m and m 15 - Hypotensive Agents

Question 1

How does the diastolic wave differ in Older vs younger patients?

Answer 1

In younger patients, reflected wave augments diastole, improving diastolic pressure. In older patient, wave returns too fast and decreases diastolic pressure (older pt will have increased systolic and decreased diastolic pressure)

Question 2

What is the significance of a widened pulse pressure in surgery?

Answer 2

Increased risk of post op renal dysfunction, increased risk of cerebral events in patients undergoing coronary bypass sx

Question 3

True or false, hypertensive crisis can cause diastolic dysfunction? What is mechanism of diastolic dysfunction?

Answer 3

True

Mechanism is inability to sequester calcium in the sarcoplasmic reticulum, therefore no relaxation

Question 4

They tow major components of BP are?

Answer 4

CO and SVR

Question 5

What is the mechanism of sodium nitroprusside?

Answer 5

As it is metabolized, it will release nitric oxide, an endogenous vasodilator

Question 6

What is the indication of inhaled nitric oxide?

Answer 6

Reversible pulmonary hypertension

Question 7

What are the products of sodium nitroprusside metabolism? Enzymatic or non-enzymatic?

Answer 7

Non enzymatic
In RBC, it gets electron from iron to make nitroprussside radical and methemoglobin, The nitroprusside radical becomes 5 cyanide ions and a nitroso group

Question 8

What is the fate of the cyanide ions made from metabolism of sodium nitroprusside? (3)

Answer 8

1) Bind methemaglobin to make cyanmethemoglobin
2) metabolized by liver rhodanase to make thiocyanate
3) Bind tissue cytochrome oxidase to block oxygen utilization

Question 9

What are the 3 hallmarks of acute cyanide toxicity?

Answer 9

Metabolic acidosis
Arrythmias
Increased venous O2 (can’t use the oxygen available)

Question 10

How does cyanide toxicity affect responsiveness to nitroprusside?

Answer 10

Tachyphylaxis occurs, less responsive to increasing doses (acute tachyphylaxis, as opposed to tachyphylaxis from long term use)

Question 11

How is cyanide toxicity treated?

Answer 11

100% oxygen

Thiosulfate or sodium nitrate (both oxidize hemoglobin to methemoglobin)

Question 12

What are signs of thiocyanate accumulation? (5)

Answer 12

Thyroid dysfunction 
Muscle weakness 
Nausea 
Hypoxia 
Acute psychosis

Question 13

What is the treatment of methemaglobinemia?

Answer 13

Methylene blue

Question 14

What is the net effect of sodium nitroprusside on the CV system?

Answer 14

Decreases preload and afterload

Question 15

What is a possible effect of sodium nitroprusside on patients with aortic regurg, mitral regurg or CHF? Mechanism?

Answer 15

It may increase cardiac output secondary to the reduction in afterload

Question 16

What is intracoronary steal and how is that related to sodium nitroprusside?

Answer 16

sodium nitroprusside can cause dilation of normal coronaries but not diseased coronaries that are maximally dilated. This will then increase flow to normal coronaries at the expense of the diseased coronaries that cannot dilate anymore

Question 17

What is the effect of sodium nitroprusside on intracranial blood flow? How can this effect be blocked?

Answer 17

Will Increase blood flow to the brain, which can increase intracranial pressure
Can block with hypocapnia

Question 18

How can sodium nitroprusside increase physiological dead space?

Answer 18

It dilates the pulmonary arteries, and decreased pulmonary artery pressure will decrease the perfusion of normally ventilated alveoli. It also prevents normal vasoconstriction in response to hypoxia - hypoxic pumonry vasoconstriction

Question 19

True or false, renin and catecholamines are released in response to sodium nitroprusside?

Answer 19

True

Question 20

How might sodium nitroprusside interfere will the action of neuromuscular blocking agents?

Answer 20

It decreases muscle blood flow, which can delay the onset and prolong duration of neuromuscular blocking agents

Question 21

How does sodium nitroprusside and nitroglycerin differ in their vascular bed targets?

