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BRS Y2 > Ischemic Heart Disease and Hypoxia > Flashcards

Ischemic Heart Disease and Hypoxia Flashcards

1
Q

Define IHD

A

The term given to heart problems caused by narrowed heart (coronary) arteries that supply blood to the heart muscle

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2
Q

What is there a mismatch between in IHD

A

Demand and supply of oxygen

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3
Q

What are other names for IHD?

A

Coronary artery disease (CAD)

Coronary heart disease (CHD)

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4
Q

What are the 2 ways IHD manifests clinically?

A

Myocardial infarction

Ischemic cardiomyopathy

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5
Q

What is a reason the prevalence of IHD has increased over time?

A

Life expectancy has gone up and its more common in the older population

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6
Q

Why does sudden death occur in IHD?

A

Due to occlusion of arteries

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7
Q

What are the main signs and symptoms of IHD?

A

Angina/chest pain
Heart rhythm problems
Nausea, sweating, fatigue or shortness of breath, weakness or dizziness
Reduced exertional capacity
Leg swelling (when left ventricular dysfunction is present)
Diaphoresis (increased sweating)

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8
Q

When does leg swelling occur in IHD?

A

When left ventricular dysfunction is present

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9
Q

How does angina manifest?

A

Aching, burning, fullness, heaviness, numbness, pressure, squeezing
Radiation in arms (usually left but also can be right), back, jaw, neck, shoulder
High or low BP
Syncope

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10
Q

What is angina often mistaken for? When does this especially happen?

A

Indigestion or heart burn, especially if the pain doesn’t radiate and localised to the centre of the chest

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11
Q

How do heart rhythm problems manifest in IHD?

A 
Palpitations 
Heart murmurs
Tachycardia 
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
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12
Q

What is S3 and S4 gallop?

A

They are sounds heard that indicate left ventricular dysfunction, S3 is heard after the mitral valve opens as blood pours into the left ventricle

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13
Q

What is diaphoresis?

A

Increased sweating

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14
Q

What are non modifiable risk factors for IHD?

A 
Age 
Gender (more common in males)
Family history
Ethnicity
Genetics (eg hypercholesterolaemia)
Past history of CVD
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15
Q

What are modifiable risk factors for IHD?

A 
BP
Cholesterol
Smoking
Diabetes
BMI
Diet (this is the biggest risk factor)
Inactivity
Stress/mental health
Low social economic state
Alcohol
Income
Social deprivation
Environment
Some medications
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16
Q

What are the 2 main causes of IHD?

A

Reduced coronary blood flow to a region due to obstruction

General decrease of oxygenated blood flow

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17
Q

What are some causes of obstruction causing reduced coronary blood flow?

A 
Atheroma
Thrombosis
Spasm
Embolus
Coronary ostial stenosis
Coronary arteritis
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18
Q

What are some causes of decreased flow of oxygenated blood?

A

Anaemia Carboxyhaemoglobulinaemia

Hypotension

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19
Q

What is the process by which an atherosclerotic plaque forms called?

A

Atherogenesis

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20
Q

What are some triggers for atherogenesis?

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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21
Q

Describe a stable plaque

A

Fibrous cap of layers of VSMC surrounded by ECM network which is an effective barrier preventing rupture
They have a small necrotic core

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22
Q

Describe a vulnerbale plaque

A

Unresolved inflammation causes thinning of the fibrous cap
Areas where thinning has occurred are prone to rupture, if this happens there is thrombus formation and this leads to clinical events

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23
Q

What are the 5 ways IHD may present

A 
Asymptomatic 
Chronic stable angina
Acute coronary syndromes (unstable angina, non ST elevation MI or ST elevation MI
Heart failure 
Sudden death
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24
Q

Once an atherosclerotic plaque has contact with flowing blood what happens?

A

Platelets can adhere to it
Fibrin is deposited
RBCs get trapped and a clot forms

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25
Q

How does hypoxia arise as a result of atherosclerosis?

A

Once the atherosclerotic plaque breaks through the endothelium and forms a clot, the clot can occlude a vessel

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26
Q

What is a coronary embolus?

A

When the clot formed by a ruptures atherosclerotic plaque breaks away and blocks a more distal artery

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27
Q

What is a collateral?

A

When small arteries anastomose together

28
Q

What happens to collaterals in an acute episode?

A

They dilate within seconds and can double by the second or third day

29
Q

How do collaterals develop in chronic atherosclerotic patients?

