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NUNA 681 Pharm II > Exam II: CV drugs - ACEIs, CCBs, and vasodilators > Flashcards

Exam II: CV drugs - ACEIs, CCBs, and vasodilators Flashcards

1
Q

Concerns with Antihypertensives and Anesthesia

Interference with the sympathetic nervous system’s activity resulting in ___ ____, or exaggerated hypotension related to _____, position change, or decreased _____ ____ (pos. pressure ventilation)

A

orthostatic hypotension
hypovolemia
venous return

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2
Q

Concerns with Antihypertensives and Anesthesia

Possible depletion of _____ stores – minimal response to indirect sympathomimetics

A

norepinephrine

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3
Q

Concerns with Antihypertensives and Anesthesia

Exaggerated response to direct sympathomimetics – due to no counter-balancing ____ ____.

A

beta2 activity

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4
Q

Historical perspective

Prior to the mid-1970’s, antihypertensives were withheld prior to surgery due to their ___ ___ nature.

A

myocardial depressant

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5
Q

Historical perspective

The drugs of the day caused severe ___ ___.

A

perioperative lability

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6
Q

Historical perspective

Today, we know that beta-blockers may ____ the outcome of patients with hypertension.

A

improve

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7
Q

Historical perspective

Other than ____, antihypertensive medications* should be continued even on the morning of surgery-fewer alterations in BP and HR, fewer _____.

A

diuretics
arrhythmias

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8
Q

Beta-adrenergic blockers – negative ___, _____

A

chronotropic, inotropic

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9
Q

Combined alpha1- and beta-adrenergic blocker (Labetalol)-negative inotropic, chronotropic, vasodilation; _________ as beta-blockers or phentolamine

A

not as potent

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10
Q

Alpha1-adrenergic blocker (prazosin, phentolamine)-_____

A

vasodilation

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11
Q

Centrally acting alpha2-adrenergic agonist (clonidine, dexmedetomidine) – decrease _____ outflow

A

sympathetic

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12
Q

ACEIs MOA:
inhibit the ACE in both the plasma and in the vascular endothelium, thus block the conversion of ____ to ____, thus preventing the vasoconstriction from angiotensin II and the stimulation of the ____,
decreased aldosterone-decreased ____ & ____ retention (however, increased K)

A

angiotensin I to angiotensin II
SNS
Na and water

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13
Q

ACEIs advantage -
minimal ___ ___ compared to beta-blockers, diuretics

A

side effects

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14
Q

ACEIs indications -
hypertension (in ____), CHF, mitral ____ (F,F,V), development of CHF (regression of ____)

A

diabetes
regurgitation
LVH

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15
Q

ACEIs CIs:
patients with ___ ____ ____ (their renal perfusion is highly dependent on angiotensin II)

A

renal artery stenosis

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16
Q

slide 10 poses question about continuing ACEI therapy. The notes provide summary:

“despite the known hypotensive effect of both ACE inhibitors and ARBs, the 2014 ACC/AHA guidelines on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery recommend ______ this therapy in the _____ period.”

A

maintaining
perioperative

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17
Q

ACEI Recommendation: _____ ACE inhibitors on the day of surgery or _____ on day before surgery

A

withhold
discontinue

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18
Q

ACEIs: Hypotension was to be controlled to within __% of baseline with fluid and vasopressors.

A

30%

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19
Q

Continuation of ACEI to day of surgery:
More intraoperative _____
No difference in ____ consequences

A

hypotension
adverse

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20
Q

Meta-analysis – both ACEI and ARBs:
Withholding prior to surgery -
____ intraoperative hypotension
___ ____ in mortality or major adverse cardiac event

A

less
No change

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21
Q

Large cohort prospective study of noncardiac surgery patients:
Continuation of either ACEI and ARBs prior to surgery - Increase in ____ or ___ ____ events

A

mortality or major adverse

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22
Q

Despite the known hypotensive effect of both ACE inhibitors and ARBs, the 2014 ACC/AHA guidelines on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery state it ___ ___ ___ ___ these drugs until time of surgery.

A

“is reasonable” to continue

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23
Q

ACE Inhibitors – Side Effects

benefit is _____ SEs, most common are c____, upper resp c____, rhinorrhea, _____ ____ symptoms.

A

minimal
cough
congestion
allergic-like

(r/t Potentiation of kinins and Inhibition of breakdown of bradykinins)

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24
Q

ACE Inhibitors – Side Effects

______ – potentially life-threatening
Epi 0.3 to 0.5 mL of __:___ dilution*

A

Angioedema
1:1,000

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25
Q

ACE Inhibitors – Side Effects

Hyperkalemia – due to decreased production of _____ (esp. CHF w/ renal insuff)

A

aldosterone

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26
Q

ACE Inhibitors – Side Effects

Angioedema may occur _____ after prolonged drug use.