Answer 21

Sodium nitroprusside - arteriolar and venous target

Nitroglycerin - venous more than arterial dilation

Question 22

What is the mechanism of nitroglyerin (and sodium nitroprusside)?

Answer 22

Increased NO, activates guanylyl cyclase, increased cGMP, decreased intracellular calcium and smooth muscle relaxation

Question 23

What are 3 indications for nitroglycerin?

Answer 23

Myocardial ischemia
Hypertension
Ventricular Failure

Question 24

Which [nitroglycerin or sodium nitroprusside] must be protected from light?

Answer 24

nitroprusside (degraded]

Question 25

Which [nitroglycerin or sodium nitroprusside] must be administered with special tubing and glass containers?

Answer 25

Nitroglycerin - adsorption to polyvinylchloride

Question 26

When is tolerance likely with nitroglycerin? 3 mechanisms?

Answer 26

Chronic use 1) depletion of reactants to make NO 2) compensatory increase in vasoconstrictors 3) volume expansion

Question 27

How can you avoid tolerance with nitroglycerin?

Answer 27

Need to have dosing holidays

Question 28

How and where is nitroglycerin metabolised?

Answer 28

Metabolised by reductibe hydrolysis by glutathione organic nitrate reductase - in liver and blood

Question 29

True or false, like nitroprusside, methemaglobinemia is possible from nitroglycerin?

Answer 29

True. Metabolic product, nitrite can make Hgb to methemoglobin

Question 30

What are 4 mechanisms by which nitroglycerin can reduce cardiac ischemia?

Answer 30

- reduced preload -> decreased end diastolic pressure and decreased myocardial oxygen demand - afterload reduction decreases o2 demand - sends blood to ischemic subendocardium - relieves coronary artery spasm

Question 31

True or false, like sodium nitroprusside, nitroglycerin can also cause coronary steal

Answer 31

False

Question 32

What is the mechanism by which nitroglycerin can treat cardiogenic pulmonary edema?

Answer 32

It reduced preload

Question 33

Which is more likely to cause rebound HTN after discontinuation, nitroglycerin or sodium nitroprusside

Answer 33

Sodium nitroprusside

Question 34

True or false, nitroglycerin decreases platelet aggregation?

Answer 34

True

Question 35

What is the mechanism, and vascular bed target of hydralazine?

Answer 35

increases cGMP mainly in arteriolar smooth muscle

Question 36

How and where is hydralazine metabolized?

Answer 36

In the liver - acetylation and hydroxylation

Question 37

What are the compensatory response to hydralazine? What patient population is this dangerous?

Answer 37

Increased HR, contractility and CO | Watch out in patients with known CAD

Question 38

What is the effect of hydralazine on cerebral blood flow?

Answer 38

Increases cerebral blood flow and intracranial pressure

Question 39

What is the mechanism of vasodilation of fenoldopam?

Answer 39

It is a D1 receptor partial agonist. Also activates alpha 2

Question 40

How does dopamine differ from fenoldopam?

Answer 40

Both are D1 agonist. However dopamine also affect beta receptors, which may explain why fenoldopam is a vasodilator and dopamine isn't

Question 41

What patient population should not get fenoldopam?

Answer 41

Pt with hx of intraoccular htn or glaucoma

Question 42

Nicardipie, clevidipine, verapamil and diltiazem. Which 2 are dihydropyridines? Are Dihydropirines protective or not for cardiac function?

Answer 42

Dihydropyridines - nicardipine and clevidipine | Yes, these 2 are "cardioprotective"

Question 43

What is special about clevidipine?

Answer 43

Ultrashort half life, rapidly titratable

Question 44

What is the receptor subtype targeted by calcium channel blockers?

Answer 44

L type calcium channels - found more on arterial vessels and venous capacitance vessels

Question 45

Which is more likely to decrease preload, calcium channel blockers or nitrates? Significance?

Answer 45

Nitrates will more likely decrease preload | Significance is that preserved preload with calcium channel blockers will more likely improve cardiac output