversion of atrial fibrillation and maintenance of sinus rhythm. Flecainide should never be prescribed in patients with reduced LV function.

• Evidence basis: RCTs showed that digoxin was beneficial for lowering the ventricular rate in the short term but no better than placebo in restoring rhythm. Beta blockers and calcium-channel antagonists benefited rate control but verapamil was much less effective than amiodarone at restoring cardiac rhythm.¹¹

Atrial flutter

The ECG of atrial flutter has a regular saw-tooth baseline ventricular rate of 150 with narrow QRS complexes. This is a 2:1 AV block. It is often misdiagnosed as SVT. Rarely, conduction occurs 1:1, giving a ventricular rate of 300/min.

Treatment for atrial fibrillation/flutter^8,9

To address rate and rhythm control and prevent stroke it is best to refer or consult a specialist. The treatment needs to control the arrhythmia either as the rate or the rhythm and also from the viewpoint of prophylaxis against thromboembolic complications. Paroxysmal or persistent atrial fibrillation confers a risk of thromboembolism similar to permanent atrial fibrillation.⁸ The AFFIRM study¹² confirmed that there was no statistically significant difference between the rate and rhythm of control groups. However, patients fare marginally better (in terms of mortality) with just rate control rather than trying to get them back into sinus rhythm if they are asymptomatic in atrial fibrillation.

Rate control

Aim for a rate <110/minute at rest.⁸

• verapamil 1 mg/min IV up to maximum 15 mg then orally

• or

• metoprolol 5 mg (1 mg/min) IV to max 20 mg (provided no evidence of heart failure and well-monitored BP)

• verapamil SR 160–480 mg (o) daily

• or

• diltiazem CR 180–360 mg (o) daily

• or

• atenolol or metoprolol 25–100 mg (o) bd

• Digoxin still has a place in the elderly, especially with cardiac failure:

• digoxin 0.0625–0.25 mg (o) daily according to age, plasma creatinine and digoxin level

Rhythm control

This should be considered if the patient is symptomatic and the arrhythmia is of recent onset—less than 6 months.

amiodarone or flecainide

If the rate cannot be well controlled despite maximal medical therapy, consider AV node ablation and a permanent pacemaker. Atrial fibrillation with a rapid ventricular response over a long period gradually causes left ventricular dysfunction.

This can be given for first-line treatment or for failed medical conversion.

(Refer to CHAPTER 131.)

The decision to use an oral anticoagulant or an antiplatelet agent (e.g. aspirin), especially in the younger patient, is difficult and should be made in consultation with a cardiologist. If aspirin is indicated, use:

• aspirin 100–300 mg (o) daily

• If oral anticoagulation is indicated, use:

• warfarin—start with a low dose (e.g. 2–4 mg) and maintain a relatively low INR of 2–3 with regular checks.

• or

• a direct-acting oral anticoagulant (DOAC)

• e.g. dabigatran

Apart from special rate-responsive pacemakers for bradycardia, there are several new modalities of treatment for complex arrhythmias, including means of blocking the re-entry phenomenon.

Surgery

Guided by electrophysiological monitoring, surgeons can dissect a small section of the AV ring to ensure that all aberrant connections between the atria and the underlying ventricular muscle are severed.

Catheter electrode ablation

Specific abnormal foci in the conducting pathways can be ablated using direct current electrical surgery or radiofrequency ‘burns’ via a catheter electrode. Radiofrequency ablation, which will probably supplant surgery as a form of treatment, is indicated for recurrent episodes of supraventricular tachycardia, accessory pathways and nodal re-entry tachycardia with success rates of up to 95%. Catheter ablation for atrial fibrillation is more complex and still evolving. Success rates at best are 60–80%.

Automatic implantable cardioverter defibrillator (AICD)

This expensive implant is the most effective therapy yet devised for the prevention of sudden cardiac death in patients with documented sustained ventricular tachycardia or fibrillation. Operative mortality should be less than 10%, after which survival at 1 year is over 90%. These new defibrillators incorporate an antitachycardia pacemaker. Patients can either be paced out of arrhythmia or, if they develop ventricular fibrillation, they can be defibrillated using higher energy.

TABLE 70.5 presents a summary of the treatment of arrhythmias.

Patients should be referred to a cardiologist¹² when:

• a sustained supraventricular tachycardia is suspected

• a sustained ventricular tachycardia is suspected

• an ECG shows sustained delta waves of WPW syndrome, even if asymptomatic

• syncope or dizziness suggests a cardiovascular cause

• a paroxysmal arrhythmia may be the cause of unexplained cardiovascular symptoms

• anticoagulation has to be considered

Hand-out sheets from Murtagh’s Patient Education 7th edition:

• Atrial fibrillation