Acute Coronary Syndromes Flashcards
In 2010, how many Americans experienced a new MI?
785,000
In 2010, how many Americans had a recurrent MI
470,000
How many silent MIs occur each year
195,000
What is the avg age of a persons first MI
64.5 for men, 70.3 for women
Abnormal thickening and hardening of vessel walls
Arteriosclerosis
Arteriosclerosis caused by build-up of fat-like deposits in the inner lining of large and middle sized aa.
Atherosclerosis
What is the usual cause of an Acute Coronary Syndrome (ACS)
Rupture of an atherosclerotic plaque
Initial event leading to atherosclerosis
Endothelial injury
What is the initial response of the vessel wall to an expanding plaque
Blood vessels expand outwardly to maintain size of lumen
At what point does a vessel stop growing outwardly when a plaque is forming
Plaque fills about 40% of the inside of the vessel
What % stenosis is required to cause symptoms in coronary aa.
70%
Features of a stable plaque
Thick fibrous cap that contains a large amount of collagen and smooth muscle but contains a relatively small lipid pool.
Feature of unstable plaques
Thin fibrous cap, thick fatty core
Events likely to trigger a plaque rupture
Extreme physical activity Severe emotional trauma Sexual activity Exposure to illicit drugs Exposure to cold Acute infection
General area in BVs likely for plaque rupture to occur
Vessel bifurcations due to speed of blood flow and turbulence created at these areas
3 vulnerable sites for plaque rupture w/in the coronary aa
Proximal part of the LAD
Near origin of the marginal branch on the RCA
Near the origin of the 1st obtuse marginal branch on the circumflex coronary a.
GpIIB/IIIA receptors link platelets via what molecule
Fibrinogen
Fibrinolytics stimulate the conversion of what to what
Plasminogen to plasmin (plasmin then dissolves the clot)
Most common cause of MI
Acute plaque rupture
Partial blockage of a coronary a. may cause what
Silent MI, unstable angina, NSTEMI or even sudden death
Complete coronary a. block causes what
STEMI
If you have a complete blockage but no ischemia, what’s the deal?
Development of collateral circulation
Other, less common causes of MIs
Coronary spasms (eg. cocaine), abnormalities of vessels, hypercoag, trauma to coronary aa. (CAs), CA emboli (rare)
How does cocaine cause an MI
Increases demand (incr. HR and contractility)
Decrease supply (vasoconstriction)
Stimulating platelet activation
Accelerating atherosclerosis
What other spasmodic dxs is Prinzmetals angia associated with
Migraines and Raynaud
What does typical angina do to the ST segment
Depression
What does Prinzmetals angina due to the ST segment
Elevation
What can you use to treat prinzmetals angina
Sublingual nitroglycerin (NTG)
What should you order before initiating treatment in any pt w/ possible ACS
12 lead EKG
What causes the pain/discomfort in pts w/ angina
Lactic acid and CO2 buildup in ischemic tissues
What are some things that do NOT describe ischemic chest discomfort
Sharp, worsened by inspiration, affected by muscle movement, pain is positional
Although indicate something other than ischemic heart probs
Common precipitating events for stable angina
Emotions, exercise, cold weather
% of MIs preceded by longstanding angina
18%
How long does unstable angina last
> 20 minutes
Innermost half of the myocardium is called what
Subendocardial
Outermost half of the myocardium is called what
Subepicardial area
What area of the heart is most vulnerable to ischemia
Endocardial and subendocardial areas
Criteria for acute MI
Rise of biomarkers (prefer troponin) w/ at least 1 of the following
Symptoms of ischemia
ECG changes indicating ischemia (ST-segment change or new LBBB)
Pathological Qs on EKG
Imaging evidence of loss of viable myocardium or new regional wall motion abnormality
Criteria for prior MI
New pathologic Qs w/ or w/out symptoms
Imaging evidence of loss of viable myocardium that is thin and fails to contract
Pathologic findings of a healed or healing MI
Who delays longer when seeking medical help for ischemic type chest discomfort, men or women?
Women
SAMPLE history
Signs and symptoms Allergies Medications/past Medical hx Last oral intake Events leading to incidence
OPQRST (pain presentation)
Onset Provocation/Palliation/Position Quality Region/Radiation/Referral Severity Timing
What day of the week is an MI most likely to happen? What season?
Monday
Winter
If a pt has an MI before age 40, be suspicious of what?
