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Orthostatic Hypotension
    โรคความดันโลหิตต่ำ

   Etiology and 
       Pathophysiology
    Symptoms, Signs, and 
       Diagnosis
    Prognosis and 
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 โรคความดันโลหิตสูง
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 Orthostatic Hypotension

โรคความดันโลหิตต่ำ ( Hypotension )
โรคความดันโลหิตต่ำพบน้อยกว่าโรคความดันโลหิตสูง
ผู้ที่มีความดันโลหิตต่ำมีอันตรายน้อยกว่าผู้ที่ความดันโลหิตสูง และมีการดำเนินชีวิตที่สบายกว่า
ผู้ป่วยที่มีความดันโลหิตต่ำจะวัดได้ดังนี้ สำหรับชายและผู้หญิง Systolic Pressure 80-100 มม.
ปรอท Diastolic Pressure 50-60 มม. ปรอท สาเหตุของความดันโลหิตต่ำ ยังไม่มีคำอธิบายที่
แน่นอน แต่ส่วนใหญ่เป็นพันธุกรรมหรือเป็นมาแต่กำเนิดหรือไม่ทราบสาเหตุแน่นอนเรียกว่า 
Idiopathic Hypotension

อาการ ส่วนใหญ่ของผู้ป่วยที่มีความดันโลหิตต่ำ มักไม่มีอาการอะไรมากนัก อาการสำคัญคือ 
จะมีอาการเวียนหัวง่าย เวลาลุกขึ้นยืนเร็วๆ เช่นเวลานั่งยองๆ แล้วลุกขึ้นยืน หรือกำลังนอนอยู่
แล้วลุกขึ้นเร็วๆ จะเกิดอาการเวียนหัวเป็นครั้งคราวชั่วระยะหนึ่ง แล้วบางครั้งก็ดูปกติดีแต่ถ้า
อดนอนหรือนอนไม่พอก็จะมีอาการเวียนหัวและอ่อนเพลียด้วย

เมื่อเปลี่ยนจากท่านอนเป็นลุกขึ้นนั่งหรือยืน จะมีอาการหน้ามืดวิงเวียนจะเป็นลมเนื่องจากเลือดไปเลี้ยง
สมองไม่พอ อาจมีคลื่นไส้ อาเจียน ตาพร่า ตาลายร่วมด้วย แต่สักครู่หนึ่งก็หายเป็นปกติ

การวัดความดันโลหิต มักพบว่าความดันซิสโตลิก (ช่วงบน) ที่วัดในท่ายืนต่ำกว่าท่านอนมากกว่า 30 
มิลลิเมตรปรอท เช่น ในท่านอนวัดได้ 130/80 แต่ในท่ายืนจะวัดได้ 90/60

การรักษา
รักษาตามสาเหตุ 
- ถ้าไม่มีสาเหตุชัดเจน อาจต้องตรวจเลือด ปัสสาวะ และอื่น ๆ ที่จำเป็น 
- ควรแนะนำให้ลุกขึ้นนั่งหรือยืนช้า ๆ อย่าลุกพรวดพราด เพื่อให้ร่างกายปรับตัว 
- ออกกำลังกายบ้าง เพื่อช่วยให้หัวใจแข็งแรง 
- ถ้ามีปัญหาเรื่องขาดอาหาร ก็ควรให้สารอาหารชดเชย เช่น 
- กรดโฟลิคจากน้ำผึ้งช่วยสร้างเม็ดเลือดแดง 
- กรดอะมิโนในสาหร่ายเกลียวทองเป็นสารอาหารที่จำเป็นต่อผนังเส้นเลือดและระบบประสาทอัตโนมัติ 
- วิตามิน เกลือแร่ ในว่านหางจระเข้ช่วยให้เกิดสมดุลของความดันโลหิต 
- วิตามินซี ช่วยในการดูดซึมแคลเซี่ยม ธาตุเหล็กและกระบวนการเมตาโบลิซึมของร่างกาย 
- วิตามินอีในเมล็ดทานตะวันช่วยลดการแตกตัวของเม็ดเลือดแดง 


An excessive fall in BP (typically > 20/10 mm Hg) on assuming the upright posture.

Orthostatic hypotension is not a specific disease but rather a manifestation of abnormal BP regulation due to various causes.

Etiology and Pathophysiology

The gravitational stress of sudden standing normally causes pooling of blood in the venous capacitance vessels of the legs and trunk. The subsequent transient decrease in venous return and cardiac output results in reduced BP. Baroreceptors in the aortic arch and carotid bodies activate autonomic reflexes that rapidly normalize BP by causing a transient tachycardia. These changes reflect primarily the sympathetic mediated increase in catecholamine levels, which augments vasomotor tone of the capacitance vessels, increases heart rate and myocardial contractility, and thereby enhances cardiac output; arterial and venous vasoconstriction are mediated by similar mechanisms. Vagal inhibition also increases the heart rate. With continued standing, ADH secretion and activation of the renin-angiotensin-aldosterone system cause Na and water retention and expansion of the circulating blood volume.

