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Anesthesia Pharm > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

SV is determined by?

A
  • Preload
  • Afterload
  • Contractility
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2
Q

What effect will an increase of B1 receptors do?

Where is it located?

A

B1 receptors are located on the heart

and activation of this receptor results in INCREASED CO

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3
Q

What does the activation of ALPHA 1 receptors do? where is it located?

A

Activation of alpha 1 receptors on the peripheral vasculature results in an increase in SVR

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4
Q

Causes of systemic hypertension

A
  • renal artery stenosis
  • Pheochromocytoma
  • withdrawal from alcohol
  • sympathomimetics
  • rebound
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5
Q

How do you manage hypertension?

A
  • Inhibit RAAS
  • direct peripheral vasodilation
  • effects of autonomic receptor
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6
Q

The patient population that should be started on B BLOCKERS as long as there is not overt HF

A

Acute Coronary Syndrome

–> as long as there is no exacerbation of HF or BB could cause worsening hypotension

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7
Q

When do you use B blockers as first-line agents for the management of hypertension

A

ACS [w/o HF]

Cardiac Dysrhythmias

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8
Q

Receptos sites where B- blockers may act upon (competitive inhibition)

B1 sites and effects

A

B1 - CARDIAC

  • Decrease heart rate (negative chronotropic effects)
  • Decrease cardiac output (negative inotropic effects)
  • Inhibit the release of renin from the kidneys
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9
Q

Where can we find B2 receptors?

A

B2 found in the vascular and bronchial smooth muscle, metabolic

  • B2 agonist –> albuterol will cause bronchial relaxation
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10
Q

Where can we find Alpha 1 receptors?

what do we get when we block alpha 1 receptors?

A

Alpha 1 is found in the vasculature

– decrease in peripheral resistance when blocked

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11
Q

Which ones are beta selective among the beta-blockers

A

MEAN

Metoprolol

Esmolol

Atenolol

Nebivolol

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12
Q

beta-blockers consideration / special population

A

beta 1 selectivity is overcome with large doses

–> if we give massive doses of metoprolol sometime we will hit the beta 2 receptors ;

  • COPD patients on high dose beta-blockers may end up with blocked beta 2 receptors and this may cause vasoconstriction
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13
Q

What is the ratio of beta:alpha blockade on IV Labetalol

how about oral?

A

Beta:alpha (IV) = 7:1

Oral: 3:1

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14
Q

ratio of Metoprolol oral:iv

A

2.5 mg oral: 1 mg IV

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15
Q

When do you use Beta-blockers that are cardioselective??

A
  • May be more preferable in patients with
    • asthma/COPD,
    • peripheral vascular disease, vulnerable to hypoglycemia
  • Tachyarrhythmias
  • Decrease risk of postoperative myocardial ischemia in patients at high risk for cardiovascular disease with perioperative administration
  • Prophylaxis against tachycardia/hypertension around procedures (e.g., laryngoscopy, tracheal intubation)
    • Esmolol
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16
Q

Common adverse effects of Beta-blockers

A
  • Hypotension
  • Bronchospasm
  • Bradycardia/heart block
  • Possible worsening CHF
  • masking of hypoglycemia (tremors and tachycardia)
  • Angina and MI –> HIGHER RISK PATIENTS upon abrupt discontinuation
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17
Q

How can poorly controlled diabetes management be affected by B- blockers?

A
  • May block the release of insulin from pancreatic β cells –> hyperglycemia
  • Initial signs of hypoglycemia (tremors, tachycardia) can be masked
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18
Q

If a patient has known CAD and at risk for MI what should you do with the beta-blocker?

A

Perioperative management of β-blockers

  • Continue in patients at risk for myocardial infarction (e.g., known CAD, perioperative stress tests, diabetes treated with insulin, LV hypertrophy) during high-risk surgery (e.g., vascular, thoracic, intraperitoneal surgery, large blood loss)
    • Pre- and post- non-cardiac surgery shown to decrease mortality, CV complications, myocardial ischemia
    • Consider baseline blood pressure, possible intraoperative complications and start low dose postoperatively
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19
Q

What are the common selective alpha 1 blockers?

