University of Groningen Patterns of orthostatic hypotension and the evaluation of syncope van Wijnen, Veera Kariina

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University of Groningen

Patterns of orthostatic hypotension and the evaluation of syncope

van Wijnen, Veera Kariina

DOI:

10.33612/diss.112725119

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Publication date: 2020

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van Wijnen, V. K. (2020). Patterns of orthostatic hypotension and the evaluation of syncope. Rijksuniversiteit Groningen. https://doi.org/10.33612/diss.112725119

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CHAPTER

8

DELAYED ORTHOSTATIC HYPOTENSION AND

VASOVAGAL SYNCOPE: A DIAGNOSTIC DILEMMA

Artur Fedorowski, Veera K. van Wijnen, Wouter Wieling

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Delayed orthostatic hypotension (dOH) is defined as a systolic/diastolic blood pressure (BP) fall of ≥20/10 mmHg occurring beyond 3 min of head-up tilt (HUT) or active standing (1). Delayed OH is not a diagnosis per se, it is rather a physical sign and test result. As far as the underlying physiological mechanisms are concerned, it has been postulated that dOH may represent a milder form of autonomic failure, especially if associated with parkinsonism (1,2). Delayed OH with a subsequent vasovagal syncope (VVS) has also been reported (3), but the physiological concept underlying this condition remains to be explained. In the following case history, we will argue that dOH can be interpreted as a vasovagal reflex preceded by a prolonged phase of hemodynamic instability (presyncope) observed in older adults.

We present a 74-year-old woman with a medical history of hiatus hernia, non-specific gastrointestinal symptoms (diarrhea) and hyperlipidemia, who was admitted to the emergency department (ED) due to syncope. The same morning, she had undergone colonoscopy, and afterwards she had gone to a restaurant where she fainted after the meal. While regaining consciousness, she felt intense nausea and vomited. Electrocardiogram (ECG) at ED showed a sinus bradycardia of 53/min and AV block 1 (PQ time 228 ms). Blood pressure was 147/82 mmHg. Echocardiogram and Holter ECG [sinus rhythm 72/min (52–124)] performed after the discharge were normal.

An additional HUT test, recommended by a syncope expert (A.F.), was performed to confirm the clinical suspicion of VVS, and to educate the patient about prodromal symptoms. Expert history taken prior to HUT revealed a total number of 11 faints, starting at the age of 49 years. She had also experienced a traumatic fall and irregular complaints of lightheadedness upon standing. The prodromal symptoms preceding syncope were perspiration and nausea, and most syncope episodes occurred during standing, the recent episode while sitting.

A detailed analysis of HUT provided the following information (Fig. 1):

-9 to -2 min (8–15 min supine): installation of venous line and collection of blood sample were

performed at 0–3 min of HUT (not shown). Stable heart rate (HR, 60 bpm) and BP (180/80 mmHg) between 8 and 15 min.

-2 to 0 min (last 2 min prior to tilt up): marked increase in BP accompanied by increase in systemic vascular

resistance (SVR). Carotid sinus massage (CSM) was performed twice. These hemodynamic changes can be interpreted as ‘‘mental stress’’ and indicate intact central and efferent autonomic pathways.

0–6 min CSM was performed twice around 1 min after HUT. Marked increases in BP persist in the

upright posture suggesting that afferent baroreflex pathways are intact.

6–19 min decrease in BP from around 190/100 mmHg to 120/60 mmHg and a minor increase in HR

to 70 bpm is observed. At around 10 min, a blood sample is taken. Pulse wave analysis indicates that BP fall can be explained by reduced SVR from distinctly increased values in the first 6 min of HUT to supine resting values. Cardiac output (CO) is stable.

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131 19–24 min BP steeply decreases to 60/40 mmHg and HR is reduced to 50 bpm. Patient faints.

Lightheadedness of recognizable character from the previous attacks precedes syncope.

24–31 min Rapid return of BP to 180/90 mmHg within 3 min after tilt down. Heart rate remains at

56 bpm for 6 min after tilt down.

