Hemorrhagic shock is a clinical syndrome resulting from decreased blood volume (hypovolemia) caused by blood loss, which leads to reduced cardiac output and organ perfusion. Blood loss can be external (e.g., externally bleeding wound) or internal (e.g., internal bleeding caused by ruptured aortic aneurysm). The severity of hemorrhagic shock and associated symptoms depends on the volume of blood that is lost and how rapidly it is lost. Generally, a blood loss of <15% of total blood volume leads to only a small increase in heart rate and no significant change in arterial pressure. When blood loss is 15 to 40%, mean arterial and pulse pressures fall, and heart rate increases, with the magnitude of these changes being related to how much blood is lost. If the hemorrhage is stopped, the arterial pressure slowly recovers and heart rate declines as long-term compensatory mechanisms are activated to restore normal arterial pressure. The time for recovery is longer when there is a greater loss of blood. Resuscitation efforts, which include the administration of fluids to increase blood volume, can speed up this recovery. A greater than 40% blood loss is life-threatening, and resuscitation is generally essential for survival because prolonged, severe hypotension leads to organ failure and death.
Compensatory mechanisms. The reduction in blood volume during acute blood loss causes a fall in central venous pressure and cardiac filling. This leads to reduced cardiac output and arterial pressure. The body has a number of compensatory mechanisms that become activated in an attempt to restore arterial pressure and blood volume back to normal. These mechanisms include:
The body can quickly sense a fall in blood pressure through its arterial and cardiopulmonary baroreceptors, and then activate the sympathetic adrenergic system to stimulate the heart (increase heart rate and contractility) and constrict blood vessels (increase systemic vascular resistance). Sympathetic activation has little direct influence on brain and coronary blood vessels, so these circulations can benefit from the vasoconstriction that occurs in other organs (particularly in the gastrointestinal, skeletal muscle and renal circulations) that serve to increase systemic vascular resistance and arterial pressure. In other words, cardiac output is redistributed from less important organs to the brain and myocardium, both of which are critical for survival. Reduced organ blood flow caused by vasoconstriction and reduced arterial pressure, leads to systemic acidosis that is sensed by chemoreceptors. The chemoreceptor reflex further activates the sympathetic adrenergic system thereby reinforcing the baroreceptor reflex. When the hypotension is very severe (e.g., mean arterial pressures <50 mmHg) and the brain becomes ischemic, this can produce a very intense sympathetic discharge that further reinforces the other autonomic reflexes
The combined effects of arterial hypotension and sympathetic activation lead to activation of humoral compensatory mechanisms. Sympathetic stimulation of the adrenal glands stimulates the release of catecholamines into the blood, which reinforces the effects of sympathetic activation on the heart and vasculature. The kidneys release more renin following hemorrhage leading to increased circulating levels of angiotensin II and aldosterone. This causes vascular constriction, enhanced sympathetic activity, stimulation of vasopressin release, activation of thirst mechanisms, and very importantly, increased renal reabsorption of sodium and water to increase blood volume. This renal mechanism is particularly important in the long-term recovery from blood loss.
Hypotension, combined with constriction of precapillary resistance vessels (small arteries and arterioles), causes a fall in capillary hydrostatic pressure. This pressure normally drives filtration of fluid from the blood, across the capillary endothelium, and into the interstitial space. When capillary hydrostatic pressure is reduced, less fluid leaves the capillaries, and when the pressure falls sufficiently low as occurs following moderate-to-severe blood loss, net reabsorption of fluid can occur from the tissue interstitium back into the capillary plasma. Although this reabsorbed fluid does not contain cells, it does contain electrolytes and some protein, and therefore increases the plasma volume. This reabsorbed fluid leads to hemodilution of the blood; therefore, red cell hematocrit falls in response to this fluid shift. This mechanism can cause up to 1 liter/hour of fluid to be withdrawn from interstitial spaces back into the plasma.
Homeostasis
Blood Pressure Regulation
Due to osmosis, water follows where Na+ leads. Much of the water the kidneys recover from the forming urine follows the reabsorption of Na+. ADH stimulation of aquaporin channels allows for regulation of water recovery in the collecting ducts. Normally, all of the glucose is recovered, but the loss of glucose control (diabetes mellitus) may result in an osmotic dieresis severe enough to produce severe dehydration and death. A loss of renal function means a loss of effective vascular volume control, leading to hypotension (low blood pressure) or hypertension (high blood pressure), which can lead to stroke, heart attack, and aneurysm formation.
The kidneys cooperate with the lungs, liver, and adrenal cortex through the renin–angiotensin–aldosterone system. The liver synthesizes and secretes the inactive precursor angiotensinogen. When the blood pressure is low, the kidney synthesizes and releases renin. Renin converts angiotensinogen into angiotensin I, and ACE produced in the lung converts angiotensin I into biologically active angiotensin II. The immediate and short-term effect of angiotensin II is to raise blood pressure by causing widespread vasoconstriction. angiotensin II also stimulates the adrenal cortex to release the steroid hormone aldosterone, which results in renal reabsorption of Na+ and its associated osmotic recovery of water. The reabsorption of Na+ helps to raise and maintain blood pressure over the longer term.
Regulation of Osmolarity
Blood pressure and osmolarity are regulated in a similar fashion. Severe hypo-osmolarity can cause problems like lysis (rupture) of blood cells or widespread edema, which is due to a solute imbalance. Inadequate solute concentration (such as protein) in the plasma results in water moving toward an area of greater solute concentration, in this case, the interstitial space and cell cytoplasm. If the kidney glomeruli are damaged by an autoimmune illness, large quantities of protein may be lost in the urine. The resultant drop in serum osmolarity leads to widespread edema that, if severe, may lead to damaging or fatal brain swelling. Severe hypertonic conditions may arise with severe dehydration from lack of water intake, severe vomiting, or uncontrolled diarrhea. When the kidney is unable to recover sufficient water from the forming urine, the consequences may be severe (lethargy, confusion, muscle cramps, and finally, death)
Recovery of Electrolytes
Sodium, calcium, and potassium must be closely regulated. The role of Na+ and Ca++homeostasis has been discussed at length. Failure of K+ regulation can have serious consequences on nerve conduction, skeletal muscle function, and most significantly, on cardiac muscle contraction and rhythm.
pH Regulation
Recall that enzymes lose their three-dimensional conformation and, therefore, their function if the pH is too acidic or basic. This loss of confirmation may be a consequence of the breaking of hydrogen bonds. Move the pH away from the optimum for a specific enzyme and you may severely hamper its function throughout the body, including hormone binding, central nervous system signaling, or myocardial contraction. Proper kidney function is essential for pH homeostasis.
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