A

“zosin”

  • Prazosin
  • Terazosin
  • Doxazosin
  • Tamsulosin
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20
Q

what is the MOA of selective alpha 1 blockers

what is the downside?

A

Mechanism of action

  • Post-synaptic α1 blockade: vasodilation of arterial and venous vessels
  • downside: Usually long/longer half-lives
    • common uses: hypertension, benign prostatic hyperplasia
    • prazosin, terazosin, doxazosin, tamsulosin
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21
Q

MOA of non-selective alpha-blockers

when is it commonly used?

A
  • Phenoxybenzamine, phentolamine

Mechanism of action

  • Post-synaptic α1 blockade: vasodilation of arterial and venous vessels
  • Pre-synaptic synaptic competitive α2 blockade–> release of presynaptic norepinephrine

Common uses: *pheochromocytoma management*

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22
Q

Adverse effects of alpha receptors blockers

A
  • orthostatic hypotension
  • Hypotension
  • exaggeration of hypotension during epidural anesthesia –> alpha 1 receptor blockers tend to have a longer half-life [mind prolong hypotension even more] but can really happen to any antihypertensive
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23
Q

How do you overcome the effects of alpha-receptor blockers in the OR?

A

use vasoactive agents with alpha1 agonist activity

—> PHENYLEPHRINE [POTENT], NOREPINEPHRINE

Other atypical agents could include (not recommended as first line): epinephrine, angiotensin II, vasopressin

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24
Q

Alpha 2 receptor agonist

A

Clonidine

Dexmedetomidine

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25
Q

MOA of Clonidine compared to Dexmedetomidine

A

Mechanism of action

Clonidine

  • Selective partial α2 agonist
    • 220:1 (α2: α1 activity) –> reason for potent BP management
    • The decreased sympathetic output from the central nervous system to peripheral tissues peripheral —-> vasodilation, decreased systemic blood pressure, heart rate and cardiac output

Dexmedetomidine

  • Selective partial α2 agonist
    • 1,600:1 α2 to α1 activity –> reason for more sedation
    • alpha 2 receptors are in the locus coeruleus of brain stem
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26
Q

If you have a patient that is bradycardic and is on clonidine what should you do?

A

take clonidine off. it may cause a decrease in HR and CO

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27
Q

alpha 2 receptor agonist

Adverse SE

CAUTIONS?

big deal with Clonidine

A
  • sedation
  • Fever –> case report; really high close to 40 C . It starts within hours to dex then a day
    • temporal, if dex is taken off usually it subsides
  • CAUTION:
    • REBOUND HYPERTENSION –> BIG DEAL WITH CLONIDINE
      • Abrupt dc can result in rebound hypertension 8-36 hours after last dose
      • most likely to occur in pts taking >- 1.2 mg/day
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28
Q

What can rebound clonidine discontinuation cause?

A
  • tachycardia but predominantly hypertension
    • Beta 1 selective blockers can only control the HR but not the unopposed alpha-receptor
      • Beta adrenergic blockade may worsen hypertension due to unopposed alpha receptors
  • Tricyclic antidepressants may exaggerate the hypertensive response
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29
Q

How do you manage rebound hypertension with abrupt d/c of clonidine?

A
  • Reinitiating clonidine
  • Initiate vasodilators
  • β- adrenergic blockade with concurrent α blockade [HR and BP control!!]
  • Gradually taper (e.g., 7 days or longer)
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30
Q

MOA of ACE Inhibitor

A

prevents ACE then we will prevent angiotensin I conversion to angiotensin II

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31
Q

Samples of Ace inhibitors

A

Captopril

Lisinopril

Enalapril

Ramipril

32
Q

ACE with the shortest half-life?

