In patients suffering from hemorrhagic shock, a decrease in central venous pressure (CVP) and pulmonary wedge pressure (PCWP), a decrease in cardiac output, a decrease in venous oxygen saturation (SVO2), and an increase in systemic vascular resistance can be observed by central blood pressure measurement. Shock caused by massive blood loss is called hemorrhagic shock, which is commonly seen in bleeding caused by trauma, peptic ulcer bleeding, rupture of esophageal varices, and bleeding caused by obstetric and gynecological diseases. Whether shock occurs after blood loss depends not only on the amount of blood loss, but also on the speed of blood loss. Shock often occurs with rapid, massive (more than 30-35% of the total blood volume) blood loss without timely replenishment. The overall effect of sympathetic excitation and increased catecholamine release on the cardiovascular system is to increase total peripheral resistance and cardiac output. However, the vascular response of different organs varies considerably. The vasculature of the skin, abdominal viscera, and kidneys is innervated by abundant sympathetic constrictor fibers. Moreover, α-receptors are dominant, thus, during sympathetic excitation and catecholamine increase, small arteries, small veins, microarterioles and precapillary sphincters in these areas contract, among which they contract most strongly due to the densest distribution of sympathetic constrictor fibers in the microarterioles, and the strongest reactivity of the precapillary sphincters to catecholamines. As a result, the precapillary resistance rises significantly, the microcirculatory perfusion decreases sharply, the average blood pressure in the capillaries decreases significantly, and only a small amount of blood flows into the microvessels and small veins through the direct pathway and a few true capillaries, and the tissues undergo severe ischemic hypoxia as a result. The distribution of sympathetic vasoconstrictor fibers in cerebral blood vessels is the least, and the density of α-receptors is also low, and the caliber may not change significantly. Although coronary arteries are also sympathetically innervated and have α and β receptors, sympathetic arousal and increased catecholamines can cause coronary artery dilation through increased cardiac activity and increased metabolic levels resulting in increased vasodilator metabolites, especially adenosine. Sympathetic arousal and decreased blood volume also activate the renin-angiotensin-aldosterone system, and angiotensin II has a strong vasoconstrictor effect, including on coronary arteries. In addition, increased catecholamines stimulate platelets to produce more thromboxane A2 (TXA2), which also has a strong vasoconstrictor effect.