Flashcards in Beta blockers Deck (47):
Where are beta receptors common?
-skeletal muscle vasculature
What does stimulation of beta receptors in skeletal muscle vasculature cause?
an inhibitory action, preventing the entry of calcium that is critical to the contraction of vascular smooth muscle
Activation of beta-2 receptors in skeletal muscle leads to relaxation and
increased perfusion of this muscle group, which is of critical importance in the fight-flight-fright response which characterizes the activity of the sympathetic nervous
What does stimulation of beta-1 receptors in the heart cause?
leads to an acceleration in heart rate and an increase in the force of cardiac
What does stimulation of beta-1 receptors on juxtaglomerular cells cause?
leads to the release of renin, which converts angiotensinogen to angiotensin I and
angiotensin II, a potent vasoconstrictor agent
In this manner, beta-blockers can
diminish hypertension due to excessive renin release.
What effect can NSAIDs have on renin release?
Chronic use of
nonsteroidal anti-inflammatory drugs will diminish the production of prostaglandins
and can have an adverse effect upon renal perfusion, especially in the elderly, by
preventing the vasoconstrictor actions instigated through renin release via beta-1-agonism.
What is intrinsic
This means that the drugs are actually weak partial
agonists that will provide some cardio stimulation but prevent excessive stimulation via the endogenous neurotransmitters epinephrine and norepinephrine
What are third-generation b-blockers?
These drugs have effects upon alpha receptors or activate other signaling systems to prevent reflexive vasoconstriction from reducing the
clinical effectiveness of beta blockade.
How does reflexive vasoconstriction occur?
Recall, baroreceptors will sense the decline in blood pressure produced by beta blockade and will activate alpha-1 mediated
A drug with an extended action will prevent this occurrence
T or F. Highly lipid soluble b-blockers tend to produce more adverse CNS effects such as bad dreams
T, although these events are also
reported, on occasion, with the less lipid soluble agents.
What are the classic non-selective 1st gen b-blockers?
Some b-blockers have membrane-depressant (quinidine-like) effects. What does this result in?
Further depression of myocardial contractility and conduction, over and above activity in
the SA and AV nodes, and may be associated with ventricular tachyarrhythmias
Which 1st gen b-blockers have membrane stabilizing activity?
propranolol (high lipid soluble) and pindolol weakly
What are the 2nd gen B-1 selective blockers?
What are the 3nd gen non-selective beta blockers with additional actions?
What are the 3nd gen B1-selective beta blockers with additional actions?
Naming convention for b-blockers
Drugs from A to M are beta-1 selective; those from N to T are non-selective, except
Those with an unusual spelling “ILOL” or “ALOL” have extended actions in
preventing alpha-mediated reflex vasoconstriction.
Which b-blockers have membrane stabilizing activity?
others with higher doses-pindolol, betaxolol, metoprolol, labetalol
Beta-blocking drugs with membrane stabilizing activity are used as what?
agents (class II)
How do the selective b-blockers stabilize membranes?
bind to and block fast sodium channels that are essential to the
initial depolarizing event in the cardiac cycle decreasing the action potential.
This is separate from their other effects
mediated via beta-1 adrenergic receptors
Which drugs have intrinsic sympathomimetic activity?
pindolol and acebutolol have this ability which allows them to slightly reverse the bradycardia and negative inotropy caused by b-bockade by partially mimicking catecholamine function (bad for prevention of secondary MI)
Some b-blockers have extended actions to further prevent reflexive vasoconstriction. Name them and what they do.
Nebivolol-NO production, antioxidant activity
Carvedilol- a-1 antagonist, Ca2+ entry blockade, antioxidant activity
Labetaolol- a-1 antagonist
Betaxolol- Ca2+ entry blockade
What are some indications for b-blockers?
-supraventricular and ventricular arrhythmias
T or F. B-blockers are most effective in
patients with high plasma renin activity
T, Beta-blockers inhibit the stimulation of renin production by catecholamines
(mediated by β1 receptors). It is likely, therefore, that drug effect is due, in part, to
depression of the renin-angiotensin-aldosterone system
Do b-blockers help HTN in those with low renin activity?
Yes, Undoubtedly some of the clinical effect might arise from the inhibition of presynaptic β-adrenoceptors
(stimulation of these receptors by epinephrine helps to augment release of NE from the pre-synaptic terminal), this would reduce sympathetic vasoconstrictor nerve
How do b-blockers prevent IHD?
They reduce cardiac work, reduce O2 demands, and slow and regularize HR
How do b-blockers prevent supraventricular and ventricular arrhythmias?
by increasing AV nodal refractory period, B-blockers slow ventricular response rates in atrial flutter and fibrillation
Which b-blockers are indicated for CHF prevention?
-Metoprolol, bisoprolol, and carvedilol
T or F. Note that abrupt discontinuation of beta-blocker treatment is ill advised
T, doses should be tapered over time. Upregulation in beta-receptor expression can lead to rebound and life-threatening cardiotoxic effects.
What are the symptoms of overdose of b-blockers?
Bradycardia and bradyarrhythmia are typical symptoms
What happens in b-blocker overdose?
beta receptors lose specificity
What happens in overdose of b-blockers with membrane stabilizing activity?
further depression of myocardial contractility and conduction and may cause ventricular tachyarrhythmias
What is a side effect of Propranolol (lipid-soluble) overdose?
seizures and coma
What happens in overdose of b-blockers with ISA?
tachycardia and HTN
What is Sotalol?
an antiarrhythmic agent that also has type III activity and when overdosed can prolong QT interval and may cause tornado de points and ventricular fibrillation
What is a common result of OD on third gen b-blockers with additional activity?
direct vasodilation contributes to hypotension
What is the typical treatment for OD of a b-blocker?
glucagon or high-dose insulin/glucose
Why could a beta blocker induce bronchospasm?
beta-2 adrenergic receptors have an important role in the
treatment of bronchospasm of asthma or COPD. Given that, non-specific beta
blockers and indeed beta-1 specific blockers (to a lesser extent) have the capacity to induce bronchospasm in such patients by removing endogenous bronchodilatory
Non-specific beta-blockers are CONTRAINDICATED in asthmatics and their use is cautioned against in patients with COPD
Likewise, beta1-adrenergic selective
beta-blockers, such as atenolol, should be used with caution in these patients,
particularly with high-dose therapy. Remember, receptor specificity is dose-related.
What kinds of b-blockers are less likely to induce bronchospasm?
-B1 selective drugs or those with ISA
Other side effects of B-blockers?
-CNS depression, resulting in mental disorders, fatigue, vivid dreams (less common with hydrophilic beta-blockers)
Other side effects of B-blockers?
How can b-blockers cause hypoglycemia?
B-2 receptors normally stimulate hepatic glycogen breakdown and precreatic glycogen release
How can b-blockers cause diabetic masking?
B-1 blockers mask the tachycardia which serves as a warning sign for insulin-induced hypoglycemia
use cautiously here
How do beta-blockers affect lipids?
Beta-blockers have been shown to increase TAG levels and decrease
plasma HDL, but they have little effect on total cholesterol and
Since b-blockers increase TAG levels, what patients are they contraindicated in?
The question at hand is to what degree the benefits of treatment
of hypertensive patients-with respect to CHD--are reduced by these lipid changes.
T or F. Cardioselective agents or those with ISA tend to have less of an effect on plasma
T. Those with both characteristics tend to reduce total cholesterol and LDL