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CVS > 20. Coronary Heart Disease, Myocardial Infarction and Embolism > Flashcards

20. Coronary Heart Disease, Myocardial Infarction and Embolism Flashcards

1
Q

What can Coronary Heart Disease lead to?

A 
• Sudden cardiac death
• Acute coronary syndrome (sudden onset of chest pain)
- acute MI
- unstable angina
• Stable angina pectoris
• Heart failure
• Arrhythmia

(all count as coronary artery disease)

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2
Q

What 2 categories do patients that present with sudden onset chest pain (in the emergency room) fall into?

A
  • Myocardial Infarction

* Progressive (Unstable) Angina

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3
Q

What is the link between myocardial damage, arrhythmia and sudden cardiac death?

A
  • Damage to heart muscle leads to scar tissue formation
  • Substrate for arrhythmia
  • Substrate for sudden cardiac death
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4
Q

Summarise the epidemiology of CVD

A
  • Number 1 cause of death
  • Mortality has decreased
  • 17m deaths per year worldwide
  • 88,000 death per year in the UK
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5
Q

Summarise the epidemiology of Stable Angina

A
  • Incidence increases with age

* 2m cases in the UK

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6
Q

What is PCI (percutaneous coronary intervention)?

A
  • Same as coronary angioplasty

* Widen narrowed/blocked arteries

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7
Q

What type of vessels are epicardial coronary arteries?

A
  • Mainly conductance vessels
  • Elastic arteries
  • Dilate in response to changes in BP
  • Also subject to vasoconstriction/dilation due to the autonomic nervous system
  • Changes in capillary resistance is responsive to myocardial metabolic stimuli
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8
Q

What is the function of the coronary circulation?

A
  • Supply the myocardium
  • Make sure flow remains constant over a wide range of perfusion pressures - autoregulation
  • Make sure coronary blood flow matches myocardial demand
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9
Q

What 2 components are the coronary arteries made up of?

A

Epicardial (large arteries out of the myocardium) and Intramyocardial (small arteries in the myocardium)

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10
Q

What is the difference in resistance between the epicardial and intracardial arteries?

A

Resistance is usually equal

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11
Q

What happens to the resistance in the epicardial component if you have stenosis and how is it compensated for?

A

• Resistance increases
• Compensated to a degree by:
- increase in diameter of intramyocardial resistance vessels
- decreases the resistance in the intramyocardial component to maintain flow

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12
Q

How does the resting coronary blood flow change with increasing stenosis?

A
  • Blood flow generally remains unchanged due to response of intramyocardial arterioles
  • After around 70% stenosis, blood flow decreases rapidly
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13
Q

What is the coronary flow reserve?

A
  • Ability of the coronary circulation to adapt to an increasing demand in the face of an increasing epicardial coronary stenosis
  • Ratio of: resting blood flow : blood flow achieved under maximal stress
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14
Q

Describe a graph of ‘Coronary Flow Reserve’ against ‘Percent Stenosis’ (including the axes)

A
  • CFR decreases at a decreasing rate, with increasing stenosis
  • Coronary Flow Reserve - y axis
  • Percent Stenosis - x axis
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15
Q

How does the threshold of stenosis change under stressful conditions?

A

Resting coronary blood flow drops at 50% instead of 70%

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16
Q

Describe the ischaemic cascade?

A
  • Myocardial oxygen demand increases with a decrease in coronary blood flow
  • Perfusion abnormality => regional diastolic dysfunction => regional systolic dysfunction => ischaemic ECG changes => ANGINA pectoris
  • Worse with increased exercise load
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17
Q

How is angina pectoris felt?

A
  • Tight feeling in the chest

* Diffuses across the jaw, shoulders, back or arms

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18
Q

What provokes angina, and how can it be relieved?

A 
• Provocations 
- physical exertion
- emotional stress
- anxiety
• Relief 
- inorganic nitrate vasodilator (reduces coronary resistance and increases blood flow)
- rest
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19
Q

How is stable CHD investigated?

A
  • Confirm clinical diagnosis - demonstrate myocardial ischaemia
  • Assess risk of future adverse cardiovascular events
  • Tests for coronary artery disease - functional (demonstrate imbalance between supply and demand) & anatomical (show how anatomical severity of narrowing within the artery compromises flow)
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20
Q

Give examples of functional & anatomical tests

A

Functional
• Non-invasive: exercise ECG, stress echo, stress MRI, PET/CT
• Invasive - CFR, pressure wire, iFR

Anatomical
• Non-invasive: CT coronary calcium score, CT coronary angiogram
• Invasive - Coronary angiogram

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21
Q

Which artery is a catheter inserted into to identify stenoses?

A
  • Radial or femoral artery

* Moved along to the left main coronary artery

22
Q

What can be used to determine the degree to which flow is impaired?

A

Computational fluid dynamics

23
Q

Which do non-invasive tests involve giving stressing agents?

A
  • Create situations of increased oxygen demand

* Can be done with iontropic agents or vasodilators as well as exercise

24
Q

How can angina be treated?

A
  • Prevention - education, lifestyle modification, aspirin, statins, ACE inhibitors
  • Reduce myocardial oxygen demand - blockers, metabolic modifiers
  • Improve blood supply - vasodilators e.g. nitrates, revascularisation e.g. stents
25
Q

What medication can be used to:

  • increase the time in diastole to improve coronary perfusion
  • decrease the amount of work that the myocardium has to do
A
  • Beta blockers

* ACE inhibitors

26
Q

What is oncosis?

