L49-therapeutic Control Of Ischemia Flashcards
Agents that improve ischemic symptoms
Inc coronary flow Inc O2 supply Vasodilators: ▪️Organic nitrates ▪️Calcium channel blockers ▪️Potassium channel openers Dec cardiac work Dec O2 demand -ve inotropes ▪️beta blockers
What do organic nitrates act on
Venular
Types of organic nitrates
Rapid acting: nitroglycerine
Short acting: isosorbide mono and dinirate
Mechanism of nitrates
Act on GSH-transferase
Release on nirite ion in endothelial cell
Act as NO donner mimicking action of endogenous NO
Functions of nitrates
Vasodilation
Cytoprotection of endothelium
Side effects of nitrates
Tachycardia
Flush and headache
Syncope
How can there be an inc myocardial oxygen supply
Dilatation of collaterals which redistributes flow
Dilatation of large and resistant vessels which dec the BP and dec afterload
What are the dihydropamines and what are they selective to
Nifedipine and amlodipine
Act on VSMCs
What acts on cardiomyoctes
Verampril
What has an intermediate action on both cardiomyocytes and VSMCs
Diltaizem
Mechanism of Ca channel blockers
Bind to: L type and T type
In VSMCs they dec entry of extracellular Ca and cause vasorelaxation dec bp and afterload
In cardiomyocytes they dec entry of Ca and dec CICR from SR dec contraction and dec hr having a -ve dromotropic effect
Why should we never use short acting nifepidine
Sudden dec in bp and reflex tachycardia which causes myocardial hypo perfusion and can lead to death
Use instead long acting amlodipine
What do K channel openers do
Vasodilator action
Opening of Atp sensitive k channels causing hyper polarization and inhibits L type ca channel which dec VSMCs contraction in arteriolar
Used as second line therapy
What do beta blockers do
-ve inotropic and chronotropic
Dec CO and afterload
Dec RAAS which dec cardiac work and O2 demand
Leads to bradycardia
Which prolongs diastole and inc coronary filling as well as perfusion time which inc myocardial O2 supply
B1 selective drugs
Nebivolol
Atenolol
Bisoprolol
Metoprolol
What can nitrates be combined with
Non dihydroprine group or with beta blockers to limit decrease blood pressure and reflex tachycardia
What can calcium channel blockers be used with
Dihydropyridines since they don’t dec contractility and given if also HF
Non-dihydropyridines since they dont cause vasodilation but dec contractility so give for angina if HF is not severe and no bradycardia can be give if hypotension exist
What can beta blockers be used with
Nitrates since they abolish its induced reflex tachycardia
With dihydropydrine calcium channel blockers but not verampril nor diltiazem for fear of conduction defect
What is the mechanism of Pfox inhibitors
The shift cardio myocytes metabolism to the utilization of carbohydrates which lower the O2 demand rather than free fatty acids to spare O2 to the ischemic myocardium
They prevent beta oxidation via inhibiting enzyme responsible for transfer of free fatty acids across the mitochondrion membranes
Agents used to prevent develop of thrombos
Aspirin or clopidogrel
To hold progression of atherosclerosis
Statins
To limit cardiac demand and dysrhythmias
Beta blockers
To dump in the RASS damaging effects specially in presence of hypertension
Ace inhibitors
What is given before and during transfer in treatment of acute myocardial infarction
GTN and sublingual up to three doses at five minute intervals
Analgesic such as morphine for pain
Chewable aspirin plus loading dose clopidogrel
If needed CPR or 02 or Ivy fluids
What is given in the ER than ICU or CCU units
To relieve symptoms : IV GTN infusion plus analgesic IV
To open occluded vessel:
pry PCI
fibrinolytics 
The drugs given to improve survival
Early beta blockers
Early statins
Ace inhibitors
