Coronary Heart Disease And Stress Echo

Front 1

draw all wall segments and be able to tell which coronary artery supplies each

Back 1

do it!

Front 2

ischemic heart disease

Back 2

narrowing of the coronoary artery so that blood supply is prevented from entering the myocardium=ishemia

Front 3

infarction

Back 3

when the narrowing the the coronary artery progresses to the point that the heart muscle is damaged

Front 4

Lt main coronary artery

Back 4

-arises from the superior aspect of the left coronary sinus of valsalva and divides into LAD and circumflex arteries

Front 5

RCA

Back 5

Right Coronary artery:
-arises from the superior aspect of the right coronary sinus of valsalva and extends inferomedially and gives rise to the posterior descending artery

Front 6

what are the echo views that are used to view wall segments?

Back 6

-PSLX
-Apical-4
-Apical-2
-PSSA(all wall segments seen in this view)

Front 7

What are the causes of ischemic heart disease?

Back 7

-atherosclerosis
-coronary artery spasm
-embolus

Front 8

name the sequence of events of ishemia to myocardial infarction?

Back 8

ischemia
diastolic dysfunction
systolic dysfunction
ECG changes
chest pain

Front 9

what are the types of myocardial ischemia?

Back 9

-acute
-chronic

Front 10

Explain acute ishema?

Back 10

-commonly caused by coronary thrombus at the site of atherosclerosis
-rapidly occluded vessel, and myocardial cells suffer hypoxic injury(MI)
-severity depends on the site of obstruction, size of infarction, and collateral circulation
-ishemia is reversible in myocardial O2 demand

Front 11

what does the severity of acute ishemia depend on?

Back 11

site of obstruction
size of infarction
collateral circulation

Front 12

what is hypoxic injury?

Back 12

lack of oxygen suffereed by myocardial cells during acute ishemia(aka MI)

Front 13

chronic ishemia

Back 13

-atheroscerosis and non-occlusive thrombi cause slow progressivenarrowing of arterial lumen
-allows myocardial cells to partially adapt to hypoxia
-allows anastamosis to develop btw ishcemic and normal vessels
-necrosis occurs, and myocardial cells are replaced by fibrous tissue decreasing compliance and contractility

Front 14

what are the qualifications in assessing wall motion?

Back 14

-endocardium must clearly be seen
-contrast agensts are used sometimes
-do not forshorten the apex!(go down an interspace)

Front 15

Myocardial infarction

Back 15

-irreversable injury to the myocardium due to prolonged ishemia
-myocardium initially becomes akinetic
-overtime(4-6 wks), myocardial segments show thinning.
-

Front 16

transumral infarction?

Back 16

>50% wall thickness
-results in definite area of akineses and wall thinning

Front 17

nontrasmural infarction

Back 17

<50% wall thickness
-results in lesser degree of wall thinning and
-hypoekineses rather than akineses

Front 18

stunned myocardium

Back 18

wall motion abnormalities persist for 24-72 hours even though irreversable damage has not occured

Front 19

hibernating myocardium

Back 19

prolonged persistence of wall motion abnormalities that can be reversed by reperfusion

Front 20

complications of myocardial infarction

Back 20

-mitral regurge
-VSD
-vetricular rupture w/ pseudoaneurysm
-pericardial effusion
-RV infarction
-LV aneurysm
-LV thrombus
(love prom)
(LLVVPRM)

Front 21

MItral regurge murmur

Back 21

-most common cause of MR murmur is papillary muscle dysfunction or papillary muscle rupture
-requires immediate surgery

Front 22

VSD

Back 22

-systolic murmur after MI
-due to necross and rupture of focal area of the septum

Front 23

Ventricular rupture

Back 23

-occurs in free wall instead of septum
-high mortality rate due to blood extraversion and acute temponade
-rupture can be contained(pseudoaneurysm)

Front 24

Pericardial effusion

Back 24

-seen as nonspecific respons to trasral infarction
-may be asymptomatic or associated w/ chest pain
-temponade can occur

Front 25

RV infarction

Back 25

-difficult to diagnose
-associated w/ inferior LV infarct
-RV hypokineses or akinesis
-RV dialation

Front 26

LV aneurysm

Back 26

-dyskinetic region w/ diastolic contour abnormality
-apical are most common
-true aneursym

Front 27

explain the difference btw true aneursyms and pseudoaneurysms?