A

Slowly as the atherosclerosis gets worse

30
Q

Why does ACS still occur even though collaterals exist?

A

Extensive atherosclerosis can damage the collaterals themselves, also if they get too big they may not be able to maintain blood supply

31
Q

Is full recovery post MI possible?

A

Yes, in about a month its possible

32
Q

How does infraction occur?

A

After occlusion there is no flow or very little flow to the muscle so function cannot be sustained

33
Q

What occurs to muscle after infraction?

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, haemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow

34
Q

How much oxygen do cardiac muscle cells need?

A

1.3ml of oxygen per 100ml of tissue

35
Q

How much blood supply is required to stop cardiac muscle from dying?

A

15-30%

36
Q

What are causes of death after MI?

A

Decreased cardiac output
Ventricular fibrillations
Rupture of infarcted area
Damming of blood in the venous system

37
Q

What is systolic stretch?

A

When there is dead muscle after MI, it is pulled on in systole and when it stretched it can become balloon shaped

38
Q

How may the heart be damaged further after MI?

A

If there is excess exertion damage may occur as the heart has reduced reserve

39
Q

How is risk of MI calculated?

A

JBS3 is used in GPs

Q risk is used in hospitals

40
Q

What clinical examinations are done when diagnosing MI?

A

Heart auscultations
BP
BMI
GPE

41
Q

What lab tests are done when diagnosing MI?

A 
LDL
HDL
Triglycerides
Lipoprotein A
C reactive protein
42
Q

What are the serum markers in patients with suspected acute cardiac events?

A

Troponins (I or T)
Creatine kinase with MB isozymes
Lactate dehydrogenase and lactate dehydrogenase isozymes
Serum aspartate aminotransferase

43
Q

What are biomarkers for predicting death?

A 
B-type natriuretic peptide
CRP
Homocysteine
Renin
Urinary albumin-to-creatinine ratio
44
Q

What is seen on an ECG for stable angina?

A

Pretty much normal

If you want to see the changes do an exercise stress test, during stress test might see ST depressions indicating

45
Q

What is seen on an ECG for unstable/NSTEMI angina?

A

ST depressions and T wave inversion

46
Q

What is seen on an ECG for acute MI/STEMI angina?

A

ST segment elevation with T wave inversion, Q waves

47
Q

What is transthoracic ECG used for?

A

Assess left ventricular function
Wall-motion abnormalities in ACS or AMI
Mechanical complications of AMI

48
Q

What is transoesophageal ECG used for?

A

Assessing possible aortic dissection in the setting of AMI

49
Q

What is stress ECG used for?

A

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

50
Q

What is coronary angiography used for?

A

In vivo assessment of coronary arteries

51
Q

How do HMG CoA reductase inhibitors work?

A

They lower LDL-C levels
and triglyceride levels
Raise serum HDL levels

52
Q

How do bile acid sequestrates work?

A

Block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol

53
Q

How do CCBs work?

A

Relaxes coronary smooth muscle and produces coronary vasodilation to increase oxygen delivery to the heart

54
Q

How do ACE inhibitors work?

A

Hypertension and atherosclerosis may be intimately linked through their effects on vascular endothelial dysfunction so they can help

55
Q

How do beta blockers work?

A

Inhibit sympathetic stimulation of the heart, reducing heart rate and contractility; this can decrease myocardial oxygen demand and thus prevent or relieve angina in patients with CAD

56
Q

How do antianginal agents work?

A

Reduces myocardial cellular sodium and calcium overload via inhibition of the late sodium current of the cardiac action potential

57
Q

How do platelet aggregate inhibitors work?

A

Exert protection against atherosclerosis through inhibition of platelet function and through changes in the hemorrhagic profile

58
Q

How do nitrates work?

A

They decrease myocardial oxygen demand by producing systemic vasodilation

59
Q

What are the 2 main revascularisation therapies?

A

Percutaneous coronary intervention

CABG

60
Q

How does percutaneous coronary intervention work?

A

Angiography and stent placement helps improve blood flow

61
Q

When is percutaneous coronary intervention used?

A

To treat stable CAD

62
Q

How does CABG work?

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

63
Q

When is CABG performed?

A

In people who have several narrowed coronary arteries

64
Q

What are some preventative measures for IHD and MI

A 
Do physical activity
Stop smoking
Healthy diet 
Reduce weight if overweight 
Reduce stress at home and work
65
Q

What do Q risk and JBS3 show?

A

Risk of MI in the next 10 years

BRS Y2 (85 decks)

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