Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm 2 > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

Idiopathic HTN

A
  • overactivity of the ANS and an interaction with RASS and factors related to Na homeostasis and intravascular volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

causes of perioperative HTN

A
  • hypercarbia
  • hypoxia
  • aortic cross clamp
  • hypervolemia
  • hypothermia
  • pain
  • airway manipulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

primary cause of peri-op HTN

A
  • increased sympathetic discharge with sympathetic vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

prevalence of peri-op HTN

A

~ 80% of cardiac surgery patients
~ 25% of non-cardiac surgery patients

  • does not have to be a diagnosis of HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

vasodilators MOA

A
  • direct smooth muscle dilation (production of smooth muscle NO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

types of vasodilators

A
  • alpha 1 antagonists (prazosin and labetalol)
  • alpha 2 agonists (clonidine, alpha methyldopa)
  • ACE inhibitors (captopril, enalapril)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how vasodilators are classified according to their predominate site of action

A
  • arterial dilators
  • venodilators
  • balanced vasodilators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hemodynamic effects of vasodilators

A
  • pure arteriole dilators cause minimal effects of preload
  • pure venodilators do not exist
  • balanced vasodilators decrease afterload and preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

reflex response to vasodilators

A
  • reflex increase in HR (baroreceptors)
  • redistribution of coronary blood flow (may improve or cause coronary steal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

coronary steal

A
  • narrowed coronaries are already max dilated. Dilating other arteries may cause blood to be shunted away from the coronary vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SNP effect on coronary steal

A
  • dilates both epicardial conductance and intramyocardial resistance vessels and in the presence of CAD, shunts blood away from the ischemic zone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

NGT and coronary steal

A
  • preferentially dilates conductance vessels and directs more blood toward ischemic zones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hydralazine effects and reflex response

A
  • direct acting arterial vasodilator (alters Ca movement and metabolism)
  • has its own receptor
  • decreases BP (diastolic > systolic) and SVR
  • reflex = (increase HR, contractility, renin activity, fluid retention, CO, SV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

who to avoid hydralazine in

A
  • avoid with CAD, increased ICP, lupus
  • increases myocardial O2 demand leading to ischemia (from reflex tachycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

side effects of hydralazine

A
  • 5-10% of patients on hydralazine will have a positive ANA (lupus) titer (butterfly rash, joint pain)
  • headache, dizziness, tremor, angina, tachycardia, flushing, palpitations, anorexia, agranulocytosis congestion, muscle cramps, edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pharmacokinetics of hydralazine

A
  • metabolized in the liver
  • excreted in kidney
  • highly protein bound
  • onset 30 min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how nitroglycerine works and what it does to the body

A
  • causes a release of nitric oxide for non-specific relaxation of the vascular smooth muscle
  • dilates veins > arteries
  • decreases PVR, venous return, myocardial O2 consumption
  • relaxes coronary vessels and relieves spasms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

nitroglycerin non-cardiac effects

A
  • dilates meningeal vessels (caution with ICP) (causes headaches)
  • decreases renal blood flow with decreased BP
  • dilates pulmonary vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pharmacokinetics of nitroglycerine

A
  • onset 1 min
  • duration 3-5 min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

nitroglycerine metabolism

A
  • metabolized by glutathione nitrate reductase in the liver
  • nitrite ion oxidizes Hgb to methemoglobin
  • arterial vessels can build tolerance but not venous vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

nitroglycerin warnings/ contraindications

A
  • PDE 5 inhibitors (Viagra, Cialis) (usually end in “fil”)
  • narrow angle glaucoma
  • head trauma / cerebral hemorrhage
  • severe anemia
  • hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

advantages of nitroglycerine

A
  • rapid onset
  • coronary vasodilator
  • dec myocardial O2 consumption
  • no toxicities
  • no coronary steal
  • reduced PVR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

disadvantages of nitroglycerin

A
  • decreased diastolic BP
  • reflex tachycardia
  • possible hypotension
  • tachyphylaxis
  • methemoglobinemia
  • intrapulmonary shunting
  • prolonged bleeding time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

sodium nitroprusside actions and effects on the body

A
  • directly vasodilates arteries and veins
  • decease BP and HR
  • inc cerebral blood flow and ICP
  • renal blood flow maintains
  • overall reduction in myocardial O2 demand
  • with abrupt discontinuation = reflex tachycardia and hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

