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Life support > CVS Angina and acute coronary syndrome > Flashcards

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
Q

What happens to coronary arterioles during exercise in an individual with stable angina?

A

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
Q

When do symptoms for stable angina appear?

A

symptoms appear after certain demand reached

27
Q

How is relief given for stable angina?

A

Relief with nitrates (e.g., GTN spray)

28
Q

What method of imaging is used for stable angina?

A

Coronary angiography

29
Q

What is variant angina caused by?

A

caused by vasospasm

30
Q

When does variant angina occur?

A

Occurs at rest

31
Q

What is variant vagina often not linked to?

A

Often not linked to coronary artery occlusion

32
Q

What are the causes of variant angina?

A

-Excessive responses to vasoconstrictors
-Endothelium dysfunction

33
Q

What is the management of stable/variant angina?

A

-CCB
-Beta blockers
-Nitrates

34
Q

What do CCBs do in the management of stable/variant angina?

A

-Decrease HR/Afterload

35
Q

What do beta blockers do in the management of stable/variant angina?

A

Reduce heart rate

36
Q

What do nitrates do in the management of stable/variant angina?

A

-Open up coronary
circulation increasing collateral flow
-Decrease afterload/preload

37
Q

How does stable angina present on an ECG in an exercise stress test?

A

Exercise stress test produces symptoms and ST depression

38
Q

What are the 3 types of acute coronary syndrome?

A

-NSTEMI (non-ST segment elevation myocardial infarction)
-STEMI (ST segment elevation myocardial infarction)
-Unstable Angina

39
Q

What initiates acute coronary syndrome?

A

Initiated by a rupture of an atherosclerotic plaque produces a thrombus in a coronary artery which reduces blood flow

40
Q

What is the presentation for acute coronary syndrome?

A

-unpredictable,
-sudden,
-lasts for >30 min,
-not relieved by GTN spray

41
Q

What is the investigation for acute coronary syndrome?

A

-ECGs – NSTEMI or STEMI
-Troponins T and I measured (often raised in NSTEMI and STEMI)

42
Q

How would an NSTEMI appear on an ECG and why?

A

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
Q

How would a STEMI appear on an ECG and why?

A

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
Q

What is troponin T and I raised in and not raised in ACS?

A

-Often raised in NSTEMI and STEMI
-Not raised in unstable angina

45
Q

What is the pharmacological therapy for unstable angina and NSTEMI?

A

-Morphine
-Anti-platelet - aspirin, clopidogrel
-Anti-thrombin - heparins, NOACs
-Long term - beta-blockers, CCBs, statins, ACEi

46
Q

Based on what decisions is revascularisation needed?

A

Decision based upon:
Risk of future STEMI, symptoms persist, angiography shows occlusions

47
Q

When would percutaneous coronary intervention(PCI, stents) be considered for the management of unstable angina and NSTEMI?

A

When 1 or 2 arteries are diseased

48
Q

When would coronary artery bypass grafting(CABG) be considered for the management of unstable angina and NSTEMI?

A

-Greater than or equal to 3 main coronary arteries diseased,
-main left CA occluded,
-occlusion position not appropriate for PCI

49
Q

How does PCI work?

A

balloon catheter inflated
in area of blockage, increase luminal size

50
Q

What is the pharmacological treatment for STEMI

A

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
Q

What is the time frame for the preferred treatment for STEMI and what is it?

A

Preferred treatment within 2 hours of symptom onset – PCI or CABG

52
Q

What are the life-threatening complications with STEMI?

A

Cardiac failure
Rupture of ventricular septal leads to blood leakage between ventricles
Arrhythmias

Life support (38 decks)

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