1. General Cardiovascular Flashcards
1
Q
Treatment of Essential HTN
A
- Diuretics
- ACE inhibitors
- Angiotensin II receptor blockers (ARBs)
- Ca channel blockers
2
Q
Treatment of HTN in CHF
A
- Diuretics (usually loop, sometimes K sparing)
- ACE inhibitors
- ARBs
- Beta blockers (OK in compensated CHF, use cautiously in uncompensated CHF, do NOT use in cardiogenic shock)
3
Q
Treatment of HTN in Diabetes Mellitus
A
- ACE inhibitors (also protective against diabetic nephropathy)
- ARBs
- Ca channel blockers
- Diuretics
- Beta blockers
- Alpha blockers
4
Q
Treatment of Malignant HTN
A
- Nitroprusside
- Fenoldopam
- Diazoxide
5
Q
Hydralazine - MOA
A
- Increase cGMP –> smooth muscle relaxation
- Vasodilate arterioles more than veins –> afterload reduction
6
Q
Hydralazine - Clinical Use
A
- Severe HTN, CHF
- First line for HTN in pregnancy with methyldopa
- Frequently coadministered with a b-blocker to prevent reflex tachycardia
7
Q
Hydralazine - Toxicities
A
- Compensatory tachycardia –> CI in angina / coronary artery disease
- Fluid retention, nausea, headache, angina
- Lupus-like syndrome
8
Q
Ca Channel Blockers - Available Drugs
A
Dihydropyridines:
- Nifedipine
- Amlodipine
Non-dihydropyridines:
- Verapamil
- Diltiazem
9
Q
Ca Channel Blockers - MOA
A
- Block voltage dependent L-type Ca channels or cardiac and smooth muscle thereby reducing muscle contractility.
- In heart reduce conduction velocity, increase effective refractory period, increase PR interval
- Vascular selectivity - Nifedipine > Diltiazem > Verapemil
- Heart selectivity - Verapemil > Diltiezam > Nifedipine
“Verapemil - Ventricle”
[Nifedipine, Amlodipine, Verapamil, Diltiazem]
10
Q
Ca Channel Blockers - Clinical Use
A
- HTN
- Angina (Nifedipine - effects similar to Nitrates) (Verapamil - effects similar to b-blockers, use in asthmatics)
- Arrhythmias, prevention of nodal ie SVT (not Nifedipine)
- Prinzmetal’s angina
- Raynaud’s
[Nifedipine, Amlodipine, Verapamil, Diltiazem]
11
Q
Ca Channel Blockers - Toxicities
A
- Cardiac depression, Sinus node depression
- AV block, CHF
- Peripheral edema
- Flushing
- Dizziness
- Constipation
[Nifedipine, Amlodipine, Verapamil, Diltiazem]
12
Q
Nitroprusside - MOA
A
- Short acting
- Increase cGMP via direct release of NO
13
Q
Nitroprusside - Clinical Use
A
Malignant HTN
14
Q
Nitroprusside - Toxicities
A
Can cause Cyanide toxicity - releases CN
15
Q
Fenoldopam - MOA
A
- Dopamine D1 receptor agonist –> relaxes vascular smooth muscle
16
Q
Fenoldopam - Clinical Use
A
- Malignant HTN
17
Q
Diazoxide - MOA
A
- K channel opener –> hyperpolarizes and relaxes vascular smooth muscle
18
Q
Diazoxide - Clinical Use
A
- Malignant HTN
19
Q
Diazoxide - Toxicities
A
- Hyperglycemia - reduces insulin release
20
Q
Nitrates - Available Drugs
A
- Nitroglycerin
- Isosorbide dinitrate
21
Q
Nitrates - MOA
A
- Vasodilate by releasing nitric oxide in smooth muscle –> increase cGMP –> smooth muscle relaxation
- Dilate veins much more than arterioles –> preload reduction
[Nitroglycerin, Isosorbide dinitrate]
22
Q
Nitrates - Clinical Use
A
- Angina
- Pulmonary edema
- Also used as an aphrodisiac and erection enhancer
[Nitroglycerin, Isosorbide dinitrate]
23
Q
Nitrates - Toxicities
A
- Reflex tachycardia
- Hypotension
- Flushing
- Headache
- “Monday disease” in industrial exposure –> development of tolerance (tachyphylaxis) for vasodilating action during work week and loss of tolerance over the weekend resulting in tachycardia, dizziness and headache on reexposure on Monday
[Nitroglycerin, Isosorbide dinitrate]
24
Q
Anti-anginal Therapy
A
- Nitrates
- b-Blockers (ie Metoprolol, Atenolol, Cavedolol) (NOT Pindolol or Acebutelol - they are partial agonists)
- Ca channel blockers
- Nifedipine effects similar to Nitrates
- Verapamil effects similar to b-Blockers, can use in asthmatics
25
Nitrates in Anginal Therapy
Affect preload
- Decrease end-diastolic volume
- Decrease BP
- Reflex increase in contractility
- Reflex increase in HR
- Decrease in ejection time
- Decrease in Myocardial O2 consumption (MVO2)
26
b-Blockers in Anginal Therapy
Affect afterload
- Increase end-diastolic volume
- Decrease BP
- Decrease in contractility
- Decrease in HR
- Increase in ejection time
- Decrease in Myocardial O2 consumption (MVO2)
27
Nitrate + b-Blocker in Anginal Therapy
- Little effect on end-diastolic volume
- Decrease BP
- Little effect on contractility
- Decrease in HR
- Little effect on ejection time
- Large decrease in Myocardial O2 consumption (MVO2)
28
Cardiac Glycosides - Available Drugs
Digoxin
29
Digoxin - MOA
- Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca antiporter --> increases intracellular Ca --> Positive inotropy.
- Stimulates Vagus nerve
30
Digoxin - Clinical Use
- CHF (increases contractility)
| - Atrial fibrillation (decreased conduction at AV node and depression of SA node)
31
Digoxin - Toxicities
- Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh)
- ECG - Increased PR, decreased QT, scooping, T wave inversion, arrhythmia, hyperkalemia
Toxicities worsened by:
- Renal failure - decreased drug excretion
- Hypokalemia - Permissive for digoxin to bind at K binding site on Na/K ATPase
- Quinidine - Decreased Digoxin clearance, and displaces Digoxin from tissue binding sites.
32
Digoxin Overdose Antidote
- Slowly normalize K
- Lidocaine
- Cardiac pacer
- Anti-Digoxin Fab fragments
- Mg
33
Digoxin - Kinetics
- 75% bioavailability
- 20-40% protein bound
- Half life = 40h
- Urinary excretion
34
Nesiritide - MOA
- Recombinant B-type natriuretic peptide (BNP) --> Increase in cGMP and vasodilation --> Increase diuresis, decrease TPR.
35
Nesiritide - Clinical Use
- Acute decompensated heart failure
36
Nesiritide - Toxicities
- Hypotension
