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Z YEAR 2 BRS CARDIO > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What is IHD?

A

term given to heart problems caused by narrowed heart (coronary) arteries that supply blood to the heart muscle.( Mismatch between demand and supply)

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2
Q

How does IHD manifest clinically?

A
  • myocardial infarction

- ischemic cardiomyopathy

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3
Q

Why do some deaths due to IHD occur suddenly?

A

due to acute coronary occlusion

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4
Q

Why do some deaths due to IHD occur overtime?

A

a period of weeks to years as a result of progressive weakening of the heart pumping process

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5
Q

What is angina in IHD?

A
  1. Aching, burning, fullness, heaviness, numbness, pressure, squeezing
  2. Radiation in arms, back, jaw, neck, shoulder
  3. High or low BP
    •Syncope
    -Indigestion or heart burn - mistkane
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6
Q

What are heart rhythm problem in IHD?

A
  1. Palpitations (irregular heartbeats or skipped beats)
  2. Heart murmurs
  3. Tachycardia (Acute coronary syndrome ACS, Acute myocardial infarction AMI)
  4. Atrial fibrillation
  5. Ventricular tachycardia or ventricular fibrillation
  6. S4gallop
  7. S3gallop
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7
Q

What is S4 gallop?

A

A common early finding of diastolic dysfunction

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8
Q

What is S3 gallop?

A

An indication of reduced left ventricular function and a poor prognostic sign

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9
Q

What are the other important signs and symptoms in IHD?

A
  1. Nausea, sweating, fatigue or shortness of breath, weakness or dizziness
  2. Reduced exertional capacity
  3. Leg swelling (when left ventricular dysfunction is present)
  4. Diaphoresis
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10
Q

Is ischemic heart disease the leading cause of death in the world?

A

yes

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11
Q

Is the distribution of death to IHD different in different countries / income / age?

A
  • yes

- causes are not the same around the world

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12
Q

What is DALY?

A
  • Disability-Adjusted Life Year

- A sum of Years of Life Lost (YLL) and Years Lost to Disability (YLP)

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13
Q

What are the non modifiable risk factors of IHD?

A
  1. Age
  2. Gender
  3. Family history of CVD
  4. Ethnicity
  5. Genetic evidence
  6. Previous history of CVD
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14
Q

What are the modifiable risk factors of IHD?

A
  1. High BP
  2. Smoking
  3. Income
  4. Total cholesterol
  5. HDL cholesterol / lipoprotein a
  6. Blood sugar / diabetes / LVH
  7. BMI
  8. Diet
  9. Exercise / physical inactivity
  10. Stress / mental health
  11. Alcohol
  12. Low socio-economic status
  13. Social deprivation
  14. Environment
  15. Certain medication
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15
Q

When does myocardial ischemia occur?

A

when there is an imbalance between the supply of oxygen ( and other essential myocardial nutrients) and the myocardial demand for these substances

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16
Q

What can coronary blood flow to a region may be reduced due to an obstruction by?

A
  1. Atheroma
  2. Thrombosis
  3. Spasm
  4. Embolus
  5. Coronary ostial stenosis
  6. Coronary arteritis
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17
Q

When might there just be a general decrease of oxygenated blood flow to myocardium?

A
  1. Anaemia
  2. Carboxyhaemoglobulinaemia
  3. Hypotension causing decreased coronary perfusion pressure
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18
Q

What is atherosclerosis?

A
  1. Complex inflammatory process
    - Accumulation of lipids
    - Macrophages
    - Smooth muscle cells
  2. In the intimal plaques in the large and medium sized coronary arteries
  3. The process is also called Atherogenesis
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19
Q

What triggers atherogenesis?

A
  1. Endothelial dysfunction
  2. Mechanical sheer stresses (HTN)
  3. Biochemical abnormalities (elevated and modified LDL, DM, elevated plasma homocysteine)
  4. Immunological factors (free radicals from smoking)
  5. Inflammation ( infection such as chlamydia, Helicobacter)
  6. Genetic alteration
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20
Q

What can a dysfunctional endothelial cells and retention of lipoproteins (LDL, VLDL etc) lead to in the fatty streak phase?

A
  1. Increased expression of monocytes interaction (Migration into intimal space)
  2. Other immune cells that mediate the internalization of LDL to form foam cells
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21
Q

What does the infiltration of the proliferation of tunica media smooth muscle cells lead to in plaque progression?