A

unexpectedly

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27
Q

ACE Inhibitors – Side Effects

Hereditary angioedema is due to __ ____ ____ deficiency

A

C1 esterase inhibitor

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28
Q

ACE Inhibitors – Side Effects

ACE inhibitor induced is due to increased availability of bradykinin because ____ ____ is blocked.

A

bradykinin catabolism

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29
Q

How is angioedema treated? (4)

(r/t ACEIs - MARVEL)

A

Epi (catecholamines, antihistamines, and antifibrinolytics may be ineffective in acute episodes)
Tranexamic acid or aprotinin – inhibits plasmin activation
Icatibant – a synthetic bradykinin receptor antagonist
FFP – 2-4 units – to replace the deficient enzyme

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30
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

PO dose:

A

12.5-25 mg PO (TC says not important to know)

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31
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

Decreased ____ – especially in renal
__, __ not effected

A

SVR
CO, HR

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32
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

Baroreceptor sensitivity ____

A

reduced (HR does not increase with decreased BP)

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33
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

May cause _____ (related to blocking of aldosterone release)

A

hyperkalemia

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34
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

Onset ___ min Duration ___ hours

A

Onset 15 min Duration 6-10 hours

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35
Q

Angiotensin-Converting Enzyme Inhibitors - Captopril (Capoten)

Cough, upper respiratory congestion, rhinorrhea, and allergic-like symptoms are most common. This is due to the ____ of ____ ____, which normally breaks down bradykinins.

A

inhibition of peptidyl-dipeptidase activity

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36
Q

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec)

PO Dose:

A

20 mg

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37
Q

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec)

Available in IV ___-___ mg

A

0.625-1.25 mg

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38
Q

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec)

Onset approx __ hour; Duration ____ hours

A

1
18-30

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39
Q

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec)

Lacks the rash and pruritus side effects of _____; rarely _____ of the face, lips, tongue and glottis; watch for hypotension

A

captopril
angioedema

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40
Q

Angiotensin-Converting Enzyme Inhibitors - Enalapril (Vasotec)

Not commonly given perioperatively. _____ onset and duration is _____ (compared to vasodilators like nipride and ntg).

A

Unpredictable
negative

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41
Q

Other ACEIs: (6)

A

Benazepril (Lotensin)
Fosinopril
Lisinopril (Prinivil, Zestril)
Moexipril
Perindopril
Quinapril (Accupril)

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42
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

MOA – blocks the binding of angiotensin II to the receptors (type AT1 – found in vascular smooth muscle) to prevent ____ and _____ release

A

vasoconstriction and aldosterone

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43
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

Similar effects as ___ ___

A

ACE inhibitors

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44
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

Risk of ____ reduction* - 25% (compared to atenolol)

A

Risk of stroke reduction* - 25% (compared to atenolol)

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45
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

Dose:

A

Dose 50 mg

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46
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

May be combined with ___ ___ or inhibitor of _____** (Entresto)

A

thiazide diuretic
neprilysin

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47
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

____ is losartan and hydrochlorothiazide—combined with diuretic.

A

Hyzaar

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48
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

Cough due to ____ ____ is significantly less than w ACE inhibitors

A

bradykinin accumulation

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49
Q

Angiotensin Receptor Blocker - Losartan (Cozaar)

*effectiveness is ___ ___ in black patients (with HTN and LVH) – LIFE study out of New Zealand

A

not seen

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50
Q

Calcium Channel Blockers - Classifications

_______ - occludes the channel (Verapamil)
_______ - arterial vascular smooth cells (Nifedipine, nicardipine, nimodipine)
_______ - AV node-?MOA (Diltiazem)

A

Phenylalkylamines
1,4-Dihydropyridines
Benzothiazepines

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51
Q

CCBs - Dihydropyridines
Treat HTN in the ____, ____ ____, and ___-____ patients

A

elderly, African Americans, and salt-sensitive

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52
Q

CCBs MOA:

Bind to the alpha1 subunit of the ____ ___-____ calcium ion channels
Block calcium entering the cardiac and vascular smooth muscle cells - _____ specific
Reduction of calcium - Fails to ____ ____ - which reduces contraction, ____ depolarization of SA and AV nodal tissue

A

slow L-type
Arterial
activate myosin
Slows

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53
Q

CCBs MOA:

Calcium ion influx is responsible for the ___ ___ of the cardiac action potential, which is important in the ____/____ ____ in cardiac and vascular smooth muscle and depolarization of the SA and AV nodal tissue

