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Pharm II- RCM > Stoelting: Chapter 19 > Flashcards

Stoelting: Chapter 19 Flashcards

1
Q

What is Phentolamine?

A
  • A substituted imidazoline derivative
  • Cause transient nonselective α-adrenergic blockade.
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2
Q

How is Phentolamine administered and what are its immediate effects?

A
  • Administered intravenously
  • It causes peripheral vasodilation
  • Decreases blood pressure within 2 min
  • Last 10-15 minutes.
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3
Q

What cardiovascular effects does Phentolamine have?

A
  • Increased heart rate.
  • Increase cardiac output due to α1 and α2 receptor blockade.
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4
Q

What are Phentolamine’s clinical uses?

A
  • Used for acute hypertensive emergencies
  • Intraoperative management of pheochromocytoma
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5
Q

Describe Phentolamine’s metabolism.

A
  • Principally metabolized in the liver.
  • About 10% excreted unchanged in urine.
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6
Q

What are some side effects of Phentolamine?

A
  • Cardiac dysrhythmias
  • Angina pectoris
  • Hyperperistalsis
  • Abdominal pain
  • Diarrhea
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7
Q

How is Phentolamine used for the extravascular administration of vasoconstrictors?

A
  • A solution containing 5-15 mg in 10 mL of normal saline
  • Is used for local infiltration.
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8
Q

What are α-Adrenergic Receptor Antagonists?

A
  • They selectively bind to α-adrenergic receptors
  • Block the effects of catecholamines and sympathomimetics.
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9
Q

What are the clinical effects of α-adrenergic blockade?

A
  • It prevents catecholamine effects on the heart and vasculature
  • Stops epinephrine’s action on insulin secretion.
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10
Q

What are the common side effects of α-adrenergic antagonists?

A
  • Orthostatic hypotension
  • Reflex tachycardia
  • Impotence.
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11
Q

How do Phentolamine, Prazosin, and Yohimbine function as α-antagonists?

A
  • They are competitive antagonists
  • Reversibly binding to receptors.
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12
Q

What is the mechanism of Phenoxybenzamine?

A
  • It binds irreversibly to α-receptors
  • Blocking them even against high levels of sympathomimetics.
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13
Q

Difference between Phentolamine, Phenoxybenzamine, Prazosin, and Yohimbine.

A
  • Phentolamine and Phenoxybenzamine are nonselective, acting on α1 and α2
  • Prazosin targets α1.
  • Yohimbine targets α2.
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14
Q

What are α- and β-Adrenergic Receptor Antagonists?

A
  • They block the interaction of neurotransmitters like norepinephrine with adrenergic receptors.
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15
Q

How do α- and β-Adrenergic Antagonists affect the sympathetic nervous system?

A
  • They attenuate sympathetic nervous system functions.
  • Leading to predictable pharmacological responses.
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16
Q

What is the role of α2 Receptors in adrenergic antagonism?

A
  • Reduces sympathetic outflow
  • Downregulating neurotransmitter release.
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17
Q

What is Phenoxybenzamine?

A
  • A haloalkylamine derivative
  • A nonselective α-adrenergic antagonist.
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18
Q

Phenoxybenzamine Pharmacokinetics:

A
  • Incomplete GI absorption
  • Peak effect takes up to 60 minutes post-IV
  • Half-time about 24 hours.
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19
Q

Cardiovascular Effects of Phenoxybenzamine:

A
  • It causes orthostatic hypotension
  • Does not significantly change systemic BP in normovolemic patients.
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20
Q

Noncardiac Effects of Phenoxybenzamine:

A
  • It prevents epinephrine’s action on insulin
  • Causes miosis, sedation, and nasal stuffiness.
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21
Q

Clinical Uses of Phenoxybenzamine:

A
  • Treats hypertensive emergencies,
  • Preoperative control in pheochromocytoma
  • Raynaud disease.
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22
Q

What is Yohimbine?

A
  • Selective α2 receptor antagonist.
  • Enhance norepinephrine release.
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23
Q

Yohimbine’s Clinical Application:

A
  • Treats idiopathic orthostatic hypotension.
  • Erectile dysfunction.
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24
Q

Neurological Impact of Yohimbine:

A
  • Can cross the blood-brain barrier
  • Potentially causing tremors and increased muscle activity.
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25
Q

Adverse Effects of Yohimbine:

A
  • Tachycardia.
  • Hypertension.
  • Rhinorrhea.
  • Paresthesias.
  • Dissociative states.
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26
Q

Yohimbine and Anesthetic Interaction:

A
  • Possible interaction with volatile anesthetics
  • Due to its effects on CNS α2 receptors.
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27
Q

What is Doxazosin used for?

A
  • Treats hypertension.
  • Benign prostatic hypertrophy (BPH).
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28
Q

Doxazosin’s Selectivity and Bioavailability:

A
  • Selective α1-receptor antagonist.
  • 65% bioavailable orally.
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29
Q

Doxazosin’s Peak Levels and Effect:

A
  • Peak levels 2-3 hours after oral intake.
  • Relaxes prostatic and vascular smooth muscle.
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30
Q

Metabolism and Excretion of Doxazosin:

A
  • Metabolized in the liver.
  • Excreted in feces.
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31
Q

Doxazosin’s Half-Life and Dosage Recommendation:

A
  • Terminal half-life is 22 hours
  • Recommended as a single daily morning dose.
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32
Q

What is Prazosin’s receptor selectivity?

A
  • Selective for postsynaptic α1-receptors.
  • minimize reflex tachycardia.
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33
Q

Effects of Prazosin on Blood Vessels:

A

Dilates arterioles and veins.

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34
Q

Onset and Duration of Prazosin:

A
  • Action starts about 30 minutes post oral intake
  • Lasting 4-6 hours.
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35
Q

How is Prazosin eliminated from the body?

A

Mainly metabolized by the liver.

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36
Q

Terazosin’s Function in Treating BPH:

A
  • A long-acting α1-adrenergic antagonist.
  • Effective in relaxing prostatic smooth muscle.
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37
Q

Mechanism of Terazosin in BPH Management:

A
  • Targets α1-mediated innervation
  • Controls prostate contraction and bladder outlet obstruction.
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38
Q

Administration Method of Terazosin:

A

Orally effective for benign prostatic hyperplasia treatment.

