More than 30 pages of the textbook on autonomic failure, edited by neurologist Sir Roger Bannister and professor of neurovascular medicine Christopher Mathias, are devoted to the subject of syncope (derived from the Greek work ‘synkoptein’) (Mathias and Bannister, 1999; 2013). Forming the overture to this work is a chapter on neurocardiology in which Harvard professor Martin A. Samuels describes, for example, how a significant number of stroke patients have authentic neurogenic electrocardiographic changes.
In this article—the third in a series on neurocardiology and the work of Sir Roger Bannister—I will give an insight into these authoritative writings, beginning with the introduction to neurocardiology and moving onto syncope (defined in the textbook as ‘a transient loss of consciousness usually resulting from a temporarily inadequate cerebral blood flow’). Both cardiac- and neurally-mediated syncope are discussed, with both being highly relevant for cardiac nurses.
The brain: profound effects on the heart
‘In 1942, Walter Bradford Cannon published a remarkable paper entitled “‘Voodoo’ death” (Cannon, 1942) in which he recounted anecdotal experiences, largely from the anthropology literature, of death from fright. These often remote events, drawn from widely disparate parts of the world, had several features in common. They were all induced by an absolute belief that an external force, such as a wizard, or medicine man, could, at will, cause demise and that the victim himself had no power to alter this course.
‘This perceived lack of control over a powerful external force is the sine qua non for all the cases recounted by Cannon, who postulated that death was caused by a ‘lasting and intense action of the sympathico-adrenal system.
‘Over the years since Cannon's observations, evidence has accumulated to support his concept that “voodoo” death is, in fact, a real phenomenon, but far from being limited to ancient peoples, may be a basic biological principle which provides an important clue to understanding the phenomenon of sudden death in modern society as well as providing a window into the world of neurovisceral disease.’
Thus begins Professor Martin Samuel's chapter on neurocardiology (Samuels, 2013). He presents powerful evidence that overactivity of the sympathetic limb of the autonomic nervous system is the common phenomenon that links the major cardiac and pulmonary pathologies seen in neurological catastrophes. He describes how deaths from primarily neurological conditions such as subarachnoid haemorrhage, status epilepticus, and head trauma are often the result of profound effects on the heart and lungs during an ‘autonomic storm’, and how the connection between the nervous system and the cardiopulmonary system provides the unifying link that allows a coherent explanation for most, if not all, forms of sudden unexpected death.
Professor Blair Grubb and clinical assistant professor Barry Karas from the Medical College of Ohio present their chapter on neurally-mediated (or vasovagal) syncope, describing how it usually occurs as an unusual reaction to the baroreflex during assumption of an upright posture, in people with no evidence of heart disease or abnormalities in the heart's conduction system, but in whom an excessive degree of venous pooling probably occurs upon standing (Grubb and Karas, 1999).
Abnormal activation of ventricular mechanoreceptors in response to the baroreflex is a possible mechanism underlying neurally-mediated syncope. Normally activated by stretch, Professor Grubb suggests that, in syncope, the mechanoreceptors are also activated by the particularly strong cellular contractions arising during their very marked ‘unloading’ upon standing (in response to excessive venous pooling) when they receive a massive sympathetic outflow. Cardiovascular centres in the brain respond by reducing sympathetic impulses (‘undoing’ the actions of the baroreflex) and blood pressure drops, leading to loss of consciousness in syncope.
In addition to standing up, Professor Grubb describes how ‘faulty’ ventricular mechanoreceptors may also be activated and trigger syncope during the low blood pressure (and resulting baroreflex) experienced after haemorrhage, a large meal, diuretic use or vigorous exercise in a warm environment. Interestingly, a surge in brain serotonin levels may be important in the process of sympathetic withdrawal seen in neurally-mediated syncope (Grubb and Kosinski, 1996).
The heart: profound effects on the brain
In 20% of those admitted to hospital with syncope, a cardiac cause is found and prognosis is worse than for those with syncope of non-cardiac origin (1-year mortality is 19-30% compared with 0-12%) (Kapoor et al, 1983).
In Mathias and Bannister, Professors Juha Hartikainen and John Camm (1999) together describe the major mechanisms of cardiac syncope, in which a sudden reduction in cardiac output leads to a transient reduction in cerebral blood flow and a loss of consciousness.
In obstructive syncope, ventricular filling or emptying is restricted and cardiac output cannot rise during exercise. Disorders which can obstruct cardiac output or cardiac filling are aortic stenosis, hypertrophic cardiomyopathy, mitral stenosis, myxoma, pulmonary hypertension, pulmonary stenosis, ventricular septal defect, tetralogy of Fallot, pulmonary embolism, cardiac tamponade and prosthetic valve malfunction.
Arrhythmic syncope occurs when the arrhythmia is associated with sufficient haemodynamic deterioration to impair blood supply to the brain. Bradyarrhythmia (through sinus node dysfunction or atrioventricular conduction defect), tachyarrhythmia (including atrial fibrillation, atrial flutter and ventricular fibrillation) and pacemaker malfunction are all possible causes.
Cerebral blood flow can also be reduced, or obstructed, when an embolus originating from the heart reaches the brain. Calcification of mitral or aortic valves is an important cause of embolus; endocarditis and thrombi from prosthetic valves can also be associated with brain embolism. Arrhythmias and cardiac wall abnormalities (perhaps resulting from acute myocardial infarction) may increase risk of embolisation.
The authors write that ‘studies on humans have shown that acute cerebral anoxia results in syncope after 5-15 seconds’. Identifying the possible cardiac disorder underlying the syncope is important in order to assess future risk and determine possible management. Taking a detailed clinical history is important, and should include ‘previous cardiac diagnoses and symptoms; a family history of arrhythmias, pacemaker, syncope and sudden death; use of medications; symptoms preceding and following the syncope and the relationship of syncope to exertion, micturition and changes in body position’ (Hartikainen and Camm, 1999).
Syncope and the National Institute for Health and Care Excellence
‘Everything National Institute for Health and Care Excellence (NICE) has said on assessing, diagnosing and referring adults and young people who have experienced a blackout in an interactive flowchart’ is the title to an excellent resource on syncope (NICE, 2019), building on the work begun by Sir Roger Bannister and his team.
According to the flowchart, and in accord with the guidance in the textbook edited by Bannister, initial assessment of the patient suffering from syncope includes asking about any other transient loss of consciousness, measuring lying and standing blood pressure, and considering medication history, especially diuretics. Electrocardiogram abnormalities to be monitored for include any degree of heart block, any ST segment or T wave abnormalities, and evidence of a long or short QT interval. Blood glucose levels and haemoglobin levels may be relevant if hypoglycaemia or anaemia are suspected. Red flags include a heart murmur, new or unexplained breathlessness and syncope on exertion.
Being interactive, the flowchart takes the clinician on different pathways according to the findings, until a diagnosis is made. Where no conclusions can be drawn, psychogenic non-epileptic seizures or psychogenic pseudosyncope may be considered and referral to a neurologist is suggested. Just as over 70 neurologists and cardiologists worked together on the textbook edited by Sir Roger Bannister and Professor Mathias, it is clear that these disciplines continue to work together on the understanding of syncope today.
NICE has also written for the public on syncope (or ‘transient loss of consciousness’), detailing tests and causes (NICE, 2010). Organisations that can provide information and support for people with syncope are helpfully listed, and these include Cardiac Risk in the Young and Syncope Trust And Reflex Anoxic Seizures.