Palpitation pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akash Daswaney, M.B.B.S[2]

Palpitations are a nonspecific symptom that are often defined as a rapid disagreeable sensation/pulsation that may be momentary or sustained and regular or irregular. It is one thing to understand the pathophysiology of palpitations as a symptom and another to understand the pathophysiology of conditions that cause palpitations. Palpitations are hypothesized to be due to neural-afferent sensory pathways located at both cardiac and extracardiac levels. It may be caused due to abnormal adjustments in the rate, rhythm and contractility of the heart.

• Palpitations are a nonspecific symptom that are often defined as a rapid disagreeable sensation/pulsation that may be momentary or sustained and regular or irregular. In other words, it is an abnormal awareness of one’s own heartbeat which may or may not be associated with symptoms such as chest pain, breathlessness, presyncope/syncope, pedal edema or lightheadedness. ^[1]
• It is one thing to understand the pathophysiology of palpitations as a symptom and another to understand the pathophysiology of conditions that cause palpitations.
• Palpitations are hypothesized to be due to neural-afferent sensory pathways located at both cardiac and extracardiac levels. ^[2]
  • Subcortical areas (thalamus, amygdala) and the base of the frontal lobes are the brain centers that possibly receive information from peripheral mechanoreceptors/baroreceptors and receptors located on the pericardium and myocardium.
  • It may be caused due to abnormal adjustments in the rate, rhythm and contractility of the heart.
  • This may be due to anomalous movements of the heart (caused by structural heart diseases) or contractions of a normal heart which may be too rapid/slow, irregular or strong. ^[3]
  • Arrythmias are due to a disturbance of the normal conduction system of the heart (spontaneous depolarization cause impulses to travel from the SA node to the ventricles via the AV Node, Bundle of His and Purkinje fibres). ^[2]
  • Aging may also cause an increased risk of arrythmia development by causing the following changes; ^[4]
    1. Decreased number of pacemaker cells in the sinoatrial node.
    2. Decreased compliance of arteries
    3. Increased afterload
    4. Impaired filling of the left ventricle
    5. Prolonged availability of intracellular calcium
    6. Decreased responsiveness of beta adrenergic receptors
    7. Increased atrial dilation.
  • Systemic conditions such as hyperthyroidism may cause an increase in myocardial oxygen demand or alter cardiac pliability. Pheochromocytomas cause an excessive release of catecholamines.
  • Psychiatric conditions such as panic disorder and generalized anxiety disorder cause an activation of the autonomic nervous system. In these cases, a ‘fight or flight’ reaction may stimulate a series of responses that causes a patient to perceive their own heartbeat. This may be viewed as a pro-arrhythmogenic effect.
  • In the case of premature ventricular contractions, an ectopic beat is followed by a compensatory pause which causes an increase in end diastolic volume. As a result, the following sinus beat is associated with an increased stroke volume.^[5]