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Mr. KH is a 53 year old gentleman who was admitted to A & E after a minor traffic accident. He sustained no traumatic injuries, and his main concern was the event preceding accident, which was a complete loss of consciousness. He had never experienced such loss of consciousness before, and he was not fatigued nor confused upon wakening. He had complete memory of events prior to the syncope, and presented with no chest pain, nausea, palpitations, nor sweating pre and post syncope.
The only precipitating factor was excessive cough, which had onset 5 weeks ago. Mr. KH has significant cardiac history of 2 Percutaneous Transluminal Coronary Angioplasty in 1991 and 1994, and had suffered Myocardial Infarction in 1999, after which a stent was placed. The review of systems did not reveal any neurological abnormalities and history of epilepsy, and physical examination showed regular strong pulse at 60 bpm and blood pressure of 150/90. ECG examination failed to show AV block, arrhythmia, and long Q-T interval.
The differential diagnosis of cough syncope was made based on patient’s history and elimination of other probable causes, including: cerebrovascular causes such as stroke, tumor, or intracranial haemorrhage, and cardiovascular causes such as arrhythmia or myocardial infarction. Mr. KH’s presentation during the attack was also consistent with criteria and symptoms of situational syncope, specifically cough syncope. Syncope is classified according to its suspected pathophysiology as follows: ?
Neurally-mediated reflex syncopal syndrome referring to a reflex that, when triggered, gives rise to vasodilation and bradykardia (1) ? Orthostatic syncope occurring when the autonomic nervous system is incapacitated resulting in a failure of vasoconstrictor mechanisms and thereby in orthostatic hypotension (1) ? Cardiac arrhythmias causing a decrease in cardiac output (1) ? Structural heart disease causing syncope when circulatory demands outweigh the impaired ability of the heart to increase its output (1) ?
Steal syndrome causing syncope when a blood vessel has to supply both part of the brain and an arm (1) Neurally-mediated reflex syncopal syndrome is the most common type (3) and is further subdivided, based on their causes, into vasovagal faint (common faint) and carotid sinus syncope including situational faint, acute haemorrhage, cough, sneeze, gastrointestinal stimulation, micturition, post-exercise, and others (1). Mr. KH’s presentation is most consistent with criteria of cough-induced neurally-mediated reflex syncopal syndrome.
Although this is the most comprehensive classification of syncope currently, it is limited by the fact that more than one pathophysiological factor may contribute to the symptoms (1). The pathophysiology of carotid sinus syncope has been studied extensively, but there is a lack of investigations in situational syncope. The fact that situational syncope is classified in same subcategory as carotid sinus syncope does not warrant same pathophysiology, because the presentations and diagnostic criteria of two syncopes are different.
Patients with carotid sinus syncope have exaggerated baroreflex (carotid sinus hypersensitivity (CSH)), which in response to carotid sinus stimulation results in bradycardia and/or hypotension (2). The diagnosis of carotid sinus syncope is confirmed by carotid sinus massage in supine position (2). Situational syncope, specifically cough syncope, does not have such diagnostic confirmation test and the diagnosis is made based on clinical presentation.
One study examined the pathophysiology of cough syncope and has found that individuals susceptible to cough syncope exhibited more profound hypotension for a longer duration with cough than did other syncope patients (4). Also the expected positive chronotropic response accompanying cough-induced hypotension tended to be suppressed in cough syncope patients compared with that observed in patients with other syncope (4).
Although these cough-induced haemodynamic and heart rate changes are similar to those observed in carotid hypersensitivity-induced carotid sinus syncope, none of the cough syncope patients exhibited hypersensitive carotid sinus responses during carotid massage, suggesting that cough syncope is mediated through different neural reflex trigger sites than those of carotid sinus syncope (4). Other proposed mechanisms include baroreflex mechanism, which explains with continuous coughing, intrathoracic pressure increase results in a decrease in venous return and a diminished cardiac output, resembling Valsalva maneuver (5).
However, this mechanism fails to account for cough syncope patients with intermittent or paroxysmal cough. The complete pathophysiology of cough syncope remains controversial, and requires further elucidation. The case of Mr. KH most probably represents cough syncope of baroreflex pathophysiology. His significant cardiac history showed a compromised heart with reduced cardiac output (limited physical activity due to breathlessness), and his syncopal episode was preceded by excessive and continuous cough.
This continuous cough increased intrathoracic pressure resembling Valsalva maneuver, and probably have decreased already-reduced cardiac output further, leading to syncope. However, given his past cardiac history and incomplete understanding of pathophysiology of cough syncope, other mechanisms are not excluded. References: 1. Brignole M, Alboni P, Benditt DG, Berefeldt L, Blanc J-J, Bloch Thomsen PE, van Dijik JG, Fitzpatrick A, Hohnloser S, Janousek J, Kapoor W, Kenny RA, Kulakowski P, Masottu G, Moya A, Raviele A, Sutton R, Theodorakis G, Ungar A, Wieling W. Guidelines on Management (diagnosis and treatment) of Syncope: Update 2004.
Europace 2004;6:467-537. 2. Anpalahan M. Neurally Mediated Syncope and Unexplained or Nonaccidental Falls in the Elderly. Internal Medicine Journal 2006;36:202-207. 3. Mosqueda-Garcia R, Furlan R, Tank J, Fernandez-Violante R. The Elusive Pathophysiology of Neurally Mediated Syncope. Circulation 2000;102:2898-2906. 4. Benditt D. G, Samniah N, Pham S, Sakaguchi S, Lu F, Lurie K, Ermis C. Effect of Cough on Heart Rate and Blood Pressure in Patients with “Cough Syncope”. Heart Rhythm Society 2005;2:807-813. 5. Sharpey-Shafer EP. The Mechanism of Syncope after Coughing. British Medical Journal 1953;2:860-863.