Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II > Vasodilators, Antihypertensives and Negative Inotropes > Flashcards

Vasodilators, Antihypertensives and Negative Inotropes Flashcards

1
Q

What are the primary actions of Calcium channel blockers?

A

Negative inotropic effect
Negative dromotropic effect (AV conduction block)
Vasodilation of systemic, splanchnic, coronary and pulmonary beds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 classes of calcium channel blockers?

A

Phenylalkylamines
Benzothiazines
Dihydropyridines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What drug is a phenylalkylamine and what is its use?

A 
Verapamil
Used for conversion of supraventricular (atrial) tachycardia
Coronary artery spasm
Aortic stenosis and IHSS
Vasospastic angina
Essential HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What drug is a benzothiazine and what is its use?

A

Diltiazem
Used for rate control of tachycardia, tachyarrhythmias
Renal protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What drugs are dihydropyridines?

A 
Nifedipine
Nicardipine
Nimodipine
Nitrendipine
Isradipine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the indications of dihydropyridines?

A

Hypertension
Afterload reduction
Cerebral vasospasm, ischemia
Renal protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is the Dihydropyridine class pure arterial or veno-vasodilators?

A

Pure arterial vasodilators but with minimal reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Cardene?

A

Potent vasodilator of systemic, coronary and cerebral circulations without important negative inotropic or dromotropic effects
An arteriole specific vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is coronary steal present with the use of Cardene?

A

No coronary steal syndrome, favorable myocardial oxygen supply/demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the pharmacokinetics of Cardene?

A

Onset: 20-30 seconds
Duration: 15-20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is Cardene useful for IV control of HTN in the PACU or ICU?

A 
Slower onset and offset that SNP
Easier to use with less swings in BP
No rebound HTN with W/D
Reflex tachycardia <10 bpm
Prolonged DOA may be a benefit postop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the advantages to Cardene?

A 
Dose dependent arterial vasodilation
No arterial cath
No coronary steal
Cerebral and coronary vasodilation
Minimal effects on contractility/conduction
Mild natriuretic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the disadvantages to Cardene?

A 
Slow onset/offset
May accumulate
Variable DOA
Hypotension
Venous irritation
May cause tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Clevidipine?

A

Newest IV CCB
A dihydropyridine
Vasodilation reduces PVR, arteriole specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the pharmacokinetics of Clevidipine?

A

Onset: <5mins
Peak: 10 mins
Duration: 10-20 minutes
Half-life: 1 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the advantages to Clevidipine?

A 
Rapid onset/offset
Reduced need for other antihypertensives
Reliable control
No dose adjustments for renal/hepatic disease
Ready to use vial
No significant myocardial depression
No effect on preload
Low potential for drug interactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the disadvantages to Clevidipine?

A 
Lipid emulsion
Continuous monitoring required
Contraindicated with egg and soy bean allergy
Pancreatitis
HLD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the max amount of Clevidipine are you allowed to give

A

No more than 1L or 21 mg/hr recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Are Dihydropidines arterial or venous vasodilators?

A

Virtually pure arterial vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which drug has the most Negative inotropy and AV block?

A

Verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the adverse effects of CCBs?

A

CNS: dizziness, HA, fatigue, insomnia, nervousness
CV: flushing, edema, palpitations, bradycardia
Respiratory: nasal congestion, dyspnea, cough
GI: NVD
Other: Arthralgias, joint stiffness, ittching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does Verapamil and Diltiazem enhance myocardial oxygen balance?

A

Decreasing myocardial oxygen consumption by afterload reduction and/or negative inotropic effect
Increasing O2 delivery through coronary vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Dihydropyridines’ effect on myocardial oxygen balance?

A

May worsen MvO2 by causing diastolic hypotension and reflex tachycardia (except Nicardipine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are CCBs effect on renal function?

A

Increase RBF and GFR and induce a naturesis

Protective in renal transplantation against a variety of nephrotoxic drugs and radiocontrast media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How can the benefits of CCBs on renal function be reversed?

A

Hypotension, reflex catecholamine release or angiotensin activation leading to decreases in RBF and GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

T/F: It is safe to continue CCBs up to the time of surgery without risk of significant drug interactions

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What may CCBs do to neuromuscular blocking agents?

A

May potentiate the effects of neuromuscular blocking agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Does Clevidipine speed up or slow down gastric emptying?

A

Reduced gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which CCB increases sedative effects of midazolam?

A

Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Droperidol, Haloperidol, and Phenothiazines can cause vasodilation how?

A

By acting at the alpha1 or DA1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do you treat reflex tachycardia and increased contractility?

A

With a BB or Trimethaphan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the actions of beta blockers?

A 
Decrease CO (HR and contractility)
Decrease renin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T/F: Beta blockers vasodilate

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the advantages of beta blockers over vasodilators?

