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+]
Explain how DHP differs from NON DHP?
- DHP [Amlodipine] will bind between the proteins on the out side of the Calcium Channel, blocking it
- NON DHP [Verapamil] will just bind directly into the channel, blocking it that way
What is the mechanism of action for Beta-Blockers?
They block the Beta receptors within the myocardium from getting stimulated by Noepi and Epi [adrenaline].
- Decreased Noepi/Epi will decrease the activation of Adenylyl Cyclase, resulting in a decreased cAMP, causing VASODILATION
- Epi will increase the HR and Contraction
What is the activity of Beta-Blockers?
Help reduce oxygen usage and depress the heart
- Main treatment in Stable Angina
Which Beta-Blockers are Cardioselective and which aren’t?
B1: Metoprolol, Atenolol, Bisoprolol, Nebivolol
[Heart Selective]
B2: Propranolol, Nadolol, Labetolol, Sotaolol,
[Lung Selective]
Mixed: Carvedilol, Labetolol
[B1, B2, A Selective]
What patients shouldn’t get a Beta-Blocker?
Patients that have Asthma, already have a LOW heart rate, Heart Failure [because of negative intropic activity]
What is reflex tachycardia?
- When the blood pressure is decreased, the heart will beat faster in an attempt the increase it.
- The vagus nerve and the carotid nerve both help with this within the arteries.
What are some medical ways that we can combat Reflex Tachycardia?
- If the blood pressure is to high, we can give a Nitrate to lower that; but HR will INCREASE [can give Beta-Blocker to help lower that heart rate]
- If CCBs increase preload too much, then we can use Nitrates to lower it
What is a Hyperpolarization-activated Cyclic Nucleotide [HCN]?
- Work within the SA node in the heart, causing th hyperpolarization of the cells by the influx of Na+
- cAMP will activate these channels
What is the action of Ivabradine?
- Will block the HCN block completely, not allowing Na+ to enter, stopping the Hyperpolarization [slowing heart rate]
What is the way that we treat Unstable Angina?
- Want to block the formation of Thrombus
- Aspirin, P2Y12, Heparin
What are the MHG-CoA Reductase Inhibitors?
“-Statins”
What is the mechanism of action for the Statins?
- They block the conversion of HMG-CoA into Mevalonate, which will decrease the formation of cholesterol, causing the decrease in plaque formation
What is the purpose of Aspirin in Unstable Angina?
- Its a COX-1 Platelet inhibitor; Blocks the TXA2 synthesis, stopping the recruitment and formation fo platelets
What is the mechanism of action for P2Y12 Inhibitors?
- They inhibit the P2Y12 ADP receptor, preventing platelet activation
What are the P2Y12 Inhibitors?
Clopidogrel, Ticagrelor, Cangrelor
What is the mechanism of action for the GP IIb/IIIa inhibitors?
- They inhibit the GP IIb/IIIa receptor, preventing the platelet aggregation