When afferent, central, or efferent portions of the autonomic reflex arc are impaired by diseases or drugs, myocardial contractility or vascular responsiveness is depressed, hypovolemia is present, or hormonal responses are faulty, these homeostatic mechanisms may be inadequate to restore the lowered BP. The initial manifestations of decreased tissue perfusion are the effects of impaired cerebral blood flow; however, postural BP changes do not reliably reflect cerebral hypoperfusion.

Hypovolemia is the most common cause of symptomatic orthostatic hypotension. Hypovolemia is often induced by excessive use of diuretics (eg, loop diuretics such as furosemide, bumetanide, and ethacrynic acid); relative hypovolemia is due to vasodilator therapy with nitrate preparations and Ca blockers (verapamil, nifedipine, diltiazem, amlodipine) or with ACE inhibitors. The hypovolemia and diminished vasomotor tone caused by protracted bed rest are also often a cause of orthostatic hypotension. Orthostatic hypotension is more frequent in diabetic than nondiabetic patients treated with antihypertensive drugs and also occurs secondary to vasodilation during febrile illnesses.

Acute or subacute severe hypovolemia caused by disease may produce orthostatic hypotension due to a decrease in cardiac output despite intact autonomic reflexes. Hemorrhage, severe vomiting or diarrhea, excessive sweating, or the osmotic diuresis in uncontrolled diabetes mellitus may lead to volume depletion, dehydration, and orthostatic hypotension unless fluid or electrolyte replacement is adequate. Hypokalemia impairs the reactivity of vascular smooth muscle and may limit the increase in peripheral vascular resistance on standing. The adrenocortical hypofunction of Addison's disease may lead to hypovolemic orthostatic hypotension in the absence of adequate salt intake. The effects of diuretics and vasodilators are discussed below.

Drugs that impair autonomic reflex mechanisms and reduce BP on standing, eg, excessive doses of antihypertensive drugs (methyldopa, clonidine, reserpine, ganglionic blocking drugs) and multiple drug use, are also frequent causes. beta-Adrenergic blockers are a rare cause, but alpha-adrenergic blockers such as prazosin may be causative, especially at the initiation of therapy (first-dose effect). Drugs that provoke postural hypotension should be initiated in small doses with gradual upward titration. Other drugs that reversibly impair autonomic reflexes and reduce BP on standing (an important adverse effect) include many of those used to treat psychiatric disorders, such as monoamine oxidase inhibitors (isocarboxazid, phenelzine, tranylcypromine) used to treat depression; tricyclic antidepressants (nortriptyline, amitriptyline, desipramine, imipramine, protriptyline) or tetracyclic antidepressants; and phenothiazine antipsychotic drugs (chlorpromazine, promazine, thioridazine). Quinidine, levodopa, barbiturates, and alcohol may also produce orthostatic hypotension. The antineoplastic drug vincristine may produce severe long-lasting orthostatic hypotension due to neurotoxicity.

Neurologic disorders that involve the autonomic nervous system interrupt the sympathetic reflex arc and impair normal adrenergic responses to standing. This is common with diabetic neuropathy, amyloidosis, porphyria, tabes dorsalis, syringomyelia, spinal cord transection, pernicious anemia, alcoholic neuropathy, Guillain-Barré syndrome (postinfectious polyneuropathy), and Riley-Day syndrome (familial dysautonomia). Surgical sympathectomy, vasospastic disorders, or peripheral venous insufficiency (particularly severe varicose veins) may result in orthostatic hypotension. The postural hypotension of Parkinson's disease may be aggravated by treatment with levodopa. Orthostatic hypotension may be a component of the vasomotor response in the postgastrectomy dumping syndrome.

Shy-Drager syndrome and idiopathic orthostatic hypotension are two possibly related primary neuropathic disorders commonly associated with severe orthostatic hypotension (see also Ch. 179). In patients with Shy-Drager syndrome, plasma norepinephrine does not increase on standing; in those with idiopathic orthostatic hypotension, norepinephrine appears to be depleted from the sympathetic nerve endings. In these conditions, widespread lesions affect the sympathetic and parasympathetic nervous systems, basal ganglia, and spinal tracts, with resultant widespread autonomic dysfunction in addition to failure of arteriolar and venous vasoconstriction; loss of sweating; bowel, bladder, and stomach atony; impotence; decreased salivation and tearing; mydriasis; and impaired visual accommodation. Paradoxically, BP may be elevated in the supine position, even when severe postural hypotension is present, because of loss of parasympathetic, as well as sympathetic, regulation of the cardiovascular system. Orthostatic hypotension is accentuated in the early morning due to overnight natriuresis and may also be more prominent postprandially and after exercise.

In many causes of secondary systemic arterial hypertension, in which BP is not controlled by the usual homeostatic mechanisms, assuming the upright posture may cause orthostasis; this is prominent in most patients with pheochromocytoma and also occurs in patients with primary hyperaldosteronism, who, paradoxically, have hypertension in the supine position as well as orthostatic hypotension.

