Definition of hypertensive emergencies
Hypertension is a serious life-threatening clinical syndrome in which the blood pressure of a hypertensive patient increases significantly or rapidly (systolic blood pressure >200 mmHg, or diastolic blood pressure >130 mmHg) during the development of the disease or under the influence of certain triggers.
or diastolic blood pressure >130 mmHg), often accompanied by functional damage to target organs such as the heart, brain, kidney and retina, is a serious life-threatening clinical syndrome.
Classification of hypertensive emergencies
I. Hypertensive emergencies that require blood pressure to be lowered to an appropriate level within 1-2 hours, including
Hypertensive crisis
hypertensive encephalopathy
Hypertension combined with stroke, intracranial hemorrhage, subarachnoid hemorrhage
hypertension combined with unstable angina pectoris, acute myocardial infarction, acute left heart failure with pulmonary edema, acute aortic coarctation
Eclampsia of pregnancy
These patients are often accompanied by acute target organ damage
II. Hypertensive sub-emergencies that require blood pressure to be lowered to an appropriate level within 24 hours, including
Hypertension grade 3
Hypertension with progressive target organ damage
Acute progressive malignant hypertension
Hypertension in pregnancy
perioperative hypertension
These patients often have no or only very mild target organ damage
Clinical manifestations of hypertensive emergencies
Hypertensive crisis
Concept: It is a series of vasopressure crisis manifested by a temporary strong spasm of peripheral arteries due to certain triggers on the basis of hypertension, which causes a further rapid rise in blood pressure and can lead to irreversible damage to vital organs in a short period of time.
Mechanism: Sympathetic nerve activity is hyperactive, and blood catecholamines, renin, angiotensin II and other vasoconstrictive substances rise sharply.
Hypertensive crisis
Clinical features
Systolic blood pressure is significantly higher than diastolic blood pressure and heart rate is significantly faster
Signs of vegetative dysfunction
- Acute damage to target organs
- Sudden onset, short duration, but easy recurrence.
Hypertensive encephalopathy
Clinical features
Elevated diastolic blood pressure, often >120 mmHg
Symptoms of cerebral edema and increased intracranial pressure
Objective examination: optic nerve papillae edema, exudation, hemorrhage
After active antihypertensive treatment, clinical signs and symptoms disappear without leaving any sequelae of brain damage
Acute malignant hypertension
Clinical characteristics
Most often seen in young men, especially heavy smokers
Rapid progression of the disease, diastolic blood pressure is often sustained ³130mmHg
Progressive renal damage
Progressive retinopathy
Hypertension combined with acute cerebrovascular disease
Regulation of cerebral blood flow in hypertension.
To maintain a certain cerebral blood flow and cerebral perfusion pressure in patients with cerebrovascular disease, it is mainly regulated by the myogenic response of contraction and diastole of cerebral arteries. The mean arterial pressure required for this automatic regulation under normal conditions (DBP about 60-150 mmHg). The small cerebral arteries respond to a prolonged increase in blood pressure with sustained constriction. Therefore, the upper and lower limits of autoregulation in hypertensive patients are shifted upward, with the result that: (i) tolerance to hypertension is enhanced, and (ii) tolerance to hypotension is reduced; and (iii) structural changes in the vessel wall occur.
Characteristics of hypertension in acute cerebrovascular disease
(1) Most stroke patients have a tendency to increase blood pressure within 24 h of onset, with marked fluctuations on the first day and a spontaneous decrease in 3 to 10 days.
(ii) Patients with a previous history of hypertension will have higher blood pressure at the onset of cerebral hemorrhage.
(③Patients with hypertension in stroke, after a spontaneous decrease in blood pressure, are still relatively higher than those without pre-morbid hypertension.
(iv) Hypertension appears earlier in acute stroke patients with impaired consciousness, suggesting a poor prognosis
Treatment of hypertensive emergencies
The advantages and disadvantages of rapid hypotensive treatment: a rapid increase in blood pressure, mean arterial pressure (MAP) > 150 mmHg occurs when the cerebrovascular hypertensive regulation response, causing cerebral small arteries spasm, ischemia, followed by dilation, exudation, causing acute cerebral dysfunction, reduced renal blood flow, renal ischemia, hypoxia, activation of the RAS system, further increase in blood pressure. Rapid hypotension section cuts off the vicious cycle, improves prognosis and reduces morbidity and mortality. However, inappropriate blood pressure lowering can cause a negative hemodynamic response with adverse clinical consequences. Ischemic damage to target organs has been reported in normal subjects when MAP decreases to <60 mmHg. Especially in elderly patients with poor vascular compliance and impaired renal function, too fast and too low blood pressure lowering can lead to excessive reduction of blood flow to the heart, brain, kidney and retina, and cause related symptoms. Therefore, the antihypertensive drugs should be selected correctly; the magnitude of the lowering should be moderate, so as not to exceed the cerebrovascular auto-regulation; the speed of lowering should be reasonable. The initial goal of treatment is to reduce 25% within a few minutes to 2 hours, and then to 160 mmHg in 2-6 hours. avoiding the induction of renal, cerebral or coronary ischemia by excessive pressure reduction.
