Ischemia Flashcards
Describe the flow of blood within the heart?
- Deoxygenated blood come into the RIGHT ATRIUM via the superior and inferior vena cava.
- It then travels to the RIGHT VENTRICLE where it is pumps out into the lungs via the pulmonary arteries.
- Oxygenated blood is returned to the LEFT ATRIUM from the lungs from the pulmonary veins.
- It then travels to the LEFT VENTRICLE where it is pumps out to the body via the atora.
- Repeat
What are the Hemodynamic Parameters?
- Preload, Afterload, Heart Rate, Contractility
- ALL affect cardiac output
What do the Hemodynamic Parameters measure?
Oxygen supply and demand to the myocardium
What is the main cause of Myocardial Ischemia?
An imbalance between Supply and Demand
- Increased oxygen consumption [caused by increased HR, Contractility, Afterload, Preload] will INCREASE demand.
- Decreased Coronary Blood Flow [caused by vasospasm, fixed stenosis, thrombus] will DECREASE supply.
What is Preload?
The amount of blood that is entering the ventricles [how much the ventricles are streched] - End Diastolic Volume
Cause and effects on Preload?
Dilation of the Veins will DECREASE preload.
- Decrease in preload will DECREASE O2 consumption [the heart isn’t stretching as much]
- Decrease in preload will INCREASE perfusion [myocytes are receiving more O2]
What is Afterload?
The resistance that the ventricles must overcome to circulate the blood [to help shoot blood out into the body]
Cause and effect on Afterload?
Dilation of the Arteries will DECREASE aferload.
- Decrease in afterload will DECREASE O2 consumption [blood is able to leave the heart easier, lowering the myocyte work load, increasing perfusion]
What is myocardial prefusion?
It is the ability of the myocytes to receive oxygen, it also shows how well blood flows through the heart.
Explain the process of the formation of atherosclerotic plaques?
-Monocytes move into the cell where they become macrophages.
- The macrophages take up the LDL, becoming a fatty streak
- Eventually the plaque will rupture forming a thrombus
What are the types of Angina?
Variant Angina [Printzmetal’s], Stable Angina [Fixed stenosis], Unstable Angina [thrombus]
Describe what happens within Variant Angina [Printzmetal’s]?
Also known as Vasospasm Angina, the arteries will spasm eventually becoming stuck closed
- SUPPLY ischemia [because of DECREASED blood flow in]
-Occurs often at rest or night
Describe what happens within Stable Angina [Fixed Stenosis]?
An atherosclerotic plaque is formed in the arteries where they become partially blocked
- DEMAND ischemia [because the supply is DECREASED so the demand is much higher]
Describe what happens within Unstable Angina [Thrombus]?
The atherosclerotic plaque ruptures resulting in platelet aggregation and the formation of the Thrombus, blocking the arteries
- SUPPLY ischemia [because of the DECREASE in blood flow]
What is a STEMI?
STEMI: ST Elevated Myocardial Infarction
- COMPLETE Blockage on the vessel due to plaque rupture and thrombus formation
- The ST wave is elevated [major sign]
What is an NSTEMI?
NSTEMI: Non-ST Elevated Myocardial Infarction
- PARTIAL Blockage on the vessel due to plaque rupture and thrombus formation
- The ST wave is NOT elevated [major sign]
How to treat angina?
INCREASE oxygen delivery:
- Vasodilators or Antithrombics [increase the supply]
DECREASE oxygen demand:
- Vasodilators and Cardiac Depressants [decrease HR, Contractility, Pressure]
What is the mechanism of action for the formation of NO?
- L-Arginine is converted into L-Citruline where NO is released from the Endothelium into the vascular smooth muscle
- It then reacts with GUANYLATE CYCLASE where it formed cGMP, and cGMP dephosphorylates MLC causing RELAXATION.
What is the activity of the Organic Nitrates?
- Mainly cause the dilation of the Veins [decreasing PRELOAD]
- Can dilate the Coronary Arteries [decreasing AFERLOAD]
With medications are the Organic Nitrates?
Glyceryl Trinitrate, Isosorbide Mononitrate, Isosorbide Dinitrate
Describe the mechanism fo Nitrate Tolerance?
Caused by frequent or high doses of GTN
- They slowly inactivate ALDH2 in mitochondria [so GTN can’t be made into NO] resulting in no vasodilation
What are the classes of Calcium Channel Blockers?
Dihydropyridines [“-pines”], Benzthiazepines [Diltiazem], Phenylalkylamines [Verapamil]
- DHP = “-pines”
- NON DHP = Verapamil and Diltiazem
What is the mechanism of action for the CCBs?
They block the extracellular Ca2+ from entering into the cell
- Decreasing the formation of the Ca + Calmodulin complex = decreasing the constriction caused by MLCK [dilation of the arteries]
What is the activity of the CCBs?
Mainly the dilation of the arteries
- NO dilation of the Veins [Veins do not use extracellular Ca2+]