warnings / contraindications w/ sodium nitroprusside

A
  • congenital optic atrophy
  • hypovolemia
  • compensatory HTN (AV shunting, aortic coarctation)
  • increased ICP
  • severe renal/ hepatic impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

presentation of cyanide toxicity w/ sodium nitroprusside

A
  • hypotension, blurred vision, fatigue
  • metabolic acidosis
  • pink skin
  • absence of reflexes
  • faint heart sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

toxic thiocyanide and cyanide levels

A
  • thiocyanate (toxic >30)
  • cyanide (toxic >2) (normal 0.2 smoker 0.4)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

treatment of cyanide toxicity

A
  • 100% O2
  • correct acidosis
  • 3% Na nitrate 4-6 mg/kg slow
  • sodium thiosulfate
  • hydroxocobalamin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

phenoxybenzamine (dibenzyline) binding and uses

A
  • nonselective alpha antagonist
  • irreversibly binds to receptor (must wait for new receptors to be made)
  • long-term preop control of pheochromocytoma
  • relieve ischemia in PVD
  • BPH to improve flow
30
Q

phenoxybenzamine (dibenzyline) effects on body

A
  • reduced PVR to reduce BP
  • secondary increases in NE due to alpha 2 blockade can increase HR and CO
  • crosses the BBB
31
Q

oral alpha 1 antagonists

A
  • prazosin
  • terazosin
  • doxazosin
  • tamsulosin
  • silodosin
  • alfuzosin
32
Q

clonidine receptor and effects

A
  • central acting alpha 2 agonist
  • decreases release of sympathetic neurotransmitters
  • inhibits renin
33
Q

clonidine actions

A
  • decrease HR, BP, CO, SVR
  • abrupt cessation may lead to rebound HTN
34
Q

clonidine withdraw

A
  • from sudden discontinuation, due to NE
  • manifests with sudden HTN, tachycardia, restlessness, insomnia, headache, nausea
  • at risk after 6 days of use
35
Q

caution with clonidine

A
  • severe coronary insufficiency, conduction disturbances, recent MI/CVA, CKD
36
Q

clonidine and anesthesia

A
  • reduced propofol and thiopental requirements
  • alternative to N2O for shortening induction time and attenuating the adrenergic response to intubation during inhaled anesthesia
37
Q

methyldopa (aldomet)

A
  • acts as a false neurotransmitter in the periphery (alpha-methyl-NE is almost as potent as NE)
  • in the CNS its metabolized to alpha-methylepinephrine (acts at alpha-2 to decrease sympathetic outflow)
  • treats HTN during pregnancy
38
Q

why hyperkalemia from ACE inhibitors

A
  • prevents angiotensin II from causing K+ excretion
39
Q

RASS pathway

A
  • angiotensinogen from the liver forms with renin from the kidney to make angiotensin 1 which forms with ACE from the lungs to make angiotensin II
40
Q

ACE inhibitors primary function and use

A
  • predominantly arterial vasodilators
  • treat CHF and MR by afterload reduction
  • used post MI
  • improves outcomes in DM
41
Q

renal function and ACE inhibitors

A
  • with HTN: decreased renal vascular resistance improves RBF and GFR
  • with hypotension: if BP is decreased renal function may deteriorate b/c compensatory constriction is blocked
  • avoid in pts with significant renal dysfunction or renal artery stenosis
42
Q

side effects of ACE inhibitors

A
  • cough, congestion, rhinorrhea
  • angioedema from increased bradykinin
  • do not use in pregnancy
43
Q

peri-op issues with ACE inhibitors

A
  • prolonged hypotension can occur
  • risk of ARF
44
Q

ACE inhibitor med interactions

A
  • increased hypotensive effects with diuretics, vasodilators and anesthetics
  • NSAIDs and ASA interaction: reduce antihypertensive effect, increased risk of hyperK and ARF
45
Q

primary action of CCB

A
  • negative inotropic effect
  • negative dromotropic effect (AV conduction block)
  • vasodilation of systemic, splanchnic, coronary and pulmonary beds
46
Q

dihydropyridines

A
  • nifedipine
  • nicardipine
  • amlodipine
  • pure arterial dilators, minimal reflex tachycardia
  • minimal negative inotropic and dromotropic effects
47
Q

nicardipine

A
  • potent vasodilator of systemic, coronary, and cerebral circulations
  • arteriole specific vasodilator
  • no coronary steal, favorable myocardial O2 supply/ demand
  • onset < 5 min
48
Q

