Autonomic Dysfunction in Cardiology: Pathophysiology, Investigation, and Management

Abstract

Presyncope and syncope are common medical findings, with greater than 40% estimated lifetime prevalence. These conditions are often elicited by postural stress and can be recurrent and accompanied by debilitating symptoms of cerebral hypoperfusion. Therefore, it is critical for physicians to become familiar with diagnosis and treatment of common underlying causes of presyncope and syncope. In some patients, altered postural hemodynamic responses are due to failure of compensatory autonomic nervous system reflex mechanisms. The most common presentations of presyncope and syncope secondary to this autonomic dysfunction include vasovagal syncope, neurogenic orthostatic hypotension, and postural tachycardia syndrome. The most sensitive method for diagnosis is a detailed initial evaluation with medical history, physical examination, and resting electrocardiogram to rule out cardiac syncope. Physical examination should include measurement of supine and standing blood pressure and heart rate, to identify the pattern of hemodynamic regulation during orthostatic stress. Additional testing may be required in patients without clear diagnosis following initial evaluation. Management of patients should focus on improving symptoms and functional status, and not targeting arbitrary hemodynamic values. An individualized structured and stepwise approach should be taken for treatment starting with patient education, lifestyle modifications, and use of physical counter-pressure maneuvers and devices to improve venous return. Pharmacological interventions should only be added when conservative approaches are insufficient to improve symptoms. There are no gold standard approaches for pharmacological treatment in these conditions, with medications often used off-label and with limited long-term data for effectiveness.

Passive standing tests for the office diagnosis of postural tachycardia syndrome: New methodological considerations

“…Postural tachycardia syndrome (POTS) is a relatively common circulatory condition, estimated to affect 0.1-1% of the population [1], disproportionately affecting women in the adolescent and young adult age range [1][2][3]. POTS can be associated with a variety of clinical syndromes including myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) [4] and Ehlers-Danlos syndrome [5,6].…”

“…The diagnosis of POTS requires an exaggerated increase in heart rate (HR) from supine to standing of at least 30 beats per minute for adults (20 years of age or older), or at least 40 bpm for adolescents over the course of 10 min upright, in the absence of orthostatic hypotension during the first 3 min [7]. The diagnosis also requires the presence of chronic orthostatic symptoms such as fatigue, lightheadedness, blurry vision, weakness, cognitive difficulties, and nausea [1][2][3][8][9][10]. Although tilt table testing was the initial method of orthostatic testing in POTS studies [8], in-office passive standing tests (PST), during which the individual leans against a wall [5,11], or active standing tests (without any support) [12][13][14][15] have also been used for several decades.…”

Refractory Hypotension post Coronary Artery Bypass Graft Unmasking Hypoaldosteronism: Case Report and Literature Review

“…(Figure 1). In our case, the autonomic insufficiency is attributed to the underlying coronary artery disease [1,2], and the CABG surgery has led to its worsening, as shown in the frequency of our patient's syncopal episodes and cardiac pauses postoperatively. The symptomatology of our patient was an overlap of two interconnected conditions, which explains partial improvement with the pacemaker placement to treat the autonomic dysfunction and complete resolution of his symptoms following fludrocortisone use.…”

“…It is well established that Heart Rate Variability (HRV) is affected by coronary artery disease, namely following a myocardial infarction [1,8]. Studies have also revealed a more pronounced reduction in HRV following cardiac and thoracic surgeries [2,9], yet it was found to be temporary and reversible within 3-6 months from the operation.…”

“…Normally, brisk changes from supine to standing position lead to pooling of blood at the periphery with subsequent activation of the RAAS and an increase in sympathetic resistance and heart rate with the aim of preventing orthostasis. Coronary artery disease is known to alter HRV (Hear Rate Variability), leading to symptoms of autonomic dysregulation such as orthostatic hypotension, arrythmias, etc [1,2].…”