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39
Q

Tamsulosin’s Role in BPH Treatment:

A
  • An α1a-adrenergic antagonist.
  • Used orally for treating benign prostatic hyperplasia (BPH) symptoms.
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40
Q

Common Side Effects of Tamsulosin:

A
  • Orthostatic hypotension.
  • Vertigo.
  • Syncope.
  • Possible sexual side effects like ejaculatory dysfunction.
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41
Q

Drug Interactions with Tamsulosin:

A

Clearance of Tamsulosin is decreased in the presence of cimetidine.

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42
Q

Alfuzosin’s Therapeutic Use:

A
  • Selective α1a-adrenergic receptor inhibitor.
  • Primarily used in treating benign prostatic hyperplasia (BPH).
  • Especially in younger populations.
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43
Q

Side Effects of Alfuzosin:

A
  • Dizziness.
  • Systemic hypotension.
  • Reflex tachycardia.
  • Sexual side effects are less common compared to similar drugs.
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44
Q

Metabolism and Excretion of Alfuzosin:

A
  • Alfuzosin undergoes extensive liver metabolism into inactive metabolites.
  • Excretion is mainly through bile (3:1 ratio)
  • Only 11% remaining unchanged and excreted by the kidneys.
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45
Q

Silodosin’s Selectivity and Use:

A
  • Highly selective α1a-adrenergic receptor antagonist.
  • Specifically targeting prostate with fewer systemic side effects.
  • Used for treating benign prostatic hyperplasia (BPH).
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46
Q

Absorption and Bioavailability of Silodosin:

A
  • Rapid oral absorption.
  • Bioavailability of only 32%.
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47
Q

Metabolism and Excretion of Silodosin:

A
  • Metabolized via two hepatic pathways.
  • Its primary metabolite is active, possessing half the activity of the parent compound.
  • The metabolites are excreted in a 3:2 ratio, primarily hepatically.
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48
Q

Tolazoline’s Pharmacological Classification:

A

Competitive nonselective α-adrenergic receptor antagonist.

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49
Q

Tolazoline’s Primary Clinical Use:

A
  • Previously used for treating persistent pulmonary hypertension in newborns.
  • Now largely replaced by nitric oxide.
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50
Q

Tolazoline’s Side Effects:

A
  • Systemic hypotension.
  • Reflex tachycardia.
  • Cardiac dysrhythmias.
  • Potential for pulmonary and gastrointestinal hemorrhages.
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51
Q

Excretion of Tolazoline:

A

Mainly excreted unchanged through the kidneys.

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52
Q

Role of α2-Adrenergic Receptor Agonists

A
  • Bind to presynaptic α2 receptors
  • Decrease norepinephrine release
  • Reduce sympathetic outflow
  • Result in hypotension and bradycardia
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53
Q

α2 Receptor Locations and Effects

A
  • Primarily in CNS, brainstem, & Locus ceruleus.
  • Peripheral inhibition affects pancreas
  • Can inhibit insulin and induce glucagon
  • Clinical effects: hypotension, bradycardia, sedation
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54
Q

Mechanism of α2-Agonists

A
  • Competitively bind to α2 receptors
  • Can be displaced for CNS effect reversal
  • Withdrawal can cause rebound hypertension
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55
Q

CNS Effects of α2-Agonists

A
  • Central sedation and mild analgesia
  • Can reverse CNS effects by displacing the drug
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56
Q

α2-Agonists Clinical Use and Side Effects

A
  • Used for hypotension and central sedation.
  • Side effects include rebound hypertension post-withdrawal.
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57
Q

α2-Agonists in Hypertension

A
  • Reduce blood pressure comparably to α1 antagonists.
  • Withdrawal needs careful monitoring
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58
Q

Clonidine Overview

A
  • Treats resistant hypertension, tremors, opioid withdrawal
  • Partial α2 receptor agonist, 400:1 α2-α1 preference
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59
Q

Clonidine Pharmacokinetics

A
  • Metabolized in liver
  • Mostly excreted unchanged in urine.
  • Variable half-life with liver/kidney dysfunction
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60
Q

Clonidine Dosage Forms

A
  • Available IV, oral, transdermal
  • Dosing depends on the treatment purpose
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61
Q

Clonidine Effects

A
  • Dose-dependent heart rate and blood pressure reduction.
  • Clinical use for cardiovascular and withdrawal symptoms
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62
Q

Monitoring Clonidine Therapy

A
  • Monitor for effects on heart rate and blood pressure.
  • Watch for variability in patients with organ dysfunction
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63
Q

Clonidine and Organ Dysfunction

A
  • Half-life can significantly vary
  • Important to adjust dosing in liver/kidney impairment
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64
Q

Dexmedetomidine Profile

A
  • Selective α2 agonist, 1600:1 α2 preference
  • Used for sedation and analgesia in ICU/OR
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65
Q

Dexmedetomidine Administration

A
  • IV infusion: 0.1 to 1.5 μg/kg/min
  • Terminal half-life: 2 hours
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66
Q

Dexmedetomidine Pharmacokinetics

A
  • Extensive liver biotransformation
  • Excreted primarily in urine
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67
Q

Dexmedetomidine and Liver Impairment

A
  • Liver impairment increases plasma levels/duration
  • Requires careful monitoring and dose adjustment
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68
Q

Dexmedetomidine Dependence

A
  • Can induce physical dependence.
  • Withdrawal can cause tachycardia, hypertension, anxiety
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69
Q

Dexmedetomidine Bolus Effect

A
  • Large IV bolus can cause paradoxical hypertension and bradycardia.
  • Crossover α1 stimulation effects similar to phenylephrine
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70
Q

Beta-Adrenergic Receptor Antagonists - Overview

A
  • Block effects of catecholamines on heart, airways, blood vessels
  • Maintain during perioperative to avoid rebound effects
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71
Q

Beta-Adrenergic Antagonists - Mechanism

A
  • Competitive inhibition at beta receptors
  • Increases receptor numbers over time, may require dose adjustment
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72
Q

Beta-Adrenergic Receptors - Function

A
  • G protein-coupled
  • Activation increases cAMP
  • Effects: ↑ heart rate, contractility, conduction, ↓ relaxation time
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73
Q

Beta Antagonists - Structure-Activity

A
  • Derivatives of isoproterenol
  • Levorotatory forms more potent than dextrorotatory forms
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74
Q

Beta Antagonists - Classification

A
  • Nonselective: affect β1 and β2
  • Cardioselective: prefer β1, better for asthma/patients with reactive airways
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75
Q

Beta Antagonists - Cardiovascular Effects

A
  • Reduce heart rate, AV node conduction, inotropy
  • Increase myocardial perfusion, reduce ischemia during exercise
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76
Q

Beta Antagonists - Risks and Side Effects

A
  • Risk of bronchospasm in reactive airway disease
  • May worsen peripheral vascular disease symptoms
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77
Q

What is the range of elimination half-time for β-adrenergic receptor antagonists?

