coronary circulation, angina and acute coronary syndrome

Question 1

circulation and their unique requirements

what do they adapt to?
what 4 things to look at when looking at them?

Answer 1

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

Question 2

coronary circulation - special requirments

what does it need a constant supply of? when does this increase?

Answer 2

Needs a high basal supply of O2 – 20x resting skeletal muscle

Increase O2 supply in proportion to
increased demand/cardiac work

Question 3

coronary circulation - special structural features

two key features?
what effect do they have together?

Answer 3

High capillary density

Large surface area for O2 transfer

Together these reduce diffusion distance to myocyte

-> t relative X2 – so transport O2 is fast

Question 4

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?

Answer 4

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%

Question 5

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?

Answer 5

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

Question 6

CO2 and oxygen unloading

what happens if more co2 produced?
how does this relate to o2 extraction in heart vs body?

Answer 6

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%

Question 7

why does more O2 demand produce more blood flow?
key reason?
what happens when more o2 is used? what effect does this have?

Answer 7

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

Question 8

coronary circulation - special problems

when does blood flow?
problem with ischemic heart disease?
what is the heart very susceptible to?

Answer 8

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

Question 9

slow and sudden obstruction of the heart

name sudden condtions
name slow condtions

Answer 9

Sudden: acute thrombosis, Acute Coronary Syndrome (ACS) including myocardial infarction

Slow: atheroma (sub-endothelium lipid plaques)
chronic narrowing of lumen, produces angina

Question 10

Why is coronary blood flow prevented during systole?

Answer 10

Pressure in ventricles is = or > aorta

- No coronary perfusion

Question 11

Why is coronary blood flow possible during distole?

key feature of aorta?
how does this maintain blood flow?

Answer 11

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

Question 12

Mechanical factors that reduce coronary flow during diastole (3)

Answer 12

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

Question 13

Issue with coronary arteries being function end-arteries

what is there a low number of?
what does this mean?
what happens if obstructions happen?

Answer 13

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

Question 14

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?

Answer 14

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

Question 15

Angina - symptoms

where is pain? other symtoms?

Answer 15

‘’Strangulation of the chest’’

Pain, crushing sensation in the chest
Radiates to neck, arms, jaw

With shortness of breath, dizziness

Question 16

Causes of Angina

main reason? causes of this reason? (3)

triggers (3)

Answer 16

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)

Question 17

different forms of angina (3)

Answer 17

stable, variant and unstable

Question 18

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?

Answer 18

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

Question 19

What happens during increased activity in healthy individual?

what is resistant like in vessels? what happens during exercise? what happens to blood flow?

Answer 19

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)

Question 20

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?

Answer 20

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

Question 21

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?

Answer 21

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)

Question 22

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)

Answer 22

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

Question 23

3 different types of acute coronary sydrome

Answer 23

unstable angina
NSTEMI (non-ST segment elevation myocardial infarction)
STEMI (ST segment elevation myocardial infarction)

Question 24

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?

Answer 24

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)

Question 25

why is the ST line isoelectric in healthy individuals

Answer 25

In healthy tissue, ventricles are uniformly depolarized, so an no current is detected on ECG

Question 26

what causes ST depression?

when does it occur? what effect does this have?

Answer 26

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

Question 27

what causes a st elevation?

when does it occur? what effect does this have?

Answer 27

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

Question 28

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)?

Answer 28

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

Question 29

What is CABG?

what 2 ways can you bypass occlusion?

which is more invasive?

Answer 29

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

Question 30

what is PCI?

can restenosis occur? how?

Answer 30

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)

Question 31

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)

Answer 31

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