33
Q

ACE with the longest half-life?

A

Ramipril

(9-18)

34
Q

ACE with active metabolites

If someone has renal metabolism issues what can happen?

A
  • Enalapril
  • Ramipril

—> may have prolonged hypotension

35
Q

ACE SE

A
  • Hypotension
  • Hyperkalemia
  • Acute Renal Failure [hold ACE]
  • Cough
  • Angio edema
36
Q

Can you give ACE to pregnant women?

37
Q

Significant Drug Interactions with

ACE

A

Potassium Supplements

Potassium-sparing diuretics

* remember that ACE causes hyperkalemia; check a BMP!

38
Q

ARB SE

A

NO COUGH

Adverse effects

ARB

  • Hypotension
  • Hyperkalemia
  • Acute renal failure
  • Angioedema

Significant drug interactions

– Potassium supplements

– Potassium-sparing diuretics

• Contraindications – Pregnancy

39
Q

MOA of Calcium Channel Blockers

w/c are potent vasodilators?

w/c have negative inotropic and chronotropic activity

A
  • Inhibits calcium influx through voltage-sensitive L-type calcium channels in vascular smooth muscle
  • Arterial specific with little effect on venous circulation
  • Dihydropyridines are potent vasodilators and may increase heart rate
  • Non-dihydropyridine are less potent vasodilators and have negative inotropic and chronotropic activity
40
Q

your patient has post-op afib and tachyarrhythmia

w/c CCB will you use?

A

Verapamil

Diltiazem

41
Q

Your patient has bradycardia which CCB are safe to give?

A
  • Nifedipine
  • Nicardipine
  • Clevidipine

–> ALSO VERY POTENT VASODILATOR

–> Nicardipine and Clevidipine –> has the greatest coronary artery dilation

42
Q

Uses for Verapamil/ Diltiazem

A

– Supraventricular tachydysrhythmias [off pressors]

– Vasospastic angina pectoris

– Hypertension

43
Q

Nifedipine

XL :CONSIDERATION

IMMEDIATE RELEASE: CONSIDERATION

A

XL: Nearly impossible to titrate!

IR: MI, STROKE – so potent!

44
Q

Whats should you consider from the anesthesia standpoint

in using CCB

how about other drugs such as Dig, BB, Amio?

A

Additive negative inotropy and peripheral vasodilation

  • Particular caution in patients with left ventricular hypertrophy or hypovolemia

Digoxin, β-blockers, amiodarone

  • Increased risk for atrioventricular block
45
Q

CCB SE

DIHYDROPYRIDINE

A

REFLEX TACHYCARDIA

46
Q

CCB SE

Non- Dihydropyridine

A

Bradycardia!

47
Q

What is the definition of Hypertensive Urgency

A

Hypertensive urgency Systolic blood pressure

(SBP) ≥ 180 mm Hg and/or diastolic blood pressure (DBP) ≥ 110 mm Hg without evidence of target organ damage

48
Q

Definition of Hypertensive Emergency

A

Hypertensive Emergency

Abrupt significant elevation of BP (often SBP >200 mm Hg and/or DBP >120 mm Hg) with concurrent target organ dysfunction

49
Q

Common Causes of Hypertensive Crisis

A
  • Intoxication
  • Withdrawal Syndrome
  • Spinal Cord Disorders
  • Pregnancy
50
Q

How do you manage Hypertensive Urgency?

time parameter?

ICU admission?

A
  • Lower BP over 24-48 h using oral medications
  • • Usually involves restarting home medications
  • No need for ICU admission
51
Q

How is Hypertensive Emergency managed?

A

Specific blood pressure targets may not be the same for all patients

  • Chronic hypertensive patients can tolerate high blood pressure
  • Lower blood pressure in a controlled fashion to avoid sudden decreases
52
Q

How do you control Acute Aortic Dissection?

