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Mo and Mik > m and m 15 - Hypotensive Agents > Flashcards

m and m 15 - Hypotensive Agents Flashcards

1
Q

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

A

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)

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2
Q

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

A

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

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3
Q

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

A

True

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

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4
Q

They tow major components of BP are?

A

CO and SVR

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5
Q

What is the mechanism of sodium nitroprusside?

A

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

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6
Q

What is the indication of inhaled nitric oxide?

A

Reversible pulmonary hypertension

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7
Q

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

A

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

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8
Q

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

A

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

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9
Q

What are the 3 hallmarks of acute cyanide toxicity?

A

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

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10
Q

How does cyanide toxicity affect responsiveness to nitroprusside?

A

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

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11
Q

How is cyanide toxicity treated?

A

100% oxygen

Thiosulfate or sodium nitrate (both oxidize hemoglobin to methemoglobin)

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12
Q

What are signs of thiocyanate accumulation? (5)

A 
Thyroid dysfunction 
Muscle weakness 
Nausea 
Hypoxia 
Acute psychosis
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13
Q

What is the treatment of methemaglobinemia?

A

Methylene blue

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14
Q

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

A

Decreases preload and afterload

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15
Q

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

A

It may increase cardiac output secondary to the reduction in afterload

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16
Q

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

A

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

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17
Q

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

A

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

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18
Q

How can sodium nitroprusside increase physiological dead space?

A

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

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19
Q

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

A

True

20
Q

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

A

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

21
Q

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

A

Sodium nitroprusside - arteriolar and venous target

Nitroglycerin - venous more than arterial dilation

22
Q

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

A

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

23
Q

What are 3 indications for nitroglycerin?

A

Myocardial ischemia
Hypertension
Ventricular Failure

24
Q

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

A

nitroprusside (degraded]

25
Q

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

A

Nitroglycerin - adsorption to polyvinylchloride

26
Q

When is tolerance likely with nitroglycerin? 3 mechanisms?

A

Chronic use

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

27
Q

How can you avoid tolerance with nitroglycerin?

A

Need to have dosing holidays

28
Q

How and where is nitroglycerin metabolised?

A

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

29
Q

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

A

True. Metabolic product, nitrite can make Hgb to methemoglobin

30
Q

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

A
  • 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
31
Q

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

A

False

32
Q

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

A

It reduced preload

33
Q

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

A

Sodium nitroprusside

34
Q

True or false, nitroglycerin decreases platelet aggregation?

A

True

35
Q

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

A

increases cGMP mainly in arteriolar smooth muscle

36
Q

How and where is hydralazine metabolized?

A

In the liver - acetylation and hydroxylation

37
Q

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

A

Increased HR, contractility and CO

Watch out in patients with known CAD

38
Q

What is the effect of hydralazine on cerebral blood flow?

A

Increases cerebral blood flow and intracranial pressure

39
Q

What is the mechanism of vasodilation of fenoldopam?

A

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

40
Q

How does dopamine differ from fenoldopam?

A

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

41
Q

What patient population should not get fenoldopam?

A

Pt with hx of intraoccular htn or glaucoma

42
Q

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

A

Dihydropyridines - nicardipine and clevidipine

Yes, these 2 are “cardioprotective”

43
Q

What is special about clevidipine?

A

Ultrashort half life, rapidly titratable

44
Q

What is the receptor subtype targeted by calcium channel blockers?

A

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

45
Q

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

A

Nitrates will more likely decrease preload

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

Mo and Mik (9 decks)

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