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What is Blood Pressure, Hypotension, Shock? |
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What is Blood Pressure? The cardiovascular system consists of three components: a pump – the heart, a carrier fluid – blood, a distribution system – the arteries, an exchange system – the capillary network, and a collecting system – the venous system. Blood pressure is the driving force that propels blood along the distribution network. Blood pressure is conventionally measured at the level of the aortic arch, where it is greatest. As the arterial tree branches out, the velocity of blood slows, until it moves extremely slowly through the capillary network. The main thrust of blood pressure comes from the contraction of the heart, around the fluid that collects in the left and right ventricles, when the pressure in the ventricles exceeds that in the aorta and pulmonary arteries, blood is projected forward. The amount of blood expelled per cycle is the stroke volume. The stroke volume is determined by the amount of blood in the heart before it starts to contract – the “preload” or end diastolic volume, the force required to overcome resistance to ejection – the “afterload”, and the ability of the heart muscle to deal with the volume “loaded” onto it – the heart muscle “contractility”. The cardiac output is the amount of blood ejected from the heart per minute, the heart rate times the stroke volume. Pressure is calculated simply as force per unit area [P=f/a]. The force in this case is the forward motion of blood, the cardiac output. The area into which the blood is being propelled is the arterial network, principally the arterioles, subdivisions of arteries that act as resistance vessels. Conventionally we call this area “the total peripheral resistance”, as the arterial network exists in a state of tonic vasoconstriction, a function of the sympathetic nervous system. The circulating volume is controlled by a number of reflex systems, extrinsic and intrinsic to the kidney. These effectively assimilate information about perfusion pressure (essentially from baroreceptors in the carotid body and aortic arch), serum osmolality (in the mid brain) and urinary sodium content (in the distal tubule of the nephron).
Blood pressure is maintained by a series of interactive autonomic and humoral reflexes that continually equate heart rate, stroke volume, total peripheral resistance and circulating volume. If there is a malfunction within this system, the other components’ function alters to compensate (after all without an adequate blood pressure vital organs will not perfuse). If a patient becomes hypotensive, compensation has failed, and external intervention is required to correct the problem. What are these compensatory mechanisms?The heart is responsive to the amount of fluid present in the ventricles at the end of a diastolic filling period. The heart muscles are stretched by the distending fluid, and the degree of stretch is directly related to the stroke volume, this is known as Starling’s Law (figure 2). If the heart rate slows down, then filling time increases, as does filling volume. The stroke volume increases. If the filling volume is reduced due to excessively fast heart rate, stroke volume falls. If the patient has a low preload, due for example to bleeding, the heart rate increases in order to compensate for the lower stroke volume. The objective of all interventions relating to the heart is to optimize stroke volume while minimizing the risk of rate or work related ischemia. The majority of patients who are hypotensive in ICU are so because of overall hypovolemia, the treatment is volume loading in order to place the patient on the most efficient part of the pressure-volume curve.
In a similar manner, if a patient becomes vasodilated for any reason (anaphylaxis, sepsis etc), then peripheral resistance falls, and heart rate and stroke volume must increase in order to maintain blood pressure. This is sometimes called “high output” cardiac failure, a somewhat incorrect term. In patients with severe sepsis, the cardiac output may increase to 10 –12 litres per minute, in order to maintain blood pressure. If, under these circumstances, the patient remains hypotensive, then either the vasodilatation is excessive, or the heart itself is not able to mount an adequate compensatory response. The interactions of the heart and peripheral vasculature are represented in figure 3.
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Please note: these tutorials are for personal study purposes only. They are not currently peer reviewed, and no responsibility will be taken for mistakes or inaccuracies. Reproduction of information is forbidden. All material is copyrighted by the GasWorks Group. |
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