A

phase 2
excitation/contraction coupling

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54
Q

Calcium Channel Blockers - effects

Negative ____, _____ effects

A

inotropic, chronotropic

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55
Q

Calcium Channel Blockers - effects

Decreased ___ node activity

A

SA

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56
Q

Calcium Channel Blockers - effects

Conduction slowed through the ___ node

A

AV

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57
Q

Calcium Channel Blockers - effects

Vasodilation, decreased ___

A

BP

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58
Q

Calcium Channel Blockers - effects

Relaxes ___ ___ spasm
Complements ____ (different MOA)

A

coronary artery
nitrates

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59
Q

CCBs Uses

treatment of coronary artery spasm, unstable ____ ____, chronic stable _____, essential _____

A

angina pectoris
angina
hypertension

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60
Q

CCBs

Increased risk with dihydropyrimidine derivatives (______)
_____ complications (placebo)
Perioperative bleeding, GI hemorrhage
Development of _____ (compared to beta-blockers, ACE inhibitors)

A

nifedipine
Cardiovascular
cancer

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61
Q

Calcium Channel Blockers - Verapamil (Calan)

derivative of _____

A

papaverine

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62
Q

Calcium Channel Blockers - Verapamil (Calan)

_____ contractility

A

Decreases

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63
Q

Calcium Channel Blockers - Verapamil (Calan)

_____ HR

A

Decreased

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64
Q

Calcium Channel Blockers - Verapamil (Calan)

Decreased conduction through ___ node

A

AV

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65
Q

Calcium Channel Blockers - Verapamil (Calan)

Relaxation of vascular _____ ____, coronary arteries

A

smooth muscle

(Vascular smooth muscle relaxation is more arterial.)

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66
Q

Calcium Channel Blockers - Verapamil (Calan)

Uses-treatment of ___ (AV node), ___

A

SVT
HTN

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67
Q

Calcium Channel Blockers - Verapamil (Calan)

Dose ___-___ mcg/kg (__-__ mg) IV slowly

A

75-150
2.5-5

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68
Q

Calcium Channel Blockers - Verapamil (Calan)

Onset __-__ minutes

A

1-3

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69
Q

Calcium Channel Blockers - Verapamil (Calan)

Oral nearly complete ____ metabolism

A

hepatic

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70
Q

Calcium Channel Blockers - Verapamil (Calan)

IV ___% renal metabolism, ___% in bile

A

70%
15%

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71
Q

Calcium Channel Blockers - Verapamil (Calan)

Elimination ½ life __-__ hours

A

6-12

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72
Q

Calcium Channel Blockers - Verapamil (Calan)

Combination with ___ ___ - has additive myocardial depressant and vasodilation effects, even in normal LV function

A

volatile anes

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73
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Vasodilation of ____ and ____ _____ (>verapamil)

A

coronary and peripheral arteries

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74
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

_____ BP

A

Decreased

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75
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Indirect ____-____ increased HR

A

baroreceptor-mediated

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76
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

____ decreased contractility, decreased chronotropic, and dromotrophic effects

A

Directly

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77
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

routes of admin

A

PO, IV or SL

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78
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Uses – angina, especially coronary artery vasospasm, hypertension emergencies (____/____ -cerebrovascular ischemia, MI, severe hypotension)

A

CAUTION/STOP

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79
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Dose __-__ mg PO or SL

A

10-20

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80
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Onset __ min

A

20

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81
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Metabolism ____ - Elim ½ life: __-__ hours

A

hepatic
2-5

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82
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Negative effects are due to ___ ____ ____ of BP

A

too rapid lowering

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83
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Side effects – f____, h____, v_____, hypotension; may cause ____ dysfunction.

A

Side effects – flushing, headache, vertigo, hypotension; may cause renal dysfunction.

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84
Q

Calcium Channel Blockers - Nifedipine (Adalat, Procardia)-dihydropyridine

Abrupt stop has caused ____ ____ ____

A

coronary artery vasospasm

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85
Q

Calcium Channel Blockers - Nicardipine (Cardene)

Selective ____ vasodilation - SVR

A

arterial

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86
Q

Calcium Channel Blockers - Nicardipine (Cardene)

Greatest _____ effects - especially _____ arteries

A

vasodilating
coronary

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87
Q

Calcium Channel Blockers - Nicardipine (Cardene)

Does not effect the __ ___ or ___ ___, minimal myocardial depressant effects

A

SA node or AV node

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88
Q

Calcium Channel Blockers - Nicardipine (Cardene)

25 mg in 240 ml solution (0.1 mg/ml)
Titrate – start at __ mg/hr (__ ml/hr), increase by ___ mg/hr every __-___* mins to a max of __ mg/hr

