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Blockers Flashcards

1
Q

Inhaled Selective Beta-2 Adrenergic Agonists relax what?

A

Primarily relax bronchiole and uterine smooth muscle.

generally lack the beta-1 effects on the heart due to selectivity for beta-2

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2
Q

What are 3 Beta-2 Selective Agonists? Which two of the three have high B2 selectivity.

A

Albuterol - high selectivity
Terbutaline - high selectivity
Metaproterenol

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3
Q

Methods of administration for: Albuterol
Metaproterenol
Terbutaline

A

Albuterol: Inhaler, PO, IV (rare)
Terbutaline : Inhaler, PO, Subq, IV (tocolytic)
Metaproterenol: PO, Subq

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4
Q

Duration of action for Albuterol and Terbutaline

A

~4 hours

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5
Q

The presence of an endotracheal tube decreases the amount of drug delivered to the trachea by a metered-dose inhaler by ~____-____%

A

50% to 70%

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6
Q

How long should the patient hold their breath when inhaling inhaled bronchodilator

A

~10sec

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7
Q

What are tocolytics?

A

IV infusion Beta2 agonists to stop premature uterine contractions.

Increasing Beta-2 activation in uterine muscle promotes relaxation slowing contractions.

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8
Q

With optimal inhalation technique, without the presence of an ET tube, approximately _____% of beta-2 bronchodilators are delivered from an inhaler to the lungs. The remainder is deposited in the mouth, pharynx and larynx.

A

12%

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9
Q

Beta two bronchodilator agonists are divided into what two categories?

A

Intermediate acting (3-6hours duration)
Long acting (>12hrs)

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10
Q

Side Effects of Beta-2 Adrenergic Agonists

A

-Widespread distribution of beta two receptors makes it likely that undesired responses may result if systemic absorption occurs.

-Primary side effect in awake patients is TREMOR.
-Increased heart rate is less common with selective beta two agonists.

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11
Q

What are acute metabolic side effects of beta-2 agonists?

A

Hyperglycemia,
hypokalemia and
hypomagnesemia

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12
Q

In severe asthma, why might you see a transient decrease in arterial oxygenation that may require supplemental oxygen when you administer a Beta-2 Agonist?

A

When parts of the lung are not getting properly ventilated hypoxic pulmonary vasoconstriction shunts blood to better ventilated areas. However, beta-2 agonists relax pulmonary vessels, inhibiting HPV, therefore reduced ventilation and diffusion into blood and lower SaO2.

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13
Q

What is the preferred selective beta-2 agonist for the treatment of acute bronchospasm due to asthma?

A

Albuterol

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14
Q

about how many mcg of Albuterol is administered per puff via MDI

A

~100mcg

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15
Q

How many puffs of albuterol is usually delivered? How often can it be repeated and what is the max dose?

A

Usually two puffs one to five minutes apart
Can be repeated every 4 to 6 hours not to exceed 16 to 20 puffs daily

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16
Q

The effects of albuterol and volatile anesthetics on broncomotor tone are?

A

Additive

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17
Q

Nebulizer albuterol, 2.5 to 5 mg can be administered every ____ minutes for 3 to 4 doses, followed by treatments hourly during initial hours of therapy

A

15 minutes

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18
Q

To treat asthma Terbutaline can be administered via?

A

PO, Subq, or inhalation

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19
Q

Subcutaneous dose of Terbutaline for asthma

A

0.25mg
Produces responses that resemble those of epinephrine but longer duration

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20
Q

What is the main function of Alpha- Adrenergic Blockers

A

Used mainly to cause smooth muscle relaxation by blocking Norepinephrine.

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21
Q

What are invariable side effects of alpha-adrenergic blockade?

A

Orthostatic hypotension, baroreceptor, mediated reflexive tachycardia, and impotence.

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22
Q

What are three reversible (aka competitive) alpha antagonists?

A

Phentolamine
Prazosin
Yohimbine

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23
Q

What is an irreversible (aka non-competitive) alpha antagonist?

A

Phenoxybenzamine

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24
Q

Describe the general mechanism of action of Alpha and Beta Blockers as whole

A

Prevent the interaction between endogenous neurotransmitters )or sympathomimetics) with their corresponding adrenergic receptors therefore reducing sympathetic nervous system outflow.