A
  1. Various growth factors e.g. TGF-beta and fibroblast growth factors (FGF) etc
  2. SMC’s are recruited to the luminal side of the lesion to form a barrier between lesioal prothrombotic factors
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22
Q

What type of fatty things are less likely to regress?

A

fibrous fatty lesions are less likely to regress than fatty acid

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23
Q

What is the fibrous cap composed of in a stable plauqe?

A

layers of smooth muscle cells ensconced in a substantial extracellular matrix network

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24
Q

What does a fibrous cap provide?

A

effective barrier preventing plaque rupture

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25
Q

What do stable plaques have?

A

small necrotic core

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26
Q

What maintains the fibrous cap?

A

production of TGF-β by T-reg cells and macrophages maintains fibrous cap quality by being a potent stimulator of collagen production in smooth muscle cell

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27
Q

What is a vulnerable plaque the result of?

A

increases and unresolved inflammatory status of core

28
Q

What does unresolved inflammation cause?

A

thinning of the fibrous cap

29
Q

What are areas of thin fibrous cap prone to?

A

rupture exposing prothrombotic components to platelets and pro-coagulation factors leading to thrombus formation and clinical events.

30
Q

What are the different stages of coronary / ischaemic heart disease presentation?

A
  1. Asymptomatic
  2. Chronic stable angiina
  3. Acute coronary syndromes
  4. Heart failure
  5. Sudden death
31
Q

What are example of acute coronary syndromes?

A
  • Unstable angina
  • Non-ST elevation MI
  • ST elevation MI
32
Q

When does acute coronary occlusion happen?

A

in people with underlying atherosclerotic disease

33
Q

What is the process of local blood clot-Thrombus formation?

A
  1. Atherosclerotic plaque breaks though the endothelium
  2. Direct contact with flowing blood
  3. Leads to:
    - Blood platelets adhere to it
    - Fibrin is deposited
    - Red blood cells entrapped to form a blood clot
34
Q

What happens to the clot?

A

grow until the artery occludes the vessel

35
Q

What is a coronary embolus?

A

when vessel breaks away and blocks a more distal artery (leads to hypoxia)

36
Q

What can also add to occlusion?

A

local muscular spasm of a coronary artery

37
Q

What happens to collaterals in an acute episode?

A
  1. Dilate within seconds during an acute episode

2. Doubling by the second or third day and often reaching normal or almost normal coronary flow within about 1 month

38
Q

What happens to collaterals in a chronic atherosclerotic patient?

A

Slow occlusion-collateral vessels can develop at the same time while the atherosclerosis becomes more and more severe

39
Q

If there are collaterals why do you still get ACS?

A
  1. Collaterals can also get atherosclerosis or the damage become so extensive that even the collaterals can not help
  2. Can cause weakening of the heart and hence heart failure
40
Q

What happens to the area of muscle after an acute occlusion?

A

area of muscle that has either zero flow or so little flow that it cannot sustain cardiac muscle function is said to be infarcted- hence the name myocardial infarction

41
Q

What is the pathogenesis of the muscle soon after the infarction?

A
  1. Small amount of collaterals open and blood seep into the infarcted area
  2. Local blood vessels dilate and area becomes overfilled with stagnant blood
  3. Muscle fibres use all the remaining oxygen, hemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow
42
Q

What is the pathogenesis of the muscle in later stages?

A
  • Vessels walls permeability increases, fluid leak and local tissue oedematous
  • Cardiac muscle cells swell and due to no blood supply die within few hours
43
Q

How much oxygen does cardiac muscle require?

A

1.3ml of oxygen per 100g of muscle tissue

44
Q

How much oxygen is delivered to normal resting left ventricle each minute so usually muscle do not die

A

8 ml of oxygen per 100 g

45
Q

What happens if 15-30% of blood supply remains?

A

muscle will not die accept in the central portion of a large infarct with no collaterals

46
Q

What are the causes of death after an MI?

A
  1. Decreased cardiac output-systolic stretch and cardiac shock (non functional muscle)
  2. Damming of blood in body’s venous system
  3. Ventricle fibrillation— can happen during first 10mins/hour
  4. Rupture of infarcted area
    Early little danger after few days infarcted area begin to degenerate heart walls become very thin stretched until finally rupture
47
Q

What is the recovery after an acute MI with a small area of ischemia?

