CH 16 + 30: Alphas, BB & CCBs Flashcards
what is first-dose phenomenon?
- when the SNS is blocked, PNS dominates
- hypotension / orthohypotension d/t decr blood flow to brain; syncope
- reflex tachycardia and nasal congestion also occur
How to prevent first-dose phenomenon?
prevention by initial therapy begun with low doses and usually given at bedtime
what do they do?
Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers
- block peripheral catecholamines
- used concurrently w/ drugs like diuretics
- relax smooth muscle bladder (detrusor) and prostate
- incr urine flow
Alpha-Adrenergic Antagonists: Selective Alpha1 Blocker - what do they do to** arterioles**?
Block vasoconstriction on vascular smooth muscle (afterload) which decr BP directly
Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - what do they do to veins?
Block vasoconstriction which decr venous return (preload) to heart and lowers BP indirectly
Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - Therapeutic uses
- Benign prostatic hyperplasia
- Pheochromocytoma
- HTN
What selective agents are used?
Selective Alpha1 Blockers: BPH therapeutic use
Alpha-Adrenergic Antagonists
2 selective agents used in BPH
1. Alfuzosin (uroxatral)
2. tamsulosin (Flomax)
don’t cure condition, need surgery
what is it?
Selective Alpha1 Blockers: Pheochromocytoma
Alpha-Adrenergic Antagonists
small tumour of adrenal medulla, causes irregular secretion of Epi & NE
- excessive secretion of catecholamine in this condition causes severe HTN
Selective Alpha1 Blockers: HTN
Alpha-Adrenergic Antagonists
used to treat severe HTN
Beta-Adrenergic Antagonists: Selective
- block only beta1 receptors
- cardioselective
- fewer noncardiac SEs
- little effect on bronchial smooth muscle
- can be safely given to pts w/ asthma and COPD
Beta-Adrenergic Antagonists: Nonselective
- block beta1 and beta2 receptors
- produce more SEs than selective beta1 antagonists
- serious SE = bronchoconstriction (caution in pts w/ COPD + asthma)
what to not do with beta-adrenergic antagonists?
- don’t stop suddenly, will go into rebound tachycardia / rebound HTN –> can lead to stroke
- stay away from grapefruit juice + statins (ARBs)
When should you not give beta-adrenergic antagonists?
- hypotension
- bradycardia
- in 2nd-3rd degree heart block
Beta-Adrenergic Antagonists: Therapeutic Uses
most therapeutic actions relate to CV system
- slow conduction velocity thru AV node
- decr HR (chronotropic)
- decr force of contractions (inotropic)
- during stress/exercise - prevents sympathetic stimulation to heart
- caution when admin CCBs concurrently bc may potentiate HF
How does it take for body to adapt to Beta-Adrenergic Antagonists?
in about 6 weeks, pts will feel like shit
Beta-Adrenergic Antagonists: AEs
- prevents hyperglycemia effect of catecholamines –> dangerous in pts w/ DM b/c can cause hypoglycemia + masks s/s hypoglycemia
- decr amount of free fatty acids available during metabolic stress - bronchoconstriction - cannot be used in pts w/ COPD, asthma
- rebound cardiac excitation may occur if beta blockers withdrawn abruptly - never stop w/o talking to HCP first
Propranolol: Considerations
Non-selective Beta1 Blockers
- monitor VS q15min to q1hr
- Hx + Px - assess for asthma + COPD
- review lab tests for kidney, liver, hematologic + cardiac functions
- watch for ADRs in older adults + in pts w/ impaired renal function
- monitor I/O & daily weights (esp in HF)
- pt edu: decr salt intake, don’t stop drug suddenly
- examine for impaired circulation: irregular rhythm, SOB, bilateral lower extremities edema
- watch for widening QRS - immediate nursing attention
Propranolol: names of nonselective beta blockers
“-olol”
- carvedilol (Coreg)
- labetalol (Normodyne, Trandate)
- sotalol (Betapace, Sorine): watch for widening QRS complex
Calcium Channel Blockers: Vascular smooth muscle effects
- prevents contraction of peripheral arterioles (vasodilation + decr BP)
- afterload reduced - decr peripheral resistence + preload = lower myocardial oxygen demand + less workload for heart
- dilation of coronary arteries = more bld flow to heart
What do CCBs do?
stop the influx of Ca into vascular smooth muscle
CCBs: Myocardium effects
reduces force of myocardial contraction (negative inotropic effect)
- reduces inward movement of calcium during plateau phase of action potential
CCBs: Cardiac conduction effects
negative chronotropic effect
- SA node generates fewer action potentials
- slows automaticity
- decr hR
Nifedipine: Drug Interactions
Dihydropyridine CCBs: selective for vascular smooth muscle & used to treat HTN + angina pectoris
- may interact w/ drugs that induce or inhibit CYP 3A4
- additive effect w/ other antiHTN drugs
- incr risk of CHF w/ BB
- incr serum levels of digoxin - bradycardia
- syncope/drop in BP w/ alcohol
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Nifedipine: Treatment of Overdose
Dihydropyridine CCBs
- rapid-acting vasopressors such as dopamine, dobutamine
- calcium infusions
Verapamil: Drug Interactions
nondihydropyridines: act on both vascular smooth muscle + myocardia
- incr digoxin levels = incr risk bradycardia
- additive hypotension / bradycardia with other antiHTN drugs
- 3x plasma concentration of buspirone
- risk of myopathy incr significantly w/ statins
- verapamil incr carbamazepine (Tegretol) levels = neurotoxicity (ataxia/seizures)
- grapefruit juice may incr levels
Drugs similar to verapamil (Calan, Isoptin, Verelan)
Diltiazem (Cardizem, Dilacor, Taztia XR, Tiazac)
- treatment of atrial dysrhythmias + HTN, stable, and vasospastic angina
- same profile as verapamil
- migraine prophylaxis off-label