Cardiac causes of sudden-onset postural hypotension include unrecognized MI or cardiac arrhythmia. Other cardiac causes of postural hypotension reflecting inability to increase cardiac output include severe dilated cardiomyopathy, aortic stenosis, constrictive pericarditis, and advanced heart failure of any cause.

In the elderly, decreased baroreceptor responsiveness, coupled with decreased arterial compliance, accounts for frequent orthostatic hypotension. The decreased baroreceptor responsiveness delays the tachycardic response. Although postural hypotension is described in about 20% of unselected elderly persons, its prevalence is much lower in healthy community-dwelling elderly. Coexistent multiple abnormalities often impair cardiovascular homeostasis in institutionalized elderly.

Symptoms, Signs, and Diagnosis

Faintness, light-headedness, dizziness, confusion, or visual blurring is evidence of a mild to moderate reduction in cerebral blood flow. With more severe cerebral hypoperfusion, syncope or generalized seizures may supervene (see also Syncope, below). Exercise or a heavy meal may exacerbate symptoms. Other associated phenomena usually relate to the underlying cause.

Orthostatic hypotension is diagnosed when symptoms suggestive of hypotension and a marked reduction in measured BP are provoked by standing and relieved by lying down. An underlying cause must be sought based on the patient's presenting circumstances and associated phenomena (eg, as described above in Shy-Drager syndrome).

Prognosis and Treatment

Prognosis depends on the underlying cause. Orthostatic hypotension due to hypovolemia or drug excess is rapidly reversed by correcting these problems. Anemia and electrolyte imbalance can be specifically treated. The orthostasis of protracted bed rest can be lessened by having patients sit up each day. Elderly patients should maintain adequate fluid intake, limit or avoid alcohol, and exercise regularly when feasible. The outlook in patients with a chronic underlying disorder is determined by the management of that disease; eg, postural hypotension appears to indicate a poor prognosis in diabetic patients with hypertension.

When the causative disease cannot be improved, management is designed to produce peripheral vasoconstriction and/or increase cardiac output. Often, this allows BP to be maintained at an asymptomatic (although reduced) level in the standing position. However, in advanced stages of Shy-Drager syndrome or idiopathic orthostatic hypotension, pharmacotherapy is often inadequate, and some mechanical form of counterpressure or a counterpulsation device may be needed. If orthostatic hypotension is related to venous pooling in the legs, fitted elastic hose may enhance the cardiac output and BP on standing. In more advanced cases, inflatable aviator-type antigravity suits, although often poorly tolerated, may be needed to produce sufficient leg and abdominal counterpressure.

With mild orthostasis, the peripheral adrenergic drug ephedrine 25 to 50 mg po q 3 to 4 h, when the patient is awake, may maintain adequate BP. Phenylephrine has also been used. An alternative or concurrent therapy is expansion of plasma volume, initially by increasing Na intake and subsequently by administering Na-retaining hormones. In the absence of heart failure, Na intake can be increased 5 to 10 g above the usual dietary level by liberally salting food or taking sodium chloride tablets. 9-alpha-Fludrocortisone 0.1 to 0.5 mg/day po improves the peripheral vasoconstrictor response to sympathetic stimulation but is effective only when Na ingestion is adequate and weight gain of 1.3 to 2.2 kg (3 to 5 lb) occurs due to Na retention and expansion of the intravascular fluid volume. The risk of this management, particularly in elderly patients or those with impaired myocardial function, is the development of heart failure; dependent edema alone, in the absence of heart failure, does not contraindicate continued therapy. An important complication is hypokalemia due to the K-wasting effect of mineralocorticoid administration accompanied by a high Na intake; K supplements may be needed. Supine hypertension is an added risk.

Propranolol therapy has been reported to enhance the beneficial effects of Na and mineralocorticoid therapy. beta-Blockade with propranolol, leading to unopposed alpha-adrenergic peripheral vascular vasoconstriction, prevents vasodilation that occurs in some patients on standing. The risk is reduction of Na excretion with development of heart failure.

Dihydroergotamine, a selective constrictor of peripheral capacitance vessels, has shown only short-term benefit; the risks include supine hypertension and extremity gangrene. NSAIDs may cause renal Na retention and inhibit prostaglandin-induced vasodilation; indomethacin 25 to 50 mg po tid may be beneficial in increasing peripheral vascular resistance. However, these drugs may cause GI symptoms and unwanted vasopressor reactions (described in patients who received indomethacin and sympathomimetic drugs concurrently). Metoclopramide may inhibit the natriuretic and vasodilator effects of dopamine excess (a rare cause of orthostatic hypotension) but may exacerbate parkinsonism. Rapid atrial pacing has had limited success, particularly in patients with slow heart rates.

Midodrine may be tried in patients with severe orthostasis unresponsive to other drugs. However, its benefit/risk profile has not been established.

Elderly patients should be encouraged to change posture slowly; sleeping with the head of the bed raised may relieve symptoms by promoting Na retention and reducing nocturnal diuresis. They should also avoid prolonged standing. Regular modest-intensity exercise promotes overall vascular tone and reduces venous pooling.


 


 






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