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25
Of the Alpha-Blockers, which are selective and which are non-selective?
Selective - Alpha1 OR Alpha2: Yohimbine, Prazosin, Tamsulosin Non-Selective- Alpha1 AND Alpha2: Phentolamine, Phenoxybenzamine, Tolazolin
26
What Alpha Receptors dose Phentolamine act on?And what are the clinical uses of Phentolamine?
Alpha1 AND Alpha2: transient nonselective a-adrenergic blockade. Tx of: -acute hypertensive emergencies, -manipulation of a pheochromocytoma -autonomic nervous system hyperreflexia. -Extravasation of vasoconstricting drugs
27
IV effects of Phentolamine only last how long?
Onset 2 min, DOA 10-15, may use a drip during intraop mgmt of pheochromocytoma resection
28
Side effects of Phentolamine?
Baroreceptor mediated tachycardia, arrhythmias, parasympathetic dominance -> abdominal pain, diarrhea
29
What Alpha Receptors dose Phenoxybenzamine act on?And what are the clinical uses of Phentolamine?
Alpha1 AND Alpha2: Irreversible (non-competitive) nonselective a-adrenergic blockade. Administered orally to control blood pressure in patient with pheochromocytoma. And diseases with cutaneous vasoconstriction such as Raynaud's disease.
30
The most beneficial clinical responses to alpha adrenergic blockade are in disease diseases with?
A large component of cutaneous vasoconstriction, such as Raynaud's disease.
31
MOA of Prazosin?
Selective POSTsynaptic Alpha1 receptor antagonist.
32
Is Prazosin more or less likely to cause reflexive tachycardia than nonselective alpha blockers?
Less Likely. Selectivity for alpha1 receptors leaves the inhibitory action of alpha2 receptors on norepinephrine release intact, and less norepinephrine- induced tachycardia results than when a nonselective α- antagonist is used. (Doesn't interfere with the Alpha2-Norepi Negative Feedback Loop)
33
MOA and Clinical Indications of Yohimbine
Alpha 2a Selective Blocker. Crosses blood brain barrier and inhibits NE reuptake by blocking the presynaptic Alpha-2 receptor. Leads to increase in NE. Tx: Idiopathic orthostatic hypotension
34
When dealing with a pt with Pheochromocytoma, which must be given first, an alpha or beta blocker? Why?
Alpha Blocker 1st. If non-selective beta blockers (B1&B2 Blocker) are given first the decreased beta two stimulation will allow the alpha one stimulation from the pheo to be "unopposed" and cause extreme vasoconstriction and high blood pressure.
35
Should Beta Blocker therapy be continued throughout the perioperative period? Why or Why not?
should be continued throughout the perioperative period to maintain desirable drug effects and to avoid the risk of sympathetic nervous system hyperactivity associated with abrupt discontinuation of these drugs
36
Chronic administration of Beta Blockers is associated with what kind of beta receptor regulation?
Increased (Up Regulation) in the number of beta receptos.
37
MOA of Beta Blockers
Beta Adrenergic Receptor Antagonists. Competitive inhibition (so can be over powered / reversed)
38
What is the principle difference in pharmacokinetics between all beta adrenergic receptor antagonists?
The elimination half-time ranging from brief for Esmolol (~20min) to hours for others.
39
MOA of Metoprolol
Selective Beta-1 Antagonist. Prevents inotropic and chronotropic effects of sympathetic NS activation (Epi and Norepi). At large doses likely to become nonselective and block Beta-2 as well.
40
How is Metoprolol absorbed and metabolized?
Readily absorbed in GI tract but substantial first-pass metabolism. Only about 40% of the drug reaches systemic circulation via PO admin.
41
MOA and Route of Admin of Esmolol
Rapid Onset, short acting beta-1 selective blocker that can only be administered IV.
42
Initial dose and Infusion dose of Esmolol
0.5-1.5mg/kg (500-1500mcg/kg) IV over 60s Infusion: 50-300mcg/kg/min
43
Esmolol therapeutic effect seen after how many minutes? How long is its duration of action?
effect seen within 5min Action ceases within 10-30min after admin is discontinued
44
What is the metabolism of Esmolol? How is it different than Succinylcholine?
Plasma esterases in RedBloodCells are responsible for the hydrolysis of esmolol. Succinylcholine is metabolized by plasma cholinesterase (pseudocholinesterase) that is in the plasma (not RBCs). DOA of Succ is not prolonged by patients received Esmolol
45
Clinical manifestations of excessive myocardial depression produced by Beta Blockade include:
Bradycardia Low CO Hypotension Cardiogenic shock
46
Excessive bradycardia and/or decreases in cardiac output due to drug-induced β blockade should be treated initially with?
Atropine
47
If atropine is ineffective at reversing excessive beta-blockade, a continuous infusion of ______ can usually overcome competitive beta blockade
Isoproterenol
48
___________ is the standard b-adrenergic antagonist drug to which all other b-adrenergic antagonists are compared.
Propranolol
49
What are some Non-Selective Beta Blockers
propranolol, nadolol, timolol, pindolol
50
What are the Cardiac Selective (Beta-1) Blockers
metoprolol, atenolol, esmolol, bisoprolol, acebutolol, betaxolol
51
b1 Receptor blockade is associated with slowing of
