Antihypertensives, Negative Inotropes, Negative Chronotropes Flashcards

1
Q

This is related to overactivity of the ANS and an interaction with the Renin-Angiotensin System alone with factors related to sodium homeostasis and intravascular volume

A

Idiopathic hypertension

  • Initially SVR normal, increased BP due to CO
  • SVR increases to prevent the increased in BP from being transmitted to the capillary bed where it would affect cell homeostasis
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2
Q

What is the primary cause of perioperative HTN?

What are complications that can occur bc of this?

A

Increased sympathetic discharge with systemic vasoconstriction

CVA, MI, ischemia, LV dysfunction, arrhythmias, increased suture tension, hemorrhage, pulmonary edema, cognitive dysfunction

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3
Q

What are 4 things to consider when choosing an antihypertensive medication?

A

Route of administration
Pharmacokinetics
Ease of titration, use, monitoring
Comorbidities

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4
Q

What is the mechanism of action of vasodilators?

A

Direct smooth muscle dilation

  • production of intracellular NO (SNP and nitrates)
  • calcium channel blockers
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5
Q

What are the 3 hemodynamic effects of vasodilators?

A

Act primarily to cause systemic vasodilation
-arterial dilatory (reduce afterload)
-venodilators (reduce preload)
Balanced vasodilators

Can cause reflex increase in HR (baroreceptors)

Redistribution of coronary blood flow - NTG may improve collateral circulation, other may cause coronary steal

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6
Q

T/F: there are “pure” venodilators available

A

FALSE

There are pure arteriole dilators and balanced vasodilators. There are no “pure” venodilators. NTG act primarily on the venous circulation, but also affect arterioles

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7
Q

What percentage of coronary artery perfusion to the LV occurs during diastole?

A

70-90%

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8
Q

What is coronary steal?

A

Narrowed coronary arteries are always maximally dilated to compensate for the decrease blood supply. Dilating the other arterioles causes blood to be shunted away from the coronary vessels.

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9
Q

What med shunts blood away from ischemic areas (coronary steal), and what med directs more blood toward ischemic zones?

A

SNP - dilates both epicardial and conductance and intramyocardial resistance vessels and in the presence of CAD, shunts blood away from ischemic zones

NTG - preferentially dilates conductance vessels and directs more blood toward ischemic zones

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10
Q

Name the 3 vasodilators

A

Hydralazine

Nitroglycerine

Sodium nitroprusside

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11
Q

This is a direct acting arterial vasodilator that increases HR, contractility, renin activity, fluid retention, CO and SV. It also. Decreases BP (diastolic > systolic), and SVR

A

Hydralazine

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12
Q

Hydralazine will increase or decrease myocardial O2 demand?

A

Increases

Avoid in pts with CAD, increased ICP, and lupus

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13
Q

This drug causes a release of nitric oxide for non-specific relaxation of the vascular smooth muscle. It dilates veins > arteries. Decreases PVR, venous return, and myocardial O2 demand. It also relaxes coronary vessels and relieves spasms

A

Nitroglycerine

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14
Q

What are 3 non-cardiac effects of nitroglycerine?

A
  • Dilates meningeal vessels (caution with increased ICP)
  • Decreases renal blood flow with decreased BP
  • Dilates pulmonary vessels (decreases PVR)
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15
Q

Tolerance to nitroglycerine can occur in _______ vessels with chronic use

A

Arterial

But won’t occur in venous vessels.

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16
Q

What can happen with chronic use of nitroglycerine?

A

Methemoglobinemia

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17
Q

What class of medications can cause fatal hypotension if taken with nitroglycerine?

A

PDE5 inhibitors - viagra, cialis

Phosphodiesterase 5 inhibitors

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18
Q

This medication directly vasodilates arteries and veins (more balanced)

A

Sodium Nitroprusside

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19
Q

There is an increase or decrease in myocardial O2 demand with sodium nitroprusside?

A

Overall reduction in myocardial O2 demand

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20
Q

What will happen with abrupt discontinuation of sodium nitroprusside?

A

Reflex tachycardia and hypertension

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21
Q

What is a potential side effect of sodium nitroprusside?

