C14: Ischemic HD Flashcards
2 causes of ischemic HD/CAD
which is more common
atherosclerosis - more common
non-atherosclerotic causes
most common symptom of CAD
angina
what is acute coronary syndrome
2 types
when the patient is having a heart attack
- STEMI - ST elevation MI
- NSTEMI - non-ST elevation MI
non-atherosclerotic causes of CAD
emboli to the coronaries traume dissection of the AO arteritis/vasculitis radiation coronary spasm which cause angina cocaine/amphetamines
describe ischemia of the heart
decreased blood supply to the myocardium or increased demand for blood
most common causes of ischemia of the heart
coronary artery disease - plaque in the vessel that impedes blood flow
increased metabolic demand - hypertrophic cardiomyopathy or AS (more work or high afterload)
describe infarction
death or necrosis of tissue due to prolonged ischemia of total occlusion of blood flow…. everything downstream of the occlusion dies unless theres collateral circulation from another vessel
is ischemia and infarct reversible
only ischemia
when does cell death start and complete w/ infarction
starts to happen w/in 1 hour and is completed by 4 hours (death in transmural w/in 4 hours)
symptoms of ischemia
MI?
SOB, fatigue
angina
same, but add sweating, nausea and vomitting, anxiety
why does angina occur
how does it feel
reduction in 02 delivery to part of the myocardium due to CA stenosis or spasm
heaviness, during or aching pain in the chest +/- left arm
what can cause coronary artery spasms
stress, exercise, alcohol, smoking, cold, cocaine
which gender tends to have atypical symptoms of angina
what are those symptoms
women
pain in the jaw, neck, arm, back
2 main types of angina w/ CAD caused by atherosclerosis
describe them
stable
- occurs when a stenosis is > 70%
- predictable and regular chest pain
- relieved w/ rest or nitro and manageable w/ medication or angioplasty
unstable
- more intense, painful and not predictable
- maybe due to plaque rupture
- may require immediate bypass or PCI
- medication helps to minimally stabilize
“stable” refers to the stability of the patient
other less common types of angina
variant angina - due to coronary A spam
microvascular angina - “cardiac syndrome x” maybe due to microvascular dysfunction
common place for CA plaque
just distal to a bifurcation
describe the plaque that typically causes un-stable angina
a thrombus has formed through a torn plaque but doesnt completely occlude the vessel
common re-perfusion options w/ an MI
how is plaque diagnosed first?
PCI - percutaneous coronary intervention (angioplasty)
angiogram
if an angiogram is + for plaque, how is an angioplasty performed
- catheter inserted into the stenosed artery
- balloon inflated to displace the plaque
- steroid producing stent placed in the artery to hold the plaque back, plaque helps the stent stick (steroid allows the endothelium to grow back through the stent)
what is done before a CABG
what does the surgery include?
angiogram and echo done first
open heart surgery, heart and lung bypass machine…
when is a CABG performed
- when the blockage is unreachable percutaneously w/ a catheter
- there are too many blockages to stent (>3 or 4)
- vessel becomes unable or ruptures during PCI
- patient presents late w/ MI (b/c cell death will already be occurring)
which vessels are usually used in a CABG
GSV or internal mammary artery used… attach one end proximal and one end distal to the blockage
disadvantages of a CABG
- higher mortality and morbidity rates… more severe risks
- longer recovery time
- cant be done on frail patients
survival rate of patient drops by what % for every minute w/ no pulse… what do you do once pulse is back
10%… thrombolytics, PCI or emergency bypass
sequence of events in cardiac arrest
MI > arrhythmias (VT, VF) . asystole
…needs CPR and defibrillator
treatment for patients post MI or ischemia
modify risk factors
medication
what risk factors should be modified post MI or ischemia
stop smoking lower fat in diet, alcohol, sat exercise manage stress lose weight lower BP
what medication is used for chest pain relief
what effect do they have
nitrates/nitroglycerines
vasodilation which lowers systemic vascular resistance since the plaque covers less surface area, but can also affect veins and lead to congestion
