coronary circulation, angina and acute coronary syndrome Flashcards
circulation and their unique requirements
what do they adapt to?
what 4 things to look at when looking at them?
Circulations are able to adapt the particular needs of end organs/tissues
e.g. circulations to brain, heart, skin, kidney lungs, skeletal muscle
All have there unique characteristics
Special requirements
Special features
Structural, Functional
Special problems
coronary circulation - special requirments
what does it need a constant supply of? when does this increase?
Needs a high basal supply of O2 – 20x resting skeletal muscle
Increase O2 supply in proportion to
increased demand/cardiac work
coronary circulation - special structural features
two key features?
what effect do they have together?
High capillary density
Large surface area for O2 transfer
Together these reduce diffusion distance to myocyte
-> t relative X2 – so transport O2 is fast
coronary circulation - special function during normal activity
what happens a lot during normal activity?
what is decreased and why is a lot of released? what effect does this have?
net effect of this compared to rest of body?
During normal activity
High blood flow - 10x the flow per weight of rest of body
Sparse sympathetic-mediated vasoconstriction + high nitric oxide released -> together helps shift towards resting vasodilatation
High O2 extraction (75%) - average body is 25%
coronary circulation - special function during increased demand
what happens during increased demand? how is symathetic vasoconstriction reduced?
what other molecule acts on vessels? what receptors?
Coronary blood flow increases in proportion to demands
Production of molecules from muscle which are vasodilators e.g. adenosine, K+, acidosis (metabolites made from more work done in muscles)
‘out-compete’ sympathetic vasoconstriction during exercise hence MORE dilation and MORE blood flow
Circulating adrenaline dilates coronary vessels
due to abundance of B2-adrenoceptors
CO2 and oxygen unloading
what happens if more co2 produced?
how does this relate to o2 extraction in heart vs body?
If more CO2 produced it will displace oxygen from oxyhaemoglobin and extract more O2 from blood
therefore with more activity more CO2 is produced which will be displaced and more O2 extracted
hence heart has 75% extraction and body has 25%
why does more O2 demand produce more blood flow?
key reason?
what happens when more o2 is used? what effect does this have?
Extraction is near max during normal activity
Therefore to provide more O2 during demand, we must increase blood flow
Myocardium metabolism generates metabolites. As more o2 used, more metabolites is produced such as adenosine, co2, H+, K+ which feedback on coronary circulation to cause an increase in vasoldilation via metabolic hyperaemia which increase blood flow
coronary circulation - special problems
when does blood flow?
problem with ischemic heart disease?
what is the heart very susceptible to?
Systole obstructs coronary blood flow
Coronary blood flow only occurs during diastole
Ischemic Heart Disease
Coronary arteries are functional end-arteries and therefore a decrease in perfusion produces major problems
Heart is very susceptible to sudden and slow obstruction
slow and sudden obstruction of the heart
name sudden condtions
name slow condtions
Sudden: acute thrombosis, Acute Coronary Syndrome (ACS) including myocardial infarction
Slow: atheroma (sub-endothelium lipid plaques)
chronic narrowing of lumen, produces angina
Why is coronary blood flow prevented during systole?
Pressure in ventricles is = or > aorta
- No coronary perfusion
Why is coronary blood flow possible during distole?
key feature of aorta?
how does this maintain blood flow?
Ventricles pressure decrease a lot but aorta maintain pressure durinf diastole due to its recoiling nature
this means that the aorta can take on blood due to elastin and when heart relaxes hence diastole, the compliance decreases and it can send the blood flow to the rest of the body e.g heart and maintain BP during diastole
Mechanical factors that reduce coronary flow during diastole (3)
1) Shortening diastole, e.g. high heart rate
2) Increased ventricular end-diastolic pressure, e.g. volume-overload heart failure
3) Reduced diastolic arterial pressure, e.g. hypotension, aortic regurgitation hence there is less difference netween arterial and ventricles so less drive for blood flow
Issue with coronary arteries being function end-arteries
what is there a low number of?
what does this mean?
what happens if obstructions happen?
Low numbers of cross-branching collateral vessels
(Arterio-arterial anastomoses)
Blood flow cannot by diverted to ischemic areas
This means functionally vessels provide o2 + nutrients to specific areas of the heart so there is no cross branching so if obstrcution happens, parts of the heart will die due to poor blood flow
Example of functional end-arteries
Total occlusion of left anterior descending coronary artery
what does it lead to? result of this? what sequent of events happen after this?
Leads to ischemic area – myocardial infarction ->
ischemic tissue, acidosis, pain (stimulation of C-fibres) -> impaired contractility -> sympathetic activation -> arrhythmias -> cell death (necrosis)
Functional end-arteries – other arteries cannot divert blood to area
Angina - symptoms
where is pain? other symtoms?
‘’Strangulation of the chest’’
Pain, crushing sensation in the chest
Radiates to neck, arms, jaw
With shortness of breath, dizziness
Causes of Angina
main reason? causes of this reason? (3)
triggers (3)
Causes – ischemia due to O2 and nutrient demands
of cardiac tissue not being met due to partial occlusion of coronary arteries
Causes of increased demand –
Increased heart rate, left ventricular contractility, wall stress
triggers – Exercise (increased heart rate, contractility,
hypertension (afterload), left ventricular dilatation (heart failure)
different forms of angina (3)
stable, variant and unstable
Partial occlusion of left coronary arteries
Stable angina upon exercise
what is partial occlusion due to plaque formation called?
why is this okay at rest?
what happens during exercise?
stenosis - partial occlusion due to plaque formation
At rest, this may be fine as body can produc compensatory mechanism that can cope with the drop in blood flow
However, during exertion, the heart must work harder hence not able to produce the compensatory mechanisms hence not enough blood flow to this area and area becomes ischemic
What happens during increased activity in healthy individual?
what is resistant like in vessels? what happens during exercise? what happens to blood flow?
