conception
In 1996, the American Autonomic Association and the American Academy of Neurology stated in a consensus that orthostatic hypotension (oh) refers to a decrease in blood pressure within 3 minutes of standing [systolic blood pressure (sbp) ≥ 20 mmhg or diastolic blood pressure (dbp) ≥10 mmhg]. In 2011, the American Autonomic Association, together with the European Federation of Autonomic Associations, the World Neurological Union Autonomic Research Group, and the Autonomic Branch of the American Academy of Neurology, supplemented the concept of oh: (1) in patients with baseline hypertension, including supine hypertension (sh), the blood pressure drop required sbp ≥ 30 mmhg; (2) the blood pressure requirements for diagnosing msa were more stringent (blood pressure drop sbp≥ 30 mmhg or dbp ≥ 15 mmhg). The onset of oh more than 3 minutes is called delayed orthostatic hypotension, the appearance of delayed hypotension means the early stages of disease development, and studies have reported that half of patients with delayed orthostatic hypotension will convert to typical oh within the next 10 years. The overall incidence of OH in people over 65 years of age in population reports is about 20%, and oh is 30% to 50% of Parkinson's patients.
Non-neurogenic postural hypotension (non-neurogenic oh) refers to oh due to non-neurologic lesions, including decreased cardiac output and decreased vasoconstriction due to various causes. Neurogenic orthostatic hypotension (noh) is due to neurological disorders involving autonomic dysfunction, such as impaired central pathways of sympathetic control, or postganglionic sympathetic degeneration leading to adrenergic receptor activation disorders, resulting in the inability to achieve reflex adjustment of blood pressure in normal postural changes, resulting in oh manifestations. Noh clinical manifestations are both OH and sh, and the heart rate response is poor.
Classification of noh
Suggestive significance of clinical manifestations for noh
When the patient has a relevant complaint or has been found oh, it should focus on two aspects. On the one hand, it is to look for more other manifestations of autonomic damage from the symptoms of the autonomic nervous system, including urination, gastrointestinal function, changes in vision, and changes in the reproductive system; on the other hand, it is to look for signs and symptoms of the nervous system, including cognition, extrapyramidal manifestations, signs of the cerebellum, and peripheral nerve diseases.
The four-step method identifies noh
1. Similar medical history and physical examination – raising awareness: 5 groups of people, 10 questions
1. When neurodegenerative disease with autonomic damage is suspected or diagnosed (PD, MSA, PAF, DLB).
2. Unexplained falls or syncope.
3. When diagnosing peripheral neuropathy with autonomic damage.
4. Elderly, frail, or with multiple medications over 70 years of age.
5. Orthostatic dizziness or non-specific standing symptoms.
1. Have you fainted recently?
2. Is there dizziness or top-heavy standing?
3. Is there a disregard barrier in the standing position?
4. Is there breathing difficulty standing?
5. Are there any weakness in the standing position?
6. Is there neck pain in the standing position?
7. Do the above symptoms improve or disappear with sitting or lying down?
8. Are the above symptoms worsened in the morning or after meals?
9. Have there been any recent falls?
10. Are there any other symptoms that appear within 3 to 5 minutes of standing and disappear with sitting or lying down?
Any of the above questions is an affirmative answer and needs to be further examined!
2. Blood pressure monitoring - find oh
●Recumbent blood pressure: standardized measurement, can be delayed to 10 minutes;
● Tilt test (hut);
●Ambulatory blood pressure monitoring (abpm);
●Average blood pressure: <75 mmhg.
3. Heart rate reactivity - identification oh/noh
●△hr＜15；
●△hr/△sbp＜0.5 bpm/mmhg。
4. Review of concomitant medications - exclusion of non-neurogenic causes (drug factors)
Related drugs
Drug class
The name of the drug
α1 antagonist
Doxazolid, piperazosin, tamsulosin, trazosin
diuretic
Furosemide, torasemide, dihydrogram urtica, acetazolamide, spironolactone
nitrate
Nitroprin, isosorbide nitrate, nitroglycerin
β blocker
Propranolol, metoprolol, atenolol, bisoprolol, carvedilol, labetolol
Tricyclic antidepressants
Amitriptyline, destriptyline, imipramine, destamine
Phosphodiesterase inhibitors
Sildenafil, Vadenafil, Tadalafil
α agonists
Clonidine, guanfacine
Adjunctive testing
Adjunctive tests for noh help confirm the diagnosis of the disease, and routine adjunctive tests include blood tests, metabolic screening, blood volume, structural and functional problems of the heart, and structural damage to the nervous system. In addition, endocrine, metabolic, tumor and inflammatory immune-related factors are also worth paying attention to.
Therapeutic goals
Instead of adjusting blood pressure to normal levels, we focus on reducing the burden of symptoms, improving life treatment, and reducing mortality and disability rates.
Treatment of noh
1. Remove the effects of the drug
2. Non-pharmacological treatment
● Lifestyle changes:
Adequate hydration: 2~3 l/d;
Acute drinking water: 240 to 480 ml in 30 minutes;
Salt intake: 2.3 to 10 g/day;
Head high: 15 to 22 cm above the foot level, or 10 to 30 °;
Physical condition: lower limb strength training, recommended spinning bike, rowing machine, treadmill is not recommended;
Food: eat less and eat more meals, low gi;
Avoid overheating of the ambient temperature, such as hot baths and saunas.
●Physical therapy (counter-stress):
Lower extremity exercises;
Breathing exercises: slow, deep breathing, nasal breathing; avoid vaslva.
●External device: waist-length elastic socks, abdominal strap.
3. Monotherapy / Combination drug therapy
Recommended processing
summary
Although noh and oh are very simple clinical phenomena, the pathophysiology mechanism is not simple, and it is manifested in a variety of diseases, which is important for differential diagnosis, and also has an impact on the quality of life of patients. Whether it is diagnosis, identification or treatment, there are standardized steps to follow, which deserve more attention and application in clinical work.
bibliography
1.kalra dk, raina a, sohal s: neurogenic orthostatic hypotension: state of the art and therapeutic strategies. clin med insights cardiol 2020, 14:1179546820953415.
2.consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. the consensus committee of the american autonomic society and the american academy of neurology. neurology 1996 may;46(5):1470. doi: 10.1212/wnl.46.5.1470.
3. roy freeman, wouter wieling, felicia b, axelrod, david g, et al. consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. clin auton res(2011) 21:69–72.
4. Expert Consensus on Blood Pressure Management in Parkinson's Disease Internal Medicine Theory and Practice 2020,15(3):176-183.
Edit | Qiao Tingting
Review | Ding Huixin