Cardio drugs Flashcards
(59 cards)
1
Q
Acetylcholine (Ach)
A
natural parasympathetic agonist
2
Q
Edrophonium
A
[parasympathetic agonist] - ACHEi (used to dx and tx SVT)
S/E = GI cramping
(not used anymore)
3
Q
Adenosine
A
[parasympathetic agonist] - incr Ach
antiarrhythmic - decr Ca current in slow response tissue (SAN, AVN)
4
Q
Scopolamine
A
[parasympathetic antagonist] at muscR - CNS effects
not used much in cardiology
5
Q
Atropine
A
[parasympathetic agonist] (muscR) –> counters vagal effect in heart and vessels:
- incr HR (blocks vagal action at SAN), decr AVN refractoriness/ERP, decr vagal-mediated vasodilation
- uses: heart block (disorders w/prolonged AVN ERP) or to prevent or stop a vagal rxn ex. in cath lab
6
Q
effect of SNS activation at… alpha 1 R
A
Skin, GI, kidney: vasoconstriction (of VSMCs)
7
Q
effect of SNS activation at… alpha 2 R
A
Skin, GI, kidney: vasoconstriction
+ platelet aggregation
8
Q
effect of SNS activation at… beta 1 R
A
Heart: incr HR (incr SAN and AVN chronotropy) incr inotropy (incr myocardial contractility)
Kidney:
incr renin production
9
Q
effect of SNS activation at… beta 2 R
A
Heart and skeletal muscle: vasodilation (decr SVR)
Airway smooth muscle cells: bronchodilation
10
Q
Epinephrine (Epi) - endogenous
A
[SNS agonist] at a1, B1, B2
- incr CO, BP (no change in SVR b/c of a1 + B1 mix)
Uses: resuscitation
11
Q
Norepi (NE) - endog
A
[SNS agonist] at a1, B1
- incr SVR –> vasoconstriction –> incr SAP/BP
- decr HR due to baroR reflex from incr SAP
(no change in CO)
Uses: distributive shock
12
Q
Dopamine (DA) - 3 doses
A
[SNS agonist] at alpha, B1
- low (renal) dose: D1 R action –> renal vasodilation (use = diuretic)
- intermed dose: B1 + D1 –> incr CO (no SVR change) –> incr BP (use = HF w/out HTN)
- high dose: a1 > D1 –> effect of NE (vasoconstriction of skin, GI, kidney –> incr SAP/BP) – S/E skin necrosis due to a1 vasoconstr., tachycardia
can get desensitization (tachyphylaxis) to DA
13
Q
Phenylephrine
A
[SNS agonist] at a1
- vasoconstriction of skin, GI, kidney –> incr SVR and MAP
- decr HR from vagal rxn to incr SVR –> decr CO (no B1 action to increase chrono- or ino-tropy to counteract this)
Use: pressor (incr SVR and MAP/BP)
14
Q
Isoproterenol
A
[SNS agonist] at B1 and B2
- incr HR and CO (B1 chronotropy and inotropy effect)
- decr SVR and MAP (B2)
Use: rare use to incr HR in shock emergency
15
Q
Dobutamine
A
[SNS agonist] at B1
- incr inotropy, modest incr HR
Use: mimic exercise to dx HR, or tx severe CHF
S/E: arrhythmias, ischemia/angina, hypotn, tachycardia, anxiety
- can densensitize, action inhibited by B blockers
16
Q
Phenoxybenzamine
A
- decr SVR –> decr BP
17
Q
Prazosin
A
- decr SVR –> decr BP
18
Q
Clonidine
A
19
Q
Propanalol
A
- decr inotropy and chronotropy (decr HR)
- decr renin secretion (decr BP)
S/E: bronchoconstriction, lethargy
NEVER use B blockers in acute MI!!
20
Q
Metoprolol
A
- decr inotropy and chronotropy (decr HR)
- decr renin secretion
- no bronchoconstriction
NEVER use B blockers in acute MI!!
21
Q
Atenolol
A
- decr inotropy and chronotropy (decr HR)
- decr renin secretion
- no bronchoconstriction
C/I: renal excretion - don’t use w/kidney failure
NEVER use B blockers in acute MI!!
