Paroxysmal tachycardias: How to address the clinical presentation of a patient with palpitations/tachycardia – Third in series

Background

Palpitations are a common symptom that should be carefully addressed in every patient. They are usually defined as the subjective perception of a faster, stronger and/or irregular heartbeat. This abnormal situation is usually associated with anxiety and the sensation that something serious is happening to the patient’s heart. Since there are many reasons that can cause palpitations, this symptom has to be taken seriously and be thoroughly explored before reaching a conclusion. On the other hand, there are many different arrhythmias that show similar clinical features, making the use of an electrocardiographic recording method a central diagnostic tool (1).
Many patients may have premature beats, but others may have non-sustained or sustained tachycardia: these patients will need to be approached in a correct and timely manner to avoid any serious complication.
In this context of complex symptoms, a thorough history, physical exam and an electrocardiogram (ECG) are needed to define the best diagnostic approach and to decide if the patient will need an early invasive approach. The present work addresses the clinical presentation but does not include the electrocardiographic analysis. 

I – History taking

As in any other clinical situation, a meticulous history is useful for diagnosis. Symptoms need to be analysed on a patient to patient basis, since the description of symptoms is usually heterogeneous. (2) General characteristics of the patient can suggest the origin of the palpitations. (3) Age, palpitations onset and gender can be clues to defining the possible arrhythmias that produce the symptom.

• Men with episodes of sustained tachycardia having begun during childhood might have a congenital condition such as an accessory pathway (overt or concealed).
• Young women that begin with paroxysmal tachycardias at the end of their adolescence or in their early adulthood might have atrio-ventricular node re-entry.
• Older patients must be evaluated for structural heart disease and ventricular tachycardias, although the most common arrhythmia in this group is atrial fibrillation.

Taking a history of heart disease is important because the presence of a structural heart disease is associated with higher risk of sudden cardiac death.

• A patient in his sixties with a history of myocardial infarction and palpitations must be assessed as soon as possible to look for a ventricular arrhythmia.
• A younger subject with a history of congenital heart disease must also be checked for ventricular arrhythmias but he might also have an accessory pathway that can be associated with an Ebstein’s anomaly, for example.

A family history of sudden cardiac death or syncope can work toward a diagnosis of long or short QT, Brugada syndrome and other channelopathies as well as other congenital cardiomyopathies that can manifest in a familial pattern.
The palpitation episode itself needs to be carefully explored. The answers to ten questions are important in order better understand the arrhythmia and its underlying mechanism. These data can point to an aetiological explanation of the symptom. The questions to ask patient are:

1. For how long have these palpitations been happening? How often do they appear?
2. How do the palpitations start? How do they stop?
3. How long do they last?
4. Is there any “timetable” or trigger for the arrhythmia?
5. Are they rapid, and if so how rapid? Are they strong?
6. Do the palpitations appear in a regular pattern or are they irregular?
7. Where does the patient feel the palpitations?
8. Do the palpitations provoke light-headedness or loss of consciousness?
9. Do they cause other symptoms such as chest pain or breathlessness
10. Do the palpitations generate hemodynamic instability?

1) For how long have the palpitations been happening? How often do they appear?

Whether the episodes have begun in childhood, the presence of premature ventricular contractions, or patters indicative of concomitant conditions are elements to look for.

• Episodes having begun in childhood: An arrhythmia that has been occurring since childhood in an adult subject is probably “benign” and well-tolerated, although the possibility of developing a tachycardiomyopathy must be considered when the episodes are frequent. (4) Most of the arrhythmias beginning in childhood are supraventricular unless there is a family history of sudden cardiac death or a congenital heart disease. If this is the case, there is a need to search for cardiomyopathies and channelopathies as well as pulmonary artery hypertension or chronic complications of a congenital heart disease.
• Premature ventricular contractions: Arrhythmias that we had traditionally considered “benign”, such as the right ventricular outflow tract (RVOT) premature ventricular contractions (PVC), are known today as inducing cardiomyopathy and ventricular dysfunction when the PVC burden is higher than 20% of the recorded beats on a Holter ECG (precise thresholds are still controversial). (5) Long term palpitations in this context correspond most of the time to some form of arrhythmia such as supraventricular or ventricular premature contractions, accessory pathway-mediated atrio-ventricular reentries, atrio-ventricular node re-entry or focal atrial tachycardias.
• Concomitant conditions: Tachycardias or palpitations might be affected by conditions that modify the autonomic drive, so they might be more frequent when the patient has another condition or illness such as infection, surgical procedure, pregnancy or other stressors that increase catecholamine levels.
  In this setting, the patient might notice some temporary pattern as well as changing frequency in the episodes. Certain conditions such as ventricular tachycardias occurring in the Brugada syndrome are prone to appear during sleep because of the vagal modulation of the refractory periods of the right ventricle epicardium and endocardium. (6,7)

It is a common perception that tachycardia episodes become more frequent with the passage of time, but there is no clear evidence to support this belief. It has been found that a small subset of subjects might even lose conduction in an accessory pathway over the course of their lifetime, for example.