A

No reflex tachycardia or widening of pulse pressure
Improved MvO2 (decrease HR and contractility)
Intrinsic antiarrhythmic activity
No effect of hypoxic pulmonary vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the Beta1 selective drugs?

A 
Metoprolol
Atenolol
Acebutolol
Bisprolol
Esmolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of action of the Beta1 selective drugs?

A

Decrease velocity of AV conduction, HR, contractility, renin release and lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the non-selective beta drugs?

A 
Propanalol
Nadolol
Timolol
Pindolol
Cartelolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do the non-selective beta drugs work?

A

On beta1

On beta-2 causing bronchoconstriction, peripheral vasoconstriction and decrease glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the combine alpha1 and non-selective beta drugs?

A

Carvedilol and labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the elimination half-life of beta blockers?

A

Long-acting (glucuronide hepatic biotransformation)
Intermediate-acting (rapidly hydroxylated by the liver, first pass effect)
Short-acting (red cell esterases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the long-acting beta blockers?

A

Nadolol

Atenolol

42
Q

What are the intermediate-acting beta blockers?

A

Propanolol

Metoprolol

43
Q

What are the ultra short-acting beta blockers?

A

Flestolol

Esmolol

44
Q

Which drugs have low lipophylicity?

A 
Acebutolol
Atenolol
Bisoprolol
Cateolol
Nadolol
45
Q

Which drugs had moderate lipophylicity?

A

Metoprolol
Pindolol
Coreg
Labetalol

46
Q

Which drugs have high lipophylicity?

A

Penbutolol

Propanolol

47
Q

What are the adverse effects of beta blockers?

A

Non-selective blockade of beta 2 receptors–>vasoconstriction and worsening PVD, bronchospasm
Myocardial depression (decreased contractility could precipitate CHF)
Life-threatening bradycardia or asystole
Hyperkalemia in renal failure

48
Q

Use BB with caution with which 2 drugs?

A

Verapamil (decrease HR and contractility)

Digoxin (decrease HR and conduction)

49
Q

What is the treatment if overdose of BBs occur?

A

Treat with atropine
May need isoproterenol, dobutamine and/or glucagon infusion
Ultimately may need pacing

50
Q

What are the preop indications of beta blockers?

A

Control intra and postop HTN and tachycardia
Rate control and/or conversion of SVT, afib and aflutter
Myocardial protection in ischemic heart disease, AS, or IHSS
Sympathetic response to ECT
Peripheral manifestations of hyperthyroidism

51
Q

Which BB is effective in limiting HTN during induction and emergence?

A

Esmolol

52
Q

What are the contraindications to BBs?

A

Severe bradycardia
>1st degree heart block
Cardiogenic shock
Raynaud’s disease

53
Q

What type of patients do you use caution with when giving BBs?

A

Asthma/COPD
Diabetes
Heart failure

54
Q

What is propranolol?

A

Proptotype non-selective BB
Lipid soluble and can penetrate CNS
Undergoes first pass effect (up to 70% metabolized by the liver)

55
Q

T/F: Esmolol is more likely than verapamil to convert afib to SR

A

True

56
Q

What are the pharmacokinetics of Esmolol?

A 
Rapid onset and offset
Metabolized by red cell esterases
Short t1/2: 9-10 minutes
Peak effects: 5-10 mins
Duration: 20-30 mins
57
Q

What is Metoprolol?

A

Beta 1 selective agent
Treatment of angina and acute MI
Antihypertensive

58
Q

How does Labetalol work?

A

Combines weak alpha blockade with weak non-selective beta blockade
Negative inotrope and chronotrope with vasodilatation provides effective antihypertension action

59
Q

What are the indications for Labetalol?

A

Hyperdynamic HTN (blunts CV response to tracheal intubation)
Treatment of aortic dissection
Tachyphylaxis with SNP
Intracranial HTN (does not increase ICP)
Toxemia of pregnancy (Not in first trimester, uterine blood flow is preserved)

60
Q

What are the adverse effects of Labetalol?

A

Unwanted negative inotropy
Prolonged DOA with high doses
Bronchospasm in high doses (not beta1 selective)
Acute hyperkamlemia in renal failure (large doses)
Use caution when treating postop HTN in hypothermic patients: when patients rewarm, persistent beta blockade may blunt increases in CO and exacerbate rewarming hypotension (vasodilatation)

61
Q

How does Coreg work?

A

Combines alpha blockade with nonselective beta blockade

Decreases myocardial O2 demand and cardiac work

62
Q

What are the uses of Carvedilol?

A

3-5 times more potent that Labetalol in decreasing BP

Treat angina, CHF and dysrhythmias

63
Q

Why do you not abruptly stop BBs?

A

Rebound HTN and tachycardia

64
Q

What might BBs mask?