A
  • varies from brief (esmolol ~10 minutes) to several hours.
  • Considered in the perioperative period for dosing intervals or drug conversion.
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78
Q

Which β-adrenergic receptor antagonists are highly protein-bound?

A
  • Propranolol and Nebivolol.
  • High volume of distribution.
  • Rapid distribution post-IV administration.
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79
Q

How are β-adrenergic receptor antagonists eliminated?

A
  • Through various pathways.
  • Renal and hepatic functions influence elimination.
  • Requires consideration in renal/hepatic dysfunction.
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80
Q

What causes interpatient variability in response to β-adrenergic receptor antagonists?

A
  • Basal sympathetic nervous system tone differences.
  • Flat dose-response curves.
  • Impact of active metabolites.
  • Genetic differences in β-adrenergic receptors.
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81
Q

What are the key effects of Propranolol on the heart?

A
  • Decreases heart rate and myocardial contractility.
  • Lowers cardiac output, especially during exercise or increased sympathetic activity.
  • Increases peripheral vascular resistance, including coronary vascular resistance.
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82
Q

Describe the pharmacokinetics of Propranolol.

A
  • Rapid and almost complete GI absorption
  • Limited systemic availability due to hepatic first-pass metabolism.
  • Variable metabolism leading to 20-fold differences in plasma concentrations.
  • Not effective via intramuscular administration.
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83
Q

How does Propranolol interact with plasma proteins?

A
  • Extensively bound (90%-95%) to plasma proteins.
  • Plasma protein binding can be altered by factors like heparin-induced increases in free fatty acids.
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84
Q

How is Propranolol metabolized and eliminated?

A
  • Primarily metabolized in the liver
  • Active metabolite is 4-hydroxypropranolol.
  • Elimination half-time is 2-3 hours.
  • Clearance affected by hepatic blood flow and enzyme activity.
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85
Q

How does Propranolol affect the clearance of local anesthetics?

A
  • Decreases clearance by reducing hepatic blood flow and metabolism.
  • Alters systemic toxicity potential of local anesthetics like bupivacaine.
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86
Q

How does Propranolol influence opioid clearance?

A
  • Reduces pulmonary first-pass uptake of opioids like fentanyl.
  • Increases the amount of opioid entering systemic circulation post-injection.
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87
Q

What are the key pharmacokinetic properties of Nadolol?

A
  • Slow and incomplete GI absorption (about 30%).
  • Mostly excreted unchanged in urine; minimal metabolism.
  • Long elimination half-time of 20-40 hours allows once daily dosing.
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88
Q

Describe Pindolol’s pharmacokinetic characteristics.

A
  • Elimination half-time of 3-4 hours.
  • Extended half-time to over 11 hours in renal failure patients.
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89
Q

What is the primary use of Timolol and its systemic effects?

A
  • Used as eyedrops for glaucoma to decrease intraocular pressure.
  • Can cause systemic effects like bradycardia and increased airway resistance.
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90
Q

Timolol’s Pharmacokinetics

A
  • Rapid and almost complete oral absorption.
  • Extensive first-pass hepatic metabolism limits systemic availability.
  • Elimination half-time is about 4 hours.
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91
Q

Metoprolol: Classification

A
  • Selective β1-adrenergic receptor antagonist
  • Less likely to cause airway resistance or peripheral vascular disease effects
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92
Q

Pharmacokinetics of Metoprolol

A
  • Oral absorption; first-pass hepatic metabolism
  • Only about 40% reach systemic circulation
  • Low protein binding (around 10%)
  • Metabolites inactive; less than 10% excreted unchanged in urine
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93
Q

Metoprolol: Effects on the Cardiovascular System

A
  • Decreases heart rate and myocardial contractility
  • Reduces cardiac output, especially during exercise or increased sympathetic activity
  • Increases coronary vascular resistance but overall reduces myocardial oxygen demand
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94
Q

Dosage Forms of Metoprolol

A
  • Metoprolol tartrate: Shorter half-life (2-3 hours), requires frequent dosing
  • Metoprolol succinate: Extended-release, allows once or twice daily dosing
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95
Q

Metoprolol: Clinical Use

A
  • Treatment of hypertension, angina, heart failure, and some arrhythmias
  • Reduces risk of myocardial infarction and death in patients with heart disease
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96
Q

Metoprolol: Side Effects

A
  • Bradycardia, hypotension, fatigue, dizziness
  • Can worsen symptoms in patients with asthma or COPD at high doses
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97
Q

Metoprolol: Drug Interactions

A
  • Can interact with other blood pressure medications,
  • Increasing risk of hypotension
  • May enhance effects of other heart medications like digoxin
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98
Q

Metoprolol: Considerations in Pregnancy

A
  • Category C: Risk cannot be ruled out
  • Consult healthcare provider for risks and benefits
99
Q

Metoprolol: Pediatric Dose

A
  • Varies based on condition
  • Typically starts low and adjusted based on response
100
Q

Metoprolol: Mechanism of Action

A
  • Blocks β1-adrenergic receptors
  • Reduce sympathetic stimulation of the heart
101
Q

Metoprolol: Elimination Half-time

A
  • Varies based on formulation
  • Important in determining dosing frequency
102
Q

Why is Atenolol particularly valued in certain patients over nonselective β-adrenergic antagonists?

A
  • Highly selective for β1 receptors
  • Maintains β2 activity
  • Beneficial for those with airway diseases
103
Q

How does Atenolol benefit patients with coronary artery disease undergoing surgery?

A
  • Reduces postoperative myocardial ischemia
  • Lowers mortality and cardiovascular complications
104
Q

What is the duration of Atenolol’s antihypertensive effect and dosing frequency?

