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Figure 5. Cardiovascular effects of epinephrine and phenylephrine. Epinephrine increases heart rate (HR) by activating beta-1 receptors in the sinoatrial node, the heart's normal pacemaker. It also activates beta-1 receptors on myocardial cells, increasing their contractility and increasing systolic blood pressure (SBP). However, at low doses such as those provided in local anesthetic formulations, it activates beta-2 receptors on systemic arteries, producing vasodilation. This decline in arterial resistance produces a reduction in diastolic pressure (DBP). The sum of these effects results in little change of mean arterial pressure (MAP). In contrast, phenylephrine activates only alpha receptors, increasing arterial resistance and diastolic pressure. Systolic pressure also rises as the heart compensates for this increase in resistance by increasing its contractility and venoconstriction increases venous return (preload). The net effect is an increase in mean arterial pressure, which is sensed in baroreceptors, and a reflex slowing of heart rate supervenes. (Adapted from Westfall et al.¹¹)

Epinephrine‐beta blocker interaction. In this illustration the following cardiovascular changes follow the administration of epinephrine in a dosage of 10 µg/min. (A) First, it is essential to understand the precise cardiovascular influences of epinephrine in a normal (control) patient. The cardiotonic effects of epinephrine are most familiar. It activates beta‐1 receptors on the sinoatrial node to increase heart rate (HR) and also activates beta‐1 receptors on myocardial cells increasing their force of contraction. This provides an increase in systolic blood pressure (SBP). In addition to its cardiotonic effects, epinephrine has the ability to activate both alpha and beta‐2 receptors on blood vessels producing constriction or dilation, respectively. Epinephrine is commonly viewed only as a vasoconstrictor by many clinicians because this is the effect it produces when injected subcutaneously or submucosally. This is because the tiny vessels found in these locations contain only alpha receptors and are constricted by epinephrine. In contrast, larger systemic arteries that determine vascular resistance and diastolic blood pressure contain both alpha and beta‐2 receptors, with the latter most prevalent. Following absorption, low doses of epinephrine found in local anesthetic formulations (eg, 20–100 µg) preferentially activate beta‐2 receptors which dilate the arteries, and diastolic blood pressure (DBP) actually declines. (B) In the presence of a nonselective beta blocker (eg, propranolol) the cardiovascular influences of epinephrine are strikingly different. This is primarily due to the blockade of beta‐2 receptors on systemic arteries. Epinephrine will now activate the remaining alpha receptors leading to vasoconstriction and an increase in diastolic blood pressure. To meet this increase in resistance, intrinsic mechanisms within myocardial cells respond with greater force and elevate systolic blood pressure as well. Together this will increase mean arterial pressure (MAP). The sudden elevation in MAP is sensed by baroreceptors within the carotid sinuses triggering a reflex slowing in heart rate, which is further accentuated by the fact that the beta‐1 receptors in the sinoatrial node are blocked.

Paced rhythm with pacer “spike.”

Medtronic MRI-compitable pacemaker.

Typical ICD and right atrial and right ventricular lead placement.

Typical 90-gauss “doughnut” magnet.