In the supine position and 10 min after tilt up, catecholamines were measured. In the supine position, plasma concentrations of norepinephrine and epinephrine were 1.7 and 0.12 nmol/L, respectively, whereas after 10 min of HUT catecholamine concentration increased to 3.1 and 0.2 nmol/L, respectively. Reference values for norepinephrine are 0.70–2.3 nmol/L at rest, and 1.6–4.8 nmol/ L on standing. For epinephrine, this is <0.7 nmol/L at rest and on standing. Normal supine values and an almost twofold increase in catecholamines after 10 min of HUT exclude autonomic failure. Vasopressin was not measured.

Fig 1. Head-up tilt test tracings of 76-year old woman with recurrent syncope. CSM = carotid sinus massage;

BP = blood pressure. Four phases of vasovagal reflex syncope are indicated.

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In this case, a clinical history of syncope accompanied by pro- and postdromes like sweating and nausea, typical triggers (orthostatic challenge, instrumentation, blood sampling), and the final hemodynamic changes indicate VVS as the correct diagnosis.

The tilt table results documented an initial transient pronounced increase in BP, followed by a progressive BP decrease, and finally a vasovagal reflex leading to syncope. A careful analysis of continuous BP recordings during orthostatic stress allows us to divide the sequence of hemodynamic events leading to VVS into four phases (4):

Phase 1: early phase of stabilization (first 0–5 min in the upright posture) with normal hemodynamic adjustments.

Phase 2: circulatory instability (early presyncope). After a variable period of initial stabilization, a susceptible patient enters into phase 2, characterized by a gradual fall in systolic BP of approximately 20 mmHg.

Phase 3: terminal hypotension (late presyncope) and syncope, characterized by a steep BP fall and bradycardia.

Phase 4: recovery of BP and HR in the supine position.

The new finding in this case is that Phase 2 can be very much prolonged in older patients. Without Phase 3 of the VVS (the terminal hypotension between the 18th and 23rd min), the HUT period between the 5th and 18th min could be labeled as dOH in this patient.

The differential diagnosis during HUT between dOH due to a milder form of autonomic failure (1,2) and dOH due to a prolonged Phase 2 of a vasovagal response (3) can only be made by inducing presyncope/syncope (5). In our case, a fall in SVR was the underlying cause of the BP fall in Phase 2. This fall in SVR can be attributed to vasovagal reaction due to instrumentation amplified by collection of a blood sample, a well-known trigger for VVS. It is to be expected that in other older patients with a prolonged Phase 2 the combination of a fall in CO due to progressive venous pooling with diminished filling and stiffer ventricles will be involved.

In conclusion, dOH due to incipient or mild to moderate autonomic failure might be a different entity compared with dOH preceding a typical vasovagal reflex in older adults. A prospective study in a large number of subjects with dOH in different clinical settings is needed to determine the frequency of these two entities. Matching the data from detailed history taking and long-term follow-up will be crucial in such a study (1).

Conflict of interest: None

The Regional Ethical Review Board in Lund, Sweden accepted the SYSTEMA study protocol (ref no 82/2008), and the patient gave her written informed consent prior to examination.

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REFERENCES

(1) Cheshire WP,Jr. Clinical classification of orthostatic hypotensions. Clin Auton Res 2017 Jun;27 (3):133-135.

(2) Gibbons CH, Freeman R. Clinical implications of delayed orthostatic hypotension: A 10-year follow-up study. Neurology 2015 Oct 20;85 (16):1362-1367.

(3) Ricci F, De Caterina R, Fedorowski A. Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment. J Am Coll Cardiol 2015 Aug 18;66 (7):848-860.

(4) Jardine DL. Vasovagal syncope: new physiologic insights. Cardiol Clin 2013 Feb;31 (1):75-87.

(5) Tellez MJ, Norcliffe-Kaufmann LJ, Lenina S, Voustianiouk A, Kaufmann H. Usefulness of tilt-induced heart rate changes in the differential diagnosis of vasovagal syncope and chronic autonomic failure. Clin Auton Res 2009 Dec;19 (6):375-380.

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