CVS Angina and acute coronary syndrome Flashcards

1
Q

How many times more supply does coronary circulation require than unstimulated skeletal muscle does?

A

Needs a high supply of O2 – 20x of unstimulated skeletal muscle

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2
Q

What do cardiac muscles have a high density of and how does this impact diffusion?

A

-Cardiac muscle has high density of fibres and capillaries
-Shorter passive diffusion distances

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3
Q

What does a high capillary density and a large surface area do together in cardiac muscle?

A

-High capillary density
-Large surface area for O2 transfer
-Together these reduce diffusion
distance of O2 to myocyte

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4
Q

What times the blood flow is present in coronary circulation during normal activity?

A
  • 10x the flow per weight of rest of body
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5
Q

How much O2 extraction is there in comparison to the average body in coronary circulation?

A

High O2 extraction (75%) - average body is 25%

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6
Q

What happens to coronary circulation during increased demand and how?

A

-Coronary blood increases in proportion to demands
-Production of vasodilator molecules from active cardiac muscle
e.g. adenosine, K+, acidosis
Produce local vasodilation
-Circulating adrenaline dilates coronary vessels due to beta-2 adrenoceptors on coronary artery vascular smooth muscle cells

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7
Q

When does coronary blood flow occur and when is it obstructed?

A

-Systole obstructs coronary blood flow
-Coronary blood flow only occurs during diastole

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8
Q

What are sudden obstructions that can occur in the heart?

A

Acute thrombosis, Acute Coronary Syndrome (ACS) including myocardial infarction

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9
Q

What are slow obstructions that can occur in the heart?

A

Atheroma (sub-endothelium lipid plaques)
chronic narrowing of lumen, produces angina

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10
Q

Why is coronary blood flow restricted during diastole?

A

Pressure in ventricles is = or > aorta
-Poor coronary perfusion

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11
Q

What are mechanical factors reducing coronary flow?

A

(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

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12
Q

What type of arteries are the coronary artery?

A

Human coronary arteries are functional end-arteries

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13
Q

What happens when there is a total occlusion of left anterior descending coronary artery?

A

-Leads to ischemic area resulting in myocardial infarction

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14
Q

Steps involved from ischaemic tissue till cell death?

A

ischemic tissue, acidosis, pain (stimulation of C-fibres) –> impaired contractility –> sympathetic activation –> arrhythmias –> cell death (necrosis)

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15
Q

What does it mean by functional end arteries?

A

Low numbers of cross-branching collateral vessels (Arterio-arterial anastomoses)

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16
Q

What are the symptoms of angina pectoris?

A

Pain, crushing sensation in the chest
Radiates to neck, arms, jaw with shortness of breath, dizziness

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17
Q

How does angina pectoris feel like?

A

‘’Strangulation of the chest’’

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18
Q

What are the 3 forms of angina pectoris?

A

Stable, unstable and variant

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19
Q

What are the causes of angina pectoris?

A

Causes are ischaemia

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20
Q

What is ischemia in angina pectoris due to?

A

due to O2 and nutrient demands of cardiac tissue
not being met due to partial occlusion of coronary arteries

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21
Q

What are the causes of increased demands of cardiac tissue

A

Increased heart rate / left ventricular contractility / wall stress
such as triggers like:
Exercise (increased heart rate, contractility)
hypertension (afterload), left ventricular dilatation (heart failure)

22
Q

What is stenosis?

A

partial occlusion
due to plaque formation

23
Q

What happens to coronary arterioles during exercise in a healthy individual?

A

In exercise, metabolic vasodilation of
arterioles reduce total R
Increased blood flow to meet
increased O2 demands

24
Q

What happens in stable angina to coronary arteries and arterioles during rest?

A

With stenosis in large coronary
artery - Resistance to flow increases
Metabolic vasodilation of arterioles occurs at
rest, so blood flow meets needs

25
What happens to coronary arterioles during exercise in an individual with stable angina?
During exercise, arterioles can dilate a little more to increase blood flow, but resistance is too high due to dominance of stenosis O2 demand CAN NOT be met, angina develops
26
When do symptoms for stable angina appear?
symptoms appear after certain demand reached
27
How is relief given for stable angina?
Relief with nitrates (e.g., GTN spray)
28
What method of imaging is used for stable angina?
Coronary angiography
29
What is variant angina caused by?
caused by vasospasm
30
When does variant angina occur?
Occurs at rest
31
What is variant vagina often not linked to?
Often not linked to coronary artery occlusion
32
What are the causes of variant angina?
-Excessive responses to vasoconstrictors -Endothelium dysfunction
33
What is the management of stable/variant angina?
-CCB -Beta blockers -Nitrates
34
What do CCBs do in the management of stable/variant angina?
-Decrease HR/Afterload
35
What do beta blockers do in the management of stable/variant angina?
Reduce heart rate
36
What do nitrates do in the management of stable/variant angina?
-Open up coronary circulation increasing collateral flow -Decrease afterload/preload
37
How does stable angina present on an ECG in an exercise stress test?
Exercise stress test produces symptoms and ST depression
38
What are the 3 types of acute coronary syndrome?
-NSTEMI (non-ST segment elevation myocardial infarction) -STEMI (ST segment elevation myocardial infarction) -Unstable Angina
39
What initiates acute coronary syndrome?
Initiated by a rupture of an atherosclerotic plaque produces a thrombus in a coronary artery which reduces blood flow
40
What is the presentation for acute coronary syndrome?
-unpredictable, -sudden, -lasts for >30 min, -not relieved by GTN spray
41
What is the investigation for acute coronary syndrome?
-ECGs – NSTEMI or STEMI -Troponins T and I measured (often raised in NSTEMI and STEMI)
42
How would an NSTEMI appear on an ECG and why?
In partial/less severe occlusion of a coronary artery, small area of ischemia which does not depolarize - leads to injury current and depression of ST segment on ECG -
43
How would a STEMI appear on an ECG and why?
In total/severe occlusion of a coronary artery there is full wall thickness ischemia which does not depolarize - leads to injury current and elevation of ST segment on ECG -
44
What is troponin T and I raised in and not raised in ACS?
-Often raised in NSTEMI and STEMI -Not raised in unstable angina
45
What is the pharmacological therapy for unstable angina and NSTEMI?
-Morphine -Anti-platelet - aspirin, clopidogrel -Anti-thrombin - heparins, NOACs -Long term - beta-blockers, CCBs, statins, ACEi
46
Based on what decisions is revascularisation needed?
Decision based upon: Risk of future STEMI, symptoms persist, angiography shows occlusions
47
When would percutaneous coronary intervention(PCI, stents) be considered for the management of unstable angina and NSTEMI?
When 1 or 2 arteries are diseased
48
When would coronary artery bypass grafting(CABG) be considered for the management of unstable angina and NSTEMI?
-Greater than or equal to 3 main coronary arteries diseased, -main left CA occluded, -occlusion position not appropriate for PCI
49
How does PCI work?
balloon catheter inflated in area of blockage, increase luminal size
50
What is the pharmacological treatment for STEMI
Morphine Anti-platelet, aspirin, heparins Thrombolytics – streptokinase, tissue plasminogen activators Cause fibrinolysis, break down fibrin-clot, increase reperfusion zone Long-term - beta-blockers, CCBs, statins, ACEi
51
What is the time frame for the preferred treatment for STEMI and what is it?
Preferred treatment within 2 hours of symptom onset – PCI or CABG
52
What are the life-threatening complications with STEMI?
Cardiac failure Rupture of ventricular septal leads to blood leakage between ventricles Arrhythmias