R is low in large coronary artery and becomes high in arterioles
During exercise, metabolic vasodilatation of arterioles reduce total R
Increased blood flow to meet increased O2 demands
(Resistances (R) in series add together)
What happens during increased activity in individual with stable agina?
what is R like with stenosis? what happens at rest?
what happens during exercise and what does this lead to?
With stenosis in large coronary artery - Resistance high
Metabolic hyperaemia occurs at rest, so blood flow meets needs via vasodilation
However,
During exercise, arterioles further dilate to reduce resistance, but total resistance is still too high
due to dominance of stenosis
O2 demand CAN NOT be met, angina develops
Stable Angina versus Variant Angina
predicatbility for both of these?
how is stable one relieved?
what does the ECG show?
what can be used to find the occlusion?
how is variant different?
what does is excessively respond to?
Stable (Exertional, typical)
Predictable – symptoms appear after certain demand reached
Relief with nitrates (e.g. GTN spray)
ECG – exercise stress test produces symptoms and ST depression
Coronary angiography to find occlusion
Variant (Vasospastic, Prinzmetal’s)
Uncommon, caused by vasospasm, occurs at rest,
often not linked to coronary artery occlusion
Excessive responses to vasoconstrictors, endothelium dysfunction (e.g less NO produced)
Management of stable/variant
3 different drugs given - what are they and their effects?
what else can be done to reduce risk? (2 drugs and something else)
Ca Channel blockers (less HR and afterload), B-blockers (less hr), nitrates (vasodilate to increase blood flow, decrease afterload, increase preload hence decrease decrease demand of the heart)
minimise risk factors – lifestyle, aspirin to reduce clots, statins to reduce cholesterol
3 different types of acute coronary sydrome
unstable angina
NSTEMI (non-ST segment elevation myocardial infarction)
STEMI (ST segment elevation myocardial infarction)
acute coronary sydrome
urgency?
what is this?
what is it initiated by? what does it produce?
how is it presented? (4)
what 2 investigations will you do?
Spectrum of potentially life-threatening conditions
Medical emergency
Sudden decrease in flow of blood through a coronary artery
Initiated by a rupture of an atherosclerotic plaque produces a thrombus in a coronary artery which reduces blood flow
Presentation – unpredictable, sudden, lasts for >30 min, not relieved by GTN spray
Investigation
ECGs – NSTEMI or STEMI
Troponins T and I measured (often raised in NSTEMI and STEMI)
why is the ST line isoelectric in healthy individuals
In healthy tissue, ventricles are uniformly depolarized, so an no current is detected on ECG
what causes ST depression?
when does it occur? what effect does this have?
In partial/less severe occlusion of a coronary artery, small area of ischemia which does not depolarize
Polarity in the wall due to -ve/+ve movement hence this goes away from the lead and causes a depression
what causes a st elevation?
when does it occur? what effect does this have?
In total/severe occlusion of a coronary artery there is full wall thickness ischemia which does not depolarize
there is an elevation as it’s +ve to +ve so the current causes an elevation
Management – Unstable angina and NSTEMI
investigations? (2)
Pharmacological therapy (4 types)
Is revascularisation needed?
when do you carry out coronary artery bypass grafting (CABG)?
when do you carry out percutaneous coronary intervention (PCI, stents)?
Investigation
ECGs – Pick up NSTEMI
Troponins T and I measured (often raised in NSTEMI but not UA)
Pharmacological therapy Morphine Anti-platelet - aspirin, clopidogrel Anti-thrombin - heparins, NOACs Long term - B-blockers, CCBs, statins, ACEi
Is revascularisation needed?
If at moderate/high risk,
If symptoms persist, if angiography shows occlusions (multiple)
Carry out coronary artery bypass grafting (CABG)
More than 3 main coronary arteries diseased, or main left CA occluded,
occlusion position not appropriate for PCI
Carry out percutaneous coronary intervention (PCI, stents)
1 or 2 arteries diseased
What is CABG?
what 2 ways can you bypass occlusion?
which is more invasive?
coronary artery bypass grafting (leg or mammary)
bypass occludion using saphenous vein graft from leg which you can attach to aorta and coronary artery downstream hence bypass occluded area to provid o2
OR use mammary artery to divert away from mammary area and bypass over occlusion from aorta
BUT Invasive, patient on cardiopulmonary bypass, heart stopped, again potential restenosis issues, less with mammary artery
what is PCI?
can restenosis occur? how?
percutaneous coronary intervention
less invasive, balloon catheter inflated in area of blockage, increase luminal (stent in occluded area)
Restenosis can occur, thickening of internal area of vessel causing blockage (as surrounding stent, the muscle can migrate and proliferate hence lead to blockage)
Management – STEMI (acute myocardial infarction)
investiagtions (2)
3 main short term Pharmacological therapy - why these?
long term Pharmacological therapy
Is revascularisation needed?
Life-threatening complications (2)
Investigation
ECGs – STEMI, Troponins T and I measured often raised
Pharmacological therapy
Morphine
Anti-platelet, aspirin, heparins
Thrombolytics – streptokinase, tissue plasminogen activators
Cause fibrinolysis, break down fibrin-clot, increase reperfusion zone
Long term - -blockers, anti-arrhythmics, CCBs, statins, ACEi
Is revascularisation needed?
Preferred treatment within 2 hours of symptom onset
Life-threatening complications
Cardiac failure (use of intra-aortic balloon)
Rupture of ventricular septal leads to blood leakage between ventricles Arrhythmias
