W3 D2 - Acute Coronary Syndrome Flashcards

1
Q

What are the 3 layers of the artery?

A

Tunica intima - inner
Tunica media - middle
Tunica externa/adventitia - outer

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2
Q

Explain the patho of ACS

A

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

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3
Q

What is unstable angina and its treatments?

A

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

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4
Q

Explain NSTEMI

A

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

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5
Q

What is variant/prinzmetal angina?

Risk factors and treatments

A

Coronary artery spasm
* can occur with or without atherosclerotic lesions

Risk factors
* alcohol, tobacco, cocaine use

Treatment
* calcium channel blocker
* allows for vasodilation

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6
Q

What happens during a myocardial infarction?

A

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

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7
Q

Explain STEMI

A

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

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8
Q

Differentiate STEMI & NSTEMI

A

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

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9
Q

What does a pathological Q wave represent?

A

Represents cardiac tissue necrosis
* wider (more than 0.4 sec) and deeper (greater than 1/4 of R wave)
* associated with STEMI

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10
Q

Where does plaque form in the heart prior to an MI?

A

Tunica intima = the inner layer of the coronary artery

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11
Q

Explain the different locations of MIs based on occlusion of certain coronary arteries

LV: anterior, septal & lateral wall, inferior, posterior, RV

A

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

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12
Q

How is cardiac output in LV effected by MI?

A

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

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13
Q

What are the criteria for diagnosing MI?

A

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

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14
Q

What diagnostic tests are used for MI?

aside from labs

A
  1. Chest x-ray
  2. Cardiac catherterization/coronary angiogram
  3. Echocardiography trans thoracic echo (TTE)
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15
Q

Compare interventions for STEMI vs NSTEMI

A

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

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16
Q

Explain medications used for MIs

morphine, NTG, anticoagulants, antiplatelets, BBs, ACE inhib., statins

A

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)

17
Q

Break down left ventricular function and ejection fraction

A

LVF grades
* 1 = > 60%
* 2 = 40-60%
* 3 = 20-40%
* 4 = < 20%

% of blood the ventricle is able to pump out with each contraction

18
Q

What are some complications of MIs?

A

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