Compensatory Mechanism for Hemorrhage

The most obvious situation faced a patient with penetrating chest wall is hemorrhage. So here I will focus on the physiological response of the body or the compensatory mechanism to hemorrhage.

Course of Arterial Blood Pressure Changes

Cardiac output decreases as a result of blood loss. If sufficient blood is lost rapidly to bring mean arterial pressure to 50 mmHg, the pressure tends to return spontaneously back toward control over the next 20 or 30 minutes. In some cases (Curve A) this trend continues, and normal pressures are regained within a few hours, especially if the hemorrhage is quickly arrested. In other cases (Curve B), after an initial pressure rise, the pressure may subsequently decline and continue to fall at an accelerating rate until death ensues. The progressive deterioration of cardiovascular function is termed shock. At some point, if hemorrhage is not stopped and blood volume restored in time, the deterioration will become irreversible.

Compensatory Mechanisms:

A. Baroreceptor Reflexes.

The reduction in mean arterial pressure and pulse pressure during hemorrhage decreases the stimulation of the baroreceptors in the carotid sinuses and aortic arch. Several cardiovascular responses are thus evoked, all of which tend to return the arterial pressure toward normal. Reduction of vagal tone and enhancement of sympathetic tone increase heart rate and enhance myocardial contractility. The increased sympathetic discharge also produces generalized venoconstriction. Sympathetic activation constricts certain blood reservoirs such as the cutaneous, pulmonary, and hepatic vasculatures which provide an autotransfusion of blood into the circulating blood stream.

Generalized arteriolar vasoconstriction is a prominent response to the diminished baroreceptor stimulation during hemorrhage. The reflex increase in peripheral resistance minimizes the fall in arterial pressure resulting from the reduction of cardiac output.

Vasoconstriction is most severe in the cutaneous, skeletal muscle, and splanchnic vascular beds and is slight or absent in the cerebral and coronary circulations. In many instances the cerebral and coronary vascular resistances are diminished and the reduced cardiac output is redistributed to favor flow through the brain and the heart. Flow through the kidneys may also be sustained because of the strong local autoregulatory response within this organ system.

Thus, patient with hemorrhage appears pale and has cold skin due to the cutaneous vasoconstriction.

B. Chemoreceptor Reflexes.

Reductions in arterial pressure below about 60 mmHg do not evoke any additional responses through the baroreceptor reflexes, because this pressure level constitutes the threshold for stimulation. However, low arterial pressure may stimulate peripheral chemoreceptors because of hypoxia in the chemoreceptor tissue consequent to inadequate local blood flow. Chemoreceptor excitation enhances the already extant peripheral vasoconstriction evoked by the baroreceptor reflexes. Also, respiratory stimulation assists venous return by the auxiliary pumping mechanism--the abdomino-thoracic pump

C. Cerebral Ischemia.

When the arterial pressure is below about 40 mmHg, the resulting cerebral ischemia activates the sympathoadrenal system. The sympathetic nervous discharge is several times greater than the maximum activity that occurs when the baroreceptors cease to be stimulated. Therefore, the vasoconstriction and facilitation of myocardial contractility may be pronounced. With more severe degrees of cerebral ischemia, however, the vagal centers also become activated. The resulting bradycardia may aggravate the hypotension that initiated the cerebral ischemia.

D. Reabsorption of Tissue Fluids.

The arterial hypotension, arteriolar constriction, and reduced blood volume during hemorrhagic hypotension lower the hydrostatic capillary pressure. The balance of these forces promotes the net reabsorption of interstitial fluid into the vascular compartment. The reabsorption of fluid can occur rather quickly

E. Endogenous Vasoconstrictors.

The catecholamines, epinephrine and norepinephrine, are released from the adrenal medulla in response to the same stimuli that evoke widespread sympathetic nervous discharge. These humoral substances reinforce the effects of sympathetic nervous.

F. Renal Conservation of Fluids and Electrolytes.

Fluid and electrolytes are conserved by the kidneys during hemorrhage in response to various stimuli, including the increased secretion of vasopressin (antidiuretic hormone). The lower arterial pressure decreases the glomerular filtration rate, and thus curtails the excretion of water and electrolytes.

Contributed by Lawrence Oh