Module 13 : Ischemic Heart Disease Flashcards
what are the 2 main causes of ischemic heart disease
- atherosclerotic (most common)
- non atherosclerotic (least common)
what are the 2 atherosclerotic causes of ischemic heart disease
- angina pectoris
- acute coronary system
what are the 2 types of angina pectoris
- stable
- unstable
what are the 2 different acute coronary syndromes
- STEMI ( ST - elevation MI)
- NSTEMI (non ST elevation MI)
what are all the causes of non atherosclerotic ischemic heart disease
- emboli into coronary artery
- trauma
- dissection of aorta
- arteritis / vasculitis
- radiation therapy
- coronary spasm
- cocaine / amphetamines
what is ischemia
- decreased blood supply to the myocardium or increased demand of blood
what are the 2 most common causes of ischemia
- coronary arterial disease \+ plaque in the vessel which impedes blood flow - increased metabolic demand \+ hypertrophic cardiomyopathy \+ aortic stenosis
what is infarction
- death or necrosis of tissue which results from prolonged ischemia or total occlusion of blood flow to the tissue
what happens to everything downstream to the obstruction what will change that
- dies
- unless there is collateral circulation from another vessel
is ischemia non reversible
- reversible
is infarct reversible
- non reversible
when does cell death start
- within 1 hour and is complete by 4 hours
what are 2 symptoms of ischemia
- SOB/Fatigue
- angina pectoris
+ due to reduced O2 to a section of myocardium
+ heaviness burning or aching pain
+ women atypical symptoms
what are the symptoms of myocardial infarct
- SOB/Fatigue
- angina pectoris
- sweating
- nausea
- vomiting
- anxiety
what are the characteristics of stable angina
- predictable regular chest pain
- stable atheromatous plaque
- relieved with rest or nitroglycerine
- manageable with medication
what are the characteristics of unstable angina
- more intense or painful
- not predictable
- result of plaque rupture
- may require immediate by pass or PCI
- medications help minimally to stable
what are 2 other types of angina
- variant angina = prinsmetal angina
+ 1-6am not related to exercise - microvascular angina
+ possibly due to microvascular dysfunction
what is the atherosclerotic plaque
- plaque progress from fatty streak on intima to a fractured cap of a plaque to superficial erosion of the endocardial layer
- usually occurs just distal to an arterial branching
what is PCI
- percutaneous coronary intervention
steps of a PCI
- catheter inserted into stenosed artery
- balloon inflated to displace the plaque
- steroid eluding stent
- steroid allows endothelium to from back through it
what is a Coronary Artery Bypass Graft CABG
- open heart surgery
- pre surgical angiogram and echo must be performed
- patient must stop taking blood thinners first to prevent bleeding
what 2 things does a CABG
- dissecting the chest
- heart-lung bypass
what vessels are used and how are they attached in CABG
- greater saphenous vein or internal mammary artery harvested
- plug one end proximal and one end distal to blockage
when is a CABG performed
- blockage in unreachable percutaneously with catheter
- too many blockages to stent > 3 or 4
- when vessels become unstable or ruptures during PCI procedure
- presents late with MI
what are some cons to doing CABG
- higher mortality and morbidity
- longer recovery time
- more severe risks
- cannot be done on frail patients
how much does the survival rate drop by with every minute without a pulse
- 10%
what are the 2 treatments of ischemic heart disease
- risk factor modification
- chest pain relief
what are some of the things to modify risk factors
- smoking cessation
- lower lipid diet
- exercise
- stress management
- alcohol reduction
- weight reduction
- salt reduction
- BP reduction
how is chest pain relief accomplished
- nitrates = nitroglycerine
\+ causes vasodilation effects
- lowers arterial resistance and effect veins
\+ administration
- pills under tongue
- spray under the tongue
\+ aspirinwhat are the 3 medical treatments for ischemic heart disease
- anticoagulation
- beta blockers
- calcium channel blockers
how does anticoagulation treat ischemic heart disease
- for prevention of risk of thrombi = but increased risk of bleeding \+ anti platelet drugs = makes more slippery \+ anticoagulants = breaks the fibrinogen strands to prevent formation of clots
how do beta blockers treat ischemic heart disease
- lower HR, BP and afterload
- improve survival by lowering O2 demand
how do calcium channel blockers treat ischemic heart disease
- lower muscle contraction including tunica media of the coronaries
- increasing lumen diameter lowering afterload
what are the 5 tests to diagnose IHD
- ECG (ST depression or elevation)
- stress test (exercise or pharmacological)
- echo (wall motion abn)
- MIBI (nuclear) stress test
- cardiac CT or MRI - perfusion defects
- coronary angiogram
which test is the gold standard for diagnosing IHD
- coronary angiogram
what does the acute phase of MI require
- blood work with enzymes
+ CKMB
+ Troponin C
what is the treatment for MI
MONA M = morphine O = oxygen N = nitrates (not for low BP, inferior MI, or viagra) A = aspirin - plus heparin - thrombosis - reperfusion
what differential diagnose should we exclude
- aortic dissection
- tension pneumothorax
- pericardial disease
- pleural effusion
what is a thrombolytic
- cuts the long chains of plasminogen
- prevents plasminogen from forming fibrinogen strands found in blood clot
what is TPA
- tissue plasminogen activator
- most effective MI clot busting
+ streptokinase
+ urokinase
what are the 2 types of MI
- STEMI
- NSTEMI
what is a STEMI
- usually transmural infarct
+ through the whole thickness of the myocardium - ST segment ELEVATED over affected area
