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Cardio Pharmacology Flashcards

memories those meds (61 cards)

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1
Q

What are the classes of Calcium channel blockers

A

Dihydropyridines (All the divines) and non-Dihydropyridines (Diltiazem and Verapimil)

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2
Q

Whats the mechanism of action of Ca channel blockers

A

Block voltage dependent L-type calcium channels of Cardiac (non-dihydropyridines) and Smooth muscles(Dihydropyridines).

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3
Q

Uses of Calcium Channel blockers by class

A

Dihydropyridines (except nimodipine): HTN, Angina, and Raynauds
Nicardipine and Clevidipine: HTN urgency and emergency
Non-Dihydro: HTN, Angina, A.fib/flutter. Verap in Migraine prophylaxis

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4
Q

Which Ca channel blocker is used in Pregnancy and postpartum

A

Nifidipine

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5
Q

Side effects of Ca channel blockers by class

A

Non-Dihydropyridines: Cardiac depression, AV block, Bradycardia, Hyperprolactinemia, constipation, gingival hyperplasia
Dihydropyridines: Oedema, flushing dizziness, reflex tachycardia

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6
Q

Which Ca channel blockers exacerbates MI

A

Nifidipine due to reflex tachycardia, avoid in Angina its

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7
Q

Uses of Nimodipine

A

used in Subarachnoid hemorrhage (prevents cerebral vasospasm)

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8
Q

Mechanism of action of Hydralazine

A

Increases cGMP which leads to smooth muscle relaxation, vasodilates arterioles more than veins
Causes afterload reduction

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9
Q

Uses of Hydralazine

A

Severe HTN (Acute), HF, safe in pregnancy

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10
Q

Side effects of Hydralazine

A

Excacerbates MI due to compensatory tachycardia, fluid retention, headache, SLE like syndrome

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11
Q

Fenoldepam Mechanism of action

A

Its a Dopamine D1 receptor agonist. causes coronary, peripheral, renal and splanchnic vasodilation.
Reduces BP and causes increased natriuresis

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12
Q

Uses of Fenoldepam

A

Post-op as an anti-HTN

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13
Q

Side effects of Fenoldepam

A

Hypotension and tachycardia

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14
Q

Nitroprusside mechanism of action

A

Increases cGMP via direct release of NO, can cause Cyanide toxicity

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15
Q

Uses of Nitroprusside

A

Hypertensive emergency

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16
Q

Nitrates Mechanism of action

A

Vasodilate by increasing NO in vascular smooth muscles, which leads to increase in cGMP and smooth muscle relaxation
Dilates Veins more than arteries
Reduce end-diastolic volume (PRELOAD), ejection time, MVO2
increases HR (reflex response)

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17
Q

Uses of Nitrates

A

ACS, Angina, and pulmonary oedema

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18
Q

Side effects of Nitrates

A 
REFLEX TACHYCARDIA (treat with B-blockers)
HYPOTENSION
FLUSHING
HEADACHE
MONDATY DISEASE
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19
Q

Contraindications of Nitrates

A

Right ventricular infarction & Hypertrophic CM

Absolute contraindication with Sildenafil

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20
Q

Why does oral Isosorbide Dinitrate requires higher doses than sublingual nitrate

A

absorbed via GI tract and undergoes extensive first pass metabolism in the liver prior to release in circulation, leading to low bioavailability

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21
Q

What are the determinants of MVO2 (Myocardial Oxygen consumption)?

A

End-diastolic volume
BP
HR
Contractility

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22
Q

Ranolazine mechanism of action

A

Reduces diastolic wall tension and oxygen consumption by inhibiting late phase of sodium current

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23
Q

Ranolazine Uses

A

Refractory Angina

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24
Q

Milrinone Mechanism of action

A

Selective PDE-3 inhibitor
In cardiomyocytes: Increas cAMP accumulation –> high Ca–> +ve Inotropy and chronotrop
In vascular smooth muscles: increase cAMP –> inhibition of MLCK activity–>general vasodilation