Treatment objectives and principles Zhengzhou University First Affiliated Hospital Emergency Center Li Li
1.Rapidly and appropriately lower the blood pressure and remove the immediate cause of the emergency as much as possible.
2.Correct the damage of target organs.
3.Consolidate the therapeutic effect-, followed by maintenance treatment.
Commonly used rapid blood pressure lowering drugs
Vasodilator
Sodium nitroprusside: 20-300 ug/min
Nitroglycerin: 10-50ug/min
Calcium antagonists
Nifedipine
Nicardipine
Diltiazem
Verapamil
Adrenergic receptor blockers
Uraldil
Phentolamine
Labetalol (Liothyronine)
Diuretics
Furosemide
Management of common hypertensive emergencies
(I) Hypertensive encephalopathy
Lower blood pressure to a systolic level of 140-160 mmHg within 2-3 hours, but not more than 25% of the mean arterial pressure. The use of this drug is limited because sodium nitroprusside requires strict monitoring conditions and can increase intracranial pressure and affect cerebral perfusion. Nicardipine can gradually lower blood pressure and maintain cerebral blood flow by injection or sedation.
(ii) Acute ischemic stroke
Cerebral thrombosis and cerebral embolism are common. In the early stage, blood pressure may rise compensatingly to ensure blood supply around the lesion, but later it may fall automatically due to dysregulation of cerebral circulation. Therefore, it is important to lower blood pressure carefully in these patients. If the diastolic blood pressure is >130 mmHg, the blood pressure can be carefully lowered to 110 mmHg. A slightly higher blood pressure is beneficial to the perfusion of the ischemic area, and the reduction of cerebral perfusion caused by too low blood pressure should be avoided, increasing the infarct area. If emergency thrombolytic therapy is considered, blood pressure should be lowered to 185/110 mmHg in order to prevent bleeding due to hypertension.
(C) Cerebral hemorrhage
Blood pressure often increases significantly immediately after cerebral hemorrhage because of the compensatory response to ensure blood supply to brain tissue when intracranial pressure is elevated, and when intracranial pressure decreases, blood pressure also decreases. Therefore, the first step is to lower the cranial pressure, including dehydration with drugs such as mannitol and tachyphylaxis, surgical elimination of hematoma and ventricular drainage. However, persistently high blood pressure can cause rebleeding or persistent bleeding, and it is currently believed that a systolic blood pressure >200 mmHg and diastolic blood pressure >130 mmHg will aggravate bleeding, and lowering the blood pressure may improve the prognosis. The lowering of blood pressure in cerebral hemorrhage should be carried out cautiously, and should be done gradually within 6-12h, with the magnitude of lowering not more than 25%. The application of sodium nitroprusside needs to pay attention to the increase of intracranial pressure and cerebral perfusion, and it is contraindicated if there is an increase of intracranial pressure.
(iv) Subarachnoid hemorrhage.
It is often accompanied by cerebral vasospasm which aggravates the fluctuation of cerebral perfusion. Analysis of controlled trials of nimodipine versus placebo groups concluded that nimodipine reduced the risk of such patients by 42% compared to the placebo group. It is advocated that blood pressure should be lowered to normal levels so as not to affect the patient’s consciousness and cerebral perfusion.
(v) Aortic coarctation
The rate of death is extremely high and requires rapid hypotension, generally requiring a systolic blood pressure of 100-120 mmHg and a mean arterial pressure of <80 mmHg. Lowering the blood pressure also reduces the decompressive effect on the aortic wall. The classical drug treatment is sodium nitroprusside combined with β-blocker to lower the blood pressure.
(vi) Acute left heart failure.
Rapidly lowering blood pressure to normal reduces left ventricular pre and afterload. Sodium nitroprusside can reduce the pre and afterload of the heart and improve cardiac function. Angiotensin-converting enzyme inhibitor (ACEI) nitrate preparations can also be used effectively.
(vii) Pheochromocytoma.
Phentolamine or labetalol is preferred, or a combination of both can effectively block alpha receptors, peripheral vasodilation, and blood pressure can be rapidly reduced.
(viii) Eclampsia of pregnancy.
It needs to be recognized that excessive lowering of blood pressure can affect the placental blood supply. If diastolic blood pressure >110 mmHg should be given to reduce blood pressure and avoid excessive lowering. ACEI and diuretics are contraindicated. Sodium nitroprusside is also contraindicated as it can cause fetal chloride toxicity. Although calcium antagonists are effective in lowering blood pressure, they can reduce uterine blood flow and inhibit uterine contractions, which can affect delivery. If such patients have convulsions, magnesium sulfate can be applied intravenously.