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Medicine Year 1 > Week 119 Coronary artery disease > Flashcards

Week 119 Coronary artery disease Flashcards

1
Q

What are the 2 layers to the pericardial sac?

A
  • fibrous

- serous

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2
Q

What layers form the serous pericardium?

A
  • Parietal (fused and inseparable from the fibrous pericardium)
  • Visceral pericardium (part of the epicardium- layer immediately outside of the heart muscle proper)
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3
Q

Where are the arteries of the pericardium derived from?

A

Internal mammary and its musculophrenic branch, and from the descending thoracic aorta

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4
Q

Where are the nerves of the pericardium derived from?

A

Vagus and phrenic nerves and the sympathetic trunks

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5
Q

What is in between the parietal and visceral layers of the pericardium?

A

Potential space- pericardial cavity; normally lubricated by a film of pericardial fluid

too much fluid in the cavity (e.g. pericardial effusion) = pericardial tamponade (compression of heart within pericardial sac)- to treat this, perform pericardectomy

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6
Q

Name 3 pericardium pathologies

A

Pericarditis resulting in pericardial friction rub

Pericardial effusion which may lead to cardiac tamponade

Cardiac tamponade as a primary pathology following trauma

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7
Q

How is pericarditis classified?

A

according to the composition of the inflammatory exudate/transudate

e.g.
serous
purulent
fibrinous
caseous
hemorrhagic
post infarction
symptoms;
chest pain
dry cough
fever
fatigue
anxiety 
(can be misdiagnosed for MI)
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8
Q

Describe pericardial effusion

A

Fluid around the heart- abnormal accumulation of fluid in the pericardial cavity

limited space in the pericardial cavity means fluid accumulation here will lead to an increased intrapericardial pressure- can negatively affect heart function

Transudative: congestive heart failure, myxoedema, nephrotic syndrome

Exudative: TB, spread from emyema

Malignant

Haemorrhagic

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9
Q

What is cardiac tamponade?

A

Cardiac tamponade also known as pericardial tamponade, is an emergency condition in which fluid accumulates in the pericardium(the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart’s ventricles from filling properly. This in turn leads to a low stroke volume. The end result is ineffective pumping of blood, shock, and often death

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10
Q

Describe invasive angiography

A 
Insertion of catheter via groin or wrist
Find coronary ostia
Inject contrast
Advantages
Good spatial resolution
Gold standard
Treatment 
Disadvantages
Complications
Radiation dose
Cost
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11
Q

What does systolic myocardial contraction do?

A

Reduces myocardial perfusion

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12
Q

When is coronary flow best?

A

During systole

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13
Q

Where do coronary arteries arise from?

A

Aorta (L and R coronary arteries)

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14
Q

Where do coronary veins drain?

A

Into Right atrium (some directly into chambers)

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15
Q

What arises from the left coronary artery?

A

Circumflex branch

Left anterior descending

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16
Q

What vein runs parallel to the circumflex branch of LCA?

A

Great cardiac vein

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17
Q

Where does the left circumflex branch run?

A

Between the left atrium and ventricle

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18
Q

Where does the LAD run?

A

Between the two ventricles

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19
Q

What arises from the LAD?

A

Marginal branches
Diagonals
Septals
(D and S supply lateral wall of LV, anterolateral papillary muscle; 37% have median ramus)

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20
Q

What arises from the right coronary artery?

A

Posterior descending artery (PDA)

Acute marginal

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21
Q

What are branches of the left circumflex artery?

A

Obtuse marginal
Posterolaterals
(supply posteriolateral LV, anterolateral papillary muscle)

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22
Q

Where is the right coronary artery origin?

A

Right aortic sinus (lower origin than LCA)

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23
Q

What are branches of the posterior descending artery?

A

Septals

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24
Q

What is amlodipin?

A

Ca2+ channel blocker - antihypertensive

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25
Q

What is aspirin?

A

Antiplatelet agent- secondary prevention of vascular events

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26
Q

What is atorvastatin?

A

Statin- secondary prevention

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27
Q

What is ramipril?

A

ACE inhibitor- antihypertensive

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28
Q

What is the management for crescendo/unstable angina?

A

Admit to wards (cardiac monitor)
–Dual antiplatelet therapy (aspirin & clopidogrel)
–Anticoagulant (clexane 65 mg bd. s.c.)
–Beta-blocker (bisoprolol 2.5 mg bd)
–Refer to Cardiac centre for coronary angiogram

further pain- GTN infusion (IV)

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29
Q

What is hypoxia?

A

condition in which the body or a region of the body is deprived of adequate oxygen supply resulting in cell injury

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30
Q

What is ischaemia?