Back 27

-pseudoaneurisms have anarrow neck(<50% of body diameter), whereas aneurysms have a wide neck
-pseudoaneurysm contain only the pericardium, not the myocardium
-flow can be seen going in and out w/ pseudoanursyms, but not w/ true aneurysms
-pseudoaneurysm has an abrupt edge, and true aneurysms have a tapered edge

Front 28

LV thrombus

Back 28

-area of increased echogenicity within the ventricle, distinct from endocardium
-usually in akinetic apex
-fresh thrombus is impossible to distinguish from blood
-may develop 72 hours post MI
-most emboli occur within the first 6 months

Front 29

what are the pitfalls in diagnosis thrombus?

Back 29

-Fibrous bands across apex
-ruptured pap muscle
-abnormally placed pap muscle
-near field artifact
-prominent LV trabeculation
(FRAN P)

Front 30

Myocardial scar

Back 30

-associated w/ thrombus(larger scar area>chance of thrombus)
-area w/ decreased motion
-thinner w/ increased echogenicity than adjacent walls

Front 31

when can acute pericarditis occur?

Back 31

in the first few days following an infarction; when the infact extends to the epicardial surface

Front 32

dressler's syndrome

Back 32

-delayed form of acute pericarditis
-occurs up to several months after the infarct
-(usually 6-12 wks after)

Front 33

kawasaki's disease

Back 33

congenital mucocutaneous lymph node syndrome
-virl in nature=coronary aneurysm

Front 34

end stage ischemic cardiac disease

Back 34

-repeated transmural and subendocardial infactions can result in a diffuse pattern of abnormal wall thickening and endocardial motion
-wen global systolic dysfunction is present, it is difficult to differential end stage ischemic disease ad systolic dysfunction due to long standing valvular disease or dialated cardiomyopathy

Front 35

what is the difference btw paradoxical septal motion, and dyskinesis?

Back 35

paradoxical septal motion still thickens in systole

Front 36

If you see an inferior wall defect, what should you consider?

Back 36

if there is RV infarction

Front 37

what do we see w/ RVVO?

Back 37

paradoxical septal motion

Front 38

HOw are myocardial infartions classified?

Back 38

-subendocardial(only inner layer of the myocardium)
-subepicardial(involving both inner and middle layers)
-trasural(extending through all layers of the myocardial wall)

Front 39

what is the most common coronary artery affected by coroanary artery disease?

Back 39

LAD

Front 40

what is seen(w/ regards to flow) w/ a VSD?

Back 40

-high flow in systole due to a change in pressure
-low flow in diastole

Front 41

what pap muscle is more likely to be affected by coronary artery disease? why?

Back 41

the posterior medial muscle because the anteriorlateral is supplied by 2 coronary artery, but the PM is only supplied by one.

Front 42

What are the 3 I's? what is seen w/ each of them on ECG?

Back 42

Ishemia-inverted t wave
Injury-elevated ST segment
Infarct-q below the baseline

Front 43

what is thromboembolic therapy?

Back 43

drug used to disolve a clot

Front 44

stress echo

Back 44

-noninvasive
-used to detect and asses known or suspected coronary artery disease that does not show on a normal echo at rest
-12 leads used
-assesses hearts function in response to stress
-areas of ishcemia develop wall motion abnormalities when the heart is under stress

Front 45

who is involved in stress echo

Back 45

-sonographer
-nurse
-cardiologist

Front 46

what are the indications for an exercise stress echo?

Back 46

-evaluate patients w/ known CAD
-evaluate patients w/ symptoms of CAD
-ambiguous stress EKG exam
-Evaluate LV systolic function
-identify viable, hybernating, or stunned myocardium
-evaluate hemodynamics in valvular/cardomyopathic heart diaseas(Ao stenosis, MR)

Front 47

What are the absolute contraindications for stress echo?

