CAD Flashcards
ischemic heart disease is a
consequence of atherosclerosis of the coronary arteries
major factors that predispose to coronary heart disease
- elevated blood cholesterol
- HTN
- Cigarette smoking
non-modifiable risk factors for CAD
- age
- sex
- genetics
what do we see in pathology in CAD
dimished coronary perfusion due to fixed atherosclerotic narrowing of epicardial arteries
pathogenesis in CAD (5)
- chronic coronary obstruction
- acute plaque change
- coronary thrombosis
- vasoconstriction
- inflammation
coronary obstructions usually occur
within the first 2 cm of the left anterior descending and the left circumflex arteries and the entire length of the right coronary artery
hallmark of CAD
coronary atherosclerotic plaque rupture or disruption
types of MI
- transmural
- subendocardial
- multifocal microinfarction
transmural infarction:
- extends from
- 3 arteries involvement
- extends from endocardium to the epicardium- LV
2. LAD, RCA or LXC
subendocardial infarction:
- affects the
- due to
- affects the inner one third to one half of the LV, usually circumferential, not necessary in the distribution of any one coronary artery
- due to hypoperfusion states
multifocal microinfarction
involves small intramural vessels in the setting of microemboli, vasculitis or vasospasm
MI in first 12-24 hr.
pallor, red blue hue (dark mottling)
wavy fibers
contraction band necrosis
deeply eosinophili
in an MI the first changes occur in the
subendocardial zone, more through the myocardium wall in the form of a wavefront
MI in 2-4 days
- mottling with yellow- tan infarct center
- PMNs
- interstitial hemorrhage and edema
- myocytes are clearly necrotic
M 5-10 days
- sahrply outlined border (hyperemic)
- central pale, yellowish necrotic region
- lymphocytes
- fibroblast proliferation with collagen deposition
risk for free wall rupture in MI is highest
5 days of onset
MI 10 days- 2 weeks
- depressed, soft, gelatinous area
- granulation tissue
risk for ventricular aneurysm formation in MI
2-8 weeks post MI
MI 2-8 weeks
- gray white scar
MI complications (6)
- contractile dysfunction-cardiogenic shock
- arrhythmias
- muocardial rupture
- aneurysms
- mural thrombosis and embolism
- pericarditis
occurs in 10-15% of patients after an acute MI, usually indicates a large infarct causing L ventricular failure, hypotension, pul. vascular congestion and transudation
contractile dysfunction cardiogenic shock
prognosis of MI
overall mortality is 30% for first year and survivors have a 3-4% with each passing year
MI therapy (3)
- thrombolytic enzymes
2, Percutaneous transluminal coronary angioplasty - coronary artery bypass grafting
reperfusion injury
new cellular damage to tissues that cells are already lethally injured
Chronic ischemic Heart disease:
- who is affected?
- what do we see
- elderly pt. with CHF, previous hx of angina and MI and post-infarct cardiac decompensation
- myocardial atrophy with inerstitial fibrosis
What are the two most common causes of death in the US?
Heart disease and cancer
What is the most common cause of heart disease?
Coronary artery disease
What is the pathological hallmark in acute coronary syndromes?
Coronary atherosclerotic plaque rupture or disruption
What type of infarction extends from the endocardium to the epicardium and conforms to the distribution of one of the three major coronary arteries?
A transmural infarction
A myocardial infarction that is 5-10 days old shows which gross macroscopic features?
A sharply outlined hyperemic border with central pale, yellowish, necrotic region
A myocardial infarction that is 2-4 days old will show which microscopic features?
PMN’s , necrotic myocytes, interstitial edema, and hemorrhage.
Which complication can occur two to eight weeks post infarction?
Ventricular wall aneurysm
Insufficient oxygen delivery relative to demand causes _______that can manifest as “angina”
myocardial ischemia
decreased oxygen delivery due to (4)
- decreased perfusion pressure
- increased coronary artery resistance to blood flow
- increased microvascular resistance to blood flow
- decreased blood oxygen
increased oxygen demand due to (4)
- tachycardia
- increased contractility
- increased LV wall stress
- ventricular hypertrophy
flow limiting disease
- stable occlusive atheroma/ acute thrombus
2. vasospasm
clinical manifestation of stable CAD
- chest pain
- SOB
- syncope
Stress Myocardial perfusion imaging
identifies flow-limiting or obstructive CAD
gold standard for dx. CAD
coronary angiography
NSTEMI
no st elevation but there might be depression
- troponin elevation
STEMI
- troponin elevation
- ST segment elevation
Typically LAD occlusion
ST Elevation:
I and aVL
V2-V5
Substantial amount of myocardium may be in jeopardy particularly for proximal LAD disease
May significantly reduce LV systolic function causing pump/heart failure
anterior stemi
Typically RCA occlusion but may alternatively be LCx
Associated GI symptoms common (e.g. burping)
ST Elevation: II, III, aVF
Nitroglycerin induced hypotension
Bradycardia from vagal influences
AV node block if AV node ischemic
Proximal RCA occlusion can cause RV infarction
inferior stemi
NSTEMI may be caused by a
demand ischemia as opposed to a new plaque rupture
Coronary artery thrombosis Can be STEMI or NSTEMI No obvious change in myocardial oxygen demand Typical symptoms of MI Elevated troponin
MI type I
Atherosclerotic blockage usually present but without coronary artery thrombosis
Transient increased myocardial oxygen demand
Tachycardia: sepsis
Elevated BP: stop meds
May not be associated with chest pain or typical symptoms
Elevated troponin
MI type II
Restoring blood flow in infarct related artery less than 6 hours from symptom onset provides survival advantage.
true
After 6-hours revascularization may improve survival while also reducing symptoms, heart failure and potentially arrhythmia.
true
acute MI interventions (3)
- PCI
- thrombolytic therapy
- surgical therapy such as a CABG
time is
muscle
which medications can lessen remodeling following infarction
ACEi and BB
Acute MI complications (4)
- Pump failure and shock
- ventricular arrhythmia
- mechanical complications
- VSD
Progressive CAD leading to another MI:
- Medical therapy for ASCVD: (2)
- Revascularization: (2)
Progressive CAD leading to another MI:
- Medical therapy for ASCVD: Statin, ASA
- Revascularization: PCI or CABG
Systolic Dysfunction leading to CHF:
- Medical therapy: (3
- Revascularization
Systolic Dysfunction leading to CHF:
- Medical therapy: ACEi, beta-blocker, Aldosterone receptor blocker
- Revascularization
Scar and Systolic Dysfunction leading to VT/VF: treatment
Defibrillator
major cause of cardiac death
ischemic heart disease
Pressure is lost owing to viscous friction along the entrance and throat of the narrowed section
Poiseuille’s law
The pressure gradient across a stenosis is determined by
the sum of viscous and separation losses
Resistance to blood flow is directly proportional to __________and inversely proportional to the _______ to the fourth power
Resistance to blood flow is directly proportional to length of stenotic segment and inversely proportional to the radius of the minimum diameter to the fourth power
Insufficient oxygen delivery relative to demand causes myocardial ischemia that can manifest as
“angina”
Provides assessment of the amount of myocardium at risk, which is proportional to outcome
myocardial perfusion imaging test
