During hemorrhage, there is minimal constriction of the renal and splanchnic blood vessels in the heart and brain. However, if this constriction persists for too long, it can have negative consequences. Patients often survive the initial hypotensive phase of severe and prolonged hemorrhage, only to succumb to kidney failure caused by reduced blood flow to the kidneys. Intestinal ischemia can also have serious effects. Even a few hours of hemorrhagic hypotension can lead to intestinal bleeding and damage to the mucosa. Moreover, decreased blood flow to the splanchnic region causes swelling of liver cells, obstructing the hepatic sinusoids and increasing portal venous pressure, which further exacerbates intestinal blood loss.

When arterial pressure drops below approximately 60 mm Hg, there are no additional responses through the baroreceptor reflexes as this pressure level serves as the threshold for stimulation. However, low arterial pressure can stimulate peripheral chemoreceptors due to inadequate blood flow leading to tissue hypoxia. This chemoreceptor excitation can amplify the existing peripheral vasoconstriction triggered by the baroreceptor reflexes. Additionally, respiratory stimulation helps enhance venous return through the auxiliary pumping mechanism described earlier.

If arterial pressure falls below approximately 40 mm Hg as a result of blood loss, cerebral ischemia activates the sympathoadrenal system. The sympathetic nerves discharge at a much higher rate compared to the maximal neural activity during cessation of baroreceptor stimulation. This leads to pronounced vasoconstriction and increased myocardial contractility. However, with more severe cerebral ischemia, the vagal centers also become activated, resulting in bradycardia that worsens the initial hypotension causing cerebral ischemia.

During hemorrhagic hypotension, the decrease in arterial pressure, arteriolar constriction, and reduced venous pressure cause the hydrostatic pressure in the capillaries to decrease. These changes promote the net reabsorption of interstitial fluid into the vascular compartment. The speed of this response is shown in Figure 19.22. When 45% of the estimated blood volume is removed over a 30-minute period, mean arterial blood pressure initially drops rapidly but is then mostly restored to nearly the control level. Plasma colloid osmotic pressure decreases significantly during bleeding and continues to gradually decrease for several hours. This reduction in colloid osmotic pressure reflects the dilution of blood by tissue fluids with low protein content.

Significant amounts of fluid can be drawn into the circulation during hemorrhage. Approximately 0.25 mL of fluid per minute per kilogram of body weight can be reabsorbed by the capillaries. Therefore, an average individual may autoinfuse around 1 L of fluid per hour from the interstitial spaces into the circulatory system after acute blood loss. Substantial quantities of fluid may also slowly shift from the intracellular space to the extracellular space. This fluid exchange is likely mediated by the secretion of cortisol from the adrenal cortex in response to hemorrhage, which is essential for fully restoring plasma volume.

Epinephrine and norepinephrine, the catecholamines, are released from the adrenal medulla in response to the same stimuli that trigger widespread sympathetic nervous discharge. Levels of catecholamines in the blood are elevated during and after hemorrhage. When arterial pressure decreases to 40 mm Hg, the levels of catecholamines can increase up to 50-fold. Epinephrine mainly originates from the adrenal medulla, while norepinephrine is produced by both the adrenal medulla and peripheral sympathetic nerve endings. These humoral substances enhance the effects of sympathetic nervous activity mentioned earlier.
The renal and splanchnic vasoconstriction during hemorrhage is least severe in the heart and brain. However, if such constriction persists too long, it may be detrimental. Frequently, patients survive the acute hypotensive period of a prolonged, severe hemorrhage, only to die several days later from the kidney failure that results from renal ischemia. Intestinal ischemia may also have dire effects. For example, intestinal bleeding and extensive sloughing of the mucosa can occur after only a few hours of hemorrhagic hypotension. Furthermore, the diminished splanchnic flow swells the centrilobular cells in the liver. The resulting obstruction of the hepatic sinusoids causes portal venous pressure to rise, and this response intensifies intestinal blood loss.
Reductions in arterial pressure below approximately 60 mm Hg do not evoke any additional responses through the baroreceptor reflexes because this pressure level constitutes the threshold for stimulation (see ). However, low arterial pressure may stimulate peripheral chemoreceptors because inadequacy of local blood flow leads to hypoxia in the chemoreceptor tissue. Chemoreceptor excitation may then enhance the already existent peripheral vasoconstriction evoked by the baroreceptor reflexes. In addition, respiratory stimulation assists venous return by the auxiliary pumping mechanism described earlier (see also
When arterial pressure falls below approximately 40 mm Hg as a consequence of blood loss, the resulting cerebral ischemia activates the sympathoadrenal system. The discharge by sympathetic nerves is several times greater than the maximal neural activity that occurs when the baroreceptors cease to be stimulated. The vasoconstriction and increase in myocardial contractility may be pronounced. With more severe degrees of cerebral ischemia, however, the vagal centers also become activated. The resulting bradycardia aggravates the hypotension that initiated the cerebral ischemia
Reabsorption of Tissue Fluids
The arterial hypotension, arteriolar constriction, and reduced venous pressure during hemorrhagic hypotension cause the hydrostatic pressure in the capillaries to drop. The balance of these forces promotes the net reabsorption of interstitial fluid into the vascular compartment (see ). The rapidity of this response is displayed in
Fig. 19.22 . When 45% of the estimated blood volume is removed over a 30-minute period, mean arterial blood pressure declines rapidly and then is largely restored to nearly the control level. Plasma colloid osmotic pressure declines markedly during the bleeding and continues to decrease more gradually for several hours. The reduction in colloid osmotic pressure reflects dilution of the blood by tissue fluids that contain little protein.
Considerable quantities of fluid may thus be drawn into the circulation during hemorrhage. Approximately 0.25 mL of fluid per minute per kilogram of body weight may be reabsorbed by the capillaries. Thus approximately 1 L of fluid per hour might be autoinfused from the interstitial spaces into the circulatory system of an average individual after acute blood loss. Substantial quantities of fluid may shift slowly from the intracellular space to the extracellular space. This fluid exchange is probably mediated by secretion of cortisol from the adrenal cortex in response to hemorrhage. Cortisol is essential for the full restoration of plasma volume after hemorrhage.
The catecholamines epinephrine and norepinephrine are released from the adrenal medulla in response to the same stimuli that evoke widespread sympathetic nervous discharge (see
Chapter 43). Blood levels of catecholamines are high during and after hemorrhage. When blood loss is such that arterial pressure is reduced to 40 mm Hg, the level of catecholamines increases as much as 50-fold. Epinephrine comes almost exclusively from the adrenal medulla, whereas norepinephrine is derived from both the adrenal medulla and peripheral sympathetic nerve endings. These humoral substances reinforce the effects of the sympathetic nervous activity listed previously.