WHAT IS THE GOAL?

within what time parameter?

A

Acute aortic dissection

Progression of dissection is dependent on arterial BP and force of left ventricular contraction

  • QUICK REDUCTION! Control HR and contractility to decrease stress on the aorta
    • Goal HR <60 bpm as soon as possible (within 5-10 min)
    • Goal SBP <100-120 mm Hg as soon as possible (within 5-10 min)
53
Q

Management of Acute Ischemic Stroke

what is the equation?

if your ICP is high what will be the CPP?

A

* THE HIGHER ICP THE LOWER THE CPP so you have drive-up your MAP

– Hypertension after a stroke is the body’s way to maintain cerebral perfusion pressure (CPP)

  • CPP=MAP–ICP
  • (ICP = intracranial pressure)
54
Q

If a person has an ischemic stroke and is a candidate for TPA what are your considerations?

what is the SBP/DBP goal?

How much should you reduce your map?

A

Treat blood pressure for specific scenarios

  • Thrombolytic therapy is needed (goal SBP <185 mm Hg and DBP < 100 mm Hg to decrease bleeding risk)
  • The occurrence of other target organ damage
  • SBP >220 mm Hg and/or DBP >120 mm Hg
  • Goal reduction in MAP 15-20% over 24 h
55
Q

Management of Intracerebral Hemorrhage

SBP goal and time

A

Elevated BP associated with hematoma expansion, neurological deterioration, and death

  • SBP <140-160 mm Hg (within 5-10 min) in patients without elevations in ICP shown to be safe and possibly linked with improved functional recovery
  • Unclear if aggressive BP targets are safe in some patients
    • SBP >220 mm Hg, patients with large hematomas, elevations in ICP [prob need to be more aggressive]
56
Q

Management of Hypertensive Emergency

57
Q

Long-acting medication for Hypertensive Emergency

A

Hydralazine

increase CO

reduction of afterload

58
Q

very good preload reducer [hypertensive emergency drug]

oftentimes used for people that have CHF exacerbation and absolutely overloaded.

may get tachyphylaxis

A

Nitroglycerin

little bit to maybe no effect on afterload

not as potent as Nitroprusside

59
Q

B1 selective medication that is easy to titrate because of fast onset and shorter duration [Hypertensive Emergency]

A

Esmolol

–> slowing the rate to give more time to fill

60
Q

Management of Hypertensive Emergency

A

Metoprolol IV Push

Labetalol can be given with boluses but does not last very long –> hypertension again within 15 mins, afterload [NON SPECIFIC BETA BLOCKER]

61
Q

Only IV ACE Inhibitor

A

Enalaprilat

LONG DURATION

*mona forgets this exist

62
Q

Why do we use Phentolamine?

A

The antidote for extravasation of pressors [potent vasoconstriction, from a drug that has alpha 1 activity]

– causes local vasodilation

63
Q

Nitroprusside

what should we absolutely be worried about?

dose and time of infusion where you may see toxicity?

A

Cyanide accumulation!

  • Toxicity associated with infusions >72 h or doses >3 mcg/kg/min
  • If not controlled by 10 mcg/kg/min after 10 min, discontinue infusion
64
Q

What are the signs of Cyanide Toxicity?

what is the TX?

A

Signs of cyanide toxicity

a(acidosis) (b)bradycardia confusion/colvusion, desaturation

Treat cyanide toxicity with sodium thiocyanate

65
Q

will Nitroprusside increase ICP?

A

YES! IT WILL INCREASE ICP

it will also cause CORONARY STEAL!

66
Q

A drug that you may use with Pregnant ladies with hypertensive emergency

A

Hydralazine

but realize that you may have prolonged effects [prolonged hypertension]

also reflex tachycardia!!!

