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41 Cards in this Set

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What is compromised blood supply or increased oxygen demand (supply-demand mismatch)?
ISCHEMIA
What is cell death due to ischemia?
INFARCTION
What is chronic ischemia +/- infarction?
ISCHEMIC HEART DISEASE
What is the main cause of Ischemic Heart Disease?
Coronary atherosclerosis

(anything that decreases oxygen delivery or increases oxygen demand)
What is the pathophysiology of Ischemic Heart Disease?
- supply demand mismatch
- myocardial ischemia in affected region
- myocardial infarction
- other complications
Coronary arteries
- RIGHT CORONARY ARTERY ( RV, Posterior LV / Septum {75%}, posterior papillary muscle, AV & SA nodes)

- LEFT ANTERIOR DESCENDING (anterior septum)

- LEFT CIRCUMFLEX (lateral LV, posterior LV / Septum {25%})
Pathophysiology of Acute MI
- acute change in coronary artery plaque

- thrombosis

- ischemic damage to myocardium

- myocyte necrosis

- other complications
PIC OF?
RUPTURE OF VULNERABLE PLAQUE
PIC OF?
RUPTURE AND THROMBOSIS OF VULNERABLE PLAQUE
PIC OF?
THROMBOSIS OF CORONARY ARTERY
PIC OF?
THROMBOSIS OF CORONARY ARTERY
PIC OF?
THROMBOSIS OF CORONARY ARTERY
Cells involved in MI
- neutrophils
- macrophages
- fibroblasts
Early changes in MI Histology (<24hrs)
- initially no visible histology

- coagulative necrosis ("Contraction Band Necrosis")

- Neutrophil response
PIC OF?
CONTRACTION BAND NECROSIS
Middle changes in MI Histology (1-3 days)
- neutrophils
- cellular debris
- macrophages
Later changes in MI Histology (3-7days)
- macrophages
- phagocytosis
- fibroblasts
When is the the greatest risk of myocardial rupture?
4-7 days

- weak tissue and blood can leak out into the pericardium
Healing changes in MI histology (>7days)
- fibroblasts
- neovascularization
- collagen / fibrin

* result is myocardial scar
PIC OF?
MI 1-3 DAYS

- Pale, soft myocardium
Coronary Atherosclerosis Timeline
- Nothing ~ 0 days

- Neutrophils ~ 1-3 days

- Macrophages ~ 3-7 days

- Fibroblasts ~ >7days

- Scar ~ weeks
Complications of MI
- arrhythmia
- myocardial rupture
- pericarditis
- mural thrombus
- ventricular aneurysm
- ventricular remodelling
Arrhythmias from MI
- MYOCARDIAL IRRITABILITY

- Heart Block (depending on location)

- Bradycardia, ventricular tachycardia, premature ventricular contractions
PIC OF?
VENTRICULAR FREE WALL RUPTURE

- Hemopericardium
PIC OF?
SEPTUM RUPTURE

- causes acute VSD with left to right shunt
PIC OF?
PAPILLARY MUSCLE RUPTURE

- leads to acute mitral valve insufficiency
What is Dressler's Syndrome?
FIBRINOUS PERICARDITIS

* after acute MI
~ 1-7 days later (acute inflammatory exudate)

~ 6-8 weeks later ("autoimmune")

- after bypass graft surgery
~ POST - PERICARDOTOMY SYNDROME
PIC OF?
MURAL THROMBUS

- Akinesis / hypokinesis of infarcted myocardium
~ blood pools on endocardial surface
~ thrombus forms

* Complication : embolization of thrombus leading to stroke or gangrene
PIC OF?
VENTRICULAR ANEURYSM

- infarcted myocardium is thinned and balloons outward with forceful contractions of adjacent myocardium

- thrombus can form in aneurysm
What is ventricular remodeling?
- infarcted myocardium dies (SCAR TISSUE)


- surrounding myocardium HYPERTROPHIES

* Result = zones of fibrosis with surrounding hypertrophy
~ myocardium can become thick and stiffened
What it the pathophysiology of sudden cardiac death?
- patient has severe coronary artery sclerosis

* NO OCCLUSIVE THROMBUS and / or NO MI

- death is due to arrhythimia and not infarction
~ typically V-Fib
Coronary artery bypass graph treatment
- Saphenous vein or synthetic vein used

- INTERNAL MAMMARY ARTERY (aka internal thoracic artery) grafted to LAD is best result
Percutaneous coronary intervention treatment
- aka percutaneous transluminal coronary angioplasty (PTCA) or angioplasty
STABLE ANGINA
- imbalance in coronary perfusion and oxygen demand

- exercise induced

- chronic atherosclerosis

* stable angina, stable plaque
UNSTABLE ANGINA
- myocardial ischemia
- thrombosis of coronary artery from plaque pathology
- "preinfarction angina"
- at rest or minimal exertion
What is Prinzmetal Angina?
- Episodic ischemia from coronary vasospasm

- occurs at rest
Reperfusion injury
- blood flow restored by PTCA, thrombolysis

- usually ~30mins to 3-4 hrs after ischemic event

- damaged myocardium is susceptible to hemorrhage, arrhythmia, further ischemia
Myocardial Stunning
- myocytes not lethally damaged can recover function in a few days with reperfusion
Myocardial Hibernating
- myocytes that have chronic sublethal ischemia may hibernate for days to weeks then recover function later
SERUM BIOMARKERS FOR MI
- TROPONIN T & I
~ sensitive and specific (bc not normally found in circulation)

- CK-MB
~sensitive but not as specific
~ MB can also be found in skeletal muscle

* best diagnosis is combo of both
SERUM BIOMARKERS TIMELINE
- MYOGLOBIN: out 1st, gone 1st; (-)sens/(-)spec

- CK-MB: out 2nd, gone 2nd; (+)sens/(-)spec

- TROPONINS: out last, gone last; (+)sens/(+)spec