Cocaine use
Most common symptom of infarction
Chest discomfort
Levine’s sign
Pt describes discomfort by placing a clenched fist against their sternum
Angina equivalents
Signs of myocardial ischemia other than discomfort Dsypnea Dizziness Dysrrhythmias Sweating Fatigue Generalized weakness Isolated arm or jaw pain Palpitations Syncope N/v
Why are diabetic pts more likely to present with atypical MI symptoms
Autonomic dysfunction
Most frequent symptom of MI reqardless of race
SOB
Goals of reperfusion therapy
Fibrinolytics w/in 30 minutes of arrival or PCI w/in 90 minutes
EKG changes associated w/ myocardial ISCHEMIA
ST-segment depression and T-wave inversion
EKG changes associated with myocardial INJURY
ST-segment elevation
EKG change in the hyperacute phase of MI
Tall T waves (often not seen because this phase has passed by the time pt receives help)
EKG change in early acute phase of MI
ST-segment elevation (occurs within first hour or few hours)
EKG change in late acute phase of MI
T-wave inversion
EKG change in fully evolved phase of MI
Pathologic Q
What is a pathologic Q
Q wave that is .04 seconds or more wide (i.e. one small box or more) or that is more than 1/3 the amplitude of the R wave
What EKG change generally remains in the healed phase of MI
Abnormal Q wave (indicates dead tissue)
Anterior wall MI
Indicative changes:V3, V4
Reciprocal changes:V7, V8, V9
Artery: Mid portion LAD
Anteroseptal MI
Indicative changes: V1-4
Reciprocal changes:V7, V8, V9
Artery: LAD proximal occlusion
Anterolateral MI
Indicative changes:I, aVL, V3-6
Reciprocal changes: II, III, aVF, V7-9
Artery: LAD
Inferior MI
Indicative changes: II, III, aVF
Reciprocal changes: I, aVL
Artery: RCA
Lateral MI
Indicative changes:I, aVL, V5, V6
Reciprocal changes: II, III, aVF
Septum MI
Indicative changes: V1, V2
Reciprocal changes: V7-9
Inferobasal (posterior) MI
Indicative changes: V7-9
Reciprocal changes:V1-3
Right ventricle MI
Indicative changes: V1R -V6R
Reciprocal changes: 1, aVL
When should you suspect a RVI
EKG suggest inferior infarct (II, III, aVF)
Clinical triad of RVI
Hypotension, JVD, clear lung sounds
NTG AEs
Headache, flushing, tachycardia, dizziness, orthostatic hypotension
Potent narcotic analgesic and anxiolytic
Morphine
Effects of morphine tx
Venodilation, decreased HR and systolic BP
This all reduces O2 demand
Preferred analgesic for pts w/ STEMI who experience persistent chest discomfort unresponsive to nitrates
Morphine
How do ACEIs help with fluid accumulation
Increase renal blood flow which helps get rid of sodium and fluid
MONA; what is it used for and what is it
Mnemonic for meds used in ACS
Morphine
O2
NTG
ASA
When should you give ASA and clopidogrel in pts experiencing ACS
As soon as possible
What should you do with a pt who presents w/ STEMI and is on NSAIDS (except for ASA)
Discontinue the NSAIDs
MOA for unfractionated heparin
Cofactor for activation of antithrombin, decreases thrombin, and decreases factor Xa
LMWH MOA
Act more via inhibition of Xa
Drug that directly inhibits Xa and is administered subQ
Fondaparinux
Direct thrombin inhibitor give IV
Bivalirudin
Contemporary percutaneous coronary intervention (PCI)
Gp IIb/IIIa inhibitors and a thienopyridine (clopidogrel)
What is Rescue PCI
PCI performed after unsuccessful reperfusion attempts w/ fibrinolytics
4 intervals of total ischemic time
- Onset of symptoms to arrival of EMS
- Arrival of EMS personnel to hospital arrival
- Hospital arrival to 12-lead EKG
- 12-lead EKG to drug/balloon
When are fibrinolytics indicated in ACS
Only for UA/NSTEMI who also have true posterior MI
Where are grafts used in CABG usually taken from
Internal mammary a., radial a. or saphenous vein
When does ventricular rupture usually occur after an MI
10-14 days
Most consistent finding for ventricular septal rupture
New loud systolic murmur heard best at LLSB, often accompanied by a palpable thrill
What kind of MI can lead to papillary muscle dysfunction
Inferior wall infarct
What often precedes cardiac tamponade in MI patients
Cardiac wall rupture
Cardiac wall ruptures are most likely to occur where?
Lateral wall of LV
Common mechanical sequelae of MIs
Ventricular aneurysm Ventricular septal rupture Papillary muscle dysfunction Cardiac wall rupture LV failure/cardiogenic shock RV failure (often due to LV failure)
Embolic complications of MIs
Stroke, DVT, PE
Inflammatory complications of MIs
Pericarditis
What can you use to treat pain due to pericarditis
ASA (other NSAIDs are contraindicated in the first 7-10 days)
