Historically, EMS professionals relied on the vital signs, specifically blood pressure, in conjunction with other physical findings to determine if a patient was in hypovolemic shock. Shock is a state of inadequate tissue perfusion. However, it has become clearer that blood pressure and heart rate may not be a good early indicator of a hypovolemic shock state and may actually mislead the EMS practitioner when considering a differential diagnosis.
Alteration in vital signs primarily results from both a reduction in blood volume and a cascade of neural and hormonal responses in an attempt to increase the blood pressure and conserve body fluid. We have always looked for profound changes in the blood pressure to assist in making a differential diagnosis of shock.
For example, a drop in the systolic blood pressure to 90 mmHg is an indication that the shock state deteriorated from a compensatory stage to a decompensatory, or progressive stage. This dramatic drop, which is a clear but late finding, represents approximately a 30% blood loss in a healthy individual. The literature suggests that a patient could be in a true shock state and not initially present with a dramatic decrease in blood pressure or increase in heart rate [1,2]. Therefore, it is imperative to understand what the blood pressure is indicating and that the signs of poor perfusion can be assessed to identify early indicators of shock.
Blood pressure changes from fluid loss
Blood pressure is determined by the cardiac output (CO) and peripheral vascular resistance (PVR). The equation BP = CO × PVR represents the interaction of the two variables. Cardiac output is the amount of blood ejected from the left ventricle in one minute. Peripheral vascular resistance is the resistance in the peripheral arteries and arterioles determined by the vessel size. A decrease in the vessel lumen will increase the resistance; whereas, a decrease in the vessel size will decrease the peripheral vascular resistance. An increase in the cardiac output or peripheral vascular resistance will lead to an increase in the blood pressure; whereas, a decrease will cause a decrease in blood pressure.
Cardiac output is an interaction of heart rate (HR) and stroke volume (SV), which is reflected in the equation CO = HR × SV. The stroke volume is defined as the amount of blood ejected from the left ventricle with each contraction and is determined by the preload, myocardial contractility and afterload. In general, an increase in heart rate or stroke volume will lead to an increase in cardiac output. Inversely, a reduction in heart rate or stroke volume will lead to a decrease in cardiac output.
The loss of blood associated with hypovolemic shock causes a reduction in the venous volume, which in turn diminishes the preload, stroke volume and cardiac output. A drop in cardiac output, which is reflected by a falling systolic blood pressure, results in a decrease in pressure in the carotid bodies and aortic arch, and triggers the baroreceptors (inhibitory stretch-sensitive receptors that constantly measure arterial pressure). When the baroreceptors sense a decrease in the arterial pressure, the sympathetic nervous system is prompted to initiate a cascade of neural and hormonal responses in an attempt to restore the pressure back to a normal state.
The direct neural stimulation and hormonal influence will increase the heart rate, increase myocardial contractility and increase peripheral vascular resistance through systemic vasoconstriction. The diastolic blood pressure is an indirect measure of peripheral vascular resistance; thus, as the vessels constrict and vascular resistance increases, the diastolic blood pressure is maintained or increases.
EMS provider assessment of blood pressure
Even though the patient is losing blood and the venous volume and pressure is decreasing, the blood pressure will look relatively stable as the heart rate, myocardial contractility and peripheral vascular resistance increase as a means to compensate. This could produce a blood pressure that is deceiving and may lead the EMS practitioner into a false sense of patient stability.
For example, a blood pressure of 102/88 mm Hg surely falls within a normal limit; however, it could also be a clear sign of hypovolemia when assessed closer. It is important to not only look at the overall blood pressure, but also the pulse pressure, which can provide valuable information about the hemodynamic state. The pulse pressure is the difference between the systolic blood pressure and the diastolic blood pressure.
For example, using the pressure discussed previously, the pulse pressure is calculated at 14 mm Hg (102 – 88 = 14 mm Hg). If the difference is less than 25 percent of the systolic blood pressure, the pulse pressure is considered to be narrow. A wide pulse pressure is considered to be greater than 50 percent of the systolic blood pressure.
A narrow pulse pressure in a hypovolemic shock patient indicates a decreasing cardiac output and an increasing peripheral vascular resistance. The decreasing venous volume from blood loss and the sympathetic nervous system attempt to increase or maintain the falling blood pressure through systemic vasoconstriction. This increase in heart rate and myocardial contractility is reflected in the decreasing systolic BP, the increasing diastolic BP and the narrowing pulse pressure. Thus, a blood pressure of 102/88 mmHg no longer appears to be “normal” and requires further assessment of heart rate, respiratory rate and other signs of perfusion, such as the skin color, temperature, condition and the patient’s mental status.
Be careful when assigning a blood pressure assessment as “normal.” The pulse pressure may provide more valuable and important information than the actual blood pressure itself. Blood pressure should be considered in the whole assessment of the patient and not purely as an independent finding.
Read next: Patient vital signs: 5 tips for EMTs, paramedics
References
1. Edelman D.A., White M.T., Tyburski J.G., et al: Post-traumatic hypotension: should systolic blood pressure of 90–109 mm Hg be included?. Shock 27. (2): 134-138.2007.
2. Victorino G.P., Battistella F.D., Wisner D.H.: Does tachycardia correlate with hypotension after trauma?. J Am Coll Surg 196. (5): 679-684.2003.
This article was originally posted Apr. 7, 2009. It has been updated.