A

is a condition of lack of blood supply from a stenotic / occluded artery or reduced venous drainage causing ischaemia

Ischaemia causes cell injury more rapidly than hypoxia.

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31
Q

What is infarction?

A

Irreversible cell damage due to ischaemia –and hypoxia

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32
Q

What are causes of cell injury?

A 
Hypoxia and Ischaemia 
•Infections
•Metabolic / Nutritional
•Trauma
•Drugs/ Chemicals
•Autoimmune
•Genetic diseases
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33
Q

What is the most common type of cardiac disease and commonest cause of death in the western world?

A

Ischaemic heart disease

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34
Q

Why is coronary artery disease fatal?

A

First presentation of it is sudden death

35
Q

From death of coronary artery disease, what is causing death?

A

Ventricle fibrillation or acute myocardial infarction

36
Q

What are the mechanisms for acute myocardial infarction?

A 
Coronaryvasospasm
•Coronary thrombosis in situ or embolisation from a distant source
•Cocaineabuse
•Viralmyocarditis
•Aortic dissection
•Autoimmunevasculitis
•Hypoxia
37
Q

What drugs are atherogenic?

A

Cocaine and methamphetamine - acute and chronic use may be a factor in sudden death with underlying coronary artery atherosclerosis

38
Q

What is an atheroma/atherosclerosis?

A

Accumulation of lipid and fibrous tissue within the intima of arteries –> plaques

39
Q

What are complications of atherosclerotic plaques of the coronary arteries?

A
  1. Gradual narrowing of the vessel
  2. Ulceration of the plaque
  3. Rupture and fissuring (showers of emboli)
  4. Superimposed thrombosis (with 2+3)
40
Q

What are risk factors for atherosclerosis?

A

Constitutional:
Age
Gender
Family Hx

Major:
Smoking
Hypertension
Hyperlidiaemia 
DM
Lesser/softer:
Obesity 
Low HDL
Personality/stress
Lack of exercise
Others
41
Q

Describe the change of appearance of heart tissue after MI after:

  • 4 hours
  • 4-12 hours
  • 12-24 hours
  • 1-3 days
  • 3-7 days
  • 7-10 days
  • Weeks-months
A
  • Normal
  • Slight mottling
  • Mottled
  • Soft, pale and yellow
  • Soft, pale and yellow + hyperaemic border
  • Soft, pale and yellow + hyperaemic border
  • Gray-white scar, progressive from periphery
42
Q

Describe the change of histological appearance of heart tissue after MI after:

  • 4 hours
  • 4-12 hours
  • 12-24 hours
  • 1-3 days
  • 3-7 days
  • 7-10 days
  • Weeks-months
A
  • normal
  • Eosinophilis + contraction bandsCoagulation necrosis begins
  • As above + early neutrophil infiltration
  • Coagulation necrosis. Neutrophils ++
  • Lesser number of neutsEarly phagocytosis by macrophages
  • Phagocytosis ++ by macrophages
  • Collagen deposition ++
43
Q

What are complications of MI?

A 
Sudden death
•Cardiac Arrhythmias
•Left ventricular failure
•Ventricular wall rupture
•Papillary muscle fibrosis / rupture
•Mural thrombus
•Ventricular aneurysm
44
Q

What are the three main types of cardiomyopathy?

A

Diilated Cardiomyopathy

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy

45
Q

Describe dilated cardiomyopathy

A

Any age, 25% 5 year survival
Causes include:
Genetic defects (30-40%), Alcohol, Idiopathic, Peripartum, Haemochromatosis, Doxorubicin, Post myocarditis.
Heart becomes enlarged and cannot pump blood efficiently. •
Impaired contractility (systolic dysfunction)•
Heart (>900g!), mural thrombi, interstitial fibrosis

46
Q

Describe hypertrophic cardiomyopathy

A

Young adults, sudden death
Causes include Genetic, Frederich ataxia, storage diseases.
Hypercontractile but impaired compliance (Diastolic dysfunction). •Cardiomegaly, septal hypertrophy, fibrous plaque on anterior MV leaflet, myocyte disarray

47
Q

Describe restrictive cardiomyopathy

A
  • Restrictive cardiomyopathy is a rare form of heart muscle disease in which the contractile function of the heart and wall thicknesses are usually normal, but the relaxation or filling phase of the heart is very abnormal.
  • This occurs because the heart muscle is stiff and does not allow the ventricular chambers to fill with blood normally.
  • This inability to relax and fill with blood results in a “back up” of blood into the atria, lungs and body causing the symptoms and signs of heart failure.
48
Q

Describe myocarditis

A

-marked by inflammation and damage of heart muscle

Causes:

  • viral infections
  • Autoimmune diseases
  • Environmental toxins
  • Adverse reactions to medications
  • rare, particularly deadly form of myocarditis= giant cell
  • myocarditis= associated with pre-existing autoimmune disease and hypersensitivity reactions to drugs
49
Q

What is stenosis?

