W3 D2 - Acute Coronary Syndrome Flashcards
What are the 3 layers of the artery?
Tunica intima - inner
Tunica media - middle
Tunica externa/adventitia - outer
Explain the patho of ACS
Acute episode of chest pain unrelieved by nitroglycerin or reversal of usual precipitating factors
* starts with coronary artery disease and athersclerosis, narrowing of arteries…
* sudden plaque rupture resulting in thrombus formation, partial or total occlusion
* medical emergency
1. platelets aggregation post rupture; adhere to the area and activate
2. fibrin is deposited to stabilize the thrombus
3. results in decrease in coronary artery blood flow
4. there is an imbalance between myocardial O2 demand and supply
5. results in myocardial ischemia, injury, or necrosis
What is unstable angina and its treatments?
Unstable angina
* plaque instability, rupture, & thrombus formation
* unstable = incomplete/partial occlusion
* with or without cause
* rule out MI with cardiac enzymes
Goal of treatment
* prevent MI; platletet inhibitors, anticoagulants, antihypertension, cholesterol lowering agents
* manage myocardial O2 supply; nitrates, CCB
* and demand; analgesia, betablockers, ACE inhibitors
* interventions: stents, balloon pumps, coronary artery bypass graft
Explain NSTEMI
Partial occlusion of coronary artery
* partial wall damage = subendocardium
* decreased perfusion & O2 to a region of the heart; ischemia
* prolonged ischemia = cell death, patchy areas of necrosis
* cells that are deprived of O2 have altered cellular metabolism
Lab changes
* T wave inversion, ST depression
* elevated troponin
What is variant/prinzmetal angina?
Risk factors and treatments
Coronary artery spasm
* can occur with or without atherosclerotic lesions
Risk factors
* alcohol, tobacco, cocaine use
Treatment
* calcium channel blocker
* allows for vasodilation
What happens during a myocardial infarction?
A NSTEMI (partial) or STEMI (full occlusion) damages the myocardium which normally pumps blood out the aorta throughout the body.
* contractility decreases from irreversible cell death d/t lack of oxygen to myocardium
Explain STEMI
Complete occlusion of a coronary artery
* irreversible cell death extending from endocardium, myocardium, epicardium
* ^ full wall thickness
* tissue death starts within 30-45 mins from symptoms
Lab changes
* peaked T waves from ischemia
* ST elevation from injured cells not repolarizing
* Pathological Q wave from necrosis
* elevated troponin
Differentiate STEMI & NSTEMI
STEMI
* complete occlusion of coronary artery
* involves all 3 layers of the heart
* ST elevation (cellular injury), pathological Q waves
NSTEMI
* partial occlusion of coronary artery
* partial wall thickness affecting subendocardium
* ST depression, T wave inversion
What does a pathological Q wave represent?
Represents cardiac tissue necrosis
* wider (more than 0.4 sec) and deeper (greater than 1/4 of R wave)
* associated with STEMI
Where does plaque form in the heart prior to an MI?
Tunica intima = the inner layer of the coronary artery
Explain the different locations of MIs based on occlusion of certain coronary arteries
LV: anterior, septal & lateral wall, inferior, posterior, RV
Anterior MI (LV)
* bottom left
* LAD
* left bundle branch block
Septal wall
* middle heart
* LAD
Lateral wall (LV)
* circumflex
Inferior wall (LV)
* bottom
* RCA or circumflex
Posterior wall
* back
* RCA or circumflex
Right ventricle
* RCA
How is cardiac output in LV effected by MI?
Contractility
* decreases
* ischemia/necrosis of myocardium
Preload
* increases
* less blood forced out during systole, heart is congested with blood
Afterload
* increases
* compensating for low CO/BP
Heart rate
* increases
* compensating for low CO/BP
What are the criteria for diagnosing MI?
Any two of the following
1. history of ischemic type chest discomfort
* central, heavy, dull, pressure, left side, tight
2. rise and fall in cardiac enzymes
* troponin
* CK-MB
3. serial 12 lead ECG changes
* STEMI; ST elevation, left BBB, pathological Q wave
* NSTEMI; ST depression, T wave inversion
What diagnostic tests are used for MI?
aside from labs
- Chest x-ray
- Cardiac catherterization/coronary angiogram
- Echocardiography trans thoracic echo (TTE)
Compare interventions for STEMI vs NSTEMI
STEMI - goal is to prevent further myocardial death
Primary percutaneous coronary intervention (PCI)
* within 90 mins, require antiplatelet therapy
* anticoagulant could be used
Fibrinolytic
* if PCI therapy delayed by more than 120 mins
* initiate within 6 hours
* dissolves clot to improve O2 supply
* tPa, tRa
* watch for hypotension, stroke
Coronary artery bypass graft (CABG)
* ongoing or recurrent ischemia
* severe HF, cardiogenic shock
Intra aortic balloon pump
* for cardiogenic shock
* not tested right now
Targeted temperature management
* indicated for cardiac arrest patients with return of ROSC
* goal is to improve neurological outcome; decrease metabolic demands of the brain by cooling
* 32-36 degrees x24 hours
NSTEMI - prevent total occlusion, plaque thromboembolism, recurrent infarction or death.
* Initial treatment: antianginal, DAPT, & anticoagulant.
High risk for another MI
* DAPT, anticoagulant, nitrates, beta blocker, & PCI CABG less than 24 hours
Low risk
* DAPT, anticoagulant, nitrates, stress testing, PCI more than 24 hours
NO fibrinolytic - no benefit, fatal
Explain medications used for MIs
morphine, NTG, anticoagulants, antiplatelets, BBs, ACE inhib., statins
Morphine
* controls pain, decreases anxiety, restlessness, SNS response, O2 oxygen
* causes vasodilation = decrease preload, myocardial workload
* decreases GI motility and delays gastric emptying = nausea
Oxygen
* routine O2 not recommended unless sat less than 90%
Nitroglycerin NTG
* for chest pain by vasodilating arteries
Anticoagulants
* prevents clot from getting larger, does not dissolve
Platelet inhibitors
* does not decrease size of clot, goal is to decrease platelet aggregation
* ASA - ordered stat, blocks thromboxane A
* P2Y12 receptor inhibitors - prevents formation of fibrin on top of platelet aggregation
* ex. ticagrelor
Beta blockers
* blocks beta 1 receptors to bring heart rate down which increases diastolic filling time & coronary artery perfusion…
* and decreases contractility, workload, and ischemia
* monitor for hypotension and bradycardia
Angiotensin converting enzymes ACE inhibitors
* angiotensin is a potent vasocontrictor = increased cardiac workload BAD
* inhibitor: cause vasodilation to decrease afterload
Statins
* lowers risk for CAD, HF, death, recurrent MI, stroke
* generally lowers LDLs & triglyceroids (ones that accumulate plaque)
Break down left ventricular function and ejection fraction
LVF grades
* 1 = > 60%
* 2 = 40-60%
* 3 = 20-40%
* 4 = < 20%
% of blood the ventricle is able to pump out with each contraction
What are some complications of MIs?
Arrhythmias
Left ventricular failure
* decreased CO
* need vasodilators
* fluid balance, BB, diuresis
Left ventricular aneurysm
* anterior MI only
* scar tissue may thin out the wall of the heart leading rupture & cardiac tamponade
* treatment: HF, treat arrhythmias, anticoagulants
Pericarditis
* inflammation of the pericardium in STEMI
* ST elevation
* manage pain and inflammaton ASA, tylenol, narcotic