67
Q

Hypertensive Emergency Drug that is useful for ischemia and hemorrhagic stroke

A

Nicardipine

  • Reflex tachycardia is a risk
  • Large amount of volume administered with infusion
  • Useful for ischemia and hemorrhagic stroke
68
Q

Hypertensive Medication that is a lipid infusion and you may not be suitable for patients that have an allergy to egg

- how is this drug metabolized?

A

Clevidipine

  • Lipid infusion that provides 2 kcal/mL
  • Caution for use in patients with allergy to soy or eggs
  • Useful for ischemia and hemorrhagic stroke
  • Needs dedicated IV line
  • Metabolized by plasma esterases
69
Q

Hypertensive Emergency

DOC for patients that has coronary ischemia/infarction, acute left ventricular failure, pulmonary edema

  • “vasospasm prophylaxis” after CABG in certain centers
A

NITROGLYCERIN

  • Tachyphylaxis is common
  • Adverse effects include flushing, headache, erythema
  • Dilates veins more than arteries
  • Can be used for coronary ischemia/infarction, acute left ventricular failure, pulmonary edema
  • “vasospasm prophylaxis” after CABG in certain centers
70
Q

Hypertensive Emergency medications that are contraindicated in decompensated HF

  1. Drug that is metabolized by plasma esterases
A

Esmolol

  • Contraindicated in decompensated heart failure
  • Should be used with an arterial vasodilator for management of BP with aortic dissection (_start esmolol before nitroprusside to due later onset of esmolol comparativel_y)
  • Metabolism is via plasma esterases
  • Useful if tachyarrhythmia present
  • Useful for coronary ischemia/infarction

Metoprolol

  • Contraindicated in decompensated heart failure
  • Should be used with an arterial vasodilator for management of BP with aortic dissection (start metoprolol before nitroprusside to due later onset of metoprolol comparatively)
  • Useful if tachyarrhythmia present
  • Useful for coronary ischemia/infarction
71
Q

ABSOLUTELY AVOID IN PREGNANCY

but maybe used for Acute left ventricular failure

A

Enalaprilat

  • Contraindicated in pregnancy
  • Risk of prolonged hypotension due to the long duration of action
  • Useful for acute left ventricular failure
72
Q

Fenoldopam

caution with patients that have what?

A
  • Reflex tachycardia is a risk
  • Caution in patients with glaucoma (can increase intraocular pressure)
  • May cause hypokalemia and flushing
  • May increase ICP
  • Mixed to no difference in data involving improvement of renal function
73
Q

Management of Hypertensive Emergency in Pregnancy

medication to decrease seizure

when do you consider hypertensive management?

SBP/DBP consistent?

which hypertensive medication will you use?

A

Pregnancy

  • Delivery of baby is treatment for severe preeclampsia
  • Magnesium can be given to decrease risk for seizures
  • Consider antihypertensives for consistent SBP > 160 mm Hg and/or DBP >110 mm Hg
  • Labetalol (preferred) and hydralazine can be used
74
Q

ABSOLUTELY CONTRAINDICATED WITH THE MANAGEMENT OF PHEOCHROMOCYTOMA

A

BETA 1 SELECTIVE BETA BLOCKERS

  • β-blockers contraindicated unless α-receptors blocked
  • Choice should include control of heart rate and blood pressure
75
Q

Hypertensive management for cocaine-induced hypertensive emergency

A

Benzodiazepines are useful to control tachycardia and hypertension

  • Diazepam 5-10 mg IV or lorazepam 2-4 mg IV
  • Phentolamine 1 mg with repeat doses every 5 min prn

Other agents to consider:

  • Nitroglycerin, nicardipine, clevidipine, nitroprusside, fenoldopam
  • Verapamil and diltiazem may decrease coronary vasospasm associated with cocaine;

labetalol may not treat coronary vasospasm

  • Use β-blockers only if α-antagonists present (due to coronary vasoconstriction) – conflicting data with labetalol

Anesthesia Pharm (25 decks)

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