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Pharm II > Vasodilators, Antihypertensives and Negative Inotropes > Flashcards

Vasodilators, Antihypertensives and Negative Inotropes Flashcards

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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

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2
Q

What are the 3 classes of calcium channel blockers?

A

Phenylalkylamines
Benzothiazines
Dihydropyridines

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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
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4
Q

What drug is a benzothiazine and what is its use?

A

Diltiazem
Used for rate control of tachycardia, tachyarrhythmias
Renal protection

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5
Q

What drugs are dihydropyridines?

A 
Nifedipine
Nicardipine
Nimodipine
Nitrendipine
Isradipine
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6
Q

What are the indications of dihydropyridines?

A

Hypertension
Afterload reduction
Cerebral vasospasm, ischemia
Renal protection

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7
Q

Is the Dihydropyridine class pure arterial or veno-vasodilators?

A

Pure arterial vasodilators but with minimal reflex tachycardia

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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

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9
Q

Is coronary steal present with the use of Cardene?

A

No coronary steal syndrome, favorable myocardial oxygen supply/demand

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10
Q

What are the pharmacokinetics of Cardene?

A

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

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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
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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
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13
Q

What are the disadvantages to Cardene?

A 
Slow onset/offset
May accumulate
Variable DOA
Hypotension
Venous irritation
May cause tachycardia
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14
Q

What is Clevidipine?

A

Newest IV CCB
A dihydropyridine
Vasodilation reduces PVR, arteriole specific

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15
Q

What are the pharmacokinetics of Clevidipine?

A

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

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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
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17
Q

What are the disadvantages to Clevidipine?

A 
Lipid emulsion
Continuous monitoring required
Contraindicated with egg and soy bean allergy
Pancreatitis
HLD
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18
Q

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

A

No more than 1L or 21 mg/hr recommended

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19
Q

Are Dihydropidines arterial or venous vasodilators?

A

Virtually pure arterial vasodilator

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20
Q

Which drug has the most Negative inotropy and AV block?

A

Verapamil

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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

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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

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23
Q

What is Dihydropyridines’ effect on myocardial oxygen balance?

A

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

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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

