Hypovolemia means diminished blood volume. Hemor- rhage is the most common cause of hypovolemic shock. Hemorrhage decreases the filling pressure of the circula- tion and, as a consequence, decreases venous return. As a result, the cardiac output falls below normal, and shock may ensue.
Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure
Above shows the approximate effects on cardiac output and arterial pressure of removing blood from the circulatory system over a period of about 30 minutes. About 10% of the total blood volume can be removed with almost no effect on arterial pressure or cardiac out- put, but greater blood loss usually diminishes the cardiac output first and later the arterial pressure, both of which fall to zero when about 40% to 45% of the total blood volume has been removed.
Sympathetic Reflex Compensations in Shock-Their Special Value to Maintain Arterial Pressure. The decrease in arterial pressure after hemorrhage, as well as decreases in pressures in the pulmonary arteries and veins in the thorax, cause powerful sympathetic reflexes. These reflexes stimulate the sympathetic vasoconstrictor system in most tissues of the body, resulting in three important effects:
1. The arterioles constrict in most parts of the system- ic circulation, thereby increasing the total peripheral resistance.
2. The veins and venous reservoirs constrict, thereby helping maintain adequate venous return, despite diminished blood volume.
3. Heart activity increases markedly, sometimes in- creasing the heart rate from the normal value of 72 beats/min to as high as 160 to 180 beats/min.
In the absence of the sympathetic reflexes, only 15% to 20% of the blood volume can be removed over a period of 30 minutes before a person dies; in contrast, a per- son can sustain a 30% to 40% loss of blood volume when the reflexes are intact.
Therefore, these reflexes extend the amount of blood loss that can occur without caus- ing death to about twice that which is possible in their absence.
Greater Effect of Sympathetic Nervous Reflexes in Maintaining Arterial Pressure Than in Maintaining Cardiac Output. Referring again to, note that the arterial pressure is maintained at or near normal levels in the hemorrhaging person longer than is the cardiac output.
The reason for this difference is that the sympathetic reflexes are geared more for maintaining ar terial pressure than for maintaining cardiac output. They increase the arterial pressure mainly by increasing the total peripheral resistance, which has no beneficial effect on cardiac output.
However, the sympathetic constriction of the veins is important to keep venous return and cardiac output from falling too much, in addition to their role in maintaining arterial pressure.
Especially interesting is the second plateau occur ring at about 50 mm Hg in the arterial pressure curve. This second plateau results from activation of the central nervous system ischemic response, which causes extreme stimulation of the sympathetic nervous system when the brain begins to experience lack of oxygen or excess buildup of carbon dioxide.
This effect of the central nervous system ischemic response can be called the “last-ditch stand” of the sympathetic reflexes in their attempt to keep the arterial
pressure from falling too low.
Protection of Coronary and Cerebral Blood Flow by the Reflexes. A special value of the maintenance of normal arterial pressure, even in the presence of decreasing cardiac output, is protection of blood flow through the coronary and cerebral circulations.
The sympathetic stimulation does not cause significant constriction of the cerebral or cardiac vessels. In addition, in both vascular beds, local blood flow autoregulation is excellent, which prevents moderate decreases in arterial pressure from significantly decreasing their blood flows.
Therefore, blood flow through the heart and brain is maintained essentially at normal levels as long as the mean arterial pressure does not fall below about 70 mm Hg, despite the fact that blood flow in some other areas of the body might be decreased to as little as one-third to one-quarter normal by this time because of vasoconstriction.
PROGRESSIVE AND NONPROGRESSIVE HEMORRHAGIC SHOCK
Above shows an experiment that demonstrates the effects of different degrees of sudden acute hemorrhage on the subsequent course of arterial pressure. The animals in this experiment were anesthetized and bled rapidly until their arterial pressures fell to different levels.
The animals whose pressures fell immediately to no lower than 45 mm Hg (groups I, II, and III) all eventually recovered; the recovery occurred rapidly if the pressure fell only slightly (group I) but occurred slowly if it fell almost to the 45-mm Hg level (group III).
When the arterial pressure fell below 45 mm Hg (groups IV, V, and VI), all the animals died, although many of them hovered between life and death for hours before the circulatory system deteriorated to the stage of death.
This experiment demonstrates that the circulatory sys- tem can recover as long as the degree of hemorrhage is no greater than a certain critical amount. Crossing this criti- cal threshold by even a few milliliters of blood loss makes the eventual difference between life and death.
Thus, hemorrhage beyond a certain critical level causes shock to become progressive. That is, the shock itself causes still
more shock, and the condition becomes a vicious cycle that eventually leads to deterioration of the circulation and to death.
Nonprogressive Shock-Compensated Shock
If shock is not severe enough to cause its own progres sion, the person eventually recovers. Therefore, shock of this lesser degree is called nonprogressive shock or com pensated shock, meaning that the sympathetic reflexes and other factors compensate enough to prevent further deterioration of the circulation.
The factors that cause a person to recover from mod- erate degrees of shock are the negative feedback control mechanisms of the circulation that attempt to return car- diac output and arterial pressure back to normal levels. They include the following:
1. Baroreceptor reflexes, which elicit powerful sympa thetic stimulation of the circulation.
2. Central nervous system ischemic response, which elicits even more powerful sympathetic stimulation throughout the body but is not activated significant- ly until the arterial pressure falls below 50 mm Hg 3. Reverse stress-relaxation of the circulatory system, which causes the blood vessels to contract around the diminished blood volume so that the blood vol- ume that is available more adequately fills the circulation.
4. Increased secretion of renin by the kidneys and formation of angiotensin II, which constricts the peripheral arterioles and also causes decreased output of water and salt by the kidneys, both of which help prevent progression of shocks.
5. Increased secretion by the posterior pituitary gland of vasopressin (antidiuretic hormone), which con- stricts the peripheral arterioles and veins and greatly increases water retention by the kidneys.
6. Increased secretion by the adrenal medullae of epi- nephrine and norepinephrine, which constricts the peripheral arterioles and veins and increases the heart rate.
7. Compensatory mechanisms that return the blood volume back toward normal, including absorption of large quantities of fluid from the intestinal tract, absorption of fluid into the blood capillaries from the interstitial spaces of the body.
conservation of water and salt by the kidneys, and increased thirst and increased appetite for salt, which make the person drink water and eat salty foods if they are able to do so,The sympathetic reflexes and increased secretion of catecholamines by the adrenal medullae provide rapid help toward bringing about recovery because they become maximally activated within 30 seconds to a few minutes after hemorrhage.