scholarly journals Diagnosis and Treatment of Supine Hypertension in Autonomic Failure Patients With Orthostatic Hypotension

2002 ◽  
Vol 4 (2) ◽  
pp. 139-145 ◽  
Author(s):  
Jens Jordan ◽  
Italo Biaggioni
2012 ◽  
Vol 116 (1) ◽  
pp. 205-215 ◽  
Author(s):  
Hossam I. Mustafa ◽  
Joshua P. Fessel ◽  
John Barwise ◽  
John R. Shannon ◽  
Satish R. Raj ◽  
...  

Severe autonomic failure occurs in approximately 1 in 1,000 people. Such patients are remarkable for the striking and sometimes paradoxic responses they manifest to a variety of physiologic and pharmacologic stimuli. Orthostatic hypotension is often the finding most commonly noted by physicians, but a myriad of additional and less understood findings also occur. These findings include supine hypertension, altered drug sensitivity, hyperresponsiveness of blood pressure to hypo/hyperventilation, sleep apnea, and other neurologic disturbances. In this article the authors will review the clinical pathophysiology that underlies autonomic failure, with a particular emphasis on those aspects most relevant to the care of such patients in the perioperative setting. Strategies used by clinicians in diagnosis and treatment of these patients, and the effect of these interventions on the preoperative, intraoperative, and postoperative care that these patients undergo is a crucial element in the optimized management of care in these patients.


Hypertension ◽  
2005 ◽  
Vol 45 (6) ◽  
Author(s):  
Michelangelo Sartori ◽  
Achille C. Pessina ◽  
Andrea Semplicini

2019 ◽  
pp. 390-393
Author(s):  
Peter Novak

This case illustrates autonomic failure in painful post-Lyme disease syndrome. Autonomic testing has shown supine hypertension, orthostatic hypotension, and hypocapnic cerebral hypoperfusion (HYCH). Small fiber neuropathy was painful, affecting sensory fibers. Patient noted improvement in the pain by about 40% after 12 month of intravenous immune globulins.


2020 ◽  
Vol 16 (1) ◽  
pp. 48-54
Author(s):  
Aamir Ahmed ◽  
Mohammed Ruzieh ◽  
Shaffi Kanjwal ◽  
Khalil Kanjwal

This article is intended to provide guidance and clinical considerations for physicians managing patients suffering from supine hypertension with orthostatic hypotension, referred to as “SH-OH”. We review the normal physiologic response to orthostasis, focusing on the appropriate changes to autonomic output in this state. Autonomic failure is discussed with a generalized overview of the disease and examination of specific syndromes that help shed light on the pathophysiology of SH-OH. The goal of this review is to provide a better framework for clinical evaluation of these patients, review treatment options, and ultimately work toward achieving a better quality of life for patients afflicted with this disease.


2019 ◽  
pp. 233-236
Author(s):  
Peter Novak

Autonomic failure manifesting as neurogenic orthostatic hypotension and supine hypertension are common manifestations of cardiovascular dysautonomia in Parkinson’s disease. Depending on the cerebral blood flow, neurogenic orthostatic hypotension can be either compensated (with stable orthostatic cerebral blood flow) and noncompensated (with reduced flow).


Author(s):  
Luis E. Okamoto ◽  
Jorge E. Celedonio ◽  
Emily C. Smith ◽  
Alfredo Gamboa ◽  
Cyndya A. Shibao ◽  
...  

BackgroundSupine hypertension affects a majority of patients with autonomic failure; it is associated with end‐organ damage and can worsen daytime orthostatic hypotension by inducing pressure diuresis and volume loss during the night. Because sympathetic activation prevents blood pressure (BP) from falling in healthy subjects exposed to heat, we hypothesized that passive heat had a BP‐lowering effect in patients with autonomic failure and could be used to treat their supine hypertension.Methods and ResultsIn Protocol 1 (n=22), the acute effects of local heat (40–42°C applied with a heating pad placed over the abdomen for 2 hours) versus sham control were assessed in a randomized crossover fashion. Heat acutely decreased systolic BP by −19±4 mm Hg (versus 3±4 with sham,P<0.001) owing to decreases in stroke volume (−18±5% versus −4±4%,P=0.013 ) and cardiac output (−15±5% versus −2±4%,P=0.013). In Protocol 2 (proof‐of‐concept overnight study; n=12), we compared the effects of local heat (38°C applied with a water‐perfused heating pad placed under the torso from 10 pmto 6 am) versus placebo pill. Heat decreased nighttime systolic BP (maximal change −28±6 versus −2±6 mm Hg,P<0.001). BP returned to baseline by 8 am. The nocturnal systolic BP decrease correlated with a decrease in urinary volume (r=0.57,P=0.072) and an improvement in the morning upright systolic BP (r=−0.76,P=0.007).ConclusionsLocal heat therapy effectively lowered overnight BP in patients with autonomic failure and supine hypertension and offers a novel approach to treat this condition. Future studies are needed to assess the long‐term safety and efficacy in improving nighttime fluid loss and daytime orthostatic hypotension.RegistrationURL:https://www.clinicaltrials.gov; Unique identifiers: NCT02417415 and NCT03042988.


2017 ◽  
Vol 264 (8) ◽  
pp. 1567-1582 ◽  
Author(s):  
Christopher H. Gibbons ◽  
Peter Schmidt ◽  
Italo Biaggioni ◽  
Camille Frazier-Mills ◽  
Roy Freeman ◽  
...  

1999 ◽  
Vol 10 (1) ◽  
pp. 35-42 ◽  
Author(s):  
JENS JORDAN ◽  
JOHN R. SHANNON ◽  
BOJAN POHAR ◽  
SACHIN Y. PARANJAPE ◽  
DAVID ROBERTSON ◽  
...  

Abstract. Supine hypertension, which is very common in patients with autonomic failure, limits the use of pressor agents and induces nighttime natriuresis. In 13 patients with severe orthostatic hypotension due to autonomic failure (7 women, 6 men, 72 ± 3 yr) and supine hypertension, the effect of 30 mg nifedipine (n = 10) and 0.025 to 0.2 mg/h nitroglycerin patch (n = 11) on supine BP, renal sodium handling, and orthostatic tolerance was determined. Medications were given at 8 p.m.; patients stood up at 8 a.m. Nitroglycerin was removed at 6 a.m. Compared with placebo, nifedipine and nitroglycerin decreased systolic BP during the night by a maximum of 37 ± 9 and 36 ± 10 mmHg, respectively (P < 0.01). At 8 a.m., supine systolic BP was 23 ± 7 mmHg lower with nifedipine than with placebo (P < 0.05), but was similar with nitroglycerin and placebo. Sodium excretion during the night was not reduced with nitroglycerin (0.13 ± 0.02 mmol/mg creatinine [Cr] versus 0.15 ± 0.03 mmol/mg Cr with placebo), but it was increased with nifedipine (0.35 ± 0.06 mmol/mg Cr versus 0.13 ± 0.02 mmol/mg Cr with placebo, P < 0.05). Nifedipine but not nitroglycerin worsened orthostatic hypotension in the morning. It is concluded that nifedipine and transdermal nitroglycerin are effective in controlling supine hypertension in patients with autonomic failure. However, nifedipine has a prolonged depressor effect and worsens orthostatic hypotension in the morning. The decrease in pressure natriuresis that would be expected with the substantial decrease in BP obtained with nitroglycerin and nifedipine may be offset by a direct effect of both drugs on renal sodium handling.


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