A

5 mg/hr
50 ml/hr
2.5 mg/hr
5-15 mins
15 mg/hr

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89
Q

Calcium Channel Blockers - Nicardipine (Cardene)

Not compatible with ____ ____

A

Lactated Ringer’s

90
Q

Calcium Channel Blockers - Nicardipine (Cardene)

*every __ _____ titration for more rapid reduction; every __ _____ otherwise

A

5 mins
15 mins

91
Q

Calcium Channel Blockers - Nicardipine (Cardene)

Contraindicated with advanced ___ ___

A

aortic stenosis

92
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

3rd generation _____

A

dihydropyridine

93
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

____ onset, _____

A

Rapid onset, titratable

94
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

___ emulsion (similar to _____)

A

Lipid emulsion (similar to propofol)

95
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

metabolism:

A

Metabolism: plasma and tissue esterases (organ independent)

96
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

Related to increased _____: maximum administration rate should not exceed ___ ____

A

triglycerides
32 mg/h

97
Q

Calcium Channel Blockers - Clevidipine (Cleviprex)

Researchers reached their target intraoperative mean arterial pressure (50-65 mm Hg) within 5 to 10 minutes in a group of adolescents using clevidipine infusion rate of 0.5 to 1 µg/kg/min, titrated by 0.5 to 1 mg/kg/min increments every 2 to 3 minutes. ____ of the patients experienced ____ _____ events that required intervention, and BP measurements returned to baseline within __ to __ _____ of stopping clevidipine infusion.

A

None
excessive hypotensive
5 to 10 minutes

98
Q

Calcium Channel Blockers - Nimodipine (Nimotop)

Highly ___ ___ to cross ___ ___ barrier

A

lipid soluble
blood brain

99
Q

Calcium Channel Blockers - Nimodipine (Nimotop)

Used to treat vasospasms related to ____ _____

A

subarachnoid hemorrhage

100
Q

Calcium Channel Blockers - Nimodipine (Nimotop)

Dose 0.7 mg/kg PO then ___ mg/kg ___ hrs for ___ days

A

0.35
q4
21

101
Q

Calcium Channel Blockers - Nimodipine (Nimotop)

If _____ compliance is a concern, an increase in ___ could occur

A

intracranial
ICP

102
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Class

A

Benzothiazepine

103
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Blocks channels in the __ ____

A

AV node

104
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Uses:

A

Uses - treatment of SVT, angina pectoris

105
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Dose ___ mg/kg IV over 2 minutes, may repeat in 15 min if needed
Infusion __ mg/hr

A

0.25
10

106
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Elimination via ___ (60%) and ____ (35%)

A

bile
urine

107
Q

Calcium Channel Blockers - Diltiazem (Cardizem, Dilacor, Tiazac)

Elimination ½ time __-__ hours

A

3-5

108
Q

Calcium Channel Blockers - Drug interactions

Additive myocardial depression and vasodilation with ___ ____, especially with preexisting ____ ____

A

volatile anesthetics
LV dysfunction

109
Q

Calcium Channel Blockers - Drug interactions

Potentiate ___ and ___ ___ ______-_____ drugs like ____ antibiotics (Ca ions are needed to release acetylcholine at the NM junction)

A

dep and non dep neuromuscular-blocking
mycin

110
Q

Calcium Channel Blockers - Drug interactions

Increased risk of ___ ____ ____ (inhibition of Na ion movement via Na channels)

A

local anesthetic toxicity

111
Q

Calcium Channel Blockers - Drug interactions

Hyperkalemia with K replacement due to ____ of ____ ____ ____ ___

A

inhibition of K moving into cell

112
Q

Calcium Channel Blockers - Drug interactions

____ and _____ cause hyperkalemia

A

Verapamil and dantrolene

113
Q

Calcium Channel Blockers - Drug interactions

Increase ____ ____ concentration – decreasing its clearance.

A

digoxin plasma

114
Q

Vasodilators Indications: (3)

A

Treat hypertension
Induce controlled hypotension
Encourage LV stroke volume

115
Q

Vasodilators Effects: (3)

A

Decrease BP
Decrease SVR (arterial)
Decrease venous return and CO (venodilator)

116
Q

Nitric Oxide

_____ cause both pulmonary and systemic vasodilation by producing ___ ____ (__).

A

Nitrovasodilators
nitric oxide (NO)

117
Q

Nitric Oxide

NO – increases intracellular ____ causing smooth muscle relaxation
Results ultimately from decreased ____ ____ (similar to the effect of cAMP from beta2 stimulation)

A

cGMP
intracellular calcium

118
Q

Nitric Oxide

Can be inhaled in the gaseous state to cause ___ ___ specifically

A

pulmonary vasodilation

119
Q

Nitric Oxide

Increased cGMP can potentially coexist with _____ due to stimulation of ___ receptors.