A
  • little or no death of muscle
  • might become non functional temporarily due to lack of nutrients
  • If mild can still have good cardiac output (but not when exercising)
48
Q

What is the recovery after an acute MI with a large area of ischemia?

A
  • Some in the centre die rapidly within 1 to 3 hours due to complete loss of blood supply
  • Immediately around is non functional area failure of contraction and impulse conduction
  • Surrounding non-functional still contracting but weak due to mild ischemia
49
Q

What is the health check programme in NCIE guidelines for IHD?

A
  • Everyone aged 40–74 years, who has not already been diagnosed with CVD, diabetes, or chronic kidney disease, is invited every 5 years for a free health check.
  • The health check includes a CVD risk assessment, an assessment of alcohol consumption, physical activity, cholesterol level, BMI), dementia in those aged 65-74 years, and screening for diabetes mellitus and chronic kidney disease in those at increased risk of developing these conditions.
  • A person’s 10 year CVD risk should be assessed using the QRISK assessment tool every 5 years (apart from people who already have CVD or are at high risk of developing it, or people aged 85 years or over).
50
Q

What is the clinical history for IHD diagnosis?

A
  1. Symptoms—chest pain type etc, any associated symptoms and signs
  2. Age, sex, Ethnicity, Smoking, 4. Ask about other risk factors, Socioeconomic, family history
51
Q

What is the clinical examination for IHD diagnosis?

A
  1. Heart auscultation
  2. BP
  3. BMI
  4. GPE
52
Q

What are the lab tests - lipid profile for IHD diagnosis?

A
  1. LDL
  2. HDL
  3. Triglycerides
  4. lipoprotein a
  5. C-reactive proteins etc
53
Q

What are the Serum markers in patients with suspected acute cardiac events (ACS, MI) for IHD diagnosis?

A
  1. Troponins(I or T)
  2. Creatine kinasewith MB isozymes
  3. Lactate dehydrogenase and 4. lactate dehydrogenase isozymes
  4. Serumaspartate aminotransferase
54
Q

What are the Biomarkers for predicting death?

A
  1. B-type natriuretic peptide
  2. CRP
  3. Homocysteine
  4. Renin
  5. Urinary albumin-to-creatinine ratio
55
Q

What would the ECG look like for a stable angina in IHD diagnosis?

A
  1. Pretty much normal ECG if you want to see the changes do an exercise stress test
  2. During stress test might see ST depressions indicating IHD
56
Q

What would the ECG look like for a unstable angina / NSTEMI in IHD diagnosis?

A
  1. ST depressions

2. T wave inversion

57
Q

What would the ECG look like for an acute MI/STEMI in IHD diagnosis?

A
  1. ST segment elevation with T wave inversion

2. Q waves

58
Q

What does a transthoracic echocardiography helps to assess in the IHD diagnosis?

A
  • left ventricular function
  • wall-motion abnormalities in the setting of ACS or AMI
  • mechanical complications of AMI
59
Q

When is Transoesophageal echocardiography used in the IHD diagnosis?

A

for assessing possible aortic dissection in the setting of AMI

60
Q

When is a Stress echocardiography used in the IHD diagnosis?

A

to evaluate hemodynamically significant stenoses in stable patients who are thought to have CAD

61
Q

When was coronary angiography first used?

A

n vivo assessment of the coronary arteries

62
Q

What is the first step for coronary angiography?

A

an iodinated contrast agent is injected through a catheter placed at the ostium of the coronaries

63
Q

How is the contrast agent viewed?

A

through radiographic fluoroscopic examination of the heart

64
Q

When is coronary angiography used?

A

detecting stenoses that may be revascularized through percutaneous or surgical intervention

65
Q

When is coronary CT angiography used?

A

detecting the presence and extent of CAD and independent predictors of significant coronary stenosis and other cardiovascular events

66
Q

What are the special features of an atherosclerotic plaque?

A
  • 68% fibrous tissue
  • Necrotic lipid-rich core (16%)
  • Foam cells (1%)
  • Calcium (8%)
  • Foam cells and inflammatory cells (1%)

Z YEAR 2 BRS CARDIO (18 decks)

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