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25
Uses of milrinone
Acute decompensated HF (short-term)
26
Side effects of Milrinone
Hypotension, arrhythmias
27
Digoxin Mechanism of action
Cardiac glycoside, inhibits NA/K ATPase exchanger, and also indirect inhibitor of Na /Ca exchanger Leading to higher Ca--> Positive Inotropy Stimulates vagus nerve (parasympathetic ganglionic transmission) --> lower HR
28
Uses of Digoxin
A.fib/flutter (reduces conduction at AV node and depression of SA node) HF (increases contractility)
29
Side effects of Digoxin
- Cholinergic--Nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block - Hyperkalaemia
30
Factors that predispose to Digoxin Toxicity
- Renal failure (low excretion) - Hyokalemia - Drugs: Verapimil, Amiodarone, Quinidine)
31
Antidote for Digoxin Toxicity
Digi-Fab fragments, Cardiac pacer, MG, slowly normalize K levels
32
Negative Chronotropic Medications
1. B-blockers 2. Non-Dihydropyridine Ca-channel blockers 3. Digoxin 4. Amiodarone & Sotalol 5. Cholinergic Agonists (Pilocarpine, Rivastigmine)
33
Class I Anti-Arrhythmic Mechanism of action
Na- channel blockers: * Slow/block conduction (depolarized cells) * Lower slope of Phase 0 in myo. AP * State dependent (selectively depress tissue that is frequently depolarized, eg. tachycardia)
34
Class IA Anti-arrhythmic names
Quinidine, Procainamide, Dysopyramide
35
Class IA Anti-arrhythmic Mechanism of action
``` Prolongs AP duration Prolongs ERP Prolongs QT interval (similar to class III actions) ```
36
Class IA Anti-arrhythmic Uses
Atrial and Ventricular arrhythmias specially SVT & VT
37
Class IA Anti-arrhythmic Side effects
``` Torsades de pointes due to prolonged QT Cinchonism with Quinidine Reversible SLE-like syndrome with Procainaide HF with Disopyramide Thrombocytopenia ```
38
Class IB Anti-arrhythmic names
Lidocaine, Mexiletine (+Phenytoin)
39
Class IB Anti-arrhythmic Mechanism of action
Decreases AP duration (sp in ischemic or depolarized purkinje and ventricular tissue)
40
Class IB Uses
Arrhythmias (post-MI), Digoxin induced arrhythmia
41
Class IB side effects
CNS stimulation/depression, cvs depression
42
Class IC Anti-arrhythmic names
Flecainide, propafenone
43
Class IC Anti-arrhythmic mechanism of action
Prolongs ERP in AV node and accessory bypass tracts Minimal effect on AP duration Prolongs QRS in a rate dependent manner (tachycardia)
44
Class IC anti-arrhythmic Uses
SVTS, VT (last resort)
45
Class IC anti-arrhythmics side effects
Proarrhythmic specially post MI (CI) | CI with structural heart disease
46
Class II Anti-arrhthmics names
Beta-blockers: | Metoprolol, Carvidelol, Labetolol, Esmolol, Atenolol, Timolol, Propranolol
47
Class II Anti-Arrhythmics mechanism of action
Decrease SA and AV nodal activity by decreasing cAMP --> decreasing Ca currents. Suppress abnormal pacemakers by decreasing slope of PHASE 4 AV node is more sensitive--> increased PR interval
48
Class II Anti-arrhthmics Uses
SVT, rate control in fib/flutter
49
Class II Anti-Arrhythmias Side effects
Impotence, exacerbation of COPD and asthma, CVS effects are bradycardia and AV block and HF CNS effects: sedation and sleep alteration. may mask signs of hypoglycemia Metoprolol- dyslipidemia Propranolol-exacerbates vasospasm in Prinzmetal angina
50
Class III Anti-arrhythmics names
``` K-channel blockers: AIDS Amiodarone Ibutilide Dofetilide Sotalol ```
51
Class III Anti-arrhythmics Mechanism of action
``` Prolongs AP duration Prolongs ERP Prolongs QT interval (similar to class IA actions) works on phase 3 in myo AP ```
52
Class III Anti-arrhythmics Uses
Afib/flutter, VT (A & S)
53
Class III Anti-arrhythmics Side effects
Sotalol & Ibutilide: Torsades de pointes Amiodarone: Pulmonary fibrosis, hypo or hyperthyroidism, hepatotoxicity, corneal deposits, blue/grey skin and photo dermatitis, neurologic effects, constipation, cvs (bradycardia, heart block, HF)
54
Class IV Anti-arrhythmics names
non-dihydropyridines- Diltiazem & Verapimil
55
Class IV Anti-arrhythmics Mechanism of action
Decreases conduction velocity Prolongs ERP Prolongs PR interval PHASES 4 & 0 in PM
56
Class IV Anti-arrhythmics uses
prevention of SVT, rate control in afib
57
Class IV Anti-arrhythmics side effects
cardiac (HF, AV block, SA depression) | constipation, flushing , oedema
58
Adenosine mech of action
Increases K leaving the cell-->hyperolarizing the cell and reducing Ca influx--> AV node conduction
59
Adenosine Uses
SVT (diagnosis and treatment)
60
Adenosine Side effects
Chest pain, feeling of impending doom, flushing, hypotension, bronchospasm (contraindicated in asthma)
61
Ivabradine mech of action
Selective inhibition of funny Sodium channels (If) prolonging depolarization phase (PHASE 4)

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