A

bronchoconstriction
M3

120
Q

Nitric Oxide

____ ____ ____ ____ – previous name for NO

A

Endothelial derived relaxing factor (EDRF)

121
Q

Nitric Oxide

Administration of NO affects ____ specifically – it doesn’t affect SVR due to rapid ____ by ____

A

PVR
uptake by hemoglobin

122
Q

Nitric Oxide - endogenous CV effects

Release of NO from endothelial cells due to ___ ___ and ____ ____ ____

A

shear stress and pulsatile arterial flow

123
Q

Nitric Oxide - endogenous CV effects

Regulates ____ and ____ – baseline

A

SVR and PVR

124
Q

Nitric Oxide - endogenous CV effects

Impacts distribution of ____ ____

A

cardiac output

125
Q

Nitric Oxide - endogenous CV effects

Autoregulation – increased ___ _____ with decreased ______

A

NO production
oxygenation

126
Q

Nitric Oxide - endogenous CV effects

____ produce more NO than ____ (IMA remains patent longer than saphenous vein grafts)

A

Arteries
veins

127
Q

Nitric Oxide - endogenous pulm effects

Broncho_____

A

Bronchodilation

128
Q

Nitric Oxide - endogenous pulm effects

Selective dilation of vessels to ___ ____

A

ventilated alveoli

129
Q

Nitric Oxide - endogenous platelet effect

Inhibits plt activation, aggregation, and adhesion (_____)

A

antithrombotic

130
Q

Nitric Oxide - endogenous nervous system effects

Neurotransmitter in ____, ___ ____ and peripheral nervous system

A

brain, spinal cord,

131
Q

Nitric Oxide - endogenous nervous system effects

May be involved in _____ and anesthetic effects

A

antinociception

132
Q

Nitric Oxide - endogenous

Produce relaxation of ___ ___ and ___ tract

A

smooth muscle
GI

133
Q

Nitric Oxide - endogenous immune response

Produced in response to activation of ______

A

macrophages

134
Q

Nitric Oxide - endogenous immune response

Can damage b____, f____, and p_____

A

bacteria, fungi, and protozoa

135
Q

Pathophysiologic effects related to NO

Essential hypertension - _____ NO release
Sepsis shock – _____ NO release
Atherosclerosis – _____ NO – platelet aggregation, vasoconstriction
Cirrhosis – _____ production of NO

A

decreased
excessive
decreased
excessive

136
Q

Anesthetic Effects on NO

Involved in the _____ neurotransmission

A

excitatory

137
Q

Anesthetic Effects on NO

Anesthetics cause _____ of formation of NO to _____ excitatory neurotransmission and ____ GABA inhibitory transmission

A

suppression
decrease
enhance

138
Q

Anesthetic Effects on NO

Administration of NO synthase inhibitors have a ___-___ ____ in MAC

A

dose-dependent reduction

139
Q

Uses of NO

Inhaled form to treat ______ ______ (use in any other than ______ is “off label” use

A

pulmonary hypertension
neonates

140
Q

Uses of NO

In neonates, its use has decreased the use of _____

A

ECMO

141
Q

Sodium Nitroprusside (SNP, Nipride)

___-___, arterial and venous vascular smooth muscle relaxant

A

Direct-acting

142
Q

Sodium Nitroprusside (SNP, Nipride)

Vasodilation of ____ and ____

A

arterial and venous

143
Q

Sodium Nitroprusside (SNP, Nipride)

A
144
Q

Sodium Nitroprusside (SNP, Nipride)

onset

A

60-90 seconds

145
Q

Sodium Nitroprusside (SNP, Nipride)

Duration short requiring ___, ____

A

infusion, titration

146
Q

Sodium Nitroprusside (SNP, Nipride)

Careful monitoring, ___ ___

A

infusion device

147
Q

Sodium Nitroprusside (SNP, Nipride)

Dose ___-___ mcg/kg/min – up to 5 mcg/kg/min (body can handle only __ ____ continuous)

A

0.25-1
2 mcg/kg/min

148
Q

Sodium Nitroprusside (SNP, Nipride)

MOA – reacts with ____ to _____ _____ and releases cyanide and nitric oxide (NO). NO causes the _____.

