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54 Cards in this Set

  • Front
  • Back
How many Anti-anginal drugs?
8
How do you remember the Anti-anginal drugs?
Nitro and ice
In Ne Va Da
Poke Rattlesnakes
What is Nitro and Ice?
The acute angina drugs
-Nitroglycerin
-Isosorbide dinitrate
What is In Ne Va Da?
The prophylactic drugs
-Isosorbide mononitrate
-Nifedipine
-Verapamil
-Diltiazem
What is Poke Rattlesnakes?
The chronic angina drugs
-Propanolol
-Ranolazine
What is Angina caused by?
Coronary ischemia/insufficiency due to an imbalance between myocardial O2 supply and demand
What do the drugs that treat angina mainly do?
-Reduce oxygen demand
(increasing oxygen supply is a minor mechanism)
What are the 3 direct determinants of myocardial oxygen demand?
1. Contractility
2. Heartrate
3. Wall tension (LaPlace)
What are the 3 determinants of Wall tension?
-LV pressure
-Ventricular volume
-Wall thickness
What happens to heart size during acute angina attacks?
The heart increases in size which increases wall tension and causes oxygen demand to go up
What do the Beta blockers tend to affect regarding oxygen demand?
Contractility and HR (not wall tension)
What else reduces contractility and heartrate?
Diltiazam and Verapamil (CCB's)
What are the 2 main determinants of Oxygen supply to the heart?
-AV oxygen difference (how much is extracted from hemoglobin)
-Myocardial distribution between Endo/Epicardial coronary vessels
Can much more oxygen be extracted from Hb in coronary circulation?
No
What are 3 ways you can increase oxygen supply to the heart?
1. Increase collateral bloodflow
2. Relieve coronary spasms
3. Reduce stenosis in stenotic vessels
What are the 2 main types of Angina?
1. Primary (Atypical)
2. Secondary (Typical)
What is Primary Atypical angina also called?
Prinzmetal's
What is Primary Prinzmetal's angina caused by?
Vasospasm of the large coronary artery
What are the symptoms of Prinzmetal's angina?
-Angina at rest
-Arrythmia
What are patients with Prinzmetal's angina at risk for?
Precipitation of acute MI
How is Prinzmetal's angina treated acutely and chronically?
Acutely - nitroglycerin
Chronic - CCB
What don't you want to give patients with Prinzmetal's? Why?
Beta blockers - because if you block the B2 receptors, you're blocking vasodilation and making the situation worse.
What is Secondary/Typical Angina caused by?
Oxygen demand in excess of the supply.
What are 2 conditions in which Oxygen demand of the heart will be in excess of the supply?
1. Large vessel stenosis or occlusion (ie CAD)
2. Subendocardial ischemia (diastolic crunch)
When is subendocardial bloodflow maximum?
During diastole
What is the main way to reduce diastolic crunch?
Slow heartrate w/ B-blockers to prolong diastole
What drugs will help situations in which plaques are partially occluding coronary vessels?
Calcium channel blockers - by vasodilating the vessel, the angina will be reduced.
If the plaque is concentric and covering the whole wall, will CCB's still be effective?
No
What happens to cardiac vessels over time as vessels are occluded?
Angiogenesis occurs resulting in development of collateral vessels.
What is Stable angina?
When pain is only felt with exercise.
What is unstable angina?
Angina at rest.
When is Prinzmetal's angina typically felt?
In the morning
What happens to coronary perfusion when a coronary artery undergoes spasm in Prinzmetal's angina?
The whole wall becomes ischemic - transmural ischemia
And what are the 3 adverse effects of transmural ischemia in Prinzmetal's?
-Anginal pain at rest
-Arrythmias
-Impaired mechanical function
What does the EKG show in patients with Prinzmetal's angina?
A huge rise in the ST segment.
And how is Prinzmetal's treated acutely? Chronicly?
-Nitrates acutely
-CCBs chronicly to prevent the vasospasm
What is used to diagnose Prinzmetal's angina?
Ergonovine - an inducer of coronary artery spasm.
What determines the bloodflow from Epicardial large coronary vessels, down into the smaller endocardial branches?
Pressure gradients
What is the normal pressure gradient between Epicardial and subendocardial coronary vessels?
80:5 - 75 mm Hg
What happens when an epicardial vessel is occluded?
After the occlusion, the pressure will be much lower - like 40 mm Hg; so now the gradient for subendocardial flow is only 35 mm Hg.
What happens as the tissue beyond the occlusion becomes ischemic?
Preload rises as cardiac function is falling, so that perfusion pressure is even worse, resulting in a classic Angina attack.
What will be the better treatment for classic angina?
An agent that reduces preload.
What change will be seen on the EKG in
-Prinzmetal's angina
-Classic Angina
Prinz: Elevated ST segment
Classic: Depressed ST segment
What is Stable angina predominantly due to?
A Fixed OBSTRUCTION - 95% obstruction, maybe 5% spasm
What is Prinzmetal's angina predominantly due to?
SPASM - 95%, and maybe 5% obstruction
What is the best acute treatment for vasospasm in Prinzmetal's?
Nitroglycerin
What is the best treatment for prophylactic prevention of spasm in Prinzmetal's?
Calcium antagonists - Diltiazem, Verapamil, Nifedipine, etc.
What 3 drugs are useful for treating classic stable angina?
-Nitrates
-B-blockers
-Calcium antagonists
What are 2 procedures to use if the spasm/occlusion in Classic angina doesn't respond to drugs?
-Dilation via PTCA (stent)
-Bypass operation
What is used to treat all unstable angina and acute attacks?
Nitrates - nitroglycerin
So to review; what are the 2 factors that are altered by the drugs that treat Angina?
1. Increase Oxygen supply to myocardium
2. Decrease Oxygen demand of Myocardium
How do the drugs increase O2 supply? (4 ways)
1. Increase subendocardial flow to the ischemic area
2. Increase collateral bflow
3. Decrease coronary spasm
4. Dilate eccentric stenosis
What are 3 ways that drugs decrease the O2 demand of the myocardium?
1. Decrease HR
2. Decrease Contractility
3. Decrease wall tension
And 2 ways the drugs decrease wall tension?
-Decrease afterload (systolic)
-Decrease preload (diastolic)