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FStCP 1 > Supporting Life > Flashcards

Supporting Life Flashcards

1
Q

How do atherosclerotic plaques form? What happens to them over time?

A

Excess cholesterol ingested in the diet goes into the bloodstream and sinks into the cracks in blood vessel cell walls.

Over the years it bulges up and out into the artery gradually reducing blood flow.

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2
Q

What happens if there is mild blockage in a coronary artery?

A

Starved surrounding cardiomyocytes send signals to the coronary arteries causing them to grow new artery extensions (angiogenesis) in order to supply that area of heart muscle with blood.

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3
Q

How quickly does angiogenesis in the heart occur?

A

Around two days.

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4
Q

What causes an atherosclerotic plaque to rupture?

A

Turbulent blood flow due to increased heart rate and respiratory rate as a result of exertion.

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5
Q

What causes a complete blockage when an atherosclerotic plaque ruptures?

A

When the plaque ruptures, the cholesterol ‘sludge’ it was covering is released. Within moments blood platelets converge on the site forming a clot. This gets larger and larger and eventually causes a complete blockage.

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6
Q

What are the clinical signs of an acute myocardial infarction?

A
  • Sense of impending doom
  • Severe central crushing pain
  • Pain radiating down the arms (mainly left), shoulders, neck or jaw
  • Feeling of heartburn or indigestion (early sign)
  • Dyspnoea (shortness of breath)
  • Heart palpitations
  • Sweating
  • Syncope
  • Increased heart rate
  • Dizziness and disorientation (later sign)
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7
Q

What causes the drastic rise in heart rate during an acute MI?

A

The brain triggers a massive release of adrenaline into the bloodstream causing the increase in heart rate.

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8
Q

What happens to oxygen starved cardiomyocytes?

A

They die and rupture releasing troponin into the bloodstream.

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9
Q

What happens when the heart can no longer keep up with the oxygen demands of the body in an acute MI?

A

Pulse becomes weaker leading to pulmonary oedema and dyspnoea (breathlessness). This causes dizziness and disorientation.

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10
Q

How many heart cells are lost each second during an acute myocardial infarction?

A

500

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11
Q

What do ambulance staff give patients suffering an acute MI as a first line treatment?

A

300mg of aspirin that is chewed and absorbed via the buccal mucosa.

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12
Q

What is given to disperse a clot in an acute MI?

A

TPA (tissue plasminogen activator)

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13
Q

What can happen when the cardiomyocytes that were starved of oxygen during an acute MI are reperfused?

A

One of the cardiomyocytes can become a pacemaker beating out of time with the rest of the heart. This can cause VF.

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14
Q

How do you correct VF?

A

By shocking the heart with 130,000 watts with the intention to stop all activity in the heart and hope that the heart will start again in the correct rhythm.

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15
Q

What are the five electrical stages of the cardiac cycle?

A

1) PR interval
2) P wave
3) QRS complex
4) ST segment
5) T wave

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16
Q

What is the PR interval?

A

Where the electrical signal in the heart moves from the SA node and travels through the atria to the AV node. There is electrical silence as it travels through the intra-ventricular system and emerges through the perkingie fibres and triggers ventricular contraction.

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17
Q

What does the P wave represent?

A

Atrial depolarisation

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18
Q

What does the QRS complex represent?

A

Ventricular contraction

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19
Q

What is the ST segment?

A

A period of electrical silence where the heart muscle repolarises after ventricular contraction.

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20
Q

What does the T wave represent?

A

The repolarisation of the ventricles.

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21
Q

What is the iso-electric line?

A

The line of electrical silence between every PQRS complex after the T wave.

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22
Q

Why is the height of the ST segment important?

A

It is used to diagnose NSTEMI and STEMI.

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23
Q

What is the normal height of the ST segment?

A

It should be the same height as the PR interval and the iso-electric line.

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24
Q

What are the cardiac specific troponins that are used to diagnose MI?

A

Troponin T and I

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25
Q

What is the coronary flow reserve?

A

The ratio between rest flow and max flow. This is the maximum amount of increase in blood flow that the heart can cope with.

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26
Q

What amount of blood flow increase are normal healthy hearts capable of sustaining?

A

5-fold increase

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27
Q

How great does artery stenosis have to be in order to affect flow reserve?

A

80%

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28
Q

In terms of coronary flow reserve; why do symptoms of angina occur upon exertion?

A

Because the basal flow rate is not affected in arterial stenosis, just maximum vasodilation which is reached during exertion.

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29
Q

What are the clinical signs of angina (myocardial ischaemia)?