A

hemoglobin to form methemoglobin
vasodilation

149
Q

Sodium Nitroprusside (SNP, Nipride)

Nipride is 44% cyanide (CN-) and during metabolism ___ ____ ____ are released making cyanide toxicity possible-causing ____ ____, _____ metabolism, and ____ acidosis

A

five cyanide ions
tissue anoxia, anaerobic metabolism, and lactic acidosis.

150
Q

Sodium Nitroprusside (SNP, Nipride) - who is susceptible to CN- toxicity

Receiving infusion of ______
Children or young adults – baroreceptor reflexes cause ____ of SNS –require ___ ___
Pregnancy - ____ cyanide toxicity

A

> 2 mcg/kg/min
stimulation
larger dose
fetal

151
Q

Sodium Nitroprusside (SNP, Nipride) - CN- toxicity S&S:

Unresponsive to previously ____ ___ of SNP
Increased MvO2 – inability of tissues to ___ ___
Metabolic ____
CNS dysfunction, ____

A

therapeutic doses
use oxygen
acidosis
seizures

152
Q

Sodium Nitroprusside (SNP, Nipride) - treatment of CN- toxicity: (4)

A

Stop infusion
100% oxygen
Sodium bicarbonate to correct met acidosis
Sodium thiosulfate to be a sulfur donor to convert cyanide to thiocyanate

153
Q

Sodium Nitroprusside (SNP, Nipride)

Nipride must be protected from the light to prevent breakdown into ____. Light-protected solutions are safe for ___ ____.

A

cyanide
24 hours

154
Q

Sodium Nitroprusside (SNP, Nipride)

CV effects - ____ arterial and venous vasodilation

A

direct

155
Q

Sodium Nitroprusside (SNP, Nipride)

Decreased ___, ___, Indirect increase in HR and contractility, May have increased ___

A

BP, SVR
CO

156
Q

Sodium Nitroprusside (SNP, Nipride)

Coronary artery vasodilation which creates ___ ___ from ischemic areas.

A

coronary steal

157
Q

Sodium Nitroprusside (SNP, Nipride)

Decrease in ____ pressure

A

diastolic

158
Q

Sodium Nitroprusside (SNP, Nipride) - CNS

Increased ____ blood flow
Increased ____ blood volume

A

cerebral
cerebral

159
Q

Sodium Nitroprusside (SNP, Nipride) - CNS

ICP increases are ____ if MAP decreases less than 30%; if >30% decrease in MAP, the ICP ____ to ____ levels.

A

maximal
returns to awake

160
Q

Sodium Nitroprusside (SNP, Nipride)

CPP = ____-____

A

CPP = MAP - ICP

161
Q

Sodium Nitroprusside (SNP, Nipride) - CNS

To prevent the increase in ICP, infuse the SNP to slowly lower BP over ___ _____ along with ____ and _____

A

5 minutes
hyperoxia
hypocarbia

162
Q

Sodium Nitroprusside (SNP, Nipride) - CNS

Once the dura is open, ICP problems are ___ ___ ____.

A

not a problem

163
Q

Sodium Nitroprusside (SNP, Nipride) - CNS contraindications

Patients with increased ___ and inadequate cerebral ____ ___, and patients with ___ ___ stenosis

A

ICP
blood flow
carotid artery

164
Q

Sodium Nitroprusside (SNP, Nipride) - pulm effects

decrease in the _____, alteration of ____ ____ ____

A

PaO2
hypoxic pulmonary vasoconstriction

165
Q

Sodium Nitroprusside (SNP, Nipride) - pulm effects

Bigger problem with ____ lungs

A

healthy

166
Q

Sodium Nitroprusside (SNP, Nipride) - pulm effects

___ ____ develop vascular changes that prevent this effect

A

COPD lungs

167
Q

Sodium Nitroprusside (SNP, Nipride) - pulm effects

Treat: add ____

A

PEEP

168
Q

Sodium Nitroprusside (SNP, Nipride) - pulm effects

Inhibits platelet aggregation (___mcg/kg/min)
No ____ ____-bleeding not increased

A

> 3
clinical significance

169
Q

Sodium Nitroprusside (SNP, Nipride) - clinical uses

Deliberate _____
Most likely to maintain ____ perfusion
Initial rate – __ to ___ mcg/kg/min
Should not exceed ___ mcg/kg/min
Combined with other agents to min. risk of CN- tox

A

hypotension
cerebral
0.3 to 0.5
2

170
Q

Sodium Nitroprusside (SNP, Nipride) - clinical uses

Hypertensive emergencies
_____ initial treatment – effective ___ ____ the cause – onset, titration, quick offset

A

Temporary
no matter

171
Q

Sodium Nitroprusside (SNP, Nipride) - clinical uses

Cardiac disease – decreased ____
MR, AR, CHF, MI with LV failure (may also need ____)

