Test 2- Main points Flashcards
Class 1C agent main points
Slow dissociation; MFP- flecainide and propafenone
pro-arrhythmics, used for ventricular and atrial arrhythmias
Class 1A agent main points
intermediate dissociation, DQP- quinidine and procainamide, atrial and ventricular tachyarrhythmias
Concerns: lupus like syndrome & cardiotoxic leading to HF
Class 1B agent main points:
Fast dissociation, LMP- lidocaine, mexiletine
used in ventricular arrhythmias
-lidocaine has CYP450 metabolism so impaired by propranolol and cimetidine or induced by barbiturates, phenytoin, or rifampin
NOT A PRO-ARRhythmic due to fast dissociation
SE of lidocaine- can prolong NMBD
What drug is used in suppression of ventricular arrhythmias associated with digitalis toxicity?
Phenytoin (Class 1B)
Class II agents main points:
beta blockers; used to treat SVT, atrial and ventricular arrhythmias; decreases SA node firing and slows through AV node; blocks at phase 4
Class III agents main points:
Potassium channel blockers; work at phase 3, lengthening repolarization; used to treat SVT & ventricular arrhythmias, afib
**Super Pro-arrhythmic- torsades
AIDDS (amiodarone, ibutilide, dofetilide, dronedarone, sotalol)
Main points regarding amiodarone:
Class III anti-arrhythmic with 1, II, and 4 properties/activities
first line for VT/Vfib
29 day half-life
Adverse effects are huge: pulmonary fibrosis, thyroid abnormalities, pro-arrhythmic
Calcium channel blockers main points:
Work at phase 2 (shortens phase 2) of cardiomyocyte on L1a type receptors; decreases contractility of the heart; Verapamil and diltiazem on AV node and nifedipine on arterial bed
not used in ventricular arrhythmias (used in SVT, afib, and aflutter)
Side effects: prolongs neuromuscular blockers, hypotension and bradycardia
Can see reflex tachycardia with nifedipine
Calcium channel blockers and drug interactions:
-myocardial depression and vasodilation with inhalational agents
-can potentiate NMBDs
-Verapamil and beta blockers can cause heart block
-Verapamil increases risk of LA toxicity
-Verapamil & dantrolene can cause hyperkalemia
-Digoxin- can increase plasma concentration of digoxin
-H2 antagonists- can increase levels of CCB
toxicity of CCB can be reversed with calcium or dopamine
Calcium channel blockers require:
slow discontinuation or else may result in coronary vasospasm
Adenosine takeaways:
binds to A1 purine nucleotide receptors and increases K+ currents; slows AV nodal conduction
contraindicated in asthma and heart block
Digoxin takeaway:
cardiac glycoside
increases vagal activity, thus decreasing activity of the SA node and prolongs conduction through AV node
SEs: arrhythmias, heart block
Phenoxybenzamine
binds covalently A1>A2; pro-drug; decreases SVR and Vasodilation
used for pts with pheo & Raynaud’s
d/t less A2 we see less associated tachycardia
Phentolamine
non-selective alpha antagonist
-cause reflex mediated AND alpha 2 associated increases in HR & CO
Used for hypertensive emergences (pheo & autonomic hyperreflexia) & extravascular admin of sympathomimetic agents
Prazosin
selective alpha 1 antagonist (less likely to cause tachy)
dilates both arterioles and veins
uses: Pheo, HF, HTN, Raynaud’s
Yohimibine
alpha 2 selective blocker; increases the release of Norepi from post-synaptic neurone; used w/ orthostatic hypotension & impotence
Terazosin & tamsulosin
selective alpha 1a for BPH
orthostatic hypotension is concern
Relative contraindications to beta blockers:
reactive airway disease; DM (masking of hypoglycemia); heart blocks or AV node blocks; hypovolemia
Propranolol:
non-selective
causes decreased HR & contractility and increased vascular resistance
chronic treatment: decreased clearance of local LAs and decreased pulm clearance of fentanyl
Metoprolol
beta 1 selective (selectivity is dose related)
good for asthmatics
Atenolol
MOST selective beta 1 antagonists with least CNS effects
used for HTN; good for asthmatics
Esmolol
rapid onset and short DOA beta 1 selective blocker