2) How do the palpitations start? How do they stop?

The pattern of initiation and termination of the arrhythmia is an important clue to distinguish between re-entrant arrhythmia and abnormal automaticity. (8) That and structural heart disease or channelopathy, liver and kidney function, or co-administration of other drugs will help decide on the class of anti-arrhythmic drug to use. The type of sinus tachycardia (appropriate or not) and AV node involvement are also elements to potentially uncover.

• Re-entrant arrhythmia: A re-entrant arrhythmia will have an abrupt initiation, many times with the sensation of a pounding chest or a palpitation that initiates the tachycardia. Since the re-entry needs another premature beat or change of physiology to depolarise the excitable gap of the re-entry circuit in order to terminate the tachycardia, the end of the tachycardia will also be abrupt.
• Abnormal automaticity: The patient needs to be very attentive to his or her arrhythmia in order to differentiate between abrupt onset related to a palpitation and abrupt onset that is unrelated to a palpitation, and to perceive whether there is an acceleration or a slowing of the arrhythmia. Real life practice shows it is very difficult to distinguish re-entry from abnormal automaticity.
• Choice of medication: While waiting for the results of an electrophysiological study or an ablation to be performed, identifying the mechanism of the arrhythmia can be helpful in deciding what class of anti-arrhythmic drug to use. Other aspects such as the presence or not of a structural heart disease or channelopathy, liver and kidney function, co-administration of other drugs, etc. are all elements to consider as well.
• Sinus tachycardia: A common finding in anxious subjects is sinus tachycardia. These patients might describe their arrhythmia as a progressive acceleration and reduction in heart rate. Whether it is inappropriate or appropriate will be defined by both the context associated to its onset and other tests. The final diagnosis of inappropriate sinus tachycardia is not always straight-forward, but it is clinically different from the abrupt beginning of a re-entry or an automatic focus. (9)
• AV node involvement: A relevant question in this regard could be if the patient did something to end the tachycardia such as a Valsalva manoeuvre or any other vagal stimulation (carotid massage, vomiting). If the tachycardia is terminated by such an intervention, the AV node is probably involved in the arrhythmia circuit.

3) How long do the palpitations last?

The duration of the episode may be indicative of sustained tachycardia, isolated premature beats, that would cause susceptibility to tachycardiomyopathy or hemodanymic instability.

• Sustained tachycardia: A sustained tachycardia (more than 30 seconds) is usually symptomatic and significant (ventricular or supraventricular). Symptoms such as diaphoresis, dizziness, or even syncope might appear as a manifestation of a low cardiac output due to the short diastolic intervals. If not treated promptly, sustained arrhythmias are capable of inducing tachycardiomyopathy but most importantly and in the case of an acute presentation, sustained tachycardias are liable to cause hemodynamic instability. The susceptibility to instability will be determined by the baseline ventricular function and other co-morbidities such as heart valve, coronary or other myocardial diseases. Atrial fibrillation, however is an exception in that it can be tolerated for years be it with physiological complications but without major symptoms. (10)
• Isolated premature beats: An isolated premature beat will not cause immediate deterioration of the ventricular function, nevertheless, some patients might describe an instantaneous chest pounding or strong heartbeat preceded by a pause or related to a pause, appearing repeatedly at irregular intervals for long periods at a time. This is a characteristic description of premature beats. The diastolic interval prior to the premature beat is short and thus the ventricular end-diastolic volume is reduced, giving the sensation of a pause or “missed beat”. The compensatory pause after the premature beat results in a higher end-diastolic volume for the next normal beat that will be felt as a momentary strong palpitation. When these premature beats are frequent or noticed by the patient, they produce anxiety and they are commonly a reason to look for medical assistance. As mentioned earlier, premature ventricular beats occurring for a long period and representing a significant arrhythmia burden, have to be considered as potentially inducing a tachycardiomyopathy. This issue has been addressed in recent works as a case indication for ablation. (5,11)

4) Is there any “timetable” or trigger for the arrhythmia?

Caffeine intake or exercise or stress related elements, electrophysiologic variables related to congenital long QT syndromes or anti-arrhythmic drugs are to be looked for as potential triggers.