A
  • A form of accidental or passive cell death that is often considered a lethal injury
  • Mechanism of myocardial death
27
Q

What is a calcific nodule?

A
  • Spikey piece of calcium that sticks out into the lumen
  • Initation site for the thrombus
  • Rare
28
Q

What is the difference between a white and red thrombus?

A

White
• platelet rich
• common in arterial thrombosis (high pressure/turbulent circulation)
• benefit from anti-platelet therapy

Red
• fibrin rich with trapped erythrocytes
• common in venous or low pressure situations (stasis)
• benefit from anticoagulant or anti-fibrinolytic therapy

29
Q

What is the effect of coronary stenosis on haemodynamics?

A 
• Narrowing 
- area of high shear 
- blood accelerates
• Energy dissipates - pressure drop
• Areas of low and oscillatory shear stress - mediate endothelial dysfunctioning and accelerate atherogenesis
30
Q

Where is tissue factor made?

A
  • Cellular constituents of the atherosclerotic plaque
  • Ischaemic heart muscle
  • Circulating inflammatory cells - humoral source
31
Q

How is Acute MI determined (following a test)?

A

Detection of a rise or fall in a biomarker (troponin) with at least one value >99th percentile reference limit and at least one of:
• Symptoms suggestive of ischaemia
• New or presumed ST-T changes or Left Bundle Branch Block (LBBB) on ECG
• Development of pathological Q waves on ECG
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
• Identification of intracoronary thrombus/angiography/autopsy

32
Q

Where is cardiac troponin normally found?

A

Part of the thin filament of the sarcomere

33
Q

What are the 3 isoforms of troponin and which of those are specific to the cardiac muscle?

A
  • I, T and C

* I and T are highly specific to cardiac muscle

34
Q

When is troponin released from the cell?

A

Proteolytic cleavage during myocardial ischaemia

35
Q

How long can troponin be detected after a MI?

A

2 weeks

36
Q

What are the 2 types of Acute Coronary Syndrome?

A
  • ST elevation - complete occlusion of coronary artery
  • No ST elevation - partial occlusion which embolises distally into the microcirculation => myocardial cell death and troponin elevation
37
Q

Where does the myocardial necrosis zone start during an infarction?

A

Inner layers of the myocardium

38
Q

Which layer of the heart gets hit first and worst during an infarction?

A

Subendocardium

39
Q

What is the difference between the subepicardial and intramyocardial pressures?

A
  • Subepicardial < Intramyocardial

* Threatens to increase the difference between supply and demand

40
Q

What does an infarction become when it has spread from the endocardium (through the myocardium) to the epicardium?

A

Transmural myocardial infarction

41
Q

What percentage of the heart muscle dies if we:
• occlude an artery and don’t recanalise it
• reperfuse a blocked artery (and what are the problems with this)

A
  • Not recanalised - 70% muscle dies
  • Reperfused - 40% muscle death
  • Some of the reperfusion causes part of the 40% injury e.g. inflammation and microinfarctions, but this can be reduced using various strategies
  • Opening an infarction can lead to cardiac arrest
42
Q

What does the remodelling of the left ventricles following MI involve?

A 
• Left ventricular dilation
- increased wall tension
- allows maintenance of CO
• Thinning of the scar
• Impairment of heart function
• Increases the risk of heart failure and arrhythmias
43
Q

What does the remodelling of the left ventricles in a non-infarcted myocardium involve?

A
  • Left ventricular hypertrophy and myofilament dysfunction
  • Altered electromechanical coupling
  • Myocardial fibrosis
  • Apoptosis
  • Inflammation
  • Abnormal blood flow
44
Q

What are the consequences of adverse Left Ventricular Remodelling?

A
  • Increased systolic & diastolic wall tension
  • Increased myocardial oxygen demand
  • Reduced myocyte shortening
  • Dysynchronous depolarisation
  • Reduced subendocardial perfusion
  • Mitral regurgitation
  • Malignant ventricular arrhythmia => sudden cardiac death
45
Q

How is acute and recurrent thrombosis treated similarly and differently?

A

• Both treated with
- oral antiplatelets (aspirin, thienopyridines etc.)
• Acute - IV anticoagulants and antiplatelets, thrombectomy
• Reccurent - Factor Xa inhibitors (anticoagulant)

46
Q

How are plaques stabilised (mechanically vs drugs)?

A
  • Mechanical - stent

* Drugs - statins and ACE inhibitors

47
Q

How is Left Ventricular Remodelling treated (non-drug vs drug)?

A 
• Non-drug
- Cardiac Resynchronisation Therapy (pacemakers or defibrillators)
- Progenitor cells
• Drugs
- Beta blockers
- ACE inhibitors
- Angiotensin receptor blockers
- Aldosterone receptor antagonists
(prevents dilation of ventricle => heart failure)
48
Q

What is a transient ischaemic attack (TIA)?

A
  • Like a stroke
  • Symptoms only last a few minutes
  • No permanent damage
49
Q

How can a deep vein thrombosis be treated?

A
  • Anticoagulation
  • Fibrinolysis
  • Thrombectomy
50
Q

What leads to air, fat, amniotic and cholesterol embolisms?

A
  • Air - iatrogenic, decompression sickness, trauma
  • Fat - trauma
  • Amniotic - pulmonary vasconstriction, inflammation
  • Cholesterol - many of microemboli from within plaque, foreign body inflammatory response

CVS (21 decks)

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