AHA recently announced guidelines on the topic of syncope. Orthostatic hypotension is a cause in about 9% of afflicted individuals. A good portion of these patients have autonomic peripheral neuropathy from advanced diabetes mellitus. You can find below more details on syncope guidelines. Statements were published in Circulation March 2017

Circulation

Guidelines

March 2017

Orthostatic hypotension (OH) involves excessive pooling of blood volume in the splanchnic and leg circulations. With standing, venous return to the heart drops, with a resultant decrease in cardiac output. Normally, the autonomic nervous system provides compensatory changes in vascular tone, heart rate, and cardiac contractility. In some individuals, this response may be defective or inadequate.

In neurogenic OH, the vasoconstrictor mechanisms of vascular tone may be inadequate because of neurodegenerative disorders, such as multiple system atrophy, pure autonomic failure, Parkinson’s disease, and autonomic peripheral neuropathies, such as those due to DIABETES MELLITUS and other systemic diseases.

Neurogenic OH may present clinically as classic or delayed OH. Most commonly, orthostatic hypotension is due to dehydration or medications, such as diuretics and vasodilators. Syncope caused by OH conditions occurs in the upright position.

Orthostatic intolerance is a general term referring to frequent, recurrent, or persistent symptoms that develop upon standing (usually with a change in position from sitting or lying to an upright position) and are relieved by sitting or lying. Most commonly, the symptoms include lightheadedness, palpitations, tremulousness, generalized weakness, blurred vision, exercise intolerance, and fatigue. These symptoms may be accompanied by hemodynamic disturbances, including blood pressure decrease, which may or may not meet criteria for OH, and heart rate increase, which may be inadequate or compensatory. The pathophysiology is quite varied. One condition of note is POTS, in which upright posture results in an apparently inappropriate tachycardia, usually with heart rates >120 bpm. Although syncope occurs in patients with POTS, it is relatively infrequent, and there is little evidence that the syncope is due to POTS.

Studies of syncope report prevalence rates as high as 41%, with recurrent syncope occurring in 13.5%. In a cross section of 1925 randomly selected residents of Olmsted County, Minnesota, with a median age of 62 years (all age >45 years), 364 reported an episode of syncope in their lifetime; the estimated prevalence of syncope was 19%. Females reported a higher prevalence of syncope (22% versus 15%, P<0.001). The incidence follows a trimodal distribution in both sexes, with the first episode common around 20, 60, or 80 years of age and the third peak occurring 5 to 7 years earlier in males.

Predictors of recurrent syncope in older adults are aortic stenosis, impaired renal function, atrioventricular or left bundle-branch block, male sex, chronic obstructive pulmonary disorder, heart failure, atrial fibrillation, advancing age, and orthostatic medications, with a sharp increase in incidence after 70 years of age. Reflex syncope was most common (21%), followed by cardiac syncope (9%) and orthostatic hypotension (OH) (9%), with the cause of syncope unknown in 37%. In patients with New York Heart Association class III–IV HF, syncope is present in 12-14% of patients.

In older adults, there is a greater risk of hospitalization and death related to syncope. The National Hospital Ambulatory Medical Care Survey reported 6.7 million episodes of syncope in the emergency department (ED), or 0.77% of all ED patients. Among patients >80 years of age, 58% were admitted to hospital. The prevalence of syncope as a presenting symptom to the ED ranged from 0.8% to 2.4% in multiple studies in both academic and community settings.

Quality of life (QoL) is reduced with recurrent syncope, as demonstrated in studies that compared patients with and without syncope. QoL associated with recurrent syncope was equivalent to severe rheumatoid arthritis and chronic low-back pain in an adult population. Similarly, pediatric patients with recurrent syncope reported worse QoL than individuals with diabetes mellitus and equivalent QoL to individuals with asthma, end-stage renal disease, and structural heart disease.

Predictors of worse QoL over time include advanced age, recurrent syncope, neurological or psychogenic reason for syncope, and greater comorbidity at baseline. Syncope-related QoL can be improved through effective diagnosis and treatment. In 1 study, use of an implantable loop recorder increased diagnostic rate, reduced syncope recurrence, and improved QoL as compared with patients who received a conventional diagnostic workup. In a second study, nonpharmacological treatment of recurrent syncope was associated with reductions in recurrent syncope and improvements in QoL.