Nifedipine is an important antihypertensive drug that has been widely used in clinical practice for many years. Due to the short duration of action of short-acting nifedipine, which requires multiple daily doses and can lead to significant fluctuations in blood pressure, its clinical application has been reduced in recent years and gradually replaced by nifedipine controlled-release or extended-release dosage forms. However, because of the low price and fast onset of action, the drug is still used more often in primary care institutions. Many doctors often use sublingual short-acting nifedipine for emergency hypertension, subacute or general hypertensive patients, which may have serious adverse effects on patients and should be avoided. 1, short-acting nifedipine characteristics of action nifedipine belongs to the dihydropyridine class of calcium antagonists, through the dilatation of blood vessels, reduce peripheral resistance and play a role in lowering blood pressure. The drug has a rapid onset of action and can exert its antihypertensive effect in a few minutes after sublingual administration. The main adverse effects are flushing, headache and tachycardia. Since sublingual nifedipine is fast-acting and easy to administer, it was a common method for treating hypertensive emergencies. 2, hypertension emergency and sub-emergency management principles Because there is no target organ damage, patients with hypertension sub-emergency generally do not need too aggressive antihypertensive treatment, blood pressure drop too fast or too large for the patient may do more harm than good. In general, blood pressure in patients with subacute hypertension can be slowly reduced to 160/100mmHg (1mmHg=0. 133kPa) within 24-48h. Most patients can be controlled by oral antihypertensive drugs and usually do not require intravenous application of antihypertensive drugs. Patients with high blood pressure, but without complications, should not be over-treated. Intravenous or high-dose oral loading doses of antihypertensive drugs can produce severe hypotension or other adverse effects on the patient and should be avoided. Unlike subacute hypertension, patients with acute hypertension are more critically ill and should be managed more aggressively and carefully. The ideal drug should anticipate the intensity and speed of blood pressure lowering and facilitate timely adjustment of the intensity of blood pressure lowering according to the patient’s blood pressure control, thus short-acting antihypertensive drugs by the intravenous route should be preferred. Because target organ damage already exists, too rapid or excessive blood pressure lowering can easily lead to lower tissue perfusion pressure and induce ischemic events, so the initial blood pressure lowering target should not be lowered to normal. A reasonable approach is to first lower their blood pressure to a relatively safe level to prevent or reduce target organ damage such as heart, brain and kidney to the maximum extent. In general, the following principles can be followed to control the magnitude and speed of blood pressure drop: the average arterial pressure drop ≤ 25% of the pre-treatment rate within 1h, followed by a drop to <160/100mmHg within 2~6h. If tolerated and clinically stable, the blood pressure will be gradually reduced to normal levels within 24~48h. 3. Sublingual nifedipine is potentially harmful to patients with acute hypertension. Based on the previously described characteristics of sublingual nifedipine and the principles of management of acute and subacute hypertension, it can be seen that sublingual nifedipine should not be used for emergency antihypertensive treatment. However, the magnitude and speed of blood pressure reduction are difficult to control and may have adverse effects on patients or even lead to serious consequences. Fan Zihang et al. reported 7 cases of hypertensive patients with severe adverse effects caused by sublingual nifedipine, whose main manifestations included hallucinations, dizziness, nausea, chest pain, chest tightness, profuse sweating, near-death feeling, impaired consciousness, stroke with hemiparesis, and blindness, etc. OMailia et al. reported 3 cases of hypertensive crisis patients with severe hypotension after sublingual nifedipine (10 mg), and 2 of them had elevated cardiac enzymes The other patient had ST-segment elevation on the ECG, and the ST-segment fell back to the baseline level when the blood pressure returned to normal. This was further confirmed by the study of Ishibashi et al. This study included 93 patients with hypertensive crisis, aged ≥65 years, all with a previous history of coronary heart disease. A significant decrease in blood pressure with increased heart rate was observed after nifedipine (5 mg) was administered. Among the 55 patients with left ventricular hypertrophy and electrocardiographic abnormalities, 6 developed myocardial ischemic symptoms. Shettigar et al. reported two patients with unstable angina who died after taking nifedipine, and autopsy confirmed that the cause of death was myocardial infarction. Peters et al. reported a case of hypotension and prolonged QT interval after nifedipine administration in a patient with hypertensive crisis and loss of consciousness after 1 h. The ECG suggested ventricular fibrillation, and it was thought that this patient developed subendocardial myocardial ischemia after nifedipine administration, leading to tip-twist type of ventricular tachycardia. Schwartz et al. reported a case of a 44-year-old male patient with blood pressure of 270/140 mmHg and no obvious neurological abnormalities, whose blood pressure dropped to 160/100 mmHg after 15 min of nifedipine (10 mg), while the patient developed mild hemiparesis of the left limb. In the other patient, blood pressure was 200/120 mmHg and decreased to 150/90 mmHg after sublingual nifedipine, and the patient developed mild hemiparesis of the right limb 2 h later. Both patients were confirmed to have new cerebral infarction by cranial CT examination. The mechanism of adverse cardiovascular and cerebrovascular events after sublingual nifedipine may involve various aspects, and the most important reasons may include the following two aspects: 1. The rapid and significant decrease in blood pressure in a short period of time in patients with severe hypertension may lead to a significant decrease in blood perfusion pressure and blood flow to vital organs; 2. 2. Nifedipine can lead to redistribution of systemic blood flow, with an increase in peripheral blood flow and a relative decrease in cardiac and cerebrovascular blood flow. In view of the fact that sublingual nifedipine may lead to serious adverse events, in 1985 the U.S. Food and Drug Administration concluded that patients with hypertension should not take sublingual nifedipine. The 6th report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of Hypertension in the United States also clearly stated that sublingual nifedipine was "unacceptable". The Chinese Guidelines for the Prevention and Treatment of Hypertension (2009 Primary Edition) also states that sublingual nifedipine should be used with caution or not in patients with acute hypertension. In China's current clinical practice, sublingual nifedipine is still commonly used for emergency antihypertensive treatment in acute or subacute hypertension, and education on this should be strengthened.