Cardiac/Renal Pharm Flashcards
What class of drug targets phase - in fast-response fibers (the fast i sodium channels)
Class I anti-arrhythmic drugs
Which class of drug targets phase 3 of cardiac muscles (repolarization) - slowing the phase down
Class III antiarrhythmic drugs
The _____ negative the threshold potential, the slower the conduction velocity.
less negative
The _____ negative the resting potential, the faster the conduction
More
What class of drug blocks phase - in slow-response fibers (SA/AV node)
Class IV antiarrhytmic drugs
Recall: this phase is due to increased Ca, not increased Na like in the cardiac muscle fibers
What (2) classes of drugs can slow phase 4 in pacemaker fibers?
Class II and IV antiarrhthmic drugs.
Recall: phase 4 is the pacemaker current - inward Na and Ca and outward K currents
MOA of Class IA
target fast Na channels in the open/activated state - increasing action potential duration (ADP) and effective refractory period (ERP)
MOA of Class 1 antiarrhtmics
Na+ Channel blockers
Name 2 Class 1A antiarrythmics
Quinidine; Procainamide
What are 2 considerations needed with Quinidine [Class 1A]
M2 blockade (inc HR and AV conduction) - need to give Digoxin first in A-Fib. Hyperkalemia (antacids) enhance effects. Also displaces Digoxin
What are 3 side effects of Quinidine [Class 1A]
Cinchonism [GI, tinnitus, ocular dysfunction];
Increased QT interval;
Increased QRS duration
Name 2 side effects of Procainamide [Class 1A]
SLE;
Hematotoxicity [thrombocytopenia, agranulocytosis] - need regular CBCs
MOA for Class IB
Blocks fast Na channels in the inactivated state [keeps them refractory]; Decrease APD therefore Increase diastole and time for recovery
Name 3 Class IB drugs and there route of administration
Lidocaine (IV);
Mexiletine; Tocainide - PO
Name 3 uses for Lidocaine [IB]
Post MI; Open heart surgery; Digoxin toxicity
What side effects are associated with Lidocaine
CNS toxicity [seizures] although it is the LEAST cardiotoxic of all anti-arrhythmics
What are 2 oral formulations of Lidocaine?
Mexiletine, tocainide
What is Class IC MOA
Block fast Na channels especially His-Purkinje. NO effect on APD
Name 1 Class 1C drug and important info
Flecainide - proarrhythmogenic - increases sudden death post MI
What is Class II MOA
Beta-blockers: Decrease slope of phase 4 of pacemakers; Decrease SA/AV node activity
Name 3 drugs (+Class) from Class II anti-arrhythmics
Propranolol [non-cardioselective];
Acebutolol + Esmolol [Cardioselective]
Indications for Class II anti-arrythymics
Prophylaxis post MI; SVTs; [Esmolol IV for acute SVTs]
MOA for Class III antiarrhythmic drugs
K+ Channel blockers: Decrease K slowing phase 3 (repolarization); Increases APD and ERP
Name 2 Class III antiarrhythmic drugs w/indications
Amiodarone [ANY arrhythmia -Half life > 80 days!];
Sotalol [life-threatening ventricular arrhythmia]
Name 6 side effects of Amiodarone [Class III]
Pulmonary fibrosis; Blue Skin; Phototoxicity; Corneal deposits; Thyroid dysfunction; Hepatic necrosis;
What is special about Sotalol [Class III]
Also has B-blockade therefore decreases HR and decreases AV conduction
What antiarrhythmic classes risk torsades
IA and Class III
Class IV MOA
Ca++ Channel blocker [L-type]. Decrease phase 0 and 4; Decrease SA and AV nodal activity
Name 2 Class IV drugs
Verapamil and Diltiazem
Use of Class IV antiarrhythmics
Supraventricular tachycardia
Side effects of Class IV antiarrhythmic [5]
Constipation (Verapamil); Dizziness; Flushing; Hypotension; AV block (additive block with B-blockers, digoxin)
What drug interacts with Class IV antiarrhythmics
Digoxin is displaced by verapamil from tissue-binding sites
What receptor does Adenosine work on and what are its effects
Adenosine receptor = Gi –> Decrease SA and AV nodal activity
Adenosine use
DOC for paroxysymal SVTs and AV nodal arrhythmias. Given IV b/c half life <10seconds)
3 Adenosine SE
Flushing; Sedation; Dyspnea
Adenosine drug interactions
Is antagonized by theophylline (tx for COPD) and cafffene
Name 4 methods of altering sympathetic activity to treat HTN
- alpha 2 agonists;
- Interfere with storage vesicles;
- Alpha 1 blockers;
- Beta blockers
Name 2 alpha 2 agonists used to treat HTN
Clonidine; methyldopa
Clonidine Class; use; SE; drug interactions
Alpha 2 agonist. Tc mild-moderate HTN and opiate withdrawl;
Decreases TPR and HR;
SE: CNS depression, edema;
Drugs interactions: TCAs decrease antihypertensive effects
Methyldopa: class, use, MOA, SE, Drug interactions
Alpha 2 agonist;
Decrease TPR and HR;
Mild-Moderate HTN and HTN IN PREGNANCY;
SE: + COOMBS TEST, CNS depression, Edema;
Drug I: TCAs decrease antihypertensive effects
Name 2 drugs that interfere with storage vesicles that are used to treat HTN
Reserpine; Guanethidine
Reserpine: MOA; SE
Destroys vesicles thus decrease NE in periphery thus decrease CO and TPR. Also decreases NE, DA, 5-HT in CNS.