- seen in ANTERIOR MI LEADS
what is NSTEMI
- infarct that causes a zone of ischemia with small zone of cell death
- usually subendocardial MI only
- ST segment DEPRESSION
what does a normal ECG look like
- ST segment is at same level as TP segment = isoelectric
what does ST segment depression indicate
- ischemia
what does ST segment elevation indicate
- infarction
what happens to the Q wave in patients with ST segment elevation who get reperfusion therapy
- end up with necrosis shown by Q wave
what happens to the Q wave in patients with NSTEMI infarcts
- less necrosis
- non q wave MI
- ECG normal
what are the other ECG changes that occur with MI
- arrhythmias
- conduction defects
+ AV block, LBBB - Q waves - old MI
- peaked T waves - acute MI
- symmetric flat or reversed T waves= chronic ischemia
what are the three main coronary arteries
- LAD = anterior IV sulcus
- Circumflex CFX = runs laterally along AV sulcus toward the posterior aspect of heart
- RCA = heads rightward laterally toward the back of the heart
what is the role of echo in wall motion analysis
- assess walls kinesis from all veins
- assess wall thickening
- measure all chamber sizes, EF, Estimate diastolic function, RVSP
- assess regurge/stenosis
what two things must happen for wall motion to be considered normal
- wall motion normal
- wall thickening normal
what is a con of WMA (wall motion anomaly)
- absence of a RWMA does not exclude the possibility of ischemia
what factors may cause abnormal septal wall motion
- LBB
- WPW
- paced rhythms
what might abnormal wall motion be caused from
- subarachnoid hemorrhage
- cardiac sarcoidosis
- takosubo CMO
what are the 5 types fo wall motion
- hyperkinesis = enhanced wall motion
- normal = > 40% wall thickening
- hypokinesis = reduced wall thickening and motion < 40% > 5 %
- akinesis = no wall thickening or little
- dyskinesis = no wall thickening moving wall opposite way
how is wall motion scoring done
- each of the 16 segment is scored a number out of 4
- score 1 = normal wall motion (>40% )
- score 2 = hypokinetic (< 40% >5%)
- score 3 = akinetic (< 5%)
- score 4 = aneurysmal
what is the wall motion scoring index WMSI equation
- sum of all wall motion scores / number of segments visuaized
- if 2 or more segments are not seen they are not counted in the sum
what does a higher WMSI mean
- lower the systolic function
what is a sigmoid septum
- basal septal focal hypertrophy
- myocardial disarray related to reduced perfusion in that segment
- more prominent in diabetes and elderly patients
what is the prognosis of a signed septum
- correlates with inreased risk for adverse cardiac events
what are 7 post MI complications
- secondary MI
- thrombus formation
- aneurysm
- dresslers
- acquired VSD due to myocardial necrosis
- CHF, sys/diast
- ventricular arrhythmia
what is RV myocardial infarction RVMI associated with
- inferior MI
- inferior wall is perfused by the RCA
what is a complication of IHD/CAD
- papillary muscle dysfunction
+ ischemia of pap muscle segment
+ improper contraction of the segment and pap muscle
+ affects MV function leading to eccentric mitral regurgitation
+ rupture more common with inferior MI
+ may also occur in right heart and TV
what are 2 complications of echo in MI
- LV thrombus
- VSD or wall rupture
what is an LV thrombus
- echo dense mass - in apec
- protruding or mural
- requires 2 views
- high frequency probe zoom
- risk of embolization
what is a VSD or wall rupture
- rupture of inter ventricular septum
- loud harsh systolic murmur left sternal border
- thrill
- high velocity flow across septum
- flow into pericardium for wall rupture
How is thrombus formed
- stagnant blood will clot
- with a new MI larger areas of the heart will no longer contract especially at apex leading to low velocity stagnant flow
what kind of MIs have more common chance of thrombus
- anterior MI
when do 50% of thrombus form post MI
- within 48 hours
when do 95% of thrombus form post MI
- first 2 weeks
describe embolization of thrombi
- 10% of all thrombi
- 1-3. months post MI
what are 4 increased risks that thrombi will embolism
- protruding
- large size
- mobile
- adjacent to hypermobile segment
characteristics of laminar thrombus
- suspect when apex thickness> septal thickness
- adjacent to hypo/akinetic walls ( anterior/septal)
- indicates older thrombus
- use color doppler
characteristics fo protruding thrombus
- recently formed thrombus
- less echogenic
- more mobile
- higher risk of embolization
- protrudes into LV cavity
what is LV contrast enhancement and when is it used
- used to help visualize LV when poor
- micro bubbles opacify the LV cavity or myocardium
what are 4 applications of contrast enhancement
- detect intracardiac shunts
- enhance doppler signals
- LV opacification
- myocardial perfusion
what are the right heart application for micro bubble contrast
- agitated saline
- used to assess for intacardiac shunts
- larger > 5 microns
- do not pass through lungs
- if bubbles seen on left means shunt
what are the left heart applications of micro bubble contrast
- smaller size < 5 microns
- LV opacification
- wall motion analysis
- myocardial perfusion
characteristics of pseudoaneruysms
- narrow neck
- wall rupture
- filled with thrombi
characteristics of true aneurysms
- wide neck
- all 3 layers of wall
- may leak into pericardium
- usually at apex
processes of wall rupture as a result of MI
- MI damages wall
- wall thins and becomes necrotic
- wall weakens
- wall ruptures
- shunt occurs
what is dresslers syndrome
- acute pericarditis post infarct
- 24-96 hours after MI
- pericardium may look bright over abs wall motion area
- related to autoimmune response to necrosis
what are 3 main features of dresslers syndrome
- fever
- pleuritic pain
- pericardial effusion
- tamponade rare