At with dose is the risk increased?

A

Thiocyanate/cyanide toxicity

Doses over 4mcg/kg/min, or > 2 days of therapy

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22
Q

Do smokers have a higher or lower threshold for cyanide toxicity?

A

They have a higher threshold

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23
Q

What is the treatment of cyanide toxicity?

A
  • Stop the infusion
  • Administer 100% O2
  • Correct metabolic acidosis
  • Give 3% sodium nitrate (will replace cyanide to make methemoglobin)
  • Give sodium thiosulfate
  • Consider Vitamin B12
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24
Q

What can be added to sodium nitroprusside to prevent cyanide toxicity?

A

Sodium thiosulfate

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25
Q

This is a non selective alpha antagonist that irreversibly binds to the receptor

A

Phenoxybenzamine

Used to decrease PVR to reduce BP

Used to for BPH to improve flow

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26
Q

This is used when there is extravasation of catecholamines

A

Phentolamine

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27
Q

Most oral alpha-1 antagonists are used for what?

A

To improve urinary outflow with BPH

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28
Q

This is a centrally acting alpha-2 agonist that leads to inhibition of sympathetic outflow.

It has a 220:1 affinity for alpha-2 over alpha-1 receptors

A

Clonidine

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29
Q

T/F: abrupt cessation of clonidine may lead to rebound HTN

A

TRUE

Due to NE. At risk if using for >6 days

30
Q

Clonidine causes an increased or decreased need for propofol and thiopental?

A

DECREASED

31
Q

This medication is used for continuous sedation, and has a 1620:1 affinity for alpha-2 over alpha-1 receptors

A

Dexmedetomindine (Precedex)

32
Q

This medication is generally used to treat HTN in pregnant women

A

Methyldopa (Aldomet)

33
Q

Methyldopa can lead to positive _______ test, which reads as a false B12 anemia.

A

Coombs test

34
Q

ACE inhibitors are predominantly _________ vasodilators

A

Arterial

35
Q

T/F: It is ok to give pts with decreased renal function or renal artery stenosis ACE inhibitors

A

FALSE

If BP decreased, renal function may deteriorate bc compensatory efferent arteriolar constriction mediated by angiotensin II is blocked and decreased glomerular filtration pressure and GRF May result in acute hyperkalemia

36
Q

This is an IV ACE inhibitor that is an active metabolite of enalapril.

A

Enalaprilat (Vasotec)

37
Q

What are 2 very common side effects of ACE inhibitors?

A

Cough - untreatable except to d/c med

Angioedema - serious side effect

38
Q

T/F: you must taper an ACE inhibitor rather than d/c abruptly

A

FALSE

Rebound HTN not seen with abrupt withdrawal

39
Q

Are ACE inhibitors safe to use during pregnancy?

A

NO!!!

They have demonstrated fetal morbidity and mortality

40
Q

Are ARF and hyper-K+ reversible with withdrawal of ACE inhibitors?

A

Yes

41
Q

What is a perioperative concern with prolonged hypotension that can occur with pt being treated with ACE inhibitors?

A

Risk of acute renal failure both intraoperative and post op

  • hypotension and hypovolemia contribute to the risk
  • hold ACEI and ARB day of surgery
42
Q

What 3 things can cause increased hypotensive effects of ACE inhibitors?

A

Diuretics
Vasodilators
Anesthetics

43
Q

Angiotensin II receptor antagonists end in what?

A

“Sartan”

Ex: losartan, irbesartan

44
Q

What group of medications hast the same hemodynamic effects and uses as ACEI, but less cough and angioedema?

A

Angiotensin II receptor antagonists

45
Q

What are 4 functions of calcium?

A
  1. Signal transduction: CNS, heart
  2. Muscle contraction: smooth muscle, cardiac muscle, vessels walls
  3. Bone health
  4. Clotting cascade
46
Q

What are the 3 primary actions of calcium channel blockers?

A
  1. Negative inotropic effect
  2. Negative Dromotropic effect (AV conduction block)
  3. Vasodilation of systemic, spanchic, coronary and pulmonary beds

*Primarily arterial vasodilator

47
Q

This class of calcium channel blockers is pure arterial vasodilator, with minimal inotropic and dromotropic effects

A

Dihydropyridines

*end in “dipine”
Ex: nicardipine, amlodipine

48
Q

T/F: nicardipine does not cause coronary steal, and is favorable for myocardial O2 supply/demand

A

TRUE

49
Q

Is nicardipine useful in emergent situations?

A

NO

It has a slower onset and offset. Useful for IV control of HTN in PACU or ICU

50
Q

Is there rebound HTN when nicardipine is d/c’d?

A

No

51
Q

This CCB is also a dihydropyridine, but is cleared faster than nicardipine and is ultra short acting

A

Clevidipine

52
Q

This CCB is in phenylalkylalmine class, and is a potent negative inotrope dromotrope and vasodilator

A

Verapamil

53
Q

This CCB (benzothiazine class) fits between verapamil (phenylakylamine) and dihydropyridines in action

A

Diltiazem (cardizem)

54
Q

This CCB is used for aortic stenosis and IHSS, conversion of atrial re-entry tachyarrhythmias, and coronary artery vasospasm

A

Verapamil

55
Q

This CCB is used as a rate-control agent for a-fib and atrial tachycardia

A

Cardizem

56
Q

How do CCBs effect myocardial O2 balance?

A

Verapamil and diltiazem enhance myocardial O2 balance

Dihydropyridine vasodilators may worse myocardial O2 consumption by causing diastolic hypotension and reflex tachycardia

57
Q

How do CCBs effect renal function?

A

Increase RBF and GFR and induce a naturesis

Benefit can be reversed if they cause hypotension —> decreased RBF and GFR

58
Q

When should CCBs be held prior to surgery?

A

Continue up to the time of surgery without risk of significant drug interactions

59
Q

What are the 3 actions of beta blockers?

A
  1. Decrease CO (HR and contractility)
  2. Decrease renin release
  3. Do NOT vasodilator
60
Q

What are 3 advantages of beta blockers over vasodilators?

A
  1. No reflex tachycardia or widening of pulse pressure
  2. Improved MvO2 (decreases HR and decrease contraction)
  3. Intrinsic antiarrhythmic activity
61
Q

Name the beta-1 selective beta blockers

A

Metoprolol
Atenolol
Esmolol
Bisoprolol

62
Q

Name non-selective beta blockers

A
Propranolol
Nadolol
Timolol
Pridolol
Careolol
63
Q

Name the combined alpha-1 and non-selective beta blockers

A

Carvedilol

Labetalol

64
Q

Name the 3 ways to classify beta blockers

A
  1. Beta-selectivity
  2. Elimination half-life
  3. Lipophylicity
65
Q

Name 4 contraindications of beta blockers

A
  1. Severe bradycardia
  2. > 1st degree heart block
  3. Cardiogenic shock
  4. Raynaud’s disease
66
Q

Beta blockers can mask symptoms of what?

A

Hypoglycemia and hyperthyroidism

67
Q

T/F: you can stop beta blockers abruptly

A

FALSE

Can get rebound HTN and tachycardia bc of up regulation of receptors

68
Q

What 4 things should of consider when pts have HTN perioperative lay?

A
  1. Check depth of anesthesia
  2. Administer sufficient analgesia
  3. R/O hypercarbia, distended bladder, hyperthermia, hypoxia, thyroid storm, MH
  4. When vasodilators are used, watch for reflex tachycardia as BP decreases
69
Q

What medication has demonstrated fetal morbidity and mortality in all 3 trimesters?

A

ACE Inhibitors

70
Q

What BP marks a HTN emergency?

A

Acute elevation of SBP>180 or DBP>120 with Target organ damage

71
Q

During HTN emergency, goal is to decrease BP by how much?

A

Reduce MAP by no more than 25% within minutes to hours. Reach 160/100 within 2-6 hours

72
Q

What are some examples of target organ damage?

A
Encephalopathy
ICH
Unstable angina
Acute MI
Acute LV failure with pulmonary edema
Dissecting aortic aneurysm
Eclampsia