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Year 2 Cardio > Ischaemic Heart Disease and Hypoxia > Flashcards

Ischaemic Heart Disease and Hypoxia Flashcards

1
Q

What ischaemic heart disease?

A

IHD is the 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

What are other names for IHD?

A

Coronary heart disease (CHD)/Coronary artery disease (CAD)

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3
Q

What are the signs and symptoms of IHD?

A 
Angina
Heart Rhythm problems
Nausea
Sweating
Fatigue
SOB
Reduced exertional activity
Leg swelling
Diaphoresis
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4
Q

Describe the chest pain in IHD?

A

Aching, burning, fullness, heaviness, numbness, pressure, squeezing
Radiation in arms, back, jaw, neck, shoulder
High or low BP
Syncope

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5
Q

What are the rhythm problems in IHD?

A

Palpitations (irregular heartbeats or skipped beats)
Heart murmurs
Tachycardia (Acute coronary syndrome ACS, Acute myocardial infarction AMI)
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
S4gallop: A common early finding of diastolic dysfunction
S3gallop: An indication of reduced left ventricular function and a poor prognostic sign

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6
Q

What is IHD often mistaken for?

A

Indigestion

Heartburn

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7
Q

What are the Non-modifiable risk factors for IHD?

A 
Age
Gender
Family history of CVD
Ethnicity
Genetics
Previous history of CVD
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8
Q

What are the modifiable risk factors?

A 
High BP
Total cholesterol
HDL
Smoking
Diabetes
Diet
High BMI
Alcohol
Physical inactivity 
Stress
Low socioeconomic state
Medication
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9
Q

What is the percentage contribution of modifiable risk factors to IHD?

A

70%

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10
Q

When does IHD occur?

A

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

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11
Q

What are the two causes of IHD?

A

Coronary blood flow to a region may be reduces due to OBSTRUCTION

A general decrease of oxygenated blood flow to myocardium

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12
Q

What causes obstruction?

A 
Atheroma
Thrombosis
Spasm
Embolus
Coronary ostial stenosis
Coronary arteritis
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13
Q

What causes general decrease in blood flow?

A

Anaemia
Carboxyhaemoglobulinaemia
Hypotension causing decreased coronary perfusion pressure

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14
Q

What is atherosclerosis?

A

Complex inflammatory process
Accumulation of lipids
Macrophages
Smooth muscle cells
In the intimal plaques in the large and medium sized coronary arteries
The process is also called Atherogenesis

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15
Q

What triggers atherosclerosis?

A

Endothelial dysfunction
Mechanical sheer stresses (HTN)
Biochemical abnormalities (elevated and modified LDL, DM, elevated plasma homocysteine)
Immunological factors (free radicals from smoking)
Inflammation ( infection such as chlamydia, Helicobacter)
Genetic alteration

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16
Q

Summarise stages of atherosclerosis pathophysiology

A

Fatty streak phase
Plaque progression
Stable plaque
Vulnerable plaque

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17
Q

How does IHD present?

A

Can be asymptomatic

Chronic stable angina

Acute coronary syndromes

Heart Failure

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18
Q

What are acute coronary syndromes?

A

Unstable Angina
Non ST elevation MI
ST elevation MI

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19
Q

How do acute coronary occlusions occur?

A

Thrombus forms

Atherosclerotic plaque breaks through the endothelium

Direct contact with the flowing blood

blood platelets adhere to it

fibrin is deposited

Red blood cells entrapped to form a blood clot

The clot grows until the artery occludes the vessel

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20
Q

Why can you still get ACS in the presence of collaterals?

A

The collaterals can also get atherosclerosis or the damage become so extensive that even the collaterals can not help

Can cause weakening of the heart and hence heart failure

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21
Q

What is the role of collateral vessels?

A

After an acute episode

Collaterals that were collapsed before start opening due to hypoxic condition

Can supply normal coronary blood flow

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22
Q

What is myocardial infarction?

A

After an acute occusion the area of muscle that has either zero flow or so little flow that it cannot sustain cardiac muscle function is said to be infarcted

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23
Q

What is the pathogenesis of MI?

A

Small amount of collaterals open and blood seep into the infarcted area

Local blood vessels dilate and area becomes overfilled with stagnant blood

Muscle fibres use all the remaining oxygen, hemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow

24
Q

What are later stages of MI?

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

25
Q

How much oxygen does cardiac muscle require?

A

1.3ml per 100g

26
Q

How much oxygen is usually delivered?