A

afterload
inotrope

172
Q

Sodium Nitroprusside (SNP, Nipride) - clinical uses

____ surgery
Treat HTN related to ___-___
? spinal cord ischemia – distal _____

A

Aortic
cross-clamp
hypotension

173
Q

Sodium Nitroprusside (SNP, Nipride) - clinical uses

Cardiac surgery
_____ period to cause vasodilation to distribute warmth to periphery
Treat pulmonary hypertension after ___ ____ (pulmonary vasodilator)

A

Rewarming
valve replacement

174
Q

Vasodilators - Nitroglycerin

____ nitrate

A

Organic

175
Q

Vasodilators - Nitroglycerin

Dilates venous side except, at ____ doses, it will relax ___ ___ ___

A

elevated
arterial smooth muscle

176
Q

Vasodilators - Nitroglycerin

MOA – produces ___ ___ (__) which causes peripheral vasodilation

A

nitric oxide (NO)

177
Q

Vasodilators - Nitroglycerin

Sublingual – onset __ ____

A

4 minutes

178
Q

Vasodilators - Nitroglycerin

Transdermal – sustained protection from ___

A

MI

179
Q

Vasodilators - Nitroglycerin

Infusion requires special ___ and ___ ____ to prevent absorption into the plastic

A

tubing and glass bottles

180
Q

Vasodilators - Nitroglycerin

Elimination ½ life – 1.5 minutes requires ____

A

infusion

181
Q

Vasodilators - Nitroglycerin

May cause the production of _____ when the nitrite metabolite oxidizes the ____ ion in hemoglobin

A

methemoglobin
ferrous

182
Q

Vasodilators - Nitroglycerin

Treatment: ___ ___ 1-2 mg/kg IV over 5 minutes to convert back to hemoglobin

A

methylene blue

183
Q

Vasodilators - Nitroglycerin CV effects

Venous ____ (up to 2 mcg/kg/min)
Decreased venous return, ____, ____
CO ____ (in normal heart with no CHF; if patient in heart failure, the CO is improved, and pulmonary congestion is relieved)

A

dilation
LVEDP, RVEDP
decreased

184
Q

Vasodilators - Nitroglycerin CV effects

Decreased ___ (related more to volume than SNP)
Decreased ___, coronary blood flow

A

BP
DBP

185
Q

Vasodilators - Nitroglycerin CV effects

Dilates larger conductance vessels of the coronary circulation – provides better blood flow to ____ ___
Relaxes ____ vessels

A

ischemic areas
pulmonary

186
Q

Vasodilators - Nitroglycerin CV effects

Baroreceptor-reflex ____, increased ____ effect (increased demand, decrease supply)

A

tachycardia
inotropic

187
Q

Vasodilators - Nitroglycerin - smooth muscle effects

Relaxes ____ smooth muscle
Relaxes biliary tract smooth muscle (___ of ___)
Relaxes ____ muscles
Relaxes uterine and ureteral smooth muscles

A

bronchial
sphincter of Oddi
esophageal

188
Q

Vasodilators - Nitroglycerin - CNS effects

_____ vasodilation
Inhibition of ___ ____

A

Cerebral
platelet aggregation

189
Q

Vasodilators - Nitroglycerin - clinical uses

____ ____ - decrease myocardial oxygen demand and vasodilate coronaries to ischemic areas (decrease size of MI-not SNP)

A

Angina pectoris

190
Q

Vasodilators - Nitroglycerin - clinical uses

Cardiac failure – decrease ____ and relieve pulmonary ____

A

preload
edema

191
Q

Vasodilators - Nitroglycerin - clinical uses

Acute hypertension – maternal patient during C-section with __ ____ on fetus

A

no effects

192
Q

Vasodilators - Nitroglycerin - clinical uses

Deliberate hypotension – less potent than SNP; decrease in diastolic is less than SNP; ____ ____ has a bigger effect

A

intravascular volume

193
Q

Vasodilators - Isosorbide dinitrate

Oral nitrate – prophylaxis of ____ ____

A

angina pectoris

194
Q

Vasodilators - Isosorbide dinitrate

Prolonged _____ effect, increased exercise tolerance up to __ ___

A

antianginal
6 hours

195
Q

Vasodilators - Isosorbide dinitrate

Vasodilation of venous circulation and dilation of coronary arteries to ___ ___ ___ to ischemic areas

A

redirect blood flow

196
Q

Vasodilators - Isosorbide dinitrate

Given preop to ____ patients

A

CABG

197
Q

Vasodilators - Hydralazine (Apresoline)

___ ___ of arterial side, some venous

A

Direct dilation

198
Q

Vasodilators - Hydralazine (Apresoline)