clevidipine

A
  • IV CCB (dihydropyridine)
  • vasodilation reduces PVR, arteriole specific
  • onset <5min, half life 1 min
  • reduces gastric emptying
49
Q

verapamil

A
  • phenylalkylamine
  • potent negative inotrope, dromotrope, and vasodilator
  • for aortic stenosis, conversion of atrial re-entry tacyarrhythmias, coronary artery vasospasms
50
Q

diltiazem

A
  • benzothiazine
  • used for rate control in a-fib and atrial tach
  • moderate CYP3A4 inhibitor, weak CYP2D6 inhibitor, weak P-gp inhibitor (tons of drug interactions)
51
Q

verapamil and diltiazem effect on myocardial O2 balance

A
  • enhance myocardial O2 balance (decrease myocardial O2 consumption by afterload reduction and or negative inotrope effect and increased o2 delivery through coronary vasodilation
52
Q

dihydropyridine vasodilators effect on myocardial O2 balance

A
  • may worsen MvO2 by causing diastolic hypotension and reflex tachycardia (except nicardipine)
  • decrease reperfusion injury after ischemia
53
Q

CCB effect on renal perfusion

A
  • increase RBF and GFR and induce naturesis
  • benefits reversed in they induce hypotension
  • reflex catecholamine release and angiotensin activation lead to decreased RBF and GFR
54
Q

recommendations with CCB

A
  • continue up to surgery without risk of significant drug interactions
  • may potentiate NMB
  • primarily block L type Ca channels in CV system (causing NDNMB to bind to P-type channels that effect Ach release)
55
Q

BB actions

A
  • decrease CO (HR and contractility)
  • decrease renin release
  • do not vasodilate
56
Q

BB advantages over vasodilators

A
  • no reflex tachycardia or widening pulse pressure
  • improve MvO2
  • antiarrhythmic activity
57
Q

beta 1 selective BB

A
  • metoprolol
  • atenolol
  • acebutolol
  • bisoprolol
  • esmolol
  • decrease velocity of A-V conduction, HR, contractility, renin release, lipolysis
58
Q

non-selective BB

A
  • propranolol
  • nadolol
  • timolol
  • pindolol
  • carteolol
  • block beta 1 and beta 2 (bronchoconstriction, peripheral vasoconstriction)
59
Q

combined alpha 1 and non selective beta

A
  • carvedilol
  • labetalol
60
Q

short acting BB elimination

A
  • red cell esterases (esmolol)
61
Q

adverse effects of BB

A
  • non-selective blockade of beta 2 = vasoconstriction and worsening PVD, bronchospasm
  • myocardial depression
  • life threatening bradycardia asystole
  • hyperkalemia in renal failure
62
Q

BB contraindications and cautions

A
  • bradycardia, heart block
  • cardiogenic shock
  • raynauds disease
  • caution with asthma, COPD, diabetes, HF
63
Q

propranolol

A
  • non-selective BB
  • lipid soluble (can penetrate CNS)
  • undergoes 1st pass (70%)
64
Q

esmolol

A
  • beta 1 selective
  • blunts cardiovascular response to intubation
  • control SVT a-fib
  • rapid onset and off
  • red cell esterase metabolism
65
Q

metoprolol

A
  • beta 1 selective
  • approved for treatment of angina and acute MI
  • antihypertensive
  • longer DOA
66
Q

Labetalol

A
  • combines a weak alpha blockade with weak non-selective beta blockade
  • negative inotrope and chronotrope with vasodilation, providing antihypertensive action
  • for aortic dissection
  • treatment of tachyphylaxis with SNP
  • intercranial HTN (does not increase ICP)
67
Q

adverse effects of labetalol

A
  • unwanted negative inotropy
  • prolonged DOA with higher dose
  • bronchospasm in high doses
  • hyperkalemia in renal failure
  • caution in hypothermic pt ( may exacerbate rewarming hypotension)
68
Q

BB warnings

A
  • negative inotropic effects and conduction delays are potentiated by general anesthetics
  • rebound HTN and tachycardia with abrupt cessation
  • mask hypoglycemia and hyperthyroidism
  • anticholinesterases may increase bradycardia
69
Q

treatment of BB overdose

A
  • glucagon
  • atropine
  • beta 1 agonists
  • high dose insulin
  • IV lipids
  • ca and bicarb
70
Q

antihypertensives and pregnancy

A
  • alpha-methyldopa is favored
  • labetalol can be used in 2nd and 3rd trimester
  • hydralazine during delivery
  • nifedipine PO

Pharm 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions