An acute hypertensive patient with blood pressure of 200/110 mmHg showed no signs of acute left heart failure. In order to lower the blood pressure, a vasodilator was used, but when the blood pressure dropped to the normal range (120/60 mmHg), the patient showed signs of acute left heart failure. Why is this? I. Body circulation and pulmonary circulation The blood circulation of human body is mainly divided into two circulations, namely, body circulation and pulmonary circulation, also called large circulation and small circulation. The important difference between the two is the difference in pressure. The body circulation is a dynamic high-pressure system, the highest pressure is the clinically measured arterial systolic pressure, up to about 100mmHg, and in the case of hypertension, up to 200mg or more. During the diastolic phase of the heart, the pressure falls back, i.e. diastolic pressure, which is also above 60 mmHg in healthy people. Therefore, from an overall perspective, the body circulation is a dynamically changing, high pressure system. The normal right ventricular pressure curve fluctuates within 30 mmHg; the normal value of pulmonary artery pressure (PCWP) is 4-12 mmHg; pulmonary stasis starts to appear at PCWP 18-20 mmHg; moderate pulmonary stasis appears at PCWP 20-25 mmHg; severe pulmonary stasis appears at PCWP 25-30 mmHg; acute pulmonary stasis appears at PCWP ＞Acute pulmonary edema appeared at PCWP >30 mmHg. Therefore, from an overall perspective, the pulmonary circulation is a low-pressure system at a low level with dynamic changes. In short, the pressure difference between the body circulation and the pulmonary circulation is obvious. Second, “people go to higher places” physics principle “people go to higher places”, one of the layers of meaning is that “beautiful things” are in the “high place “, people want to pursue the good things, should go to the “high place”. In clinical treatment, the fluid infused from the vein (from the low place) must also be transported to the “high place” (arterial system) in order to function, and cannot exist in the “low place”, otherwise it will not play its proper role. From the “low” to the “high”, only “pump” can be used, the “left heart” in the human body is a The “left heart” in the human body is a “pump”, responsible for “lifting” the blood from the low pressure area (pulmonary circulation) to the high pressure area (body circulation). This process is determined by three factors: time, volume and differential pressure. (A) time factor First of all, the time problem, that is, the rate problem. Clinically, too fast intravenous infusion rate can cause acute pulmonary edema. The mechanism is: rapid infusion through the vein, the liquid through the large vein to the right heart, and then to the pulmonary circulation. The left heart is the pump that “lifts” the fluid to the body circulation and then to the peripheral capillaries. If the infusion speed is too fast, the left heart pump will not be able to “lift” it to the body circulation, and the fluid will be “trapped” in the low-pressure lungs, which will naturally cause pulmonary stasis or pulmonary edema. Therefore, in clinical treatment, the body needs time to “digest” and “balance” the infused fluid. If the time is too short, the fluid will not be able to transfer, it will be retained in the low-pressure pulmonary circulation. (B) Volume factors The total amount of clinical infusion is too much, although very slow, can also cause acute pulmonary edema. The mechanism is: the body circulation is a dynamic high-pressure system, the pressure of the pulmonary circulation is relatively low, and there is a significant pressure step difference between the two. When the systemic volume is too much, “water flows to the lower part”, the low-pressure pulmonary circulation will naturally retain relatively more fluid, thus causing pulmonary stasis or pulmonary edema. Therefore, in clinical treatment, the total amount of fluid infused needs to be controlled, otherwise too much fluid will be retained in the low-pressure pulmonary circulation relatively more. (iii) Differential pressure factor The greater the pressure difference between the body circulation and the pulmonary circulation, the more effort the left heart pump will take to “lift” the blood from the pulmonary circulation to the body circulation, and the speed of fluid transfer from the pulmonary circulation to the body circulation will be slowed down. Therefore, when hypertension, the speed of infusion is slightly accelerated, there is a possibility of pulmonary edema, and this is the reason. Therefore, in the circulatory system, the transfer of fluid between the body circulation and the pulmonary circulation is determined by three factors: time, volume and differential pressure, that is, the ability of the “left heart pump” and the surrounding environment. This is also one of the important differences between arterial and intravenous infusion, arterial infusion should give priority to the total amount, followed by the speed; intravenous infusion should give priority to the speed, followed by the total amount. Third, the physics of “water flows to the lower part of the” “water flows to the lower part of the”, refers to the flow of liquid to the lower pressure area. In the circulatory system, the blood flow in the pulmonary circulation is also determined by two other factors, the pressure of the pulmonary artery and the pulmonary vein. (i) Pulmonary artery In the pulmonary circulation, the pulmonary artery is equivalent to a “valve” located in front of the lung tissue and is the first regulating valve of the pulmonary circulation. In patients with hypertensive emergencies, the constriction of small systemic arteries is often accompanied by constriction of the pulmonary artery; the latter may be a protective mechanism to reduce the effect of the high pressure state of the body circulation on the pulmonary circulation by reducing the blood flow to the lungs. After the application of vasodilators, the peripheral blood vessels expand and the vascular resistance of the body circulation decreases; if the pulmonary artery is still in a constricted state, the blood flow to the lungs remains at the original low level, the left heart may appear to be “idle” and the cardiac output may decrease. Therefore, when treating hypertension with vasodilators, the “non-isometric decrease” in systemic peripheral vascular resistance and pulmonary vascular resistance may cause the cardiac output (CO) to remain unchanged or decrease, which may aggravate the condition. In the treatment of hypertension with vasodilators, if the systemic peripheral vascular resistance and pulmonary vascular resistance are “isometric decrease”, the cardiac output (CO) can be unchanged or increased, which may be an ideal state. In other words, vasoactive drugs that dilate both peripheral blood vessels and pulmonary arteries are better antihypertensive drugs. There are six main categories of drugs currently used to lower blood pressure, namely diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, calcium antagonists, and a-blockers. There are also some compounded drugs containing the above ingredients, such as Fuzheng Tablets, Zhenju Antihypertensive Tablets, Beijing Antihypertensive 0, Hedgea, Ambonox, etc. But only calcium antagonists have any effect on the lung. However, only calcium antagonists may have a more pronounced effect on pulmonary vascular resistance, with the potential for an “isometric decrease”; because the newer guidelines for the treatment of pulmonary hypertension only leave calcium antagonists in the category of vasodilators. Therefore, the intravenous calcium antagonist antihypertensive drug, nicardipine, may have unparalleled advantages over other drugs in the treatment of hypertensive emergencies. （In the pulmonary circulation, the pulmonary vein is equivalent to a “valve” located behind the lung tissue, which is the second regulating valve of the pulmonary circulation, and its resistance is one of the factors determining the amount of fluid retained in the lungs. In the treatment of hypertensive emergencies, if there is obstruction of the pulmonary veins, the systemic application of vasodilators can cause the pulmonary arteries to dilate, resulting in increased pulmonary blood flow, which leads to pulmonary edema. This should be noted in clinical practice. The main diseases that cause pulmonary vein changes are: 1, pulmonary vein obstruction: pulmonary vein occlusion disease, congenital pulmonary vein stenosis, mediastinal tumor or granuloma, mediastinitis. 2, left heart disease: left heart insufficiency (wind heart disease, coronary heart disease, high heart disease, etc.), mitral valve stenosis or incomplete closure, left atrial mucinous tumor, etc. The pulmonary venous hypertension caused by these disorders was named as postcapillary pulmonary hypertension in the past classification, which is still relatively common in clinical practice. (iii) Status of pulmonary vessels The status of pulmonary vessels is also an important factor affecting pulmonary circulation. For example, in the early stage of pulmonary hypertensive lesions, vascular smooth muscle contraction often exists and responds better to vasodilator therapy; in the late stage of pulmonary hypertensive lesions, intimal and mid-layer fibrosis and thrombosis restrict vasodilation and respond poorly to therapy, or even paradoxically. Therefore, the responsiveness of pulmonary vessels should be considered before treatment with vasodilators. Secondly, hypertensive patients with chronic lung disease or interstitial lung disease, whose pulmonary hypertension is likely to be due to hypoxia, and areas of poor ventilation in the lungs are often accompanied by vasoconstriction, should use vasodilators with caution. This is because vasodilator therapy can cause an imbalance in the ventilation-to-blood flow ratio, which can aggravate hypoxemia. In conclusion, the treatment of any disease such as hypertension should be individualized and pathophysiologically oriented. The patient’s underlying pulmonary circulation status, the effect of drugs on the pulmonary circulation, and the interaction between the body circulation and the pulmonary circulation are issues that must be considered in the course of clinical treatment.