• transient episodes of myocardial ischemia
• due to impbalances in myocardial oxygen supply and demand

stable

variant

unstable

• narrowing of epicardial coronary A.
• ischemia present upon exertion or stress
• occurs at predictable level of exercise, hence stable

• rupture of atherosclerotic plaque
• platelet adhension and aggreation leading to decreased coronary blodo flow
• must be treated expeditiously to prevent becoming MI

• arteriole-venous oxygen difference
  • under normal conditions, it cant put out much more as it is
• coronary blood flow

• contractile state (change in force at a given preload)
• HR
• wall tension (Laplace's law) 
  • LV pressure
  • LV volume

• whenever we increase tension, we increase oxygen demands

• CBF = (aorta diastolic P - LV pressure)/ coronary vascular resistance

1. increase NO
2. increase guanylate cyclase
3. increase cGMP
4. dephosphor. MLC
5. decrease contractile state smooth muscle

Mainly works on venules, and to a lesser extent arterioles.

• dilate venules leading to reduced preload and reduced pressure within ventricle during diastole
  • increase in pressure gradient btw aorta and endocardial surface of cardiac muscle cause increase blood flow, reducin ischemia and angina
• reduce preload with organic nitrates will decrease oxygen demands of cardiac muscle by decreasin tension
• no coronary steal
  • coronary steal is when there is a global vasodilation to the point where you dilate the ischemic and the non-ischmeic tissue (wasteful)
    • this could decrease driving P and reduce flow to eischemic areas
  • the nitroglycerine will only vasodil. large coronary arteries, permiting autoreg. to act and increase blood flow only to inadequately perfused areas

• intermittent treatments allow retainment of efficacy (continued/frequent exposure cause marked attention of response)
• interupt dosing for 8-12 hrs each day (usually at night to restore efficacy of drug)
  • some pateints could still develop angina during nitrate free periods and may need other anti anginal drugs

headaches

dizziness

weakness

• very low
  • high capacity heaptic organic nitrate reductase
  • sublingual route avoids first past effects
• half life after being absorbed: 2-8 minutes

1. influx Ca, releas from SR
2. Ca bind to calmodulin
3. increase MLCK
4. phosphory. MLC
5. constriction of vessels

Mainly act on arterioles, but also on venules.

verapaminl

diltiazem

nifedipine

• increase coronary vasodil.
• increase peripheral vasodil.
• decrease HR
• decrease contractility
• decrease rate of recovery of Ca channels
• slows AV conduction

• increase coronary vasodil. (VERY POTENT)
• increase peripheral vasodil (VERY POTENT)
• reflex tachycardia (vasodil. leads to increase symp. output and decrease parasymp. output via baroR reflex)
  • increase HR  
  • increase conractility
• no change in rate of recovery of Ca channels
• no change in AV conduction

• dihydropyridine Ca channel blocker
• high affinity for cerebral vessels
  • reduce vasospasm and mortality after subarachnoid hemorrhage

• phosphorylate I(f) channel, so increase influx of Na, Ca
• reduce threshold of depol.

• block symp. influence on SA nodal cells
• decrease PK, less phosphorylation of voltage gated Ca channels, less release from SR, decrease Ca

DECREASE HR, DECREASE CONTRACTILE STATE

• HTN
• prior MI

Usually, you have an overlap with these two conditions with stable angina

• beta blockade leading to decrease HR will cause increase preload
• nitrates will cause the venodilation, this will decrease the preload