A
  • Prolonged effect allows once-daily dosing
  • Suitable for treating hypertension
105
Q

Does atenolol significantly penetrate the central nervous system (CNS)?

A
  • Minimal CNS entry
  • May cause fatigue
  • Mental depression
106
Q

Can atenolol be used in diabetic patients with hypertension?

A
  • Safe for diabetics
  • Does not enhance insulin-induced hypoglycemia
107
Q

What are the key pharmacokinetic properties of atenolol?

A
  • 50% oral absorption rate
  • Peak concentration in 1-2 hours
  • Primarily renally excreted
108
Q

What is the elimination half-life of atenolol and its implications in renal failure?

A
  • 6-7 hours under normal conditions
  • May exceed 24 hours in renal failure
109
Q

What makes betaxolol suitable for patients with airway diseases?

A
  • Cardioselective β1 antagonist
  • Less bronchoconstriction risk compared to nonselective β blockers
110
Q

What is betaxolol’s absorption rate and how often should it be administered for hypertension?

A
  • Nearly complete oral absorption
  • Once daily dosing due to long action
111
Q

What is the elimination half-life of betaxolol and its primary clearance method?

A
  • 11-22 hours elimination half-life
  • Mainly metabolized, less renal elimination
112
Q

How is betaxolol used in the treatment of glaucoma?

A
  • Topical form for chronic open-angle glaucoma
  • Alternative to timolol with fewer airway risks
113
Q

Why is Bisoprolol particularly effective for patients with heart conditions?

A
  • Highly β1-selective
  • Minimal intrinsic agonist activity
114
Q

What is the elimination half-time of Bisoprolol and how is it excreted?

A
  • Elimination half-time is 9-12 hours
  • Equally by renal and nonrenal mechanisms
115
Q

What conditions is bisoprolol commonly prescribed for?

A
  • Essential hypertension
  • Congestive heart failure, with noted survival improvement
116
Q

Are the metabolites of bisoprolol pharmacologically active?

A

No, metabolites are inactive

117
Q

What is the selectivity of Nebivolol?

A

Very potent, selective β1-antagonist.

118
Q

How does Nebivolol’s selectivity compare to Bisoprolol?

A

3.5 times more selective than Bisoprolol.

119
Q

Does Nebivolol exhibit any β2 antagonism?

A

Yes, at doses above 10 mg or certain genetic profiles.

120
Q

What is the elimination half-life of Nebivolol?

A

12 to 19 hours.

121
Q

How often should Nebivolol be taken?

A

Once daily, with flexible dosing.

122
Q

How is Nebivolol metabolized and excreted?

A
  • Urine (unchanged)
  • Feces (inactive metabolite).
123
Q

What is Nebivolol currently approved to treat?

A

Essential hypertension.

124
Q

What is Esmolol?

A
  • Is a rapid-onset and short-acting selective β1-adrenergic receptor antagonist.
125
Q

How is Esmolol administered?

A

Esmolol is administered only intravenously (IV).

126
Q

What is the typical initial dose of Esmolol IV?

A

0.5 mg/kg IV over about 60 seconds.

127
Q

When does the full therapeutic effect of Esmolol become evident?

A

Within 5 minutes after administration.

128
Q

How long does the action of Esmolol last after administration is discontinued?

A

Ceases within 10 to 30 minutes after administration is discontinued.

129
Q

When is Esmolol useful in clinical settings?

A
  • Is useful for preventing or treating adverse systemic blood pressure.
  • Heart rate increases that occur intraoperatively in response to noxious stimulation, such as during tracheal intubation.
130
Q

How does Esmolol affect heart rate and systolic blood pressure during tracheal intubation?

A
  • Protects against increases in both heart rate and systolic blood pressure.
131
Q

What are alternative drugs for blunting the increase in systolic blood pressure associated with laryngoscopy and tracheal intubation?

A
  • Lidocaine.
  • Fentanyl.

Both are effective alternatives

132
Q

Does lidocaine or fentanyl influence heart rate during tracheal intubation?

A

No, heart rate is not influenced by lidocaine or fentanyl.

133
Q

Besides tracheal intubation, in what other situations can Esmolol be used?

A
  • In preventing perioperative tachycardia and hypertension, during electroconvulsive therapy,

Management of conditions like:

  • Pheochromocytomas
  • Thyrotoxicosis
  • Pregnancy-induced hypertension, and more.
134
Q

What adverse effects are associated with the use of β-adrenergic receptor antagonists for excessive sympathetic nervous system activity?

A
  • Fulminant pulmonary edema
  • Irreversible cardiovascular collapse may occur.
135
Q

What is the β1 selectivity of Esmolol?

A

selective β1-adrenergic receptor antagonist.

136
Q

How does Esmolol interact with patients chronically treated with β-adrenergic antagonists?

A
  • It does not produce additional negative inotropic effects when administered to such patients.
137
Q

How does Esmolol affect the plasma concentration of propofol required to prevent patient movement in response to a surgical skin incision?

A
  • significantly decreases the plasma concentration of propofol required.
138
Q

What is the mechanism of action of Esmolol?

A
  • Is a β1-adrenergic receptor antagonist.
  • It blocks the effects of epinephrine on β1 receptors.
139
Q

In what form is Esmolol available for administration?

A

is available for IV (intravenous) administration only.

140
Q

Besides Esmolol, which other β-adrenergic antagonists can be administered IV?

A
  • Propranolol and metoprolol are the other β-adrenergic antagonists that may be administered IV.
141
Q

What is the pH range of the commercial preparation of Esmolol?

A

pH 4.5 to 5.5.

142
Q

Why may pain occur on injection of Esmolol?

A
  • The pH range of Esmolol’s commercial preparation (4.5 to 5.5) may be one of the factors responsible for pain on injection.
143
Q

What is the elimination half-time of Esmolol?

A

About 9 minutes.

144
Q

How is Esmolol metabolized and excreted in the body?

A
  • Rapidly hydrolyzed in the blood by plasma esterases
  • Independent of renal and hepatic function.
  • Less than 1% of the drug is excreted unchanged in urine
  • About 75% is recovered as an inactive acid metabolite.
145
Q

Is methanol formed as a result of Esmolol’s metabolism?

A

Yes, clinically insignificant amounts of methanol can occur from the hydrolysis of Esmolol.

146
Q

How long does it take for the heart rate to return to predrug levels after discontinuing Esmolol?