how are nitroglycerines administered
pills, spray
medical treatment post MI or ischemia
anticoagulants - breaks the fibrin strands to avoid clotting
antiplatelets - makes platelets more slippers
beta blockers - improve survival by lower demand for 02
calcium channel blockers - lower muscle contraction
how can we diagnose IHD (ischemic HD)
- ECG: ST depression or elevation
- stress test
- echo
- MIBI (nuclear stress testing)
- cardiac CT or MRI to look for profusion defects
- coronary angiogram
gold standard for diagnosis of IHD
coronary angiogram
why does an acute MI required bloodwork
to look for enzymes released w/ myocardium injury and when the cells start to die:
creatine kinase myocardial band
troponin
when could creatine kinase myocardial band and troponin be increased w/ an MI
acute stress
acute MI management
MONA - morphine, oxygen, nitrates, ASA/aspirin
heparin or thrombolysis
re-perfusion
which differential diagnoses for MI need to be R/O
AO dissection
tension pneumothorax
pericardial disease
pleural effusion
which type of thrombolytic is the most effective MI clot busting medication
what does it do
TPA - tissue plasminogen activator
cuts (“lyse”) the long chains of plasminogen to prevent it from forming fibrin strands in blood clots (also used for DVT and PE)
types of TPAs
streptokinase
urokinase
describe an STEMI MI
- MI w/ ST elevation over the affected area on ECG… usually a transmural infarct from endocardium to epicardium
- often an anterior MI, look at anterior leads
describe an NSTEMI MI
- MI w/o ST elevation on ECG… can cause the ST segment to become depressed instead of elevated, usually a subendocardial infarct only
- the infarct causes a zone of ischemia w/ a small zone of cell death only
what causes the ST segment to become depressed w/ an STEMI
the area of cell death around the zone on ischemia which is irritated
the ST segment is isoelectric w/ which other segment
PR segment or TP segment (?)
in general, what does ST depression mean
ischemia
in general, what does ST elevation mean
infarction
how will the Q wave change w/ both a STEMI and NSTMI
STEMI - abnormal Q wave, will be larger
NSTEMI - normal Q wave
unstable angina an be confused w/ what cardiac events
STEMI and NSTEMI
general ECG changes seen w/ MI or ischemia
arrhythmias - originating in the ventricle due to irritated tissue
conduction defects like AV block and LBBB
peaked T waves (acute MI)
symmetric flat or reversed T waves (chronic ischemia)
what could a LBBB potential indicate
MI
describe 1st, 2nd and 3rd degree block
1: PR segment is prolonger
2: PR gets progressive longer until the QRS is dropped
3: P and QRS dissociation
how does the LAD run on the surface of the heart
what does it mainly supply
along the anterior IVS… supplied most of the anterior wall and septum
how does the circumflex run on the surface of the heart
gives rise to which artery 10% of the time (left dominant)
runs laterally along the AV sulcus towards the posterior of the heart
PDA
how does the LAD run on the surface of the heart
gives rise to which artery 90% of the time (right dominant)
which areas of the conduction system does it supply
runs laterally towards the back of the heart
PDA
supplied the SA and AV nodes
how do we asses the kinetics of the walls
can perfusion be adequate at rest
wall motion index or strain
yes
good tool to use if you cant tell if the walls are thickening or moving well
m-mode
does the absence of a resting wall motion abnormality excuse the possibility of ischemia
no
define hypokinesis
reduced wall thickening and motion - <40% but > 5%
normal is > 40% thickening
how do we score each of the 16 segments on motion
from 1-4
1: normal
2: hypokinetic
3: akinetic
4: dyskinetic or aneurysmal
how do you do a wall motion score index
take the sum of all wall motion scores and divide it by the # of segments visualized
…if segment not seen in at least 2 views then dont include it in the denominator
what does a higher wall motion score mean
higher = lower systolic function of the LV
what is a sigmoid septum
focal basal septal hypertrophy due to myocardial disarray… more common in diabetics and old patients
what can cause myocardial disarray
reduced perfusion to that segment
how does the movement of a a sigmoid septum often appear