• Common triggers: Some patients are able to identify specific triggers or conditions that can induce the tachyarrhythmia. It is important to ask about caffeine consumption, cola refreshments or “energy” drinks, but also about exercise-related, stress-related triggers.
• Congenital long QT syndromes: Autonomic modulation of might also explain certain patterns. In this regard, some patients with congenital long QT syndromes might experience tachycardia related to exercise, auditory stimuli or emotional stress. It is important not only to ask the patient about these features, but also recommend patient that they be avoided until an effective therapy can be initiated.
• Anti-arrhythmic drugs: The pro-arrhythmic effects of anti-arrhythmic drugs are well known and usually monitored. It is also common to associate palpitations to decongestants and bronchodilators, but it is less frequent to think about antihistamine drugs and some combinations such as antibiotics with decongestants or H1 blockers, and antipsychotics for example. These agents are known to prolong the QT interval and are associated with a higher risk of ventricular tachycardia. It is recommended to check the specialised data banks to have up-to-date information regarding the QT-prolonging drugs, as well as other pro-arrhythmic combinations. (12)

   5) Are the palpitations rapid, and if so, how rapid? Are they strong?

Asking a patient whether palpitations are fast or strong, where they originate, whether there is a slow neck vein pounding, may point to AV node re-entrant tachycardia, atrio-ventricular dissociation in a tachycardia or atrio-ventricular block with A-V dissociation.

• AV node re-entrant tachycardia: Sometimes, patients are concerned about a strong pounding in the chest or neck. That symptom might be related to hypertension or to some arrhythmia. When the patient mentions this, it is important to differentiate between “fast” and “strong” palpitations. Fast palpitations usually are due to some sort of tachycardia, if they are strong as well it is important to ask for their location, since the patient might be describing a “frog sign”. Patients might describe a strong pounding in the neck as a result of jugular “cannon waves” that result from the atrial contraction against a closed atrio-ventricular valve. This is common in AV node re-entrant tachycardia, were the jugular beating is also visible to the observer (the “frog sign”). (13-15)
• Atrio-ventricular dissociation in a tachycardia: The presence of a relatively “slow” neck vein pounding with fast arterial pulse might suggest atrio-ventricular dissociation in a tachycardia.
• Atrio-ventricular block with A-V dissociation: A strong but within a “normal rate” palpitation might be related to anxiety, hypertension or other causes, but not necessarily to an arrhythmia. When this symptom occurs in the presence of a slow heart rate, searching for an atrio-ventricular block with A-V dissociation is mandatory.

The heart rate has been used as an indication of the probable arrhythmia, for example to differentiate between an A-V node re-entrant tachycardia and an atrio-ventricular re-entry. It is now known that there is considerable overlap between the cycle lengths of different tachycardias, making the heart rate a rather non-specific feature.

6) Do the palpitations appear in a regular pattern or are they irregular?

A distinctive feature of atrial fibrillation is the sensation of uneven or irregular heartbeat. Other arrhythmias might be referred as fast but regular heartbeats.

The premature beats might also induce the sensation of irregular heartbeat, but unless they appear in bursts, they will be of very short duration. (16)

Sometimes it can be useful to ask the patient to “reproduce” the arrhythmia tapping in a surface so the description is more accurate and the comprehension of the symptom easer.

7) Where does the patient feel the palpitations?

The sensation of palpitations in the neck and the presence of “frog sign” or visible palpitations in the neck in the context of a sudden onset tachycardia, in a young woman, with tachycardia episodes beginning in late adolescence strongly suggests an AV node re-entrant tachycardia. This sort of palpitation can be also be felt in the epigastrium. It must be kept in mind that the symptoms related to tachyarrhythmia are very subjective and anxiety-related in many cases.

8) Do the palpitations provoke light headedness or loss of consciousness?

In some settings, the presence of light-headedness or syncope has been used to presume the ventricular origin of a tachycardia. As with heart rate during tachycardia however, the presence of light-headedness or syncope and ventricular origin do not show a good diagnostic correlation.
The low cardiac output state induced by the tachycardia, even in a structurally normal heart, might compromise not only the organ perfusion pressure itself, but also the autonomic regulation of regional blood flows. Other phenomena such as the release of atrial natriuretic peptide as a result of increased atrial pressure could reduce the plasma volume, even if it might be only one of the multiple phenomena to explain hypotension in a patient with tachycardia.
A syncope induced by an arrhythmia usually has a rapid onset and no previous symptoms, although some patients might feel palpitations prior to the loss of consciousness. Syncope in subjects with depressed ventricular function is usually a marker of a bad prognosis. (17)
These symptoms suggest that there is a rapid tachycardia that compromises cerebral perfusion, but they do not allow to make any assumption as to the origin of the arrhythmia.

9) Do the palpitations induce other symptoms such as chest pain or breathlessness?

