Coronary Artery Disease Exam #4 Flashcards
Evaluating CAD in 2D can do a few things (3)
- determine location/extent of LV wall motion abnormatities
- estimate systolic/diastolic function
- assess lv function changes after infarct/rperfusion therapy
*identify complications
what is acute myocardial ischemia
it is a REVERSIBLE imbalance of oxygen (demand to supply) in myocardium
obstructed coronaries can usually compensate for demands at rest… when they exceed this percentage, certain demands cannot be met.
70% narrowing, can’t keep up with:
-exercise
-pharmacologic interventions
- mental stress
consequences of acute myocardial ischemia (7)
- artery obstruction
- diastolic dysfunction
- impaired relaxation / decreased compliance
- increased LVEDP
- Decreased left ventricular EF (reduction of endocardial motion, impaired systolic thickening)
*** contraction is OUT OF SYNC, “DESYNCHRONOUS” - possible lv dilation
- large infarctions
- increase in LVEDP
- CHF develops
How to describe wall motion abnormalities… (3)
- hypokinesis: increase in systolic wall thickening <40%
- Akinesis: systolic wall thickening <10%
- Dyskinesis: present when wall moves outward during ventricular systole and has wall thinning
MI is divided into 3 categories:
subendocardial - inner layer of myocardium only
subepicardial - inner and middle layers
transmural - extends through all 3 layers of myocardial walls
Acute myocardial ischemia - EKG FINDINGS:
T wave inversion suggests…. ischemia
Elevated ST segment represents….. acute MI
Prominent peaked T waves show…. acute MI
Pathologic Q waves show…. “old” MI
*may also see ventricular arrhythmias or other conduction defects
If MI is uncomplicated, a physical exam may be
NORMAL!
***symptoms usually occur last… chest pain, SOB, nausea, vomiting, asymptomatic
CK lab values after MI, describe time process
levels rise when muscle or heart cells are injured
levels begin to rise 4-6 hours after MI
highest levels are 18-24 hours after
will return to normal 2-3 days
can also be seen with skeletal muscle damage
More specific test needed if CK is high!
CK aka
TOTAL CK (creatine kinase) also known as CPK
Lab values of CK-MB aka
CK MB, CPK MB, creatine kinase - MB
- helps differentiate between heart damage/other muscle damage
- shows if clot dissolving drugs are working
- higher than 2.5-3.0 indicates heart muscle damage likelihood
- some skeletal muscle injury can be severe enough to raise CK-MB levels (broke a bone, etc)
Lab Values of Troponin, aka
AKA Tn1, TnT, Cardiac specific Troponin 1 and T
- usually ordered along with other cardiac markers
- starting to replace CK and CK-MB because it is more specific for heart injury
- elevated for longer period of time, 1-2 weeks after heart attack
- other muscle damage does not affect these levels
Sonographer needs this info for 2D Doppler Exam:
clinical history
prior cardiac events
cardiac murmurs
evidence of CHF
systolic BP
Pulmonary artery cath info in CCU (hemodynamic info)
12 leak EKG for presume infarct location
some important echo information (4):
lv and rv size and function
wall motion abnormalities
valve integrity/regurg
lv diastolic filling parameters
in transmural infarction, this 2D evidence is always seen
abnormal wall motion
wall motion abnormalities may or may not be seen where ischemia occurs in the subendocardial myocardium. true or false
TRUE
Complications of MI - Pericarditis, may or may not see effusion… true or false
TRUE
Complications of MI - What is Dressler’s syndrome?
Delayed form of pericarditis 1-12 weeks post MI
Recurrence common, tamponade is rare
symptoms
fever
pleuropericardial pain
malaise
pericarditis
pleuritis
Complications of MI - These hemodynamic signs resemble those of cardiac tamponade… but it isn’t cardiac tamponade. It is
RV infarction
Complications of MI - What is super common with any sort of Left heart infarction?
Mitral regurgitation
It is common of acute or recent MI
pap muscle rupture can cause MR (flail leaflet)
Complications of MI: LV aneurysm (5)
may form at infarction site
LV anterior wall and apex are the most common sites
Distortion of LV contour at end diastole/end systole
thrombus frequently forms
“hinge point” demarcates the INFARCT ZONE and aneurysm formation from normal myocardium
LV thrombus after MI (2)
Higher incidence with aneurysm formation
thrombus can spontaneously resolve, or resolve after anticoagulant therapy
Complications of MI: LV pseudo aneurysm (3)
- Myocardial rupture contained by parietal pericardium
- True aneurysm involves myocardium
- Usually seen post recent MI
LIKELIHOOD OF RUPTURE
(small communicating neck creates gradient, thrombus may extend into neck and increase size)
In what other cases can a LV pseudo aneurysm be seen? (4)
cardiac trauma
myocarditis
infective endocarditis
cardiac surgery
Differential diagnosis for LV pseudo aneurysm (3)
Located pericardial effusion
pericardial cyst
lv diverticulum
What is LV diverticulosis (3)
- rare CONGENITAL cardiac malformation which may be confused with aneurysm
- small circular echo free space arising from LV with all 3 layers in tact
- doppler may demonstrate low velocity, systolic-diastolic flow within the chamber
Complications of MI - VSD or ventricular septal rupture post MI
- new systolic murmur after acute MI (rupture or severe MR) signs of hypo perfusion to accompany
Complications of MI - LV free wall rupture predisposing factors (4)
- large MI (lateral or posterolateral)
- elderly patient
- post MI hypertension
- No prior CAD
Complications of MI - LV free wall rupture (4)
- seen within 48 hours of acute MI
- rupture site is between zone of necrotic and normal myocardial tissue
- cardiac tamponade can develop (causes hypotension and bradycardia)
- survival is RARE
