Dr. Enrique Asensio-Lafuente
As for any other cardiovascular symptom, palpitations must be carefully analysed when examining a patient. History taking will seek to uncover onset, termination, duration, contextual period(s), triggers, and whether palpitations are associated with signs and symptoms of a low cardiac output. Review here how to address the potential findings of the ten questions to include in anamnesis. Physical examination will follow. Important aspects regarding the timing of examination, arterial and jugular pulse, heart sounds and systolic blood pressure will also be reviewed for the reader.
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.
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.
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 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:
Whether the episodes have begun in childhood, the presence of premature ventricular contractions, or patters indicative of concomitant conditions are elements to look for.
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.
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.
The duration of the episode may be indicative of sustained tachycardia, isolated premature beats, that would cause susceptibility to tachycardiomyopathy or hemodanymic instability.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Here are the main elements to keep in mind when approaching a patient with palpitation:
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.
Dr. Enrique Asensio-Lafuente MDCardiology-ElectrophysiologyHead, Internal Medicine DepartmentHospital Medica TEC-100Queretaro, MexicoMember of the Sociedad Mexicana de Electrofisiología y Estimulación Cardiaca, Sociedad Española de Cardiología/European Society of Cardiology, Member of the Heart Rhythm Society, Ex-Fellow, Arrhythmia unit, Hospital Clinic, Barcelona, Spain.Author’s disclosures: None declared.
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