A sense of urgency grips the trauma team. The 17-year-old girl on the stretcher is covered with blood. Paramedics found her unconscious in her home with both wrists slit. She lost a large percentage of her blood volume before reaching the ED and has slipped into hypovolemic shock. Her skin is as white as the sheets, she has no palpable peripheral pulses and her central pulses are weak and thready. Paramedics couldn’t obtain a peripheral IV line, and the ED physician is struggling to secure a central line. Without rapid venous access and aggressive fluid resuscitation, the girl’s chances for survival are slim.
Humans have a small circulating blood volume. A man weighing 175 pounds has a blood volume of about 5.3 liters.1 A 130-pound woman has as little as 3.6 liters.1 This blood volume is essential to life because oxygen is carried from the pulmonary system to the tissues via the blood. Diminished circulating volumes, called hypovolemia, equate to diminished tissue oxygenation. This is compounded by the fact that the heart is volume responsive. Lower blood volumes decrease stretching of the myocardium, and this results in decreased cardiac output, further compounding tissue hypoxia. Any decrease in circulating volume results in decreased tissue oxygenation and reduced cardiac output.
Hypovolemia occurs for a variety of reasons. Nausea, vomiting or diarrhea can deplete intravascular volumes. Excessive diuresis from diabetes insipidus or diabetic ketoacidosis can also reduce intravascular volumes. However, absolute blood loss remains the most common cause of shock
and death in trauma patients, secondary to blood loss from sustained injuries.2
As blood volume falls, the blood vessel walls are under less stress. This reduction in stretching of the vessel walls is sensed by the baroreceptors, mainly in the aortic arch and the carotid sinus. The baroreceptors in turn send impulses via the glossopharyngeal nerve to the cardiovascular control centers of the medulla, stimulating the sympathetic nervous system. The sympathetic nervous system, the “fight-or-flight” system, causes numerous changes in the body:
Peripheral vasoconstriction: Smooth muscles within vascular walls constrict, especially in the extremities and GI tract, to concentrate remaining volume to the more essential organs, such as the lungs, heart and brain.3
Improved cardiac output: Sympathetic stimulation causes increased heart rate, improved cardiac contractility and enhanced automaticity (the rate at which electricity moves through the electrical system of the heart); all contribute to increased cardiac output.4
Improved pulmonary gas exchange:
Increased respiratory rate, coupled with bronchodilation, improves oxygen and carbon dioxide exchange in the lungs.5 (Level B)
Diaphoresis: The sympathetic nervous system prepares the body to “fight or take flight,” and since either activity is likely to generate heat, prophylactic sweating usually occurs with stimulation of this system.6
Glucogenolysis: In preparation for the expenditure of energy associated with “fight” or “flight,” glycogen stored in the liver is broken down into glucose in a process known as glycogenolysis so that extra energy is available to the cells.3
Continued blood loss, coupled with the vasoconstriction of sympathetic stimulation, ultimately, causes the glomerular filtration rate to drop. When this occurs, the glomeruli of the kidneys release renin. Eventually, renin is converted to angiotensin II, a potent vasoconstrictor that causes further vasoconstriction above and beyond what is seen within the sympathetic nervous system. Angiotensin II also stimulates the release of aldosterone from the adrenal glands. Aldosterone acts on the tubules of the kidneys to increase sodium reabsorption from urine back to the blood. Because water follows sodium, as sodium is reabsorbed, blood volumes increase.3
The increases in blood pressure secondary to vasoconstriction — as well as increased cardiac output, improved pulmonary gas exchange and reabsorption of water and sodium in the kidneys — can quickly counteract the effects of mild hypovolemia. In fact, if blood loss is less than 30%, these changes may elevate the blood pressure to normal and partially mask hypovolemia. This is referred to as compensated shock because the body is able to compensate for the fluid losses.7
Compensatory mechanisms are effective for a while, but if blood loss is not recognized or treated in a timely manner, these mechanisms begin to fail. The vasoconstriction of compensated hypovolemic shock can further deplete peripheral cells of oxygen. For a time, these cells will function in an anaerobic state, but ultimately the metabolic waste products of anaerobic metabolism — such as lactic acid — overtake the cell, causing cell death. When the cell dies, it releases inflammatory mediators that cause capillary permeability and vasodilation in the tissues around it. When enough inflammatory mediators are released throughout the body, this capillary permeability, as well as vasodilation, becomes systemic, and the blood pressure plummets even further. This is the decompensatory stage, when the compensatory mechanisms fail.3
Not Always Obvious
At times, diagnosis of hypovolemic shock is straightforward. The signs may be more apparent in a patient who is actively bleeding from an external source. But hypovolemia is not always that obvious. Patients with abdominal or chest injuries or fractures may bleed internally. In these cases, it takes an astute practitioner to recognize the subtle signs of early hypovolemic shock and intervene before compensated shock progresses to decompensated shock.
The clinical manifestations of hypovolemic shock can closely match the effects of sympathetic stimulation as well as renin-angiotensin stimulation. Vasoconstriction can be detected in the blood pressure. The diastolic pressure is a measurement of forces within the blood vessels during cardiac diastole, or when the heart is relaxed.8 The greater the vessel dilation, the less pressure exists in these vessels during cardiac relaxation, thus lowering the diastolic pressure. Conversely, the more constricted blood vessels are, the higher the pressures within the vasculature are, causing an increase in diastolic pressure. Therefore, elevated diastolic pressures are associated with vasoconstriction.
Systolic pressure measures pressures within the blood vessels when the heart is contracted.8 The more blood in the system, the more blood is contracted, causing higher systolic pressures. Therefore as hypovolemia progresses, systolic pressure will begin to fall to reflect these losses. Vasoconstriction directs more blood back to the heart. This can keep systolic pressures at a deceptively normal rate for a time.
Pulse pressure is the difference between systolic and diastolic pressure, calculated by subtracting the diastolic pressure from the systolic pressure. The pulse pressure of a patient whose blood pressure is 120/80 mmHg is 40 mmHg. If systolic pressures are staying fairly steady secondary to vasoconstriction or falling slightly due to fluid losses, yet diastolic pressures are elevating due to vasoconstriction, the pulse pressure will decrease. A patient whose blood pressure is initially 132/84 mmHg (pulse pressure is 48 mmHg) who 30 minutes later has a blood pressure of 126/92 (pulse pressure 34) is displaying possible signs of vasoconstriction that may indicate underlying hypovolemia.8
When a patient decompensates and inflammatory mediators cause vasodilation, the diastolic pressure will drop. Similarly, the capillary leaking associated with inflammatory mediators will decrease intravascular fluid volume, causing the systolic blood pressure to drop. Significant declines in both systolic and diastolic pressure should be of major concern in the hypovolemic patient, heralding the possible onset of decompensation9.
Elevations in the pulse rate and the respiratory rate secondary to sympathetic stimulation may also be indications of underlying hypovolemia, as will diminished urinary output secondary to activation of the renin-angiotensin system. Vasoconstriction coupled with diaphoresis will often make the skin cold, clammy and pale.7
In early compensatory shock, sympathetic stimulation may result in excitability, and the patient may be hyperalert and anxious. But as the hypotension of decompensation sets in, hypoxia to the central nervous system will cause diminishing levels of consciousness.7