Vasodilates (5) things

A

coronary, cerebral, renal, and splanchnic, pulmonary vessels

199
Q

Vasodilators - Hydralazine (Apresoline)

MOA – interference with ____ ion transport

A

calcium

200
Q

Vasodilators - Hydralazine (Apresoline)

Decreases ____ more than ____ pressure

A

diastolic
systolic

201
Q

Vasodilators - Hydralazine (Apresoline)

Increases in HR (baroreceptor and direct), SV, CO (can cause MI, prevented with ___-___)

A

beta-blocker

202
Q

Vasodilators - Hydralazine (Apresoline)

Onset 10 to 20 minutes (_____)
Duration 2 to 4 hours (_____)
Dose 10 to 20 mg

A

prolonged
unpredictable

203
Q

Vasodilators - Hydralazine (Apresoline)

Mostly ____ metabolism

A

hepatic

204
Q

Vasodilators - Hydralazine (Apresoline)

Side effects – ___-___ ____, peripheral neuropathies, vertigo, diaphoresis, nausea, tachycardia – uncommon in ____ use

A

Lupus-like syndrome
intermittent

205
Q

Vasodilators - Trimethaphan

Ganglionic blocker – blocks ____ nervous system reflexes

A

autonomic

206
Q

Vasodilators - Trimethaphan

Vasodilation of ___ ___ vessels
Decreases CO, ___

A

venous capacitance
SVR

207
Q

Vasodilators - Trimethaphan

Blocks receptors for ____

A

acetylcholine

208
Q

Vasodilators - Trimethaphan

May have ____ that offsets the benefit of decreased BP

A

tachycardia

209
Q

Vasodilators - Trimethaphan

Historical use in ____ ____

A

deliberate hypotension

210
Q

Vasodilators - Adenosine

______ _____ in all cells – maintain the balance of oxygen supply and demand of the heart and other organs

A

Endogenous nucleoside

211
Q

Vasodilators - Adenosine - Effects

Dilation of coronary arteries (___ possible)
Negative ____

A

steal
chronotropic

212
Q

Vasodilators - Adenosine

MOA- stimulation of __ ____ in supraventricular cells to hyperpolarize atrial cells and slowing of SA node
Can also stimulate release of ___ from endothelial cells

A

K+ channels
NO

213
Q

Vasodilators - Adenosine - Uses

SVT – paroxysmal SVT and narrow complex tachycardia (not atrial fib or v. tach)
Dose _________
Can repeat within ___ ____
Elimination ½ life ___-___ ____

A

Dose 6 mg IV, then 12 mg, then 18 mg*
Can repeat within 60 seconds
Elimination ½ life 0.6-1.5 seconds

214
Q

Vasodilators - Adenosine

Deliberate _____
____ responsiveness, onset and recovery
Decreased SVR, increased HR*, coronary flow increased**, cardiac filling pressures unchanged
____ mcg/kg/min – no _____

A

hypotension
Rapid
220
tachyphylaxis

215
Q

“Adenosine infusion evokes a receptor-specific sympatho-excitatory reflex in humans that overrides its ___ ___ ___ effect.”

A

direct negative chronotropic

216
Q

Principle Adenosine effects - A1 (4)

A

Slowing of the rhythm Negative inotropic effects
Vasoconstriction
Bronchoconstriction
Sedation Anticonvulsive effectDecrease of neurotransmitter release

217
Q

Principle Adenosine effects - A2 (5)

A

Vasodilation
Bronchodilation
Complex stimulant effects
Increase of neurotransmitter release
Platelet aggregation inhibition

218
Q

A1 receptors – located in ______ (more in atrial membranes than ventricular) – produce negative chronotropic, dromotropic and inotropic effects. The activation of the A1 receptors inhibits ____ ____, decreases the concentration of intracellular cAMP and induces opening of potassium channels, which indirectly ____ ____ ____ into the cell.

A

cardiomyocytes
adenyl cyclase
reduces calcium penetration

219
Q

A2 receptors – in endothelial and vascular smooth muscle – produce coronary artery vasodilation and vascular smooth muscle relaxation -The stimulation of the A2 receptors has an opposite effect, it activates ____ ____.

A

adenyl cyclase.

220
Q

Adenosine - Adverse reactions (seen in ___ of ____):
Most common: ____ ____, ___ pain (awake patient), and dyspnea – duration averages 50 seconds

A

1/3 of patients
facial flushing
chest

221
Q

Adenosine - If brady arrhythmias persist, can treat with _____ – antagonizes receptor. ______ will be ineffective

A

aminophylline
Anticholinergics

NUNA 681 Pharm II (12 decks)

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