Hemorrhagic Shock 

Hemorrhagic shock is a condition of reduced tissue perfusion, resulting in the inadequate delivery of oxygen and nutrients that are necessary for cellular function. Whenever cellular oxygen demand outweighs supply, both the cell and the organism are in a state of shock.

On a multicellular level, the definition of shock becomes more difficult because not all tissues and organs will experience the same amount of oxygen imbalance for a given clinical disturbance. Clinicians struggle daily to adequately define and monitor oxygen utilization on the cellular level and to correlate this physiology to useful clinical parameters and diagnostic tests.

The 4 classes of shock, as proposed by Alfred Blalock, are as follows:^[1]

• Hypovolemic
• Vasogenic (septic)
• Cardiogenic
• Neurogenic

Hypovolemic shock, the most common type, results from a loss of circulating blood volume from clinical etiologies, such as penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Humans are able to compensate for a significant hemorrhage through various neural and hormonal mechanisms. Modern advances in trauma care allow patients to survive when these adaptive compensatory mechanisms become overwhelmed.

Well-described responses to acute loss of circulating volume exist. Teleologically, these responses act to systematically divert circulating volume away from nonvital organ systems so that blood volume may be conserved for vital organ function. Acute hemorrhage causes a decreased cardiac output and decreased pulse pressure. These changes are sensed by baroreceptors in the aortic arch and atrium. With a decrease in the circulating volume, neural reflexes cause an increased sympathetic outflow to the heart and other organs. The response is an increase in heart rate, vasoconstriction, and redistribution of blood flow away from certain nonvital organs, such as the skin, gastrointestinal tract, and kidneys.

Concurrently, a multisystem hormonal response to acute hemorrhage occurs. Corticotropin-releasing hormone is stimulated directly. This eventually leads to glucocorticoid and beta-endorphin release. Vasopressin from the posterior pituitary is released, causing water retention at the distal tubules. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Hyperglycemia commonly is associated with acute hemorrhage. This is due to a glucagon and growth hormone–induced increase in gluconeogenesis and glycogenolysis. Circulating catecholamines relatively inhibit insulin release and activity, leading to increased plasma glucose.

In addition to these global changes, many organ-specific responses occur. The brain has remarkable autoregulation that keeps cerebral blood flow constant over a wide range of systemic mean arterial blood pressures. The kidneys can tolerate a 90% decrease in total blood flow for short periods of time. With significant decreases in circulatory volume, intestinal blood flow is dramatically reduced by splanchnic vasoconstriction. Early and appropriate resuscitation may avert damage to individual organs as adaptive mechanisms act to preserve the organism.

Age

Hemorrhagic shock is tolerated differently, depending on the preexisting physiologic state and, to some extent, the age of the patient. Very young and very old people are more prone to early decompensation after loss of circulating volume.

• Pediatric patients have smaller total blood volumes and, therefore, are at risk to lose a proportionately greater percentage of blood on an equivalent-volume basis during exsanguination compared to adults. The kidneys of children younger than 2 years are not mature; they have a blunted ability to concentrate solute. Younger children cannot conserve circulating volume as effectively as older children. Also, the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to coagulopathy.
• Elderly people may have both altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood loss. Atherosclerosis and decreased elastin cause arterial vessels to be less compliant, leading to blunted vascular compensation, decreased cardiac arteriolar vasodilation, and angina or infarction when myocardial oxygen demand is increased. Older patients are less able to mount a tachycardia in response to decreased stoke volume because of decreased beta-adrenergic receptors in the heart and a decreased effective volume of pacing myocytes within the sinoatrial node. Also, these patients frequently are treated with a variety of cardiotropic medications that may blunt the normal physiological response to shock. These include beta-adrenergic blockers, nitroglycerin, calcium channel blockers, and antiarrhythmics.
• The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the presence of near-normal serum creatinine. Concentrating ability may be impaired by a relative insensitivity to antidiuretic hormone. These changes in the heart, vessels, and kidneys can lead to early decompensation after blood loss. All of these factors in concert with comorbid conditions make management of elderly patients with hemorrhage quite challenging.