Factors affecting blood pressure

Typical measurement of blood pressure is relative to a recurring cardiac cycle of atrial and ventricular contractions and relaxations (Figure 21-1). The cycle is divided into the systolic phase and the diastolic phase. The systolic phase is the portion in which ventricular contraction occurs, resulting in ejection of blood through the aorta. Conversely, diastole is the period of ventricular relaxation and blood filling. Systolic blood pressure (SBP) is the peak pressure reached during ventricular ejection, and diastolic blood pressure (DBP) is the lowest pressure reached right before ventricular ejection. Arterial pressure is typically recorded as SBP/DBP, for example, 120/80 mm Hg. Mean arterial pressure (MAP) refers to the pressure that drives blood into the tissues averaged over the entire cardiac cycle. Because the cardiac cycle is pulsatile rather than continuous and because two-thirds of the normal cardiac cycle is spent in diastole, MAP is not the arithmetic mean of the SBP and DBP. MAP is defined as the product of cardiac output (CO) and systemic vascular resistance (SVR), as follows:

< ?xml:namespace prefix = "mml" />[2(DBP) + SBP]/3 or MAP = CO × SVR

Systemic vascular resistance is used to define the resistance to flow of the vasculature that must be overcome to push blood through the peripheral circulation. Cardiac output is the amount of blood that is ejected into the aorta and travels through the systemic circulation per unit of time. Cardiac output is dependent on the sum of all local blood flow regulations and is shown in the following equation as the product of heart rate (HR) and stroke volume (SV). Stroke volume is the amount of blood ejected from the heart during systole. Changes in any of these components may alter the effects of the others.

CO = HR × SV

Summing up all components that affect the MAP, the following equation may better illustrate how these components relate to blood pressure:

MAP = HR × SV × SVR

The use of therapies such as fluids, vasopressors, and inotropes to maintain cardiovascular stability is directed toward altering each of these components, as seen in Table 21-2. The various vasopressors currently on the market have different affinities for the various receptors located within the body and exert different effects on the hemodynamic parameters, as seen in Table 21-3. Vasopressors and inotropes are not always first-line therapy; on the contrary, fluids are the mainstays for improving hypotensive episodes. Vasopressors and inotropes have considerable side effects, and certain medications interact with various vasopressors and inotropes, leading to alterations in hemodynamic parameters as seen in Table 21-4.

In addition to vascular tone, another component that may affect changes in tissue perfusion is vascular volume. Intravascular volume depletion may influence stroke volume and affect MAP as well. This component may be indirectly measured as the pulmonary capillary wedge pressure (PCWP), central venous pressure, or preload. In other words, using a device called a pulmonary artery catheter, a measurement of the amount of fluid returning to the heart can be used to estimate the PCWP. With this measurement, the clinician can evaluate a patient-specific response to fluid therapy and vasoactive therapy. The use of a pulmonary artery catheter is associated with complications such as infection, pneumothorax, bleeding, or thrombus formation.

Norepinephrine (Levophed) and epinephrine (Adrenalin Chloride) are endogenous catecholamines that are secreted by the adrenal medulla. Epinephrine is ultimately synthesized by the catalytic actions of tyrosine hydroxylase, which converts the amino acid tyrosine to levodopa and subsequently to dopamine, norepinephrine, and epinephrine.^1,2 These neurotransmitters travel to sympathetic nerve endings, where they are released to stimulate other nerve fibers and to stimulate an excitatory response. Norepinephrine and epinephrine stimulate α receptors on the vasculature and β receptors, also located within the vasculature as well as in the myocardium. α receptors within the vasculature cause vasoconstriction, whereas β receptors cause vasodilation. Most vascular beds within the body contain β receptors; however, they are outnumbered by α receptors, so any epinephrine and norepinephrine stimulation of β receptors is negligible or of no effect, yielding a net response of vasoconstriction. In addition, β receptors more densely populate the myocardium compared with α receptors, leading to a net effect of tachycardia.^3,4

Dobutamine is indicated for the short-term treatment of decompensated heart failure secondary to depressed contractility. Dobutamine is a synthetic catecholamine that is chemically related to dopamine; however, in contrast to dopamine, it is not metabolized to norepinephrine, and it does not stimulate dopamine receptors.⁴ Its pharmacologic actions are due to the effects of its racemic components. The (R)-isomer is responsible for its activity on the β₁ and β₂ receptors, causing predominant positive inotropic and chronotropic effects and vasodilatory effects, respectively. This combination of effects enhances cardiac output and stroke volume. The (S)-isomer is responsible for its activity on the α₁ receptors, causing vasoconstriction.^1,6 The vasodilatory β₂-adrenergic effects counterbalance the vasoconstrictive α₁ effects, leading to minor changes in systemic vascular resistance usually seen at lower doses. With increasing doses, the β₂-vasodilatory actions predominate over the α₁-vasoconstrictive effect, causing a decrease in systemic and pulmonary vascular resistance. The decline in systemic and pulmonary vascular resistance may also be secondary to enhanced cardiac output.

As an inotropic agent, dobutamine has adverse cardiac effects, which include arrhythmias, increase in myocardial oxygen consumption and demand, tachycardia, and hypotension. A limiting factor when dobutamine is used for more than 72 hours is tachyphylaxis; this may be due to a downregulation of β₁ receptors and may be overcome by increasing the dose. In patients with sulfite sensitivity, allergic reactions such as anaphylaxis or life-threatening asthmatic episodes may occur because dobutamine formulations contain sulfites.⁴

Ablation with radiofrequency current