Back 47

-Acute MI(within 2 days)
-unstable angina
uncontrolled cardiac arrythimias
-severe Aortic stenosis
-aortic dissection
-pregnancy
-congental anomalies
-significant PE or tamponade

Front 48

what are some relative contraindications for stress echo?

Back 48

-lt main coronary artery stenosis
-moderate stenotic valvular heart disease
-electrolyte balence
-outflow tract obstructions
-mental/physical imparement leading to inability to exercise
(LE MOM)

Front 49

what does the 2D of a normal post exercise echo look like? what images are taken? why?

Back 49

-decreased LV size
-hyperdynamic wall motion
-increased EF
IMAGES TAKEN:
-PSLX
-PSSA(pap level)
-APICAL 4
-APICAL 2
So that all walls are demonstrated

Front 50

what does the 2D look like on an abnormal post exercise exam?

Back 50

-increased LV size
-myocardium has variable degrees of hypokinesis
-reduced EF

Front 51

why are some patients unable to exercise?

Back 51

-peripheral vascular disease
-musculoskeletal or neurological disorders
-pulmonary disease
-obesity

Front 52

what is an alternate method for stress echo? explain it?

Back 52

Doubutamine(most common drug used):
-augments myocardial contractility=increasing the work of the heart and myocardial oxygen requirements
-rapid onset of action within 2 minutes-peak at 10 minutes
-safe and well tolerated
-infused w/ infusion pump
-HR and BP monitored every 3 minutes

Front 53

what echo images are obtained w/ dobutamine?

Back 53

-rest
-each infusion level
-drug recovery

Front 54

what is another drug used for stress echo?

Back 54

atrophine

Front 55

what are some contraindications for dobutamine?

Back 55

-class 3 and 4 heart failure
-high grade AV block
-angina at rest

Front 56

what are the causes for false negatives in stress echo/dobutamine?

Back 56

-uncommon
-unable to reach max heart rate
-inadequate exercise-dobutamine
-rapid reperfusion as a reprofusion as a result of extensive collaterals

Front 57

what are false positives for strss echo?

Back 57

-uncommon, but more common than false negatives
-cardiomyopathy
-inadequate exercse in elderly
-early myocardial dysfunction
-LVH-LV fibrosis
-aging of the heart
-high BP
-severe hypertension

Front 58

what are the pitfalls and artifacts associated w/ stress echo?

Back 58

-reqires quick and precise sonographer
-Left bundle branch block causes abnormal septal wall motion(looks like a bounce)
-LVH
-atypical acoustic windowns-low parasternal window=anteroseptal hypokinesis
-apex seen best at apical view(don't forshorten)-false RV dialation
-gain settings need to be constant
-subconstal view best for RV size.

Front 59

angina

Back 59

Demand for oxygen increases, eg.exercise, the narrowed coronary vessels restrict blood flow.
Pain fibers in the heart are stimulated.
Pattern of crushing chest pain, radiating to left arm = angina pectoris

Front 60

thrombolytic therapy

Back 60

Drug that breaks up or dissolves blood clots which are the main cause of both heart attacks and stroke
Reperfusion therapy = thrombolytic therapy

Front 61

what are the strategies for CAD?

Back 61

Thrombolysis during angiography
Transluminal angioplasty
Severe obstruction requires coronary bypass surgery

Front 62

subacute cardiac rupture

Back 62

Slow leakage of blood into pericardium
Slow evolution of cardiac tamponade
Association with regional wall motion abnormalities

Front 63

what are the pathophysiologic events that occur w/ stress to the heart

Back 63

1. Myocardial perfusion becomes nonhomogenious, decreasing in myocardium- supplied by the obstructed vessel
2.Change in diastolic function
3.Slowed relaxation, increased stiffness, increased end-diastolic pressure
4.Contractile failure = segmental hypokinesis
5.Significant shifts of the ST segment ECG
6.Chest pain