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25
How can the benefits of CCBs on renal function be reversed?
Hypotension, reflex catecholamine release or angiotensin activation leading to decreases in RBF and GFR
26
T/F: It is safe to continue CCBs up to the time of surgery without risk of significant drug interactions
True
27
What may CCBs do to neuromuscular blocking agents?
May potentiate the effects of neuromuscular blocking agents
28
Does Clevidipine speed up or slow down gastric emptying?
Reduced gastric emptying
29
Which CCB increases sedative effects of midazolam?
Diltiazem
30
Droperidol, Haloperidol, and Phenothiazines can cause vasodilation how?
By acting at the alpha1 or DA1 receptors
31
How do you treat reflex tachycardia and increased contractility?
With a BB or Trimethaphan
32
What are the actions of beta blockers?
``` Decrease CO (HR and contractility) Decrease renin release ```
33
T/F: Beta blockers vasodilate
False
34
What are the advantages of beta blockers over vasodilators?
No reflex tachycardia or widening of pulse pressure Improved MvO2 (decrease HR and contractility) Intrinsic antiarrhythmic activity No effect of hypoxic pulmonary vasoconstriction
35
What are the Beta1 selective drugs?
``` Metoprolol Atenolol Acebutolol Bisprolol Esmolol ```
36
What is the mechanism of action of the Beta1 selective drugs?
Decrease velocity of AV conduction, HR, contractility, renin release and lipolysis
37
What are the non-selective beta drugs?
``` Propanalol Nadolol Timolol Pindolol Cartelolol ```
38
How do the non-selective beta drugs work?
On beta1 | On beta-2 causing bronchoconstriction, peripheral vasoconstriction and decrease glycogenolysis
39
What are the combine alpha1 and non-selective beta drugs?
Carvedilol and labetalol
40
What is the elimination half-life of beta blockers?
Long-acting (glucuronide hepatic biotransformation) Intermediate-acting (rapidly hydroxylated by the liver, first pass effect) Short-acting (red cell esterases)
41
What are the long-acting beta blockers?
Nadolol | Atenolol
42
What are the intermediate-acting beta blockers?
Propanolol | Metoprolol
43
What are the ultra short-acting beta blockers?
Flestolol | Esmolol
44
Which drugs have low lipophylicity?
``` Acebutolol Atenolol Bisoprolol Cateolol Nadolol ```
45
Which drugs had moderate lipophylicity?
Metoprolol Pindolol Coreg Labetalol
46
Which drugs have high lipophylicity?
Penbutolol | Propanolol
47
What are the adverse effects of beta blockers?
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
Use BB with caution with which 2 drugs?
Verapamil (decrease HR and contractility) | Digoxin (decrease HR and conduction)
49
What is the treatment if overdose of BBs occur?
Treat with atropine May need isoproterenol, dobutamine and/or glucagon infusion Ultimately may need pacing
50
What are the preop indications of beta blockers?
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
Which BB is effective in limiting HTN during induction and emergence?
Esmolol
52
What are the contraindications to BBs?
Severe bradycardia >1st degree heart block Cardiogenic shock Raynaud's disease
53
What type of patients do you use caution with when giving BBs?
Asthma/COPD Diabetes Heart failure
54
What is propranolol?
Proptotype non-selective BB Lipid soluble and can penetrate CNS Undergoes first pass effect (up to 70% metabolized by the liver)
55
T/F: Esmolol is more likely than verapamil to convert afib to SR
True
56
What are the pharmacokinetics of Esmolol?
``` 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
What is Metoprolol?
Beta 1 selective agent Treatment of angina and acute MI Antihypertensive
58
How does Labetalol work?
Combines weak alpha blockade with weak non-selective beta blockade Negative inotrope and chronotrope with vasodilatation provides effective antihypertension action
59
What are the indications for Labetalol?
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
What are the adverse effects of Labetalol?
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
How does Coreg work?
Combines alpha blockade with nonselective beta blockade | Decreases myocardial O2 demand and cardiac work
62
What are the uses of Carvedilol?
3-5 times more potent that Labetalol in decreasing BP | Treat angina, CHF and dysrhythmias
63
Why do you not abruptly stop BBs?
Rebound HTN and tachycardia
64
What might BBs mask?
Hypoglycemia and hyperthyroidism
65
What do you do if your patient becomes hypertensive intraop?
Check depth of anesthesia and administer sufficient analgesia R/O hypercarbia, distended bladder, hyperthermia, hypoxia, thyroid storm, malignant hyperthermia
66
What is the first line therapy of intraop HTN?
``` 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
Which antihypertensive is favored in pregnancy?
Alpha-methyldopa
68
T/F: ACEI can be used in the 2nd and 3rd trimesters
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
What is a hypertensive emergency?
Acute elevation of SBP >180 or DBP >120
70
What is the goal if you have a hypertensive emergency?
Reduce MAP by no more than 25% within minutes to hours. Reach 160/100 within 2-6 hours
71
What happens if you have excessive correction of HTN?
Renal, cerebral, coronary ischemia
72
What is a hypertensive urgency?
Accelerated, malignant, or perioperative increase in BP without target organ damage
73
What type of therapy is preferred for a hypertensive urgency?
PO therapy and immediate BP lowering is not required
74
These are drugs used to control the primary determinants of myocardial oxygen consumption in ischemic heart disease
Negative inotropes and chronotropes
75
What is the mechanism of action for negative inotropes/chronotropes?
``` Beta1 antagonists (propranolol, esmolol, metoprolol) Calcium channel antagonists Direct effects (inhaled anesthetics) ```
76
What are the hemodynamic effects of negative inotropes/chronotropes?
Decrease contractility and HR | Decrease CO and BP and may increase RA and LA pressures
77
T/F: Calcium channel blockers are vasodilators and will decrease arterial resistance
True
78
What are the indications for negative inotropes/chronotropes?
Decrease myocardial O2 consumption Treatment of arrhythmias (sinus tach, SVT) Myocardial preservation
79
What are the contraindications to using negative inotropes/chronotropes?
Low CO Bronchospastic pulmonary disease Prolonged conduction block (2nd degree heart block may progress to 3rd degree block with beta blockers or verapamil)
80
Myocardial ischemia represents what?
A mismatch of oxygen delivery and oxygen demand on a regional or global basis
81
What is resting fractional O2 extraction from myocardial capillary blood?
65-75%
82
How is O2 delivery determined?
Arterial O2 content x CBF
83
How is CBF determined?
CPP/coronary vascular resistance
84
What is the essence of myocardial perfusion?
CPP
85
How is CPP determined?
Driving pressure - intramyocardial pressure
86
Myocardial blood flow can increase 5 fold by what?
By local metabolic vasodilation
87
Patients with CAD, vascular resistance is more fixed and depends on what?
Atheromatous stenosis Active coronary vasomotor tone Collateral blood flow
88
Duration of ___ regulates the time available for coronary perfusion to the LV endocardium
Diastole
89
MvO2 is primarily regulated by what?
Wall stress (preload and afterload) Contractility Heart rate
90
___ work requires more energy than ___ work
Pressure | Volume
91
Increased HR, contractility or pressure work by 50% increases MvO2 how much?
50%
92
Increasing volume work by 50% increases MvO2 how much?
<5%
93
The force or load acting to stretch ventricular fibers at end-diastole
Preload
94
The force that myocardial fibers sense that opposes fiver shortening once contracting is initiated
Afterload
95
What is used as an index of afterload instead of ventricular wall stress?
SVR
96
T/F: in a normal ventricle, inotropes increase contractility and reduce ESV, EDV, and ultimately wall stress and MvO2
False, in a dilated ventricle
97
T/F: in a normal ventricle, heart size and wall stress are not substantially reduced by an inotrope so MvO2 parallels the increased contractility
True
98
Does an increased or decreased HR reduce EDV and consequently SV so that CO remains constant
Increased HR
99
T/F: Increasing HR decreases MvO2 and the extent of myocardial ischemic injury
False, increasing HR increases MvO2
100
What are the therapeutic goals for myocardial ischemia?
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)

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