A

Hypoglycemia and hyperthyroidism

65
Q

What do you do if your patient becomes hypertensive intraop?

A

Check depth of anesthesia and administer sufficient analgesia
R/O hypercarbia, distended bladder, hyperthermia, hypoxia, thyroid storm, malignant hyperthermia

66
Q

What is the first line therapy of intraop HTN?

A 
BBs then...
Vasodilators (hydralazine, NTG, SNP)
CCBs
Diuretics (for patients with evidence of pulm edema or with increased ICP and HTN)
Alpha2 agonists
ACE inhibitors
67
Q

Which antihypertensive is favored in pregnancy?

A

Alpha-methyldopa

68
Q

T/F: ACEI can be used in the 2nd and 3rd trimesters

A

False, cause fetal morbidity and mortality

Labetalol can be used in 2nd and 3rd trimesters. BBs are associated with growth retardation in 1st trimester

69
Q

What is a hypertensive emergency?

A

Acute elevation of SBP >180 or DBP >120

70
Q

What is the goal if you have a hypertensive emergency?

A

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

71
Q

What happens if you have excessive correction of HTN?

A

Renal, cerebral, coronary ischemia

72
Q

What is a hypertensive urgency?

A

Accelerated, malignant, or perioperative increase in BP without target organ damage

73
Q

What type of therapy is preferred for a hypertensive urgency?

A

PO therapy and immediate BP lowering is not required

74
Q

These are drugs used to control the primary determinants of myocardial oxygen consumption in ischemic heart disease

A

Negative inotropes and chronotropes

75
Q

What is the mechanism of action for negative inotropes/chronotropes?

A 
Beta1 antagonists (propranolol, esmolol, metoprolol)
Calcium channel antagonists
Direct effects (inhaled anesthetics)
76
Q

What are the hemodynamic effects of negative inotropes/chronotropes?

A

Decrease contractility and HR

Decrease CO and BP and may increase RA and LA pressures

77
Q

T/F: Calcium channel blockers are vasodilators and will decrease arterial resistance

A

True

78
Q

What are the indications for negative inotropes/chronotropes?

A

Decrease myocardial O2 consumption
Treatment of arrhythmias (sinus tach, SVT)
Myocardial preservation

79
Q

What are the contraindications to using negative inotropes/chronotropes?

A

Low CO
Bronchospastic pulmonary disease
Prolonged conduction block (2nd degree heart block may progress to 3rd degree block with beta blockers or verapamil)

80
Q

Myocardial ischemia represents what?

A

A mismatch of oxygen delivery and oxygen demand on a regional or global basis

81
Q

What is resting fractional O2 extraction from myocardial capillary blood?

A

65-75%

82
Q

How is O2 delivery determined?

A

Arterial O2 content x CBF

83
Q

How is CBF determined?

A

CPP/coronary vascular resistance

84
Q

What is the essence of myocardial perfusion?

A

CPP

85
Q

How is CPP determined?

A

Driving pressure - intramyocardial pressure

86
Q

Myocardial blood flow can increase 5 fold by what?

A

By local metabolic vasodilation

87
Q

Patients with CAD, vascular resistance is more fixed and depends on what?

A

Atheromatous stenosis
Active coronary vasomotor tone
Collateral blood flow

88
Q

Duration of ___ regulates the time available for coronary perfusion to the LV endocardium

A

Diastole

89
Q

MvO2 is primarily regulated by what?

A

Wall stress (preload and afterload)
Contractility
Heart rate

90
Q

___ work requires more energy than ___ work

A

Pressure

Volume

91
Q

Increased HR, contractility or pressure work by 50% increases MvO2 how much?

A

50%

92
Q

Increasing volume work by 50% increases MvO2 how much?

A

<5%

93
Q

The force or load acting to stretch ventricular fibers at end-diastole

A

Preload

94
Q

The force that myocardial fibers sense that opposes fiver shortening once contracting is initiated

A

Afterload

95
Q

What is used as an index of afterload instead of ventricular wall stress?

A

SVR

96
Q

T/F: in a normal ventricle, inotropes increase contractility and reduce ESV, EDV, and ultimately wall stress and MvO2

A

False, in a dilated ventricle

97
Q

T/F: in a normal ventricle, heart size and wall stress are not substantially reduced by an inotrope so MvO2 parallels the increased contractility

A

True

98
Q

Does an increased or decreased HR reduce EDV and consequently SV so that CO remains constant

A

Increased HR

99
Q

T/F: Increasing HR decreases MvO2 and the extent of myocardial ischemic injury

A

False, increasing HR increases MvO2

100
Q

What are the therapeutic goals for myocardial ischemia?

A

Maintain normal value of CPP with the smallest heart size possible
Any therapy that decreases CPP below normal values or increases CPP to supranormal values will increase the amount of injury

Pharm II (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions