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CV 2 Exam 3 > Adrenergics lecture > Flashcards

Adrenergics lecture Flashcards

1
Q

Dopamine effects

A

Renal Afferent Blood Vessels
D1 – Dilation
Increase blood flow to kidney

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2
Q

Baroreceptor Reflex Control of Heart Rate and Blood Pressure

A

b1 stimulation of heart rate & force
muscarinic-decrease in heart rate
a1- vasoconstriction
b2 -vasodilation

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3
Q

alpha 1 adrenergic agonists

A

alpha-adrenergic agonists are Pressor Agents **
Phenylephrine (Neosynephrine) Prototype
Over-the–counter nasal decongestant **

Midodrine (Pro Amatine)
oral – pts w/ autonomic insufficiency

Mixed Acting Alpha agonists
Metaraminol (Aramine)

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4
Q

Phenylephrine (prototype alpha agonist) Effects:

A

vasoconstriction
increase peripheral resistance; increase BP
increased blood pressure causes reflex bradycardia (blocked by atropine)

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5
Q

Phenylephrine Uses

A

to maintain BP in hypotensive states
spinal anesthesia
paroxysmal atrial tachycardia
induces baroreceptor reflex slowing of rate

Nasal decongestant –over the counter cough and cold medications

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6
Q

Dopamine Pharm effects

A

blood vessels: *** vasodilates renal, coronary, & mesenteric vascular beds (D1 receptors)
increase blood flow to kidney
heart: mild increase in rate & force (partial agonist beta 1 and increases release of NE)
blood vessels: high doses cause vasoconstriction & increased BP (alpha 1)-in the situation of “shock”, this is an undesirable effect bec. Decrease tissue perfusion

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7
Q

Dopamine Clinical uses

A

Shock; cardiogenic shock, unstable CHF
Increases cardiac output and enhances perfusion of kidney
Must monitor BP carefully because higher infusion rate or dose causes vasoconstriction and decreased tissue perfusion
Sometimes used in manage acute crisis in chronic CHF

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8
Q

Dobutamine

A

beta1 selective agonist

positive inotropic & some increase in rate
Cardiac output increases
little vascular effect

Clinical Use: cardiogenic shock, MI, CHF
Adverse effects: may increase size of infarct
potential arrhythmias
Increases the work/O2 requirement

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9
Q

Alpha 1 receptor blockers clinical use, effects- good and bad

A

Clinical use = 2nd or 3rd line treatment of essential hypertension; added to other agents from different class

Effects
↓PVR, ↓venous return, ↓ preload
Usually do not ↑ heart rate or cardiac output
Do not ↑ NE release (no a2 block)
Favorable effects on lipids
↓LDL & triglycerides; ↑HDL

Adverse Effects
Can cause marked postural hypotension & syncope, orthostatic hypotension, especially with initial doses
Usually given at bedtime to minimize hypotensive effects

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10
Q

beta 1-selective Beta Blockers 2nd Generation

A 
beta 1-selective = Cardioselective
* Atenolol 
* Metoprolol
Bisoprolol
* Esmolol - very short acting
Others
Acebutolol 
partial agonist, ISA
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11
Q

Non-selective Vasodilating beta Blockers3rd Generation

A

Alpha and Beta Blockers

  • Labetolol
  • Carvedilol

Vasodilating
Carteolol
Bucindolol (not available in USA)

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12
Q

Beta Blockers: Clinical uses

A
  • Hypertension. Decreases CO and produces ** slow ** decrease in peripheral resistance.
  • Ischemic Heart Disease: Angina, myocardial infarction, acute coronary syndromes. Reduces cardiac work and O2 consumption.
    MI & Post-MI prophylaxis
    protects against arrhythmias & limits infarct size
    Acute MI: assess LV function
    5-12 days after MI, reduces O2 demand & spread of infarct zone
  • Congestive Heart Failure
    Improves morbidity and mortality
  • Arrhythmias: sinus tachycardia and supraventricular ectopic beat
    Recurrent VT, VF - especially when due to ischemia
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13
Q

Beta blockers and thyrotoxicosis

A

hyperthyroid patients have increased beta receptor sensitivity
Beta blockers reduces sensitivity of myocardium to adrenergic stimulation in hyperthyroid patients.

Adjunctive treatment for anxiety (panic) attacks
reduces peripheral sympathetic signs and symptoms, e.g., palpitations
Migraine headache (Prophylactic treatment)
Pheochromocytoma

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14
Q

Properties of Beta Adrenergic Receptor Blockers

A

Propranolol- prototype beta blocker

competitive antagonists at b-1, b-2, & b-3 receptors. b blockers differ in their degree of receptor selectivity
b blockers differ in relatively lipid solubility; this effects their relative distribution to the CNS
These drugs differ in their bioavailability, biotransformation, and thus their pharmacokinetic properties
Some b blockers have intrinsic sympathomimetic activity (ISA), i.e., partial agonist activity
Some b blockers at high therapeutic doses may also have a non-receptor related quinidine-like or membrane-stabilizing effects.

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15
Q

Pharmacological Effects of beta blockers

A

The effect of antagonists are due to blocking existing sympathetic tone.
Effects are greater if sympathetic tone is high, e.g., during stress (MI) or exercise.
Effects are different in normal subjects compared to patients with hypertension or myocardial ischemia.

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16
Q

Pharmacological Effects of beta blockers on the heart

A

depend on existing sympathetic tone

Heart- decreases rate, CO, exercise tolerance, rate of depolarization of ectopic pacemakers, o2 demand, AV nodal conduction (can produce AV block), infarct size & re-infarction- prevent sudden death

17
Q

Pharmacological Effects of beta blockers: CV

A

Cardiovascular- short-term: decreases CO, HR; increased PVR to maintain BP as a result of blockade of beta 2 receptors & compensatory reflexes
long-term- PVR returns to initial values or decrease in patients with HTN. alpha/ beta blockers- CO is maintained with greater decrease in PVR

18
Q

Pharmacological Effects of beta blockers: Rhythm and automaticity

A

Rhythm and automaticity: decreases sinus rate, spontaneous rate of depolarization of ectopic pacemakers. Sloo conduction velocity in the atria and AV node. Increases functional refractory period of AV node

19
Q

Pharmacological Effects of beta blockers: Exercise tolerance

A

blunt the increase in HR and contractility that normally occurs with exercise
Cardiac output (CO) is less affected because stroke volume is increased
b blockers decrease work capacity
b1-selective agents have lesser effects on exercise tolerance than nonselective agents
Coronary blood flow increases during exercise to meet the demands of the heart
* Increased catecholamines during exercise or stress (MI) increase the work of the heart and myocardial oxygen demand*
Patients with coronary artery disease have fixed narrowing of these vessels which attenuates the expected increase in flow, leading to myocardial ischemia.

20
Q

Pharmacological Effects of beta blockers: Myocardial Oxygen Consumption

A

*** decrease myocardial oxygen demand
However, b blockers may tend to ↑ oxygen demand by increasing end-diastolic pressures and systolic ejection time period
Usually, the net effect is to improve the relationship between cardiac supply and demand; exercise tolerance is improved in patients with angina, whose capacity to exercise is limited by chest pain

21
Q

Pharmacological Effects of beta blockers: antihypertensive

A

do not usually lower BP in patients with normal BP but are effective treatment for patients with HTN ***
Mechanisms for this effect are not well understood

22
Q

Pharmacological Effects of beta blockers: plasma renin

A

Catecholamines stimulate b1 receptors in kidney juxtoglomerular apparatus to increase release of renin; b blockers block this increase in renin

Relevance of this effect to BP lowering is not clear.
However, BP is decreased the most in pts with elevated renin
b blockers are effective in lowering BP in patients with low or normal renin levels
Pindolol is an effective antihypertensive agent even though it has little effect on renin levels

23
Q

beta blocker antihypertensive mechanisms

A

Although b blockade would not be expected to decrease contractility of vascular smooth muscle, long term administration of these drugs to hypertensive pts ultimately leads to ↓ PVR
The mechanism for this effect is not known, but ↓ PVR in the face of persistent reduction in CO appears to account for much of the antihypertensive effect.
A CNS effect has been hypothesized – but there is little evidence to support this idea and drugs that penetrate into the CNS poorly are still effective.

24
Q

beta blocker Peripheral Vasodilation Effects

A

Non-selective vasodilating b blockers
Carteolol, * carvedilol, bucindolol, * labetolol

b1-selective vasodilating b blockers
* Betaxolol, celiprolol, nebivolol
These drugs produce peripheral vasodilation through a variety of mechanisms
↑NO
Activate b2 receptors
Block of a1 receptors
Block Ca++ entry
Open K+ channels
Antioxidant activity
Antiproliferative effects
25
Q

Vasodilating b blockers also are associated with

A
  • a decreased incidence of:

Bronchospasm, impaired lipid metabolism, impotence, reduced regional blood flow, increased vascular resistance, and withdrawal symptoms.

A lower incidence of these adverse effects is particularly beneficial in patients with insulin resistance, diabetes mellitus, and metabolic syndrome.

These effects are also being intensively investigated in relation to treatment of patients with congestive heart failure and peripheral arterial disease.

26
Q

Treatment of Ischemic Heart DiseaseAngina and MI

A

b blockers are effective in reducing the severity and frequency of attacks of exertional angina & in improving survival in patients who have had an MI.
– Not useful for vasospastic angina –may worsen
Timolol, metoprolol, atenolol, and propranolol have been shown to exert cardioprotective effects

Beneficial effects due to:

    • **Fall in myocardial oxygen demand & increased flow to ischemic areas
    • ↓HR, ↓contractility, ↓arterial BP (especially during exercise or stress

Both acute and long-term treatment with b blockers has been repeatedly shown to decrease mortality from MI by as much as 25% or more.

27
Q

Congestive Heart Failure and beta blockers

A

Beta blockers prevent HF in >50%, strokes reduced by >38%, occurrence of CAD and other CV events significantly decreased, improve ventricular remodeling

28
Q

beta blocker relative contraindications

A

Bronchial Smooth Muscle
Block sympathomimetic bronchodilation
precaution or contraindication in asthma & COPD

Metabolic
Blocks beta receptor effects on lipolysis and glycogenolysis.
May mask signs of hypoglycemia, e.g., tachycardia, BP changes, tremor. Delays recovery from insulin-induced hypoglycemia.

29
Q

beta blocker side effects

A 
Common: 
dizziness, fatigue, diarrhea, constipation, nausea, depression, sexual dysfunction, bizarre dreams
Severe but rare
purpura, rash, fever
May Interfere with SGOT and BUN tests
Chronic use increases VLDL & ↓HDL 
effects vary among agents
30
Q

beta blockers contraindications

A

Sudden Withdrawal: rebound hypertension, anginal attack & possibly MI if drug suddenly withdrawn after chronic therapy. Beta receptor synthesis is increased by beta blocker use. Example of receptor up-regulation, supersensitivity.

Other Contraindications: Acute treatment of decompensated heart failure; 2nd and 3rd degree heart block, and cardiogenic shock.

31
Q

Beta Blockers : Drug Interactions

A

Other hypotensive medications
reserpine, guanethidine, methyldopa

Other antiarrhythmic agents
calcium channels blockers
lidocaine

Insulin and oral hypoglycemic drugs
prolongs hypoglycemia and masks signs

Masks symptoms of hyperthyroidism

32
Q

Other Nonselective beta Blockers

A

Nadolol (Corgard) - longer acting; once-per-day dosing
Timolol (Blocadren) - more potent than propranolol
Pindolol (Visken) - partial agonist; partial blockade
less incidence of rebound hypertension
less bradycardia
Carteolol – has vasodilating properties

33
Q

beta 1 selective blockers

A

All are more potent at B1 than B2 receptors
at higher doses, block B2 as well
lessen risk of bronchospasm -still contraindicated in asthmatic
do not usually prolong hypoglycemia

Atenolol and Metoprolol

34
Q

esmolol

A

beta1 selective with very rapid onset & short duration of action ***

Used as IV infusion for peri-operative tachycardia and hypertension, arrhythmias
Used in electroconvulsive therapy

35
Q

labetolol

A

selective alpha 1 blocker
nonselective beta 1 and 2 blocker
partial agonist at beta 2

Clinical Uses:
hypertension
pheochromocytoma

36
Q

Carvedilol

A 
Nonselective b-blocker + a-blocker
Very lipid soluble
Also has antioxidant properties
Very dramatic results in CHF clinical trials
Decreased mortality by 65%
37
Q

alpha 2-selective Receptor Agonists

A

Centrally Acting Antihypertensive Agents

Brain stem a2-receptors
Control (inhibit) sympathetic outflow to periphery
Decrease sympathetic tone

Methyldopa- pregnancy hypertension

Clonidine- sudden withdrawal causes hypertensive crisis

CV 2 Exam 3 (23 decks)

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