A
  • Sudden onset central chest pain radiating to the left arm and/or jaw lasting LESS THAN 20-30 minutes
  • Pain disappears during rest
  • Shortness of breath
  • Pain relief from GTN spray
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30
Q

What happens to patients that are given IV adenosine to combat tachycardia?

A

They experience constricting chest pain.

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31
Q

What is the association between ATP and angina?

A

In myocardial ischaemia, the ATP is not ‘recharged’ because there is not enough oxygen for the oxygen transport chain. This causes ADP to break down into adenosine.
High levels of adenosine in the heart is one of the contributing factors to angina.

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32
Q

For a given cardiac output, as the heart gets more diseased the heart compensates by having a higher _________________________?

A

Left ventricular end-diastolic pressure.

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33
Q

What does a higher left-ventricular end-diastolic pressure in ischaemic heart disease cause?

A

Increased pressure in venule end of capillaries –> increased mean pressure of capillaries –> hydrostatic pressure exceeds oncotic pressure –> net movement of fluid from capillaries to alveoli –> diffusion is prevented

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34
Q

How do atherosclerotic plaques form?

A

1) Activated macrophages (and sometimes smooth muscle cells) ingest oxidised LDLs as they thing it is a foreign body.
2) Phagocytosis causes inflammation.
3) Enzymes break down the extracellular matrix (fibrous cap).
4) Eventually the macrophages die and contribute to the ‘gruel’ in the middle of the plaque.

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35
Q

What is the prevention against atherosclerotic plaque formation?

A

Statins to lower the LDL in the blood.

36
Q

What is the risk with using TPA (tissue plasminogen activator)?

A

The drug affects the whole body, not just the site of the clot causing a significant risk of intracerebral and GI haemorrhage.

37
Q

What is the more modern procedure for stopping an MI?

A

Patients are taken to specific heart attack centres (bypassing A&E) where they undergo primary percutaneous coronary intervention.

38
Q

What is percutaneous coronary intervention?

A

Where catheters are passed through the radial artery into the stenosed coronary artery where it is expanded with a wire balloon and a stent.

39
Q

What are the two difference between STEMI and NSTEMI?

A

STEMI = whole artery occlusion; ST elevation = MUCH WORSE

NSTEMI = SOMETIMES part artery occlusion; no ST elevation

40
Q

If someone present to A&E with chest pain but the ECG shows no ST elevation, what does this mean?

A

There are no completely occluded coronary arteries so you have no way of knowing if the patient is having an NSTEMI, or if the patient has unstable angina.

41
Q

How can you tell if someone is having an NSTEMI?

A

By measuring their troponin levels. If they are elevated, they are having an NSTEMI.

42
Q

Why is an ECG repeated 12-72 hours after the inital ECG to determine ST elevation?

A

To measure the Q wave.

43
Q

What is an aborted ST-elevation MI and why is it rare?

A

Where a person with an occluded coronary artery has blood flow restored before troponin is released into the bloodstream.

Rare because troponin tests are very sensitive.

44
Q

What do STEMI and NSTEMI have in common?

A

Both cause cardiac troponin (T&I) to be found in the blood.

45
Q

What is the criteria for diagnosing myocardial infarction?

A

Detection of troponin in the blood associated with at least one of:

  • Symptoms of ischaemia
  • Development of pathological Q waves
  • Imaging evidence of new loss of viable myocardium
  • Identification of intracoronary thrombus by angiography or autopsy
  • ECG changes indicative of ischaemia
46
Q

What is type 1 a NSTEMI?

A

A spontaneous MI caused by plaque rupture, ulceration, erosion or dissection.

47
Q

What is a type 2 NSTEMI?

A

A MI secondary to ischaemic imbalance (imbalance between myocardial oxygen supply and demand).

48
Q

What is a type 3 NSTEMI?

A

MI causing death before biomarkers are available.

49
Q

What is a type 4a NSTEMI?

A

MI related to percutaneous coronary intervention (PCI).

50
Q

What is a type 4b NSTEMI?

A

MI related to stent thrombosis.

51
Q

What is a type 5 NSTEMI?

A

MI related to coronary artery bypass surgery (CABG).

52
Q

What is Atorvastatin?

A

A statin used to lower cholesterol

53
Q

What is Ramipril?

A

An ace inhibitor used to lower BP

54
Q

What is Bisoprolol?

A

A beta blocker used to lower BP

55
Q

What type of drug is aspririn?

A

Anti-platelet and NSAID

56
Q

What is Ticagrelor?

A

A platelet ADP receptor antagonist used as an anti-platelet.

57
Q

What are the modifiable risk factors for acute MI?

A
  • Smoking
  • High cholesterol
  • High BP
  • Diabetes
  • Obesity/diet/lack of exercise
  • Excess alcohol
58
Q

What is an atheroma?