the sinus rate, slowing of conduction of cardiac impulses through the atrioventricular node, and a decrease in inotropy.
52
How does the slowing of conduction and inotropy of Beta-1 Blockers help the heart?
Results in decreased myocardial oxygen demand, also increases diastolic perfusion time, which may enhance myocardial perfusion.
53
What is a noncardiac acting drug that can reverse excessive beta blockade? What is it's dose and MOA?
Glucagon 1-10mg IV followed by 5mg/hr IV Increases cyclic AMP independent of beta receptors.
54
How do non-selective beta blockers affect airway resistance?
Non-selective beta blocker, such as propranolol, increase airway resistance/bronchoconstriction due to blockade of beta 2 receptors( which normally cause bronchodilation.)
55
Why are non-selective beta blockers not recommended for patient with diabetes who may be at risk for developing hypoglycemia?
Non-selective beta blockers can't interfere with glycogenolysis, thereby reducing blood glucose levels AND the important warning sign of hypoglycemia, tachycardia, is blunted by the beta blockers.
56
What two drug classes has Propranolol been shown to alter their clearance or uptake?
Amide Local Anesthetics - reduces hepatic blood flow Opioids- pulmonary first pass uptake of fentanyl substantially decreased in chronic propranolol use. Much more systemic uptake of fentanyl.
57
The interaction between inhaled anesthetics and beta blockers is not usually excessive. What medication is the exception?
timolol - profound bradycardia has been observed in the presence of inhaled anesthetics
58
What two Beta Blockers are less lipid soluble than other β-adrenergic antagonists and thus may be associated with a lower incidence of central nervous system effects?
Atenolol and Nadolol
59
Perioperative β-adrenergic receptor blockade is recommended for patients considered at risk for?
myocardial ischemia (known coronary artery disease, positive preoperative stress tests, diabetes mellitus treated with insulin, left ventricular hypertrophy) during high-risk surgery – Vascular surgery – Thoracic surgery – Intraperitoneal surgery – Anticipated large blood loss
60
Standard IV Push Dose for Metoprolol, Atenolol, and Propranolol
Metop: 5mg IV Aten: 5-10mg IV Propran: 1-10mg IV
61
What 2 Beta Blockers are effective for controlling the ventricular response rate to atrial fibrillation and atrial flutter (Effective for controlling atrial dysrhythmias following cardiac surgery)
Esmolol and Propranolol (weird... not seen clinically, on Dr. C slides)
62
What are two combined Alpha and Beta Adrenergic Receptor Antagonists?
Labetalol Carvedilol
63
MOA of Labetalol and Carvedilol
Antihypertensive that exhibits Selective Alpha-1 Blockade and NONselective Beta1 and Beta2 Blockade. CO maintained.
64
What is the Beta to Alpha Blocking ratio of PO and IV Labetalol
PO. 3:1 IV: 7:1 IV Labetalol much more Beta Blocking than Alpha Blocking.
65
Do you see reflex tachycardia from Labetalol?
No, due to concurrent Beta Blockade
66
Time until peak effect of IV push Labetalol?
5-10min
67
Is Labetalol safe for asthmatics?
Bronchospasm is possible is susceptible patients but not likely to be the cause of an acute exacerbation
68
Most common side effect of labetalol
orthostatic hypotension
69
Pts treated with longer term beta blocker therapy usually is paired with what other class of medication?
Diuretic due to fluid retention
70
metoprolol-induced increases in airway resistance (High Doses) are more readily reversed with b2-adrenergic agonists such as
Terbutaline
71
What is the difference between meto­ prolol tartrate and metoprolol succinate?
Elimination Half-Time Tartrate has short half-life and requires more frequent dosing.
72
Which beta blocker is the most Beta-1 Selective?
Atenolol
73
Esmolol, Lidocaine, and Fentanyl can all be used to attenuate the sympathetic response from intubation, What is different about esmolol's response?
Lidocaine and Fentanyl will inhibit increases in SBP but Esmolol blunts both HR and SBP increases.
74
Which IV Beta Blocker has been associated with pain on injection?
Esmolol low pH
75
The principal contraindication to administration of b-adrenergic antagonists is?
preexisting atrioventricular heart block or cardiac failure not caused by tachycardia.
76
The development of cold hands and feet is a common side effect of?
Nonselective Beta Blockade (Blocker Beta2 cause vasoconstriction in periphery and unopposed alpha-1 stimulation)
77
Stimulation of b2-adrenergic receptors seems to facilitate movement of which ion intracellularly?
Potassium (so if you block beta2, like propranolol, you could see increases in potassium)
78
Can beta-blockers cross the placenta?
Yes Can cause bradycardia, hypotension, and hypoglycemia of fetus
79
Release of renin from the juxtaglomerular apparatus that occurs in response to stimulation of b2 receptors is prevented by nonselec- tive b-adrenergic antagonists such as?
Propanolol
80
After acute myocardial infarction, What is considered to be one of the most scientifically substantiated, cost-effective preventive medical treatments?
Beta Blockers

Anesthesia Pharmacology (24 decks)

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