Confounders of vasovagal syncope: orthostatic hypotension

Abstract

A syncope evaluation should start by identifying potentially life-threatening causes, including valvular heart disease, cardiomyopathies, and arrhythmias. Most patients who present with syncope, however, have the more benign vasovagal (reflex) syncope. A busy syncope practice often also sees patients with neurogenic orthostatic hypotension presenting with syncope or severe recurrent presyncope. Recognition of these potential confounders of syncope might be difficult without adequate knowledge of their presentation, and this can adversely affect optimal management. This article reviews the presentation of the vasovagal syncope confounder and the putative pathophysiology of orthostatic hypotension, and suggests options for nonpharmacologic and pharmacologic management.

Fig. 1

Head-up tilt test traces from a patient with VVS and nOH. (A) With VVS, the heart rate (HR) and BP increase a little bit at the onset of tilt, and they are maintained for more than 25 minutes before a sudden precipitous drop in BP before the table is returned to the supine position. (B) With nOH, the BP falls almost immediately when the table is tilted up with only minimal changes in HR. (From Raj SR, Sheldon RS. Head-up tilt-table test. In: Saksena S, Camm AJ, editors. Electrophysiological disorders of the heart. 2nd edition. New York: Saunders; 2012. p. 73–6–73–8; with permission.)

Fig. 2

Physiology of standing: healthy and orthostatic hypotension. (A) With standing, there is a downward shift of approximately 500 mL of blood, which results in decreased venous return, decreased stroke volume (SV), and eventually decreased BP. This “unloads” the baroreceptors, and triggers reflex sympathetic nervous system (SNS) activation with an increase in HR and systemic vasoconstriction (countering the initial decline in BP). In a healthy individual, the net effect of assumption of upright posture is an increase in HR of 10 to 20 bpm, a minimal change in systolic BP, and an approximately 5 mm Hg increase in diastolic BP. (B) In patients with OH, the SNS and parasympathetic nervous system (PNS) cannot be adequately engaged, so the counterregulation is absent, and a drop in BP occurs. CO, cardiac output; TPR, total peripheral resistance.

Fig. 3

Cardiac sympathetic nerve integrity. Cardiac sympathetic nerve integrity can be assessed with m-iodobenzylguanidine (MIBG) scans with a chest view at 4 hours postinjection. MIBG is taken up by intact presynaptic norepinephrine transporters on postganglionic sympathetic neurons, and is not present in the setting of significant postganglionic sympathetic neuropathy. In MSA (A), the lesions are central and preganglionic. Because there is not postganglionic involvement, the heart takes up MIBG avidly. In contrast, patients with pure autonomic failure (PAF) (B) have a significant postganglionic sympathetic neuropathy, and the heart cannot be seen because it cannot take up MIBG. (C) Scan of a patient with Parkinson disease. Although the motor features of Parkinson disease are caused by central nervous system lesions, the autonomic failure is caused by a peripheral postganglionic sympathetic neuropathy, with poor cardiac uptake of MIBG.

Fig. 4

Valsalva maneuver. During the Valsalva maneuver, the patient is asked to blow and generate approximately 40 mm Hg of Valsalva pressure (VP) for 15 seconds while continuously monitoring HR and BP. In a healthy individual (A), the BP and pulse pressure initially decease because of the drop in venous return, but this hypotension triggers an increase in sympathoneurally mediated vasoconstriction. The BP starts to recover in late phase II (II_L). After release of VP (and with it increased venous return) the BP overshoots in phase IV (IV) before returning to baseline. A patient with nOH (B) might not be able to generate the appropriate sympathoneurally mediated vasoconstriction in response to the initial hypotension. Patients with nOH typically lack the late phase II BP recovery and the phase IV BP overshoot.