SE: Severe depression (suicide); Edema; inc GI secretions
Guanethidine: MOA, sE [2]; Drug interaction
Inhibit NE release;
SE: diarrhea, edema;
DI: TCA block reuptake into nerve endings
Describe how alpha 1 blockers tx HTN; 3 SE; and one advantage
Prazosin; doxazosin; terazosin;
MOA: Decrease arteriolar and venous resistance –> decreases preload. GET REFLEX TACHYCARDIA;
SE: 1st dose syncope, orthostatic hypotension, urinary incontinence;
Advantage: Lipids - increases HDL and lowers LDL
What 2 drugs work through NO and are direct-acting vasodilators [used for HTN]
Hydralazine, nitroprusside
What drug is used IV for HTN emergencies?
Nitroprusside
Hydralazine MOA, indications, SE [3]
MOA: decrease TPR via ARTERIOLAR DILATION
moderate-severe HTN
SE: SLE-like symptoms; edema; reflex tachy
Nitroprusside MOA; SE; Use
MOA: decrease TPR via BOTH arteriolar venule dilation;
DOC IV HTN emergency;
SE: Cyanide toxicity - must coadminister nitrites and thiosulfates
What 2 drugs can you use to tx HTN that open K+ channels
Minoxidil and Diazoxide
Minoxidil MOA, Indication; 3 SE
Direct acting to open K+ channels, hyperpolarization of SM -> ARTERIOLAR vasodilation;
Severe HTN; Baldness;
SE: Hypertichosis; edema; reflex tachycardia
Diazoxide MOA; indication; 3 SE
Direct acting to open K channels - hyperpolarization of SM - ARTERIOLAR vasodilation;
HTN emergencies;
SE: Hyperglycemia, edema, reflex tachycardia
Name 3 Ca_ channel blockers
Verapamil, Diltiazem; Dihydropyridines (nifedipine)
Verapamil and Diltiazem MOA, indications, SE
Decrease CO and TPR; [Ca+ Channel blocker]
HTN; Angina; Antiarrhythmic;
SE: Constipation
Nifedipine MOA; 2 indications, 2 SE
Ca channel blocker - decrease TPR;
HTN; Angina;
SE: Reflex tachy, Gingival hyperplasia
Captopril: MOA; Use (3); SE 4
ACEi: Block formation of Angiotensis II –> Dec Aldosterone; Vasodilate
Use: HTN; CHF; Protective of Diabetic neuropathy
SE: DRY COUGH, Hyperkalemia, Angioedema, Contraindicated in pregnancy
Losartan: MOA,Use 3; SE3
ARB: Block AT1 receptor (NO Bradykinin issues);
Use: Mild-moderate HTN, CHF, protective of diabetic neuropathy;
SE: Hyperkalemia, Angioedema, Contraindicated in pregnancy
Aliskiren: MOA; use 1; SE3
Renin inhibitor –> Blocks formation of Angiotensin 1 (no effect on bradykinin);
Use: HTN
SE: Hyperkalemia, Angioedema, contraindicated in pregnancy
What is the big issue with ACEi’s and ARBs?
Can cause acute renal failure in renal artery stenosis
Name 3 treatments of pulmonary HTN
Bosentan (ETA receptor antagonist); Epoprostenol (PGI2); Sildenafil (PDE inhibitor)
Bosentan: MOA, SE4, Special consideration
ETA receptor antagonist (endothelin = powerful vasoconstrictor);
SE: HA, flushing, hypotension, reflex tachycardia;
Contraindicated in pregnancy
Epoprostenol: MOA; Special consideration
Prostacyclin PGI2;
Contraindicated in pregnancy;
Sildenafil: MOA
Inhibits type V PGE –> increases cGMP –> Pulmonary artery relaxation
DOC (class) for chronic management of CHF
ARBs & ACEi
DOC (class) for acute CHF
Inotropes
Treatment for Wolff-Parkinson-White Syndrome
Class Ia or III
Inamrinone; Milrinone: MOA, use
Phosphodiesterase inhibitors –> increases cAMP. Is an inotrope for heart failure
Dobutamine MOA
Beta 1 receptor agonist (rapidly desensitizes) - used in Heart failure
Digoxin: Direct effect
inhibit cardiac Na/K ATPase –> inc intracellular Na –> dec Na/Ca exchange therefore intracellular Ca increases –> inc actin-myosin interation therefor increased contractile force
Digoxin: indirect effect
Inhibit neuronal Na/K ATPase:
increases vagal tone - dec HR - more filling = inc CO;
Increases sympathetic stimulation via Beta 1 +NE
Digoxin: dosing information
Long half life - need LD;
Renal clearance: caution with renal impairment;
Large Vd - displaced by verapamil, quinidine
Digoxin can be used for: 2
CHF; Supraventricular Tachy
Digoxin: SE6
anorexia, nausea, ECG change –> disorientation (drunk), ‘halos’, cardiac arrhythmia
Nitrates: MOA for angina
prodrug of NO - cGMP relaxes SM around veins - venodilation - lower preload, lower O2 requirements;
Dec infarct size and post-MI mortality
Name the 2 nitrates and route of administration
Nitroglycerin: sublingula, IV, transdurmal;
Isosorbide: oral for chronic use
SE of nitrates: 6
Flushing, HA, orthostatic hypotension, reflex tachycardia, fluid retnetion, Methemoglobinemia
Dosing issue with Nitrates
Tachyphylaxis - run out of GSH - tolerance
What drug can you not administer with Nitrates
Sildenafil –> cardiovascular toxicity
What calcium channel blocker is great for vasospastic angina
Nifedipine
What drug is contraindicated in vasospastic angina
Beta-blockers
Beta blockers + what drug is good for Angina of effort
Carvedilol