A

A soft pool of extracellular lipid, cell debris and activated immune cells.

59
Q

Where do atherosclerotic plaques form generally?

A

In the proximal region of coronary arteries within 6cms of the aorta.

60
Q

What is stable angina?

A

Where you have atherosclerosis in a coronary artery restricting blood flow to the heart. This plaque is not at risk of rupture.

61
Q

What are the clinical signs of stable angina?

A

A crushing sensation in the chest that is brought on by stress or exercise.

62
Q

What is the most common form of angina?

A

Primary angina (angina of effort)

63
Q

What drug stops the symptoms of primary angina?

A

GTN spray (glycerol tri-nitrate)

64
Q

Why are vasodilatory drugs ineffective in primary angina?

A

Because the atherosclerotic plaque is unable to dilate.

65
Q

What chemical change occurs in cardiac tissue as a result of a lack of oxygen?

A

Release of protons –> decrease in pH –> release of bradykinin –> TRPV1 activation on sensory nerves –> pain

Release of substance P –> vasodilation

66
Q

Clinical signs/symptoms of angina develop when stenosis in the arteries reaches ____.

A

> 70%

67
Q

What are three features of mixed (variable threshold) angina?

A

1) It is unpredictable - symptoms appear at different levels of exercise
2) Vasodilators sometimes help
3) Common

68
Q

What is the cause of mixed (variable threshold) angina?

A

Atherosclerosis and vasospasm as a result of worn epithelium = more susceptible to vasoconstrictive stimuli.

69
Q

What are three features of vasospastic (Prinzmetal’s) angina (including cause)?

A

1) Caused by spasm of coronary arteries as a result of damage, not a plaque
2) Occurs at rest, often at night = unpredictable
3) Rare

70
Q

What for of angina occurs more commonly in women?

A

Microvascular (Syndrome X)

71
Q

What causes microvascular (Syndrome X) angina?

A

Endothelial dysfunction - the microvasculature is constricted.

72
Q

What type of stable angina shows a normal coronary angiogram?

A

Microvascular (Syndrome X)

73
Q

What is a sequela?

A

A condition which is the consequence of a previous disease or injury.

74
Q

What is the main mechanism for the pharmacological treatment of angina?

A

Decrease cardiac oxygen demand.

75
Q

What is the secondary mechanism for the pharmacological treatment of angina?

A

Increase the oxygen supply to the ischaemic area of heart muscle by decreasing the heart rate and increasing blood flow in the coronary arteries.

76
Q

What are the three stages of prophylaxis for stable angina?

A

1) β-blocker or CCB (calcium channel blocker)
2) β-blocker AND vascular selective CCB
3) β-blocker AND vascular selective CCB AND long-acting nitrate/ivabradine/nicorandil/ranolazine

77
Q

What is the effect of Ivabradine?

A

It blocks the ‘funny’ current in the SA node which reduces cardiac pacemaker activity, selectively slowing the heart rate and allowing more time for blood to flow to the myocardium.

78
Q

What is the effect of Ranolazine?

A

It blocks Na channels leading to less intracellular Ca. This reduces tension in the heart wall, leading to reduced oxygen requirements for the muscle and lower cardiac output.

79
Q

What effects do nitrates have on the heart?

A
  • Dilate veins = lower central venous pressure
  • Decreases end diastolic pressure, wall tension and oxygen demand
  • Increases coronary blood flow by vasodilation
80
Q

What effect do β-blockers have on the heart?

A

Lower cardiac contractility –> lower oxygen demand –> lower energy consumption

81
Q

Blood is supplied better to the 1)________ especially during 2)_____. During 3)_____, blood is not flowing to the 4)______ due to the sheer tension in the squeezing of the walls. This closes down the 5)______ that are flowing through the walls of the heart to supply the endocardium. By slowing down the heart, you increase the 6)_____________ and therefore the perfusion of blood into the heart, especially the 7)________.

A

1) Left ventricle
2) Diastole
3) Systole
4) Left ventricle
5) Arterioles
6) Length of diastole
7) Left ventricle

82
Q

What are the effects of Ca2+ channel blockers & KATP channel activators?

A

They are arterial vasodilators which reduce afterload –> reduced TPR –> reduced blood pressure.

83
Q

What drugs would you use to treat coronary vasospasm found in some forms of stable angina?

A

Ca2+ channel blockers and/or KATP channel activators

84
Q

What are the side effects of organic nitrate drugs?

A
  • Headache
  • Facial flush
  • Fall in BP –> trigger baroreceptor reflex –> increase heart rate = tachycardia
85
Q

What are coronary collaterals and intraarterial anastomoses other names for?

A

Coronary angiogenesis

FStCP 1 (4 decks)

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