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C H A P T E R 18 VASOACTIVE MEDICATIONS DAVE NEILIPOVITZ AND PIERRE CARDINAL You are treating a 45-year-old woman whopresented to the hospital with a decreased level of consciousness. She was in severe respiratory distress and required intubation, Presently, she is hypotensive with a blood pressure of 70/45 and a heart rate of 145 despite repeated fluid boluses of over 6 litres of isotonic crystalloid solutions. Peripherally, she has very poor perfusion. You do notfind any evidence of obstructive process such as a tension pneumothorax or cardiac tamponade. She is deterioratingin front of you. What should you do? Vasopressors or inotropes? Dopamine or norepinephrine? These are questions physicians ask themselves when confronted with the need for vasoactive medications. Unfortunately, anxiety and confusion with these drugs can cause delays with potentially detrimental consequences. However, these medications can save lives so a rational approach is essential for criticallyill patients. Vasoactive medications primarily affect the cardiovascular system.Thebasicpurpose ofthe heart and blood vessels is to supply the cells of the body with oxygen and other essential nutrients. In order to do this, the cardiovascularsystem must generate both pressure and flow. Whichof these two factors is more important is debatable,but clearlyboth arenecessary. Without pressure there isnoflow,and pressure alone will not supply the cells.Ideally,fluidadministration alone would be sufficient to improve both flow and pressure but this is not always so. Thus, the purpose of vasoactive medications is to improve either the pressure (i.e., blood pressure), the flow (i.e.,cardiac output) or both. Although some drugs can raise both hemodynamic variables, most medications tend to preferentially increase one or the other. The choice of which vasoactive drug to use thus depends on which variable one is hoping to improve. 179 • Basic Principles andPhysiology A. Pressure The blood pressure (BP) is the product of the cardiac output and the systemic vascular resistance (SVR). Thus, the BP can be increased by increasing either the SVRor the cardiac output. Since the SVRis primarily a reflection of the peripheral arterial tone, drugs that increase the arterial tone will raise the BP. Vasopressors are the medications that cause vasoconstriction of these arterialor resistancevessels by activating alpha 1 receptors. Drugs that increase the cardiac output, without decreasing the SVR, can raise the BP.Unfortunately, many drugs which increase the cardiacoutput do soby also lowering the SVR and thus can paradoxicallylower the BPdespite increasing the total bloodflow. B. Flow Theblood flow to the tissues is primarilya reflection of the cardiac output (CO). CO is calculated as a product of heart rate and stroke volume. Although moderate increases in the heart rate will initially raise the CO,rates above 120 bpm will haveminimal benefit, and rates above 150bpm actuallycause it to decrease.1 As the heart rate increases, the total time spent in diastole decreases, which thus reduces the filling of the ventricles (i.e., lowers the preload). Decreases in preload will in turn lower the CO (Starling's law of the heart). A disadvantage of raising the heart rate is that it increasesmyocardial oxygen consumption and can reduce the oxygen supply to the heart because the left ventricle is only perfused during diastole.2 The increased demand and decreased supply can predispose patients to myocardial ischemia.Therefore, unless the heart rate is low,increasing the rateisnot the preferred manner for increasing the CO. Rather,it is preferableto raise the COby increasing the stroke volume. The stroke volume is primarily influenced by preload, contractility and afterload. Preload refers to the amount of stretch exerted on the myofibrils of the heart at the end of diastole.3 '4 Simply, it is the amount of blood that fills the heart at the end of diastole and reflects venous return and blood volume. Starling's law of the heart describes how an increase in preload will increase the CO (Figure 18.1). Greater filling of the ventricle increases the force of cardiac contraction.3 "5 A point is, however, reached Figure 18.1 -Starling's Law of the Heart Figure 18.1 illustrates the basis of Starling's law of the heart, whereby an increase in preload — namely the end diastolic volume of the ventricle — will increase the output of the ventricle. As can be seen, there is a point where further increases in preload do not increase the cardiac output. Although controversial, some believe that the cardiac output may start to decrease once preload becomes too high (see text for details). where too much stretch...

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