metabolized by plasma esterases
does not cross BBB or placenta
treats HTN & tachy with laryngoscopy & thyroid storm, thyroidtoxicosis, and pheo
Timolol
non-selective beta blocker used to treat glaucoma
eye drops can cause decreased BP, HR and increased airway resistance
Betaxolol
cardioselective beta 1 blocker; better for pts with glaucoma and asthma
Labetalol
alpha and beta 1 & 2 nonselective antagonist
used for HTN in OR but effects last longer than esmolol
no increase in HR b/c of beta 1 block
can cause bronchospasm, heart block, hypotension, CHF, bradycardia
Centrally acting agents
reduce sympathetic outflow from vasomotor centers
clonidine is main one- used for HTN, sedation, decrease in anesthetic requirements, analgesia
can see rebound HTN with abrupt cessation
SEs: bradycardia, sedation, hypotension, dry mouth
Vasopressin
endogenous- released in response to increased osmolality or hypovolemia
V1-vasoconstriction
v2- water reabsorption
v3- corticotropin
Uses: bleeding with Von Willebrand, refractory hypotension, cardiac shock following bypass, diuresis with diabetes insipidus
Concerns: GI ischemia, skin & digitalis ischemia, decreased CO
Sodium nitroprusside
spontaneous breakdown to NO & cyanide
relaxation of arterial and venous smooth muscle
will see slight increase in HR, increased CBF and ICP
Uses CHF, controlled hypotension, HTN crisis, acute MI (limited d/t coronary steal)
Adverse effects: profound hypotension, cyanide toxicity (tissue anoxia, confusion, death), methemoglobinemia (tissue hypoxemia), thiocyanate accumulation (CNS related effects)
drug interactions: negative inotropes, general anesthetics, circulatory depression, phosphodiesterase 5 type inhibitors, guanylate cyclase stimulators
Organic nitrates- nitroglycerin
require metabolism step to go through pathway
VENOUS capacitance vessels, dilates coronary arteries
will develop tolerance when you run out of metabolism factors
uses: angina, HTN, controlled hypotension during surgery, non STEMI, MI, HF
Adverse effects: HA, increased ICP, orthostatic hypotension, REFLEX TACHYCARDIA, methemoglobinemia
drug interactions: antihypertensive drugs, selective PDE-5 inhibitors, guanylate cyclase stimulating drugs
Milrinone
inhibits breakdown of cAMP
inotropic, vasodilation
uses: HF, cardiogenic shock, heart transplant bridge or post op
adverse effects: arrhythmias, hypotension
ACE-I
blocks the conversion of ANG I to ANG II–> prevents vasoconstriction, aldosterone secretion, decreasing NA & water retention
used for: CHF, HTN, Mitral regurg, post MI, diabetic neuropathy
useful for DM pts
NO REFLEX TACHY
“prils”
drug interaction: K+ sparing diuretic & K+ supplements
SEs: Hyperkalemia, hypotensive, contraindicated in bilateral renal artery stenosis, dry cough, angioedema, teratogenic
ARBs
sartans- competitive antagonist at AT1 receptor
blocks effects of Ang II mediated by At1R
clinical effects, uses, drug interactions, and contraindications are same as ACE-I
Aldosterone antagonist: spironolactone, eplerenone
competitive antagonist at mineralcorticoid receptor
effects: increased Na+, H20 excretion, mild diuresis, K+ reabsorption
uses: HTN, HF, K+ sparing diuresis, hyperaldosteronism, spironolactone has off label uses
AEs: hyperkalemia & broad with spironolactone
Minoxidil
directly relaxes the arteriolar smooth muscle (no effect on venous capacitance) & increases efflux of K+ from VSMC resulting in hyperpolarization and vasodilation
used for HTN
AEs: tachycardia, increased myocardial workload, palpitations, angina, fluid retention
warnings: fluid retention, pericardial effusion/tamponade, rapid BP response sinus tachy, elderly
Hydralazine
release of NO from endothelial cells, inhibition of Ca release
effects: vasodilates arterioles, minimal venous effect, decreased SVR, DBP reduced> SBP, increase HR, SV, CO
Clinical uses: HTN, HF
adverse effects: reflex tachy, tolerance, tachyphylaxis, sodium and water retention, angina, lupus, HA, sweating, palpitations
Contraindications: CAD, mitral valve, RH disease