A

Narrowing of a channel

50
Q

What is the relation between angina and coronary artery disease?

A

Angina is caused by obstructive coronary artery disease sufficient to cause myocardial ischeamia by reducing myocardial o2 supply

51
Q

What is the proportion of stenosis that causes angina?

A

Luminal stenosis of >70%= angina

Some less severe lesions (>50%) may cause angina by further exacerbating ischeamia

52
Q

What is ischaemia?

A

Inadequate blood supply to an organ

53
Q

What causes increased ischaemia?

A

Reduced blood supply
Anaemia
Coronary spasm
Increased metabolic demand- LVH, tachycardia
Increasing area of ischaemia- proximal lesions subtend a larger area of ischaemia

54
Q

What reduced ischaemia?

A
  • Development of collateral blood supply from other arterial territories
  • Reduction in area of ischaemia: more distally located lesions/previous infarction in area of arterial supply
55
Q

What is ACS?

A

Acute coronary syndrome:

coronary plaque rupture/dissection with intra-luminal thrombus formation. Covers unstable angina to myocardial infarction

56
Q

What is AMI?

A

Acute myocardial infarction

acute chest pain with ECG changes of ischaemia, evidence of myocardial necrosis, evidence of new regional wall motion abnormality or loss of viable myocardium

57
Q

What is CHD?

A

Coronary heart disease

  • most common cause of death
  • 1/5 men 1/7 women
  • most common cause of premature death 19% men 10% women
58
Q

Describe the epidemiology of CHD

A

Decreasing death rate from CHD in the UK since the early 1970s (still exceeds that in many Western countries).

  • Over 2 million people are living with CHD in the UK.
  • More than 275,000 people have a myocardial infarction annually
59
Q

What does the prevalence of angina depend on?

A

Age (65+)
Gender (male)
Ethnicity (South West Asians)

60
Q

Describe the process of atherosclerosis

A

Oxidised LDL from plasma taken up by macrophages, forming foam cells.

  • Inflammatory process resulting in VSM cell migration from media to intima, forming a fibrous cap.
  • Ulceration of the cap with clot formation occludes artery causing an ACS/AMI.
  • Repeated cycles of rupture/healing lead to formation of high grade stenosis

weakened vessel wall can give rise to coronary artery aneurysms or true aneurysms in the thoracic/abdominal aorta

61
Q

What are the complications of plaque rupture?

A
  • Unstable angina

- MI

62
Q

What are the classifications of MI?

A

Type 1:
-spontaneous MI related to ischaemia due to primary coronary event such as plaque erosion/rupture, fissuring or dissection

Type 2:
-MI secondary to ischaemia due to either increased o2 demand/decreased supply e.g. coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension

63
Q

What are biomarkers of myocardial necrosis?

A

Troponin I or T

ECG, Hx

64
Q

What is the difference between ACS and stable angina?

A

Stable: pain on exertion

ACS: Acute presentation with chest pain that is unprovoked and unremitting. Mortality risk is highest early after presentation and emergency treatment saves lives

65
Q

What is the Hx for stable angina diagnosis?

A
  • Exertional chest pain, sometimes SOB–> radiates to throat/left arm, settling rapidly with rest or GTN spray.Reproducible with exercise, non-pleuritic.
  • Exertional dyspnoea (anginal equivalent)

Palpitations (ischaemia-driven arrhythmia, eg AF/VT/V.Ectopy)

Presyncope/ syncope (ischaemia-driven conduction disease)

66
Q

What are cardiac risk factors for stable angina?

A 
Tobacco smoking
Diabetes mellitus Hypertension
Hyperlipidaemia
Family History
Recreational Drug use, eg cocaine
67
Q

What would you observe on examination for stable angina diagnosis?

A 
Pulse, JVP
Blood pressure
Corneal arcus/xanthomata/ xanthelesma
Exclude Murmur PSM/ESM (Aortic stenosis/Hypertrophic Cardiac myopathy/ ischaemic MR/Ventricular septal defect ) and CCF
Periperal pulses
68
Q

What is HOCM?

A

genetic cond where septum of heart thickens so it blocks outflow tract of blood in through aortic valve compared to posterior wall- lack of blood supply up aorta= hypertophic cardiomyopathy

69
Q

How can you measure the probability of CHD?

A

Diamond and Forrester algorithm provides a probability estimate of CAD based on the disease prevalence (%)in Western populations.
•Based on age, gender and typicality of symptoms

70
Q

What do you ask during the Diamond-Forrester algorithm?