A

Within 15 minutes after discontinuing Esmolol.

147
Q

Why is Esmolol’s transfer into the central nervous system (CNS) or across the placenta limited?

A
  • Has poor lipid solubility
  • Which limits its transfer into the CNS or across the placenta.
148
Q

What are the common side effects associated with β-adrenergic antagonists?

A
  • Cardiovascular effects.
  • Altered airway resistance.
  • Changes in carbohydrate and lipid metabolism.
  • Shifts in extracellular ions.
149
Q

Do β-adrenergic antagonists pose a risk of hypoglycemia?

A

Yes, β-adrenergic antagonists may cause hypoglycemia.

150
Q

When β-adrenergic antagonists are used with anesthesia drugs, what additive effects may occur?

A
  • Sedation
  • Bradycardia
  • Hypotension

When β-adrenergic antagonists are combined with anesthesia drugs

151
Q

Do many β-adrenergic antagonists penetrate the blood-brain barrier?

A

Yes, many β-adrenergic antagonists can cross the blood-brain barrier.

152
Q

What gastrointestinal side effects may be associated with β-adrenergic antagonist use?

A
  • Nausea.
  • vomiting.
  • Diarrhea.
153
Q

List some other effects associated with chronic β-adrenergic antagonist treatment.

A
  • Fever
  • Rash
  • Myopathy
  • Alopecia
  • Thrombocytopenia
  • Also affect lipid levels by decreasing high-density lipoproteins
  • Increase triglycerides and uric acid levels.
154
Q

What is the principal contraindication for the administration of β-adrenergic antagonists?

A
  • Preexisting atrioventricular heart block
  • Acute cardiac failure not caused by tachycardia.
155
Q

When should caution be exercised with β-adrenergic antagonist administration regarding hypotension?

A
  • To hypovolemic patients with compensatory tachycardia.
  • It may lead to profound and resistant hypotension.
156
Q

Are nonselective β-adrenergic antagonists or high doses of selective β-adrenergic antagonists recommended for patients with reactive or obstructive airway disease?

A
  • No, They are not recommended for patients with any diagnosis of reactive or obstructive airway disease.
157
Q

What is the risk associated with β-adrenergic blockade in patients with diabetes mellitus?

A
  • May mask the signs of hypo- or hyperglycemia.
  • Potentially delaying clinical recognition.
158
Q

What are the primary cardiovascular effects of β-adrenergic antagonists?

A
  • Produce negative inotropic and chronotropic effects.
  • Slow conduction through the atrioventricular node.
  • Decrease spontaneous phase 4 depolarization.
159
Q

How do β-adrenergic antagonists affect preexisting atrioventricular heart block?

A
  • Likely to be accentuated by β-adrenergic antagonists.
160
Q

What is the mechanism behind the cardiovascular effects of β-adrenergic blockade?

A
  • Effects result from the removal of sympathetic nervous system innervation to the heart (β1-blockade).
  • Nonselective β-blockade may also impede left ventricular ejection due to α-adrenergic receptor-mediated peripheral vasoconstriction.
161
Q

How do β-adrenergic antagonists affect heart rate during exercise?

A
  • The tachycardia of exercise is consistently attenuated by β-adrenergic antagonists.
  • Age-adjusted maximal heart rate should be further adjusted down by 10 beats per minute.
162
Q

Do patients with peripheral vascular disease tolerate β2-receptor blockade well?

A
  • Patients may develop cold hands and feet as a common side effect of nonselective β-adrenergic antagonists.
163
Q

What is the principal antidysrhythmic effect of β-adrenergic blockade?

A
  • Prevents the dysrhythmogenic effect of endogenous or exogenous catecholamines or sympathomimetics

By decreasing sympathetic nervous system activity.

164
Q

How should excessive myocardial depression due to β-adrenergic blockade be initially treated?

A

Atropine in incremental IV doses of 7 μg/kg. (initially)

165
Q

What are some alternative treatments for myocardial depression caused by β-adrenergic antagonists?

A
  • Continuous infusion of isoproterenol (for pure β-blockade)
  • Dobutamine (for β1-adrenergic effects)
  • Glucagon
  • Calcium chloride.
166
Q

How does glucagon reverse myocardial depression caused by β-adrenergic antagonists?

A
  • Stimulates adenylate cyclase
  • Increases intracellular cAMP concentrations independent of β-adrenergic receptors

Making it effective in reversing myocardial depression.

167
Q

When should hemodialysis be considered in the treatment of β-adrenergic antagonist overdose?

A
  • Hemodialysis should be reserved for patients refractory to pharmacologic therapy
  • Is used to remove minimally protein-bound, renally excreted β-adrenergic antagonists.
168
Q

What effect do nonselective β-adrenergic antagonists like propranolol have on airway resistance and why?

A
  • Increase airway resistance via bronchoconstriction.
  • Due to β2 receptor blockade.
  • Effects exaggerated in obstructive airway disease.
169
Q

How do selective β1-adrenergic antagonists compare to nonselective ones regarding airway resistance?

A
  • Less likely to increase airway resistance.
  • Examples: bisoprolol, metoprolol, esmolol.
  • Do not block β2 receptors responsible for bronchodilation.
170
Q

How do β-adrenergic antagonists affect carbohydrate and fat metabolism?

A
  • Interfere with glycogenolysis during hypoglycemia.
  • Blunt tachycardia response to hypoglycemia.
  • Altered fat metabolism; reduced free fatty acid release.
171
Q

Why are nonselective β-adrenergic antagonists not recommended for diabetic patients on insulin or oral hypoglycemics?

A
  • Increase hypoglycemia risk due to glycogenolysis interference.
  • Mask hypoglycemia warning signs like tachycardia.
172
Q

How does β-adrenergic blockade affect extracellular potassium distribution?

A
  • Inhibits potassium uptake in skeletal muscles.
  • Can increase plasma potassium concentration.
  • Selective β1 antagonists less likely to impair potassium uptake.
173
Q

What is the interaction between β-adrenergic antagonists and anesthetics?

A
  • Potential additive myocardial depression.
  • Clinical experience shows it’s not excessive.
  • Safe to continue β-antagonists perioperatively.
174
Q

How do β-adrenergic antagonists impact the nervous system?

A
  • Can cross blood-brain barrier.
  • Side effects: fatigue, lethargy, vivid dreams.
  • Rarely cause psychotic reactions or memory loss.
175
Q

What are the fetal risks associated with β-adrenergic antagonists?

A
  • Can cause fetal bradycardia, hypotension, hypoglycemia.
  • Effects vary by drug lipophilicity and protein binding.
  • Some β-antagonists safe for use in pregnancy and breastfeeding.
176
Q

What happens with acute discontinuation of β-adrenergic antagonist therapy?

A
  • Excess sympathetic activity within 24-48 hours.
  • Due to upregulation of β-adrenergic receptors.
  • Continuous infusion can maintain therapeutic levels.
177
Q

What are the clinical uses of β-adrenergic antagonists in the perioperative period?

A
  • Multiple therapeutic effects.
  • Recommended to continue uninterrupted perioperatively.
  • Beneficial for high-risk myocardial ischemia patients during surgery.
178
Q

How do β-adrenergic antagonists treat essential hypertension?

A
  • Gradual systemic blood pressure decrease.
  • Lowers cardiac output and heart rate.
  • Often combined with vasodilators to balance effects.
179
Q

What is the role of β-adrenergic antagonists in managing angina pectoris?

A
  • Decrease likelihood of myocardial ischemia.
  • Lower myocardial oxygen requirements.
  • Effective dose reduces resting heart rate to <60 bpm.
180
Q

Discuss β-adrenergic antagonists in acute coronary syndrome treatment.

A
  • Recommended post-myocardial infarction.
  • Contraindicated in severe bradycardia, left ventricular failure, AV block.
  • Caution in asthma, depression, fatigue, peripheral vascular disease.
181
Q

What are the contraindications and considerations for β-adrenergic antagonists in acute coronary syndrome?

A
  • Not recommended within first 8 hours of ST elevation myocardial infarction.
  • Risk of cardiogenic shock.
  • Decreases incidence of nonfatal reinfarction.
182
Q

What is the cardioprotective mechanism of β-adrenergic antagonists?

A
  • Antidysrhythmic actions.
  • Nonselective β-antagonists prevent epinephrine-induced potassium decrease.
  • Useful in reducing ventricular dysrhythmias.
183
Q

What is the role of β-adrenergic receptor blockade in perioperative care?

A
  • Recommended for at-risk patients during high-risk surgery.
  • Aim for resting heart rate between 65-80 bpm.
  • Reduces perioperative myocardial ischemia and mortality.
184
Q

How should β-adrenergic receptor blockade be managed preoperatively?

A
  • Oral atenolol, bisoprolol, or metoprolol.
  • IV atenolol or metoprolol if initiated on surgery day.
  • Esmolol for intraoperative and ICU care.
185
Q

What are the concerns with starting β-blockers in the acute preoperative setting?

A
  • Risk of increased all-cause mortality.
  • Potential cerebrovascular events.
  • Low-dose regimens recommended for preoperative initiation.
186
Q

How are β-adrenergic receptor blockers used in treating intraoperative myocardial ischemia?

A
  • Titrate to achieve heart rate around 60 bpm.
  • Options: esmolol, metoprolol, atenolol, propranolol.
  • Esmolol preferred for heart rate titration.
187
Q

What is the role of β-adrenergic receptor blockers in suppressing cardiac dysrhythmias?

A
  • Control ventricular response in atrial fibrillation/flutter.
  • Effective post-cardiac surgery for atrial dysrhythmias.
  • Propranolol for torsades de pointes in prolonged QTc.
188
Q

How do β-adrenergic antagonists manage congestive heart failure?

A
  • Improve ejection fraction and survival.
  • Examples: metoprolol, carvedilol, bisoprolol.
  • Start with minimal doses, gradually increase.
189
Q

Describe the use of β-adrenergic blockers for preventing excessive sympathetic nervous system activity.

A
  • Attenuate heart rate/blood pressure changes during intubation.
  • Treat hypertrophic obstructive cardiomyopathy, pheochromocytoma, hyperthyroidism.
  • Reduce cyanotic episodes in tetralogy of Fallot.
190
Q

How is propranolol used in preoperative preparation of hyperthyroid patients?

A
  • IV or oral administration.
  • Rapid suppression of sympathetic nervous system activity.
  • Avoids need for iodine or antithyroid drugs.
191
Q

What are the characteristics and effects of Labetalol?

A
  • Selective α1 and nonselective β1/β2 antagonist.
  • Spares presynaptic α2 receptors.
  • Lower potency compared to phentolamine (α-blocker) and propranolol (β-blocker).
192
Q

Describe the pharmacokinetics of Labetalol.

A
  • Metabolized by glucuronic acid conjugation.
  • 5% excreted unchanged in urine.
  • Elimination half-time: 5-8 hours; prolonged in liver disease.
193
Q

What are the cardiovascular effects of Labetalol?

A
  • Lowers blood pressure by decreasing vascular resistance (α1-blockade).
  • Prevents reflex tachycardia (β-blockade).
  • Cardiac output remains unchanged.
194
Q

Discuss the clinical uses of labetalol.

A
  • Treats hypertensive emergencies.
  • Controls hypertension in epinephrine overdose.
  • Used in angina pectoris treatment.
195
Q

How is labetalol administered in surgical settings?

A
  • IV doses of 0.1-0.5 mg/kg to attenuate heart rate and blood pressure.
  • Can be used for controlled hypotension.
  • Effects may be accentuated by anesthetic drugs.
196
Q

What are the side effects of Labetalol therapy?

A
  • Common: Orthostatic hypotension.
  • Possible bronchospasm in susceptible patients.
  • Less severe congestive heart failure, bradycardia, heart block risks.
197
Q

What are the key features and uses of carvedilol?

A
  • Nonselective β-adrenergic antagonist with α1-blocking activity.
  • No intrinsic β-adrenergic agonist effect.
  • Used for mild to moderate congestive heart failure and essential hypertension.
198
Q

Describe the pharmacokinetics of carvedilol.

A
  • Extensively metabolized post-oral administration.
  • Elimination half-time: 7-10 hours.
  • High protein binding.
199
Q

What is the mechanism of action of calcium channel blockers?

A
  • Interfere with calcium ion movement across cardiac and vascular smooth muscle cells.
  • Bind to L, N, and T type calcium channels, maintaining them in a closed state.
  • Reduce calcium influx, leading to reduced intracellular calcium.
200
Q

How are calcium channel blockers classified and what are their effects?