22
Q
Carvedilol
A
- decr inotropy, decr HR & decr SVR by vasodilating skin, GI and kidney (blocking a1)
Uses: HTN, post-MI, stable angina, arrhythmia that is not complete heart block/hx of SVT
NEVER use B blockers in acute MI!!
23
Q
Cardiac glycosides
A
Digitalis/Digoxin = (1) [INOTROPE]: incr inotropy w/out incr HR, and (2) [ANTI-ARRHYTHMIC]
(1) Incr contractility –> incr LVEF –> incr CO
(MOA= inhibit Na/K pump (Na cant get out –> [Na] high –> Ca/Na-X can’t pump Na in/get Ca out –> incr Ca in cell)
*Use: palliative for sx-atic HF
(2) Incr vagal tone/parasymp agonist at MuscR => AVN delay & decr SNS activation –> baroR’s less desensitized –> better HR variability (+ thus BP control)
* Use: acute tx for Afib (due to Ach/vagal/parasympathetic-mimetic action => delays AVN conduction)
BUT: no mortality benefits
C/Is: toxicity (esp w/hypokalemia or hypoMg), bradycardia, AV block (due to slowing AVN and SAN conduction at toxic levels)
24
Q
Sympathetic (SNS) agonists as inotropes (5)
A
Epi, NE, Isoproterenol, DA, Dobutamine as [INOTROPES]
- all work to incr SNS activity (incr HR and inotropy)
- MOA: agonist SNS R’s –> incr cAMP/PKA/phospholamban –> incr SERCA activity –> incr Ca release from SR –> incr contractility and faster relaxation
- also incr HR via SAN/AVN incr chronotropy (incr Ca)
Uses: advanced HF (palliative)
25
Milrinone
[Phosphodiesterase 3 inhibitor] (PDE-3 i) = [INODILATOR]
MOA: blocks cAMP breakdown by PDE --> incr intracellular Ca from SR --> incr contractility
+ vasodilates smooth muscle
Use: advanced HF (palliative)
S/E: hypotension (Amrinone - thrombocytopenia)
C/I: renal excretion - decr dose w/renal failure
26
Procainaminde, Quinidine
[Class IA anti-arrhythmic: Na+ and K+ channel blocker]
- decr excitability in FAST response tissue (myocardium, His-Pur)
- incr APD/ERP in fast tissue (decr repolarizing K+ current)
Uses: A fib, torsade de pointes, ventricular tachycardia w/scar reentry, AVRT
27
Lidocaine
[Class IB anti-arrhythmic: Na+ channel blocker] (weakest)
- decr excitability in FAST tissue (less likely to depolarize ventricle due to decr Na current)
Uses: A fib, ventricular tachy w/scar reentry, AVRT
28
Flecainide
[Class IC anti-arrhythmic: Na+ channel blocker]
- decr excitability in FAST tissue (less likely to depolarize ventricle due to decr Na current)
Uses: A fib, ventricular tachycardia w/scar reentry, AVRT
29
Atenolol
[Class II anti-arrhythmic: Beta blocker]
MOA: decr Ca, K and I-f currents in SLOW tissue --> slow SAN phase 4 depolarization =>
(1) decrease HR (SAN rate)
(2) increase AVN ERP
(3) decr AVN excitability
Uses: sinus tachycardia, AVNRT, AVRT, A fib
30
Dofetilide
[Class III anti-arrhythmic: K+ channel blocker]
-incr APD/ERP in FAST tissue (myocardium and H-P)
Uses: AVRT, ventric tachy w/scar reentry, A fib, Torsade de pointes
31
Amiodarone
[Class III anti-arrhythmic: K+ and Ca channel blocker + alpha- and beta-antagonist]
- incr APD/ERP in FAST tissue (myocardium, H-P)
- mild decr HR
Uses: AVRT, ventric tachy w/scar, A fib, Torsade de Pointes
32
Sotalol
[Class III anti-arrhythmic: K+ channel and B blocker]
- incr ventricular (FAST tissue) ERP
- decr HR
Uses: AVRT, ventric tachy w/scar, A fib, Torsade de Pointes
33
Verapamil
[Class IV anti-arrhythmic: Non-dihydropyridine Ca channel blocker (NDHP CCB)]
- blocks cardiac Ca channels --> decr cardiac contractility (and thus myocardial O2 demand) and conduction
- decr SVR (and incr coronary blood flow)
Uses: HTN in pts w/SVT (primarily a HTN drug)
34
Diltiazem
[Class IV anti-arrhythmic: NDHP CCB]
less potent version of Verapamil: decr cardiac contractility, conduction, and decr SVR
- anti-arrhythmetic (for SVT) > decr SVR/BP to tx HTN
35
Adenosine
[Anti-arrhythmic]: causes transient heart block at AVN level
- decr Ca current, incr K+/Ach current
Uses: dx (ID rhythm) in SVT, and terminate AVRT, AVNRT (and sometimes atrial tachycardia)
36
Thiazide (hydrochlorothiazide), Furosemide
[Thiazide diuretic (HCTZ), Loop diuretic (Furosemide)]
Incr natriuresis: blocks Na/Cl transporter in nephron --> inhibits Na reabsorption (eventually RAAS increases to incr CO, but BP stays low due to NO vasodilation)
Toxicities: incr plasma glucose, TG, LDL; hypoK+
37
Verapamil, Diltiazem
[Non-dihydropyridine Ca channel antagonist (CCB)]
- Bind active/open Ca channels = higher affinity for heart
- decr cardiac contractility (decr myocard O2 demand) > decr SVR
- Verapamil used more for HTN > SVT
- Diltiazem used more for SVT > HTN (less potent)
38
Nifedipine, Amlodipine
[Dihydropyridine ("-ipine") CCB]
- Bind resting Ca channels = higher affinity for peripheral SMCs --> peripheral vasodilation --> decr SVR --> decr BP
S/E: worry about reflex tachycardia!! (from big decr SVR/BP)
- Nifedipine: flushing, palpitations, headache, dizziness
C/I: post-MI, CHF
Uses: HTN (use w/B-blocker to prevent reflex tachyc)
39
Nitrates
[Direct vasodailtor]
- Venodilator
HUGE decr in SVR/BP --> get a huge reflex tachycardia and RAAS activation: doesn't overcome strong drug, but give w/BB or ACEi or ARB to even out response
Use: HTN emergencies
40
Hydralazine
[Direct vasodilator]
- Arterial dilation
- toxicity: SLE-like syndrome (esp if >6mo on tx)
HUGE decr in SVR/BP --> get a huge reflex tachycardia and RAAS activation: doesn't overcome strong drug, but give w/BB or ACEi or ARB to even out response
Use: HTN emergencies
41
Sodium nitroprusside
[Direct vasodilator]
- Arterial and venodilator
MOA: metabolized by VSMCs into NO
- Toxicity: cyanide (always give w/thiosulfates to break down cyanide)
HUGE decr in SVR/BP --> get a huge reflex tachycardia and RAAS activation: doesn't overcome strong drug, but give w/BB or ACEi or ARB to even out response
Use: #1 choice for HTN emergencies
42
Sympatholytics:
4 categories (drug name-s)
- general MOA/effect
```
alpha blockers (Prazosin, Doxazosin, Terazosin)
- vasodilation => decr PVR
```
central alpha antag (Clonidine)
- total decr sympathetic outflow --> decr PVR/HR/CO/BP
combo a & B antag: Carvedilol
- decr PVR (a), decr HR (b), decr BP (from decr renin) (b)
```
B blockers (propanalol, metoprolol, atenolol)
- decr HR, decr BP (from decr renin)
```
43
Enalapril
[ACE-I] "-april"
Use: anti-HTN
MOA: blocks ACE conversion of Ang I --> Ang II (decr RAAS to decr BP)
- blocks AT1R to decr: vasoconstriction, inflammation, remodeling, thrombosis, oxidative stress
(also blocks AT2R to decrease beneficial things: vasodilation, NO release, tissue repair, decr inflamm)
- decr cleavage of bradykinin --> incr vasodilation
- may cause S/E: cough
- most serious S/E: angioedema (can occlude airway, cause asphyxia)
(ACE escape: over time other enzymes incr [Ang II], but BP remains low due to bradykinin effect)
44
Losartan
[Angiotensin Receptor Blocker (ARB)] "-artan" = ARB
Use: anti-HTN
MOA: Selectively blocks AT1, preserves beneficial AT2 action (NO release, vasodil, decr inflamm, tissue repair)
No bradykinin effect on BP & no S/E cough/angioedema
45
Aliskiren
[Direct renin inhibitor]
Use: anti-HTN
MOA: cuts off RAAS at rate limiting step (angiotensinogen --> Ang I via renin): decr plasma renin, Ang I and Ang II, decr BP
BUT no shown CV or renal benefit
46
Spironolactone
[Aldosterone antagonist] (mineralocorticoid R antagonist)
Use: anti-HTN
- decr aldosterone --> incr Na and H2O excretion --> decr fluid volume: decr BP and decr SV
47
Simvastatin, Atorvastatin (Statins!)
