Morgan & Mikhail Chap 15(Hypotensive Agents)

Question 1

Hypotensive Agents

Answer 1

A multitude of drugs are capable of lowering blood pressure, including volatile anesthetics, sympathetic antagonists and agonists, calcium channel blockers, β-blockers, and angiotensin-converting enzyme inhibitors. Blood pressure is the product of cardiac output and systemic vascular resistance. Agents that lower blood pressure reduce myocardial contractility or produce vasodilatation of the arterial and venous capacitance vessels, or both.

Question 2

Older verse Younger Patient

Answer 2

Question 3

Beta Blockers

Answer 3

β-Blocker therapy should be maintained perioperatively in patients who are being
treated with β-blockers as a part of their routine medical regimen. The American College of Cardiology/American Heart Association guidelines for β-blocker use perioperatively should be followed (see Chapter 14). β-Blockers (esmolol, metoprolol, and others) were previously discussed for the treatment of transient perioperative hypertension and are routinely used during anesthesia

Question 4

Perioperative Hypertension

Answer 4

Perioperative hypertension may be the result of pain, anxiety,
hypoxemia, hypercapnia, distended bladder, and failure to continue prescribed
antihypertensive medications. These primary etiologies should be considered and
addressed when treating perioperative hypertension.

Question 5

SODIUM NITROPRUSSIDE

Answer 5

Sodium nitroprusside (and other nitrovasodilators) relax both arteriolar and venous smooth muscle. Its primary mechanism of action is shared with other nitrates (eg, hydralazine and nitroglycerin). As nitrovasodilators are metabolized, they release nitric
oxide, which activates guanylyl cyclase

Nitric oxide, a naturally occurring potent vasodilator released by endothelial
cells (endothelium-derived relaxing factor), plays an important role in regulating
vascular tone throughout the body.

Inhaled nitric oxide is a selective
pulmonary vasodilator that is used in the treatment of reversible pulmonary
hypertension.

The last of these reactions underlies the development of acute cyanide toxicity, characterized by metabolic acidosis, cardiac arrhythmias, and increased venous oxygen content (as a result of the inability to utilize oxygen). Another early sign of cyanide toxicity is the acute resistance to the hypotensive effects of increasing doses of sodium nitroprusside (tachyphylaxis). Cyanide toxicity is more likely if the cumulative daily dose of sodium nitroprusside is greater than 500 mcg/kg or if the drug
is administered at infusion rates greater than 2 mcg/kg/min for more than a few hours.
Patients with cyanide toxicity should be mechanically ventilated with 100% oxygen to
maximize oxygen availability.

INTRACORONARY STEAL– stealing blood away from ischemic areas where coronary arterioles are already maximally dilatated.

The pulmonary vasculature also dilates in response to sodium nitroprusside infusion. Reductions in pulmonary artery pressure may decrease the perfusion of some normally ventilated alveoli, increasing physiological dead space. By dilating pulmonary vessels, sodium nitroprusside may prevent the normal vasoconstrictive response of the
pulmonary vasculature to hypoxia (hypoxic pulmonary vasoconstriction

Usually diluted to a concentration of 100mcg/ml and infused at a rate of 0.25-5mcg/kg/min

Question 6

NITROGLYCERIN

Answer 6

Nitroglycerin relaxes vascular smooth muscle, with venous dilation predominating over
arterial dilation. Its mechanism of action is similar to that of sodium nitroprusside:
metabolism to nitric oxide, which activates guanylyl cyclase, leading to increased cGMP, decreased intracellular calcium, and vascular smooth muscle relaxation.

Nitroglycerin reduces myocardial oxygen demand and increases myocardial oxygen supply by several mechanisms:
* The pooling of blood in the large-capacitance vessels reduces the effective
circulating blood volume and preload. The accompanying decrease in ventricular
end-diastolic pressure reduces myocardial oxygen demand and increases endocardial perfusion.
* Any afterload reduction from arteriolar dilation will decrease both end-systolic pressure and oxygen demand. Of course, a fall in diastolic pressure may lower
coronary perfusion pressure and actually decrease myocardial oxygen supply.
* Nitroglycerin redistributes coronary blood flow to ischemic areas of the subendocardium.
* Coronary artery spasm may be relieved.

Preload reduction makes nitroglycerin an excellent drug for the relief of cardiogenic pulmonary edema. Heart rate is unchanged or minimally increased.

Rebound hypertension is less likely after discontinuation of nitroglycerin than following
discontinuation of sodium nitroprusside.

Concentration of 100mcg/ml. infusion rates of 0.5-5mcg/kg/min

Question 7

HYDRALAZINE

Answer 7

Hydralazine relaxes arteriolar smooth muscle in multiple ways, including dilation of precapillary resistance vessels via increased cGMP.

The body reacts to a hydralazine-induced fall in blood pressure by increasing
heart rate, myocardial contractility, and cardiac output.

Lowering PVR causes drop in ABP with a reflex increase in HR, CO and Contractility. (BAD FOR ELDERLY and Pts with CAD)

Onset of action is about 15min and DOA is 2-4 hours.