A
  • Classified as phenylalkylamines, dihydropyridines, benzothiazepines.
  • Phenylalkylamines and benzothiazepines: selective for AV node.
  • Dihydropyridines: selective for arteriolar beds.
  • Common effects: slow heart rate, reduce myocardial contractility, relax vascular smooth muscle.
201
Q

What are the common side effects of calcium channel blockers?

A
  • Systemic hypotension.
  • Peripheral edema.
  • Flushing.
  • Headache.
202
Q

Describe the role of calcium in cardiac and vascular smooth muscle cells.

A
  • Key in electrical excitation.
  • Involved in excitation/contraction coupling.
  • Calcium influx through L-type channels is critical for cardiac action potential phase 2.
203
Q

What are the pharmacologic effects of calcium channel blockers?

A
  • Decrease myocardial contractility.
  • Decrease heart rate and sinoatrial node activity.
  • Slow conduction through atrioventricular node.
  • Cause vascular smooth muscle relaxation and vasodilation.
  • Reduce systemic blood pressure.
204
Q

How do calcium channel blockers help in treating coronary artery spasm and angina pectoris?

A
  • Increase coronary blood flow by decreasing vascular smooth muscle contractility.
  • Reduce systemic vascular resistance and blood pressure.
  • Effective in chronic stable angina and unstable angina pectoris.
  • Complement nitrates in coronary artery spasm treatment.
205
Q

Which calcium channel blockers have the most significant negative inotropic effects?

A
  • Verapamil and diltiazem.
  • Exert strong negative effects on myocardial contractility.

Negative inotropic effect: This decreases the strength of the heart’s contractions. Imagine the heart pumping with less force, like turning down the power on a pump.

206
Q

Describe the binding mechanism and action of phenylalkylamines like verapamil on calcium channels.

A
  • Bind to intracellular part of L-type channel α1 subunit in an open state.
  • Verapamil: synthetic papaverine derivative, affects slow calcium channels.
  • Dextroisomer acts on fast sodium channels; levoisomer specific for slow calcium channels.
207
Q

Side effects and contraindications of Verapamil?

A
  • Major depressant effect on atrioventricular node.
  • Negative chronotropic effect on sinoatrial node.
  • Negative inotropic effect on cardiac muscle.
  • Not advised for heart failure, severe bradycardia, sinus node dysfunction, AV nodal block.
208
Q

What are the clinical uses of verapamil?

A
  • Treats supraventricular tachydysrhythmias, vasospastic angina, essential hypertension.
  • Mild vasodilator, less active on vascular smooth muscle than Nifedipine.
  • Useful in hypertrophic cardiomyopathy treatment.
209
Q

Describe the pharmacokinetics of verapamil.

A
  • Oral bioavailability: 10-20% due to hepatic first-pass metabolism.
  • Oral dose ~10 times IV dose.
  • Peaks in 30-45 mins orally, 15 mins IV.
  • Elimination half-time: 6-12 hours, prolonged in liver disease.
  • Highly protein-bound (90%).
210
Q

What is the action mechanism of dihydropyridines like nifedipine?

A
  • Prevent calcium entry into vascular smooth cells via extracellular modulation of L-type calcium channels.
  • Focus on peripheral arterioles, minimal effect on venous vessels.
  • Can cause reflex tachycardia due to sympathetic activity or baroreceptor reflexes.
211
Q

Describe the clinical uses and pharmacokinetics of Nifedipine.

A
  • Treats angina pectoris, especially coronary artery vasospasm.
  • Oral dose: 10-30 mg, effect in 20 mins, peaks in 60-90 mins.
  • Absorption ~90%, highly protein-bound.
  • Hepatic metabolism, elimination half-time: 3-7 hours.
212
Q

What are the side effects of Nifedipine?

A
  • Common: Flushing, vertigo, headache.
  • Less common: Peripheral edema, hypotension, paresthesias, muscle weakness.
  • Rare: Glucose intolerance, hepatic dysfunction.
  • Abrupt discontinuation may cause coronary artery vasospasm.
213
Q

What is the impact of Nicardipine on the sinoatrial and atrioventricular nodes, and its overall effect on the heart?

A
  • No effect on sinoatrial and atrioventricular nodes.
  • Minimal myocardial depressant effects.
  • Prominent coronary artery vasodilation.
214
Q

How is Nicardipine used in combination therapy for angina?

A
  • Combined with β-adrenergic antagonists.
  • Does not significantly depress the sinoatrial node.
  • Helps manage residual hypertension and angina.
215
Q

Describe the pharmacokinetics of Nicardipine.

A
  • High lipophilicity; nearly complete GI absorption.
  • Bioavailability ~35% due to first-pass metabolism.
  • IV half-lives: α – 2.7 min, β – 44.8 min, γ – 14.4 hours.
216
Q

What are the side effects of Nicardipine?

A
  • Similar to Nifedipine.
  • Includes vasodilation-related effects like headache and flushing.
217
Q

What are the clinical uses of Nicardipine?

A
  • Previously used as a tocolytic.
  • Administered for electroconvulsive therapy to blunt acute hemodynamic responses.
  • Treats angina and hypertension.
218
Q

What is the recommended dosage and administration method for Nicardipine in different clinical settings?

A
  • IV administration: 40 μg/kg for electroconvulsive therapy.
  • Oral and IV forms available.
  • IV functional vasodilation lasts 9-15 minutes; adjust oral doses every 72 hours.
  • Dosage adjustments necessary for liver metabolism and high protein binding.
219
Q

What are the key characteristics and uses of Clevidipine?

A
  • Third-generation dihydropyridine; extremely lipophilic, ultrashort acting.
  • FDA approved for acute, severe hypertension.
  • Administered intravenously.
220
Q

Describe the pharmacokinetics of Clevidipine.

A
  • Metabolized by plasma esterases; half-life ~1 minute.
  • Clearance unaffected by liver or kidney function.
  • Pseudocholinesterase deficiency significantly delays metabolism.
221
Q

How is Clevidipine dosed?

A
  • Starts at 1-2 mg/hour; doubled every 90 seconds until BP nears goal.
  • Median range: 4-8 mg/hour; up to 32 mg/hour possible.
  • Requires nutritional adjustments at higher doses.
222
Q

What are the side effects and cautions associated with Clevidipine?