hypokinetic
what can a sigmoid septum cause
subAO stenosis and LVOT acceleration, especially if the patient is hypovolemic
prognosis for sigmoid septum
correlated w/ increased risk for adverse cardiac events
another name for sigmoid septum
septal knuckle
post MI complications
secondary MR due to pap muscle dysfunction from ischemia thrombus formation aneurysms Dresslers syndrome acquired VSD from myocardial necrosis CHF systolic and diastolic dysfunction ventricular arrhythmia
is an isolated RV MI rare
what is it usually associated w/
yes
inferior MI - perfused by the RCA
is an RV MI associated w/ more pap muscle dysfunction than an LV MI
yes
IHD/CAD complications
pap muscle dysfunction
what does pap muscle dysfunction cause
improper contraction of the pap muscles and underlying wall segment leading to functional, eccentric MR
rupture of a pap muscle is more common in which type of MI
inferior
another name for ischemic MR
functional MR
were is a thrombus usually located post MI
types
apex - will look like an echo dense mass
protruding or mural/laminar
in how many views must you see a thrombus to diagnoses
at least 2
what type of frequency should you use to assess a clot at the apex
high frequency
describe a VSD or wall rupture post MI
what might you see, or hear w/ auscultation
- rupture of IVS, usually the inferior septum
- will hear a loud harsh systolic murmur @ L sternal border
- thrill
- high velocity flow across septum
- flow into pericardial w/ wall rupture
why do clots often form at the apex w/ a new MI
large ares of the heart no longer contracting…. and the lowest velocity flow is there.. risk drops w/ use of antithrombotics
clots are more common when the MI affects which area of the heart?
anterior - most common
inferior
at what time to clots form post MI
50% w/in the first 2 days
95% w/in 2 weeks
when would an emboli most likely embolize
1-3 months post MI (10% of thrombus embolize)
what increases the risks for embolization
protruding clot
larger size
mobile
adjacent to a hypermobile segment
how does a laminar thrombus appear at the apex
do laminar thromboses tend to be acute or chronic
flat, but apex gets thicker
chronic, press flattens it out over time
when should you be very suspicious of a laminar thrombus
if the anterior and septal walls are akinetic
how should you investigate a thrombus at the apex
zoom
use a higher frequency
use colour doppler and lower the scale… if not a clot colour will enter the suspected area, if it is, colour will stop where the clot begins
describe a protruding thrombus
is it likely acute or chronic
may be less echogenic than laminar thrombus and more mobile… protrudes into LV cavity
acute
can a clot be transitioning b/w protruding and laminar?
yes, it could have characteristics of both
4 applications of contrast
- detect shunts
- enhance doppler signals
- LV opacification
- myocardial perfusion to assess CA and defects
…helps to visualize the LV when visibility is porr
Rt heart applications for contrast
what type of contrast is used
look for shunts
agitated saline w/ bubbles > 5 microns that don’t pass through the lungs
what does it mean if the agitated saline bubbles are seen in the Lt heart
theres a possible shunt
Lt heart applications for contrast
what type of contrast is used
LV opacification and wall motion analysis
smaller size, 1-5 microns that pass through the heart
are true and false aneurysms a post Mi complication
yes
describe a pseudoaneurysm
abrupt wall rupture… has a narrow neck that connects to the pericardium sometimes
may be filled w/ thrombus
describe a true aneurysm
where is it usually located
all 3 layers are involved… has a wide neck and tapering appearance
may leak into pericardium
apex
how does a VSD or wall rupture happen post Mi
MI damages the wall and it becomes thin and necrotic… the wall weakens and ruptures creating a shunt, or leaking into pericardium
what is Dresslers syndrome
w/ what type of MI is it more common
post MI acute pericarditis due to an autoimmune rxn to the necrotic tissue…. often occurs w/ an anterior MI
3 main features of Dresslers syndrome
- fever
- pleuritic pain (lungs)
- pericardial effusion
- tamponade (rare)
appearance of pericardium w/ Dresslers syndrome
bright over an area of abnormal wall motion