Patients with rapid heart rates and secondary hypotension might experience chest pain as a result of increased oxygen consumption in the myocardium and a deficiency in coronary perfusion pressure. The imbalance between oxygen demand and availability might be present even in a patient without coronary heart disease, although the chest pain might prompt a search for myocardial ischemia if the patient has known risk factors. A tachycardia able to induce angina is possibly related to a high ventricular rate.
Breathlessness is also a common symptom that might be related to the heart rate itself during an episode of tachycardia. In subjects with left ventricle dysfunction (systolic or diastolic), the short diastolic intervals can increase end-diastolic pressure and thus increase pulmonary capillary pressure.

These two symptoms might be aggravated if the patient has myocardial ischemia or other cardiomyopathies.

10) Do the palpitations generate hemodynamic instability?

Patients with low ventricular ejection fraction usually have very little tolerance for high heart rates. Thus a tachycardia (ventricular or supraventricular) might induce an early drop in cardiac output and symptoms of hemodynamic instability such as hypotension, low urinary output and altered mental status or loss of consciousness
It is a well described phenomenon that new-onset atrial fibrillation induces symptomatic heart failure in compensated patients with a low left ventricular ejection fraction. Patients with a structurally normal heart can also experience low output symptoms when the arrhythmia is very rapid (supraventricular) or ventricular, but they might tolerate such high ventricular rates without major symptoms until there is tachy-cardiomyopathy.

II - Physical examination

Timing of exam, arterial pulse, jugular pulse, heart sounds and systolic blood pressure are the parameters to assess in the physical examination of a patient with palpitations.

1) Timing of exam

A physical exam in periods between episodes of palpitations will probably not show any significant findings in a patient with a normal heart. Patients with heart disease might show the clinical data consistent with their condition. It is thus important to perform the exam even if the patient has no tachycardia at that moment. Patients might show signs and symptoms of other systemic diseases that could explain the presence of the arrhythmias, such as thyroid disease and many other conditions. Specific findings are likely to suggest the origin of the arrhythmia, and the ECG should be considered as a part of that examination.
If the patient seeks medical attention during an on-going tachycardia, an immediate ECG is mandatory, except perhaps in cases with an obvious life-threatening condition.

2) Arterial pulse

The arterial pulse will be rapid during a tachycardia, although its intensity and regularity may be variable according to the underlying arrhythmia. Atrial fibrillation and atrial flutter with variable A-V conduction will show an irregular pulse. These arrhythmias will be related to changes in the pulse intensity according to the diastolic intervals and left ventricular preload. Rapid tachycardias with low cardiac output might show low pulse amplitude because the ventricle’s preload is deficient owing to short diastolic intervals.
Patients with premature beats might show pauses corresponding to the premature beat itself and the compensatory pause in peripheral pulses, but the central pulses will probably show a low intensity pulse wave corresponding to the premature beat. Some authors mention that premature atrial beats will show short pauses, difficult to distinguish from a normal RR interval because the compensatory pause is incomplete, while the ventricular premature beat will induce a longer pause because of the full compensatory pause.

3) Jugular pulse

The presence of prominent a waves or “cannon waves” has already been discussed when in the presence of an A-V node re-entrant tachycardia or an accessory pathway-mediated tachycardia (i.e the “frog sign”). The absence of the “a” wave and “x” down slope might suggest atrial fibrillation, as well as an irregular neck vein pulsation.

4) Heart sounds

The auscultation can show changes in the first sound’s intensity in the presence of atrial fibrillation. The first sound in the mitral area might be louder when there is normal ventricular function and a short PR interval.

5) Systolic blood pressure

As is the case with arterial pulse, systolic blood pressure might change on a beat-to-beat basis in the presence of atrial fibrillation and variable conduction atrial flutter. Ventricular tachycardias usually are associated with a reduction in blood pressure, but as discussed earlier, supraventricular tachycardias might also show this.

Conclusions

Here are the main elements to keep in mind when approaching a patient with palpitation:

• As for any other cardiovascular symptom, palpitations must be carefully addressed.
• The history should include key questions as to how do the palpitations begin and terminate, how long do they last, over what period have they been happening, are there any triggers, and if they are associated with signs and symptoms of a low cardiac output.
• The diagnostic accuracy of the palpitation characteristics and the signs related to them is low, but these are important features that together allow a better selection of diagnostic tools and therapeutic strategies.

Further to a thorough interrogation about the symptoms and phenomena that are associated with the tachycardia, an adequate physical exam will be necessary in which the timing of the examination, arterial pulse, jugular pulse, heart sounds and systolic blood pressure will be factors to consider.

In all, this initial approach is likely to lack in diagnostic precision, but it may suggest an origin of the tachycardia, allow for a better understanding of the arrhythmia mechanisms, and help to better define the final diagnostic and therapeutic approach that will improve patient safety and lead to effective therapy in all timeliness.