Ischaemic Heart Disease Flashcards
1
Q
What are the areas supplied by the coronary arteries?
A
- LAD: anterior LV, anteror RV, anterior 2/3 septum
- circumflex: lateral LV
- Posterior descending: posterior and inferior LV, posterior 1/3 septum
2
Q
What factors affect myocardial O2 supply?
A
- O2 content of blood
- myocardial blood flow
- proportional to perfusion pressure (aortic diastolic pressure)
- inveresely proportional to vascular resistance
- subendocardial muscle is most susceptible to ischaemia bc it experiences the greatest pressure
- increased by vasodilation (PGI2, NO)
- influenced by local metabolites (adenosine, lactate, hydrogen ions), vasoconstrictors (endothelin), sympathetic innervation
3
Q
What factors affect myocardial O2 demand?
A
- ventricular wall stress
- increased myocardial pressure increases stress (hypertension, aortic stenosis)
- increased radius increases stress (dilation)
- decreased if wall thickens (LVH)
- heart rate
- contractility
4
Q
What are acute coronary syndromes?
A
- unstable angina
- sudden cardiac death
- myocardial infarction
5
Q
What are chronic coronary syndromes?
A
sometimes referred to as ischaemic heart disease
- stable angina
- chronic cardiac failure
- some arrhythmias
6
Q
stable angina
A
- pain from acute ischaema on exertion
- can be due to chronic vessel narrowing/fixed vessel narrowing, ~70%
- may be accompanied with minor degree of left ventricular failure causing pulmonary congestion and shortness of breath
7
Q
unstable angina
A
- ischaemic pain at rest, increased frequency and duration
- no infarction
- thrombus formation
- acute narrowing
- rupture
- coagulation cascade activation
- thromboxane A2 secretion by platelets (vasoconstriction)
8
Q
myocardial infarction
A
- acute plaque event with thrombus formation (99%)
- narrows or occludes the vessel
- acute ischaemia
- ATP depletion
- ROS generation
- +Ca2+
- causes myocyte death after 20-40mins
- full infarct is transmural, 6-8 hours after onset
- usually subendocardial, regional (area supplied by blocked vessel)
- circumferential if triple-vessel coronary narrowing w/severe ischaemia
- can also occur in shock if BP drops following haemorrhage, coronary perfusion drops
9
Q
What are the cardiac markers for MI?
A
- cardiac troponin (elevated: 3-4 hours, peak: 36 hours, normal: 10-14 days)
- myocardial creatine kinase (elevatied: 3-4 hours, peak: 24 hours, normal: 4 days)
10
Q
sudden cardiac death
A
- unexpected fatal event
- occurs within 1 hour of symptoms, or with no symptoms
- healthy w/o predictive severe desease
- most sudden deaths
- due usually to coronary disease (atherosclerosis)
- can be caused by large pulmonary embolism
- in 25% first indication of atherosclerosis or IHD
- if resuscitated, usually no infarct
11
Q
What is the pathophysiology of sudden cardiac death?
A
- automaticity of diseased ventricular myocardium
- wave propogation of ventricular impulses is impeded by diseased muscle
- may initiate intraventricular re-entry
- abnormalities of repolarization
12
Q
What are the possible mechanisms of sudden cardiac death?
A
- arrhythmic cardiac arrest
- VF due to acute ischaemia in LV myocytes, leading to dysfunction of Na/K pumps causing electrical instability
- asystole, v-tach
- myocardial scarring, myocarditis (viral), ischaemia in hypertrophied myocardium
- mechanical
- blood in pericardial sac causing tamponade w/pulseless elctrical activity (ECG shows QRS but there is no CO)
13
Q
What are the morphological changes over time post-MI?
A
- 12 hours: pale
- 1-2 days: creamy, whitish yellow, may be some haemorrhage and vasodilation from inflammation
- 6-8 weeks: more anr more scar tissue, thinned wall
14
Q
What are the histopathological changes over time post-MI?
A
- 1 day: dead fibres more eosinophilic, some neutrophils
- 2 days: more neutrophils, nuclei karyolyse/fade
- 1-2 weeks: granulation tissue
- months: fibrous scar w/few capillaries, not many cells, few fibroblasts
15
Q
What are the morphologic complications of MI?
A
- fatal arrhythmia
- v-fib, f-tach - no blood moving through
- w or w/o infarct
- cardiac failure within a few hours
- leads to pulmonary congestion and dyspnea
- thrombus formation in LV
- endothelial damage, local changes in flow
- can embolise, cause cerebral infarct
- pericardial inflammation
- vasodilation and fibrinous exudate (1-2 days)
- can cause chest pain
- muscle rupture of LV
- tamponade, sudden cardiac death
- papillary rupture, septal rupture
- mitral incompetence
- failure
- murmur
**ruptures likely occur at maximal weakeness before collagen is deposited (within 1-10 days)
- aneurysm w/thrombus of LV
- doesn’t rupture, impedes contraction causing failure