[Lipid lowering]
HMG-CoA Reductase Inhibitors (inhibits rate lim step of cholesterol synthesis)
- decr chol synth in liver = decr chol pool in liver --> upregulate LDL-R on hepatocytes --> incr chol uptake from plasma --> decr [plasma LDL]
Use: lower LDL-C (1st line)
S/E: myalgias, myopathy, rhabdomyolysis (incr in CK can cause renal failure in most severe cases)
48
Ezetimibe (Cholesterol Absorption Inhibitor)
[Cholesterol Absorption Inhibitor, CAI]
- binds and blocks NPC1L1 = regulator of chol uptake into enterocytes --> decr chol absorption from gut --> decr liver pool --> upreg LDL-R on hepatocytes --> incr chol uptake from plasma --> decr [plasma LDL]
Use: with statins to lower LDL-C
49
Colesevelam (anything starting with Col, Chol)
[Bile acid sequestrants (BAS), Resins]
- bind bile salts in gut, prevent their reabsorption and incr their excretion --> liver receives less (75% of chol comes form entero-hepatic recirculation), upregulates synth, taps into its own pool --> decr hepatic chol pool--> upreg LDL-R on hepatocytes --> incr chol uptake from plasma --> decr [plasma LDL]
Use: with statins to decr LDL-C
S/E: no toxocity (not systemically absorbed), but constipation, bloating, incr TGs
50
Fenofibrate
[Fibric acid derivative/Fibrate]
- PPAR-alpha agonist (in liver esp) -->
incr HDL production
decr VLDL prod + incr VLDL clearance
incr activity of LPL --> decr TGs
Use: decr TGs in pts with very high TG
S/E: myopathy if w/statin, incr liver transaminases
No proven decr in CVD risk
51
Omega 3 fatty acids (fish oils)
Adjunct to decr TG
no proven CV benefit
52
Nicotinic acid/Niacin/Vit B3
Increase HDL
MOA: decr FFA release and flux ot liver --> decr lipoprotein-a and incr HDL
No decr MI so rarely used
S/E: flushing
53
Heparin
[Anticoagulant]: direct coagulation cascade inhibitor
- Inhibits thrombin (factor IIa) and factor Xa (requires cofactor antithrombin/factor IIIA)
* blocks clot from getting worse but doesn't break it down
Use: NSTEMI, STEMI
54
LMWH
[Anticoagulant]: direct coagulation cascade inhibitor
- Inhibits factor Xa
* blocks clot from getting worse but doesn't break it down
Use: NSTEMI, STEMI
55
Bivalirudin
[Anticoagulant]: direct coagulation cascade inhibitor
- Direct thrombin (factor IIa) inhibitor
* blocks clot from getting worse but doesn't break it down
Use: NSTEMI, STEMI
56
Aspirin
[Antithrombotic]
- COX inhibitor in platelets, prevents platelet activation
Use: post-MI to prevent future thrombi; post-stent; upon presentation with MI to break up clot
57
Clopidogrel (Thienopyridine)
[Antithrombotic]
- blocks ADP pathway to prevent platelet activation
Use: post-MI to prevent future thrombi; post-stent; bolus upon presentation with MI to break up clot
58
Eptifibatide (Platelet IIb/IIIa inhibitor)
[Antithrombotic]
- inhibits the function of activated platelets
- binds to integrins expressed on activated platelets that make them sticky --> prevent platelet attachment to fibrinogen or cell surface Rs
Use: extreme thrombus risk
Risk: high bleeding risk (IIb/IIIa > clopidogrel > aspirin)
59
Fibrinolytics
[Thrombolytic/Fibrinolytic drugs]
Use in place of PCI if no cath lab is available to break up clots upon presentation with MI