A

1) . Is there constricting discomfort in the front of the chest, or in the neck, shoulders, jaw, or arms?
2) . Is pain precipitated by physical exertion?
3) . Is pain relieved by rest or GTN within about 5 minutes?

3/3 yes= typical anginal pain
2/3 yes= atypical anginal pain
1/3/none yes= non-anginal pain

71
Q

How can you assess chest pain for stable angina?

A

Clinical assessment, using Diamond-Forrester algorithm.

  • Non-invasive functional testing, eg treadmill exercise test (ETT), myocardial perfusion scintigraphy with SPECT (MPS), stress echocardiogram, stress magnetic resonance scanning (stress MRI).
  • Anatomical testing, eg 64-slice CT coronary angiography or coronary angiography for obstructive coronary artery disease.
72
Q

What are differential diagnoses of chest pain?

A

Chest wall: musculoskeletal

  • Gastro-intestinal: eg gastro-oesophageal reflux disease, peptic ulcer, cholecystitis, pancreatitis
  • Lungs: pulmonary embolism, pneumonia, pneumothorax
  • Aortic dissection, pericarditis
73
Q

What are opening investigations for chest pain presentations?

A

Blood tests: FBC, Urea and Electrolytes, glucose, LFT’s, Lipids (TC, LDL, HDL).

  • ECG
  • +/-CXR (stable vs acute presentation)
  • For acute chest pain: troponin T on admission and 6-9 hours later
74
Q

What ECG changes are present in stable angina?

A

often normal ECG. Possibly evidence of old MI (Q waves, bundle branch block, fixed ST/T wave abnormalities). Ensure no evidence of hypertrophic cardiomyopathy.

75
Q

What ECG changes are present in unstable angina?

A

normal ECG or ST depression/ arrhythmia-AF, ventricular ectopics, ventricular dysrrhythmia. Possibly evolving changes.

76
Q

What ECG changes are present in acute MI?

A

ST elevation or depression, new left bundle branch block. Q waves develop later. Possibly evolving changes or arrhythmia.

77
Q

What 3 pt groups are narrowed down after investigation?

A
  1. Typical angina and pre-test probability of >90%: no further investigation required for diagnosis but may need it for prognostic stratification.
  2. Very low probability of CHD: no further investigation required.
  3. Doubt as to if angina: investigate further.
78
Q

What is the gold standard anatomical test for investigating CHD?

A

Coronary angiography

Others include multi-slice CT coronary angiography

79
Q

Describe Ca++ scoring using electron -beam CT scanning

A

Coronary artery calcification is characteristic of CAD and will also predict the presence of lipid-rich plaques.

  • Quantification of coronary artery calcification can be undertaken using EBCT scanning or multislice CT scanning, with the generation of the Agatston score or Volume score.
  • Higher Ca-scores predict increased frequency of coronary events in the next 30 months
80
Q

Describe pros and cons of Ca++ scoring

A

Quick non-invasive assessment (5 min) with minimal radiation exposure (1.5-3 mSv)compared to multislice CT

  • Does not assess severity of lesion or viability of myocardium
  • Studies suggest a sensitivity of 99% and specificity of 28% for Ca-scoring predicting the presence of obstructive CAD.
81
Q

Describe multislice CT coronary angiography

A

If Ca-score>0, will need to proceed to multislice-CT coronary angiography.

  • Uses x-ray analysis of coronary blood flow with computer-analysis of images to generate a 3D image of the heart.
  • Requires use of Iodine-containing contrast and higher radiation exposure (12-15 mSv).
  • Image quality is optimised by slowing the heart rate using beta-blockers
82
Q

How is stress caused to the heart during a stress functional test?

A

1.Exercise

2.Pharmacological
•Dobutamine: β1 adrenoceptor agonist
•Adenosine, Dipyridamole: coronary vasodilators which increase myocardial blood flow in normal coronary arteries but not in arteries distal to stenoses.

83
Q

What are treatment options for angina?

A
  1. Optimal medical therapy (OMT)
    •Intensive life-style change
    •Pharmacological therapies
  2. Revascularisation
    •Percutaneous intervention (PCI)
    •Coronary artery bypass graft surgery (CABG)
84
Q

Describe types of PCI for stable coronary artery disease

A

Depending on lesion severity and degree of calcification, can consider:
•direct stenting
•predilatationwith a non-compliant balloon
•severely fibrotic or calcified lesions may require pre-treatment with rotablation.
•Acute ischaemiadue to coronary dissection can be corrected with stents.
•Emergency CABG is necessary in <0.1%.

Medicine Year 1 (13 decks)

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