A
  • Common side effects: Hypotension, tachycardia.
  • Not recommended in hyperlipidemic states, pancreatitis, heart failure with reduced ejection fraction.
  • Higher doses may cause negative inotropic effects.
223
Q

What are the properties and clinical uses of Nimodipine?

A
  • Lipid-soluble analogue of nifedipine.
  • Enters CNS, blocks calcium ion influx in cerebral arteries.
  • Used in subarachnoid hemorrhage treatment.
224
Q

How does Nimodipine work in treating cerebral vasospasm?

A
  • Dilates cerebral arteries, preventing/attenuating vasospasm after subarachnoid hemorrhage.
  • Oral dose: 0.7 mg/kg initially, then 0.35 mg/kg every 4 hours for 21 days.
  • Can be administered via nasogastric tube if necessary.
225
Q

What is the role of Nimodipine in cerebral protection?

A
  • Evaluated for cerebral protection after global ischemia, like cardiac arrest.
  • Improves neurologic outcomes in subarachnoid hemorrhage.
  • IV dose: 10 μg/kg followed by 1 μg/kg per minute.
226
Q

What are the side effects and administration considerations for Nimodipine?

A
  • Side effects: Peripheral vasodilation, systemic hypotension.
  • Possible increase in intracranial pressure due to cerebral vasodilation.
  • Effective even with decreases in blood pressure.
227
Q

What are the key properties and clinical applications of Amlodipine?

A
  • Dihydropyridine derivative, oral administration.
  • Used for acute coronary syndrome treatment.
  • Can be combined with β-blockers for myocardial ischemia.
228
Q

Describe the pharmacokinetics of Amlodipine.

A
  • Oral dose: 5-10 mg.
  • Peak plasma concentration: 6-12 hours.
  • Elimination half-time: 30-40 hours.
  • 90% hepatically metabolized to inactive products.
229
Q

What are the effects of Amlodipine on myocardial contractility?

A
  • Minimal detrimental effects on myocardial contractility.
  • Provides anti-ischemic effects similar to β-blockers.
230
Q

What are the properties and actions of Benzothiazepines like Diltiazem?

A
  • Act at L-type calcium channels, blocking calcium entry.
  • Additional actions: affect sodium-potassium pump, inhibit calcium-calmodulin binding.
  • Intermediate effects between Verapamil and dihydropyridines.
231
Q

What are the clinical uses of Diltiazem?

A
  • First-line medication for supraventricular tachydysrhythmias.
  • Chronic control of essential hypertension.
  • IV administration for angina pectoris.
232
Q

Describe the pharmacokinetics and recommended dosing of Diltiazem.

A
  • Excellent oral absorption; onset in 15 mins, peak in 30 mins.
  • IV dose: 0.25-0.35 mg/kg over 2 minutes, repeatable in 15 mins.
  • Continuous infusion: 10 mg/hour for up to 24 hours.
  • 70-80% protein bound; excreted in bile and urine.
  • Elimination half-time: 4-6 hours (parent drug), 20 hours (metabolites).
233
Q

What are the drug interactions and considerations for Diltiazem?

A
  • May enhance atrioventricular heart block with β-blockers or digoxin.
  • Interactions with volatile anesthetics may exaggerate myocardial depression, peripheral vasodilation.
  • Continue use until surgery; watch for preexisting heart conditions.
234
Q

What are the considerations for using calcium channel blockers with anesthetic drugs?

A
  • Vasodilators and myocardial depressants.
  • Caution needed in patients with left ventricular dysfunction or hypovolemia.
  • Interact with volatile anesthetics, inhibiting calcium channels.
235
Q

How do calcium channel blockers affect anesthetized patients with cardiac issues?

A
  • Can lead to myocardial depression, decreased cardiac output.
  • Further decrease in ventricular function with verapamil or diltiazem during surgery.
  • Cardiac protection related to calcium overload prevention.
236
Q

What are the effects of calcium channel blockers on cardiac dysrhythmias and conduction in anesthetized patients?

A
  • Transient decreases in systemic blood pressure.
  • Infrequent P-R interval prolongation.
  • Use cautiously with digitalis or β-adrenergic blocking drugs.
237
Q

How do β-adrenergic agonists interact with calcium channel blockers in the context of anesthesia?

A
  • Increase the number of functioning slow calcium channels in myocardial cells.
  • Counter the effects of calcium channel blockers.
  • No increased anesthesia risk for patients treated with calcium channel blockers.
238
Q

How do calcium channel blockers interact with neuromuscular blocking drugs?

A
  • Do not produce skeletal muscle relaxant effect alone.
  • Potentiate effects of both depolarizing and nondepolarizing neuromuscular blockers.
  • Similar to potentiation by mycin antibiotics.
239
Q

What is the role of local anesthetic effects in the potentiation of neuromuscular blocking drugs?

A
  • Verapamil and diltiazem inhibit sodium ion flux, contributing to potentiation.
  • May affect patients with compromised neuromuscular transmission.
  • No evidence of inhibition of physical function in frail elderly.
240
Q

How do calcium channel blockers affect potassium levels and potassium-containing solution administration?

A
  • Slow inward movement of potassium ions.
  • May cause hyperkalemia with lower doses of exogenous potassium.
  • Does not affect plasma potassium increases from succinylcholine in animals.
241
Q

What is the interaction between calcium channel blockers and platelet function?

A
  • May interfere with calcium-mediated platelet function.
  • Interaction with clopidogrel via P450 enzyme 3A4 metabolism.
  • Reduced conversion of clopidogrel, increasing risk of cardiac events.
242
Q

How do calcium channel blockers affect the plasma concentration of digoxin?

A
  • Increase plasma concentration of digoxin.
  • Decrease plasma clearance of digoxin.
243
Q

What is the interaction between calcium channel blockers and H2 antagonists?

A
  • Cimetidine and ranitidine may increase plasma concentrations of calcium channel blockers.
  • Alters hepatic enzyme activity and/or hepatic blood flow.
244
Q

What is the role of calcium channel blockers in cytoprotection?

A
  • Protect against ischemic reperfusion injury.
  • Decrease calcium ion entry, limiting oxygen free radical accumulation.
  • May attenuate renal injury from nephrotoxic drugs.
  • Increase renal blood flow and glomerular filtration rate, favoring natriuresis.

Pharm II- RCM (2 decks)

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