Silverstein Ischemia stuff Flashcards
What does ischemia look like on an ECG?
T wave inversions that are >1mm and are symmetric
What does strain look like on an ECG?
asymmetric inverted T waves
HTN, BBB, etc
Which leads will show ST elevation in an inferior infarct? What vessel is likely infarcted?
II, III, aVF
RCA
Which leads will show ST elevation in an anteroseptal infarct? What vessel is likely infarcted?
V1-V4
LAD
Which leads will show ST elevation in an lateral infarct? What vessel is likely infarcted?
I, aVL, V5, V6
varies*
What is an important consideration in treating pts with right ventricular infarctions? What will this look like on an ECG?
these pts are preload dependent
giving nitro will cause their BP to drop
inferior MI with V1 ST elevation >V2 or with a depressed V2
What is a Q wave due to?
necrotic tissue will not produce electrical current (not viable)
Q wave reflects current from tissue opposite the infarct
what are the differences in a normal vs abnormal Q wave?
Normal Q wave:
- left to right depolarization of the septum
- small normal in I, aVL, V5, V6
Abnormal Q wave:
>1 box wide and 2 boxes deep
>25% of depth of QRS complex
-seen in V1-3
What will Pericarditis present with?
diffuse ST elevation
PR depression
TP segment is most isoelectric
What will early depolarization look like on an ECG?
Smiley face, concave shape from J point to apex with ST elevation <0.5 mm in limb leads
no reciprocal changes
Which walls of the heart are related to each precordial lead?
V1-2=septal
V3-4 =anterior
V5-6=lateral
NONE for posterior!!
What are the risk factors for CAD?
History of known CAD Age (Men 60+; Women 70+) HTN Hypercholesterolemia Tobacco Diabetes
How does hypertension increase risk of CAD?
Endothelial injury –> inc permeability to lipoproteins
increase in scavenger receptors on macrophages–> inc foam cells
increased production of proteoglycans which retain LDL
Angiotensin II stimulates NADPH oxidases–> increases oxidative stress + proinflammation
How does diabetes increase risk for CAD?
Glycation of lipoproteins–> increase cholesterol uptake by scavenger macrophages
Prothrombotic; antifibrinolytic
Reduced NO
Increased leukocyte adhesion
What are the 4 major characteristics of stable angina?
- quality: pressure, heaviness squeezing or burning (NOT sharp)
- -> Levine’s sign (arm over chest) - exacerbation by increase O2 demand (exercise or emotional stress and sometimes cold weather or large meals)
- relief with rest or sublingual nitroglycerin
- accompanying symptoms of SOB (due to increased LVEDP–> inc. pulm P), nausea (vagal stimulation), diaphoresis (sympathetic stimulation
How long does the pain from stable angina typically last?
2-10 minutes
Where is angina pain normally felt?
Retrosternal
Diffuse
(Patient points to location with 1 finger-> probably NOT angina)
Can radiate to shoulder, jaw, neck, arm
- Especially left
- Sometimes epigastric
What is the difference between stable and unstable angina (onset and duration)?
stable=triggered by exercise and only lasts about 2-10 minutes with rest
unstable=brought on by light exertion or at rest and lasts up to 20 minutes
How does exercise increase myocardial O2 demand?
increase HR and contractility
increase wall stress
What percentage of the vessel is narrowed in stable angina? Unstable?
stable=70-90%
unstable = > 90%
asymptomatic= <60%
What test should be ordered for suspected CAD?
If this is does not confirm your diagnosis, what should be ordered next? Why?
Exercise Tolerance Test (stress test) (only 65-70% sensitive)
> 1mm horizontal or downsloping ST depression –> angina
if inconclusive, order imaging (nuclear stress test and ECHO) –> more sensitive than stress test
If the pt cannot exercise, what medication should be given during stress tests? What do these medications do?
adenosine–> vasodilation
ECHO: Dobutamine (beta agonist) –> increase the O2 demand by inc. HR and contractility
What is the first line of treatment for chronic stable angina? What does this medication do?
beta-blocker
decrease contractility and HR and increase the time spent in diastole
also improve mortality in post-MI pts
When is revascularization the first line treatment for angina? (3 conditions)
(refractory symptoms or increased risk)
left main
3 vessel diseases with reduced ejection fraction
multi-vessel disease with diabetes
What additional pharm treatments should be given in chronic stable angina?
aspririn –> decrease likelihood of thrombus
high dose statin==> decrease lipid content and decrease inflammation
What are the characteristics of a “vulnerable” plaque?
larger lipid pool
thin fibrous cap
many inflammatory cells
often rupture with plaque formation leading to MI
What are the 4 classes of the grading of angina?