A

8 ml of oxygen per 100 g

27
Q

What percentage of normal oxygen supply can the muscle survive with?

A

If 15 to 30 percent of blood supply remains, muscle will not die accept in the central portion of a large infarct with no collaterals

28
Q

What are the causes of death - after MI?

A

Decreased cardiac output-systolic stretch and cardiac shock

Damming of blood in body’s venous system

Ventricle fibrillation— can happen during first 10 minutes or
After 1 hour or so—

Rupture of infarcted area

29
Q

What happens when there is a small area of ischaemia?

A

little or no death of muscle. Might become non functional temporarily due to lack of nutrients

30
Q

What happens when there is a large area of ischaemia?

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

31
Q

What are the risk assessment tools for IHD?

A

QRisk 2018

32
Q

What are the NICE guidelines for IHD?

A

5 year health check for those over 40

CVD risk assessment, an assessment of alcohol consumption, physical activity, cholesterol level, BMI

QRisk

33
Q

What is involved in a clinical history for IHD?

A

Symptoms—chest pain type etc, any associated symptoms and signs
Age, sex, Ethnicity, Smoking, Ask about other risk factors, Socioeconomic, family history

34
Q

What is involved in a clinical examination for IHD?

A

Heart auscultation, BP, BMI, GPE

35
Q

What lab tests are done with IHD?

A

LDL, HDL, Triglycerides, lipoprotein a, C-reactive proteins etc

36
Q

What serum markers are looked at when acute event is suspected?

A

Troponins(I or T)
Creatine kinasewith MB isozymes
Lactate dehydrogenase and lactate dehydrogenase isozymes
Serumaspartate aminotransferase

37
Q

What biomarkers can predict death in IHD?

A 
B-type natriuretic peptide
CRP
Homocysteine
Renin
Urinary albumin-to-creatinine ratio
38
Q

What investigation can diagnose IHD?

A

ECG
Echocardiography
Coronary Angiography

39
Q

What doe you see on an ECG in stable angina?

A

Pretty much normal ECG if you want to see the changes do an exercise stress test
During stress test might see ST depressions indicating IHD

40
Q

What doe you see on an ECG in unstable angina/NSTEMI?

A

ST depressions and T wave inversion

41
Q

What do you see on an ECG in acute MI/STEMI?

A

ST segment elevation with T wave inversion

Q waves

42
Q

What does Transthoracic echocardiography help to assess?

A

left ventricular function

wall-motion abnormalities in the setting of ACS or AMI

mechanical complications of AMI

43
Q

What is Transoesophageal echocardiography most used for?

A

assessing possible aortic dissection in the setting of AMI

44
Q

When is stress echocardiography used?

A

Stress echocardiography can be used to evaluate hemodynamically significant stenoses in stable patients who are thought to have CAD

45
Q

How is angiography conducted?

A

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

The contrast agent is then visualized through radiographic fluoroscopic examination of the heart

46
Q

What is ultrasonography?

A

Ultrasonography of the common and internal carotid arteries is a noninvasive measure of arterial wall anatomy that may be performed repeatedly and reliably in asymptomatic individuals.

47
Q

What are the different medications for IHD?

A

HMG-CoA reductase inhibitors

Bile Acid Sequestrants

Calcium channel blockers

ACE Inhibitors

Beta-blockers

Antianginal Agents

Platelet aggregate inhibitors

Nitrates

48
Q

What are revascularisation therapies?

A

Percutaneous coronary Intervention

CABG

49
Q

What happens in PCI?

A

Involves angiography and stent placement:
Common to treat stable CAD
Improves blood flow by placing a stent and compressing the plaque

50
Q

What happens in CABG?

A

A vessel from another part of your body to create a graft that allows blood to flow around the blocked or narrowed coronary artery. This type of open-heart surgery is usually used only for people who have several narrowed coronary arteries.

51
Q

What are the WHO recommendations for prevention?

A 
30 mins of physical activity
Avoid tobacco
Healthy diet
Normal body weight
Reduce stress
52
Q

How does typical angina present?

A

Precipitated by physical exertion
Constricting discomfort in the front of chest, in the neck shoulders, jaw or arms
Relieved by rest

53
Q

What is prinzmetal angina?

A

The pain from variant angina is caused by spasm in the coronary arteries caused by exposure to cold, stress, smoking etc.

54
Q

What is the most powerful independent risk factor in CVD?

A

Advancing age

55
Q

What is diaphoresis?

A

Sweating

Year 2 Cardio (10 decks)

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