I: angina with strenuous/prolonged exercise
II: angina w/exercise
III: angina w/ everyday activity
IV: angina w/ any activity or rest
Pt that are _____ likelihood of CAD by history should undergo a stress test.
intermediate
What heart sounds are commonly heard during episodes of ischemia?
S4 (atrial contraction against a non-compliant ventricle)
S3 due to systolic dysfunction
Mitral regurgitation murmur
What EKG changes indicate a high likelihood of CAD?
STEMI or ST depression > 1mm
marked symmetric T wave inversions
dynamic EKG changes with pain
intermediate:
T-wave inversion > 1mm, ST depression .5-1 mm
What is Wellen’s sign?
deep symmetric T wave inversions in V 2-4
What is the main mechanism by which nitroglycerin helps ischemia?
A. Reduced preload
B. Reduced afterload
C. Coronary vasodilation
A. reduced preload (by increasing systemic venodilation)
What will help you determine between unstable angina and NSTEMI?
Troponin!!
unstable angina will NOT have + troponins
How do you distinguish between stable and unstable angina?
clinical presentation
How do you distinguish between a NSTEMI and a STEMI?
EKG findings
STEMI=ST elevation–> Q waves
NSTEMI=ST depression and/or T wave inversion
What lab results are necessary to rule out an NSTEMI?
2 negative serial troponins at least 6 hours apart
What is the early treatment for ACS?
Aspirin
Nitrates IF ongoing pain
Beta-blockers (latest guidelines oral preferred)
Platelet receptor inhibitors (clopidogrel/ticagrelor; prasugrel if intervention)
Anticoagulant (enoxaparin, fondaparinux, heparin; bivalirudin if intervention)
High dose statin (atorvastatin 80 based on PROVE-IT trial)
When is an aldosterone antagonist indicated in ACS?
if the ejection fraction is LOW
What is the TIMI Score used for?
What is it comprised of?
Used to determine angiogram (high risk) vs. stress test (low risk)
AMERICA pneumonic
Age >65
elevated bioMarker (troponin/CKMB)
ST segment deviations on Ekg
> or 3 Risk factors
2+ anginal episodes (Ischemia) in the last 24 hours
known Cad >50%
use of Aspirin in prior 7 days
When is early invasive strategy recommended?
TIMI 3+
elevated biomarkers
new ST depression
heart failure, new/worse MR, LVEF ≤ 40
Shock
VT
recurrent severe angina despite aggressive therapy*
Prior MI, stent or bypass surgery, heart failure
If none of above: can do stress test pre-discharge
What is the discharge treatment for unstable angina or an NSTEMI?
Dual Anti-platelet (aspirin + plavix) x 12mo
Statin
Beta-blocker
Lifestyle modification
ACE inhibitor
What type of coronary lesion causes ST elevation?
plaque with occlusive thrombus
What medication should immediately be given to any patient with chest pain?
Aspirin (unless the pt has an allergy)
What is the major treatment for STEMI? How can this be achieved (2)?
re-open the vessel
fibrinolysis (alteplase, reteplase, tenecteplast, streptokinase) or a stent placement
What are the complications of an RCA injury? (4)
Sinus bradycardia
Atrioventricular block
Right ventricular infarction
Posteromedial papillary muscle rupture
(RCA supplies the right ventricle)
What are the complications of an LAD injury?
Bundle branch blocks
Left ventricular free wall rupture
Ventricular septal rupture
Ventricular aneurysm
Stroke
What are the complications of BOTH an RCA and LAD injury?
V fibrillation
CHF/cardiogenic shock/pericarditis/dressler
