Ischaemic Heart Disease and Hypoxia Flashcards

1
Q

what is ischaemic heart disease?

A

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

IHD manifests clinically as?

A

MI

ischaemic cardiomyopathy

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3
Q

Signs and symptoms of IHD

A

chest pain/angina
heart rhythm problems
general symptoms

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4
Q

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

heart rhythm problems of IHD

A

Palpitations
Heart murmurs
Tachycardia
Atrial fibrillation
Ventricular tachycardia or ventricular fibrillation
S4gallop: early finding of diastolic dysfunction
S3gallop: indication of reduced left ventricular function and a poor prognostic sign

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6
Q

general IHD symptoms

A

Nausea, sweating, fatigue or shortness of breath, weakness or dizziness
Reduced exertional capacity
Leg swelling (when left ventricular dysfunction is present)
Diaphoresis

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7
Q

highest prevalence of IHD by age

A

80-89

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8
Q

highest incidence of IHD by age

A

85-95+

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9
Q

IHD is a very high common cause of death where geographically?

A

eastern europe, north africa, india, russia

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10
Q

over __% of CVD is caused by modifiable risk factors

A

70

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11
Q

non-modifiable risk factors of IHD

A
age
gender
family history
ethnicity
genetics
previous history of CVD
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12
Q

modifiable risk factors of IHD

A
high BP
cholesterol
stress
smoking
diabetes
BMI
low socioeconomic status
diet
exercise
alcohol
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13
Q

Highest risk risk factor

A

dietary risk

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14
Q

Coronary blood flow to a region may be reduces due to OBSTRUCTION caused by?

A
Atheroma
Thrombosis
Spasm
Embolus
Coronary ostial stenosis
Coronary arteritis
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15
Q

A general decrease of oxygenated blood flow to myocardium due to?

A

anaemia
Carboxyhaemoglobulinaemia
Hypotension causing decreased coronary perfusion pressure

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16
Q

Fibrous fatty lesions are ____ likely to regress than fatty streaks.

A

less

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17
Q

Fibrous cap of an atherosclerotic plaque is composed of?

A

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

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18
Q

Fibrous cap as an effective barrier prevents?

A

plaque rupture

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19
Q

The production of what maintain fibrous cap quality?

A

TGF-β by T-reg cells and macrophages

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20
Q

By what mechanism is the fibrous cap maintained?

A

potent stimulation of collagen production in VSMC

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21
Q

How does a vulnerable plaque rupture?

A

increased + unresolved inflammatory status > thinning of the fibrous cap > prone to rupture exposing prothrombotic components to platelets and pro-coagulation factors > thrombus formation

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22
Q

presentation of coronary/ischaemic heart disease

A
asymptomatic
chronic stable angina
unstable angina
NSTEMI
STEMI
heart failure
sudden death
23
Q

coronary embolus

A

blood clot can break away and block a more distal artery

24
Q

thrombus formation

A

atherosclerotic plaque breaks up > direct contact with flowing blood > platelets adhere to it, fibrin deposited, RBC trapped to form clot

25
blood clots in coronary arteries can grow to cause?
acute coronary occlusion
26
collaterals in an acute episode
dilate within seconds, doubling by every 2nd or 3rd day usually reaching normal coronary flow in 1 month
27
what are coronary collaterals?
“natural bypasses,” anastomotic connections w/o an intervening capillary bed between portions of the same coronary artery and between different coronary arteries
28
collaterals in chronic atherosclerotic patients
Slow occlusion-collateral vessels can develop at the same time while the atherosclerosis becomes more and more severe.
29
with the presence of collaterals, why do patients still get issue?
collaterals can also get atherosclerosis or damage is so extensive that even collaterals can't help > can cause weakening of the heart > HF
30
after acute occlusion > ischaemia > ?
infarction
31
pathogenesis of myocardial infarction (soon after)
Small amount of collaterals open + blood seep into the infarcted area > local blood vessels dilate and area becomes overfilled with stagnant blood > muscle uses all O2, Hb > deoxy & blood vessels appear engorged despite lack of blood flow
32
pathogenesis of myocardial infarction (later stages)
Vessels walls permeability increases, fluid leak and local tissue oedematous Cardiac muscle cells swell and due to no blood supply die within few hours
33
causes of death following a myocardial infarction
decreased cardiac output - systolic stretch and cardiac shock, damming of blood in venous system, ventricle fibrillation, rupture of infarcted area
34
effects of small area of ischaemia
little or no death of muscle. Might become non functional temporarily due to lack of nutrients
35
effects of large area of ischaemia
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
36
risk assessment tools for cardiovascular
JBS3 | QRISK
37
clinical history for IHD
symptoms: chest pain type, associated symptoms and signs, age, sex, ethnicity, smoking, FH
38
clinical examination for IHD
heart auscultation BP BMI GPE
39
lab tests for IHD (lipid profile)
``` LDL HDL triglycerides lipoprotein A C reactive proteins ```
40
Serum markers in patients with suspected acute cardiac events (ACS, MI)
Troponins (I or T) Creatine kinase with MB isozymes Lactate dehydrogenase and lactate dehydrogenase isozymes Serum aspartate aminotransferase
41
Biomarkers for predicting death were the following:
``` B-type natriuretic peptide CRP Homocysteine Renin Urinary albumin-to-creatinine ratio ```
42
what would you see on ECG with stable angina?
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
43
what would you see on ECG with unstable angina/NSTEMI?
ST depression and T wave inversion
44
what would you see on ECG with acute MI/STEMI?
ST elevation with T wave inversion | Q waves
45
transthoracic echocardiography helps to assess?
left ventricular function wall-motion abnormalities in the setting of ACS or AMI mechanical complications of AMI
46
transoesophageal echocardiography is used for assessing?
possible aortic dissection in the setting of AMI
47
stress echocardiography can be used to assess?
evaluate hemodynamically significant stenoses in stable patients who are thought to have CAD
48
coronary angiography procedure
iodinated contrast agent injected through catheter placed at ostium of coronaries > contrast visualized through radiographic fluoroscopic heart examination
49
coronary angiography is gold standard for?
detecting stenoses that may be revascularized through percutaneous or surgical intervention
50
ultrasonography
the common and internal carotid arteries is a noninvasive measure of arterial wall in asymptomatic individuals > combined thickness of the intima + media associated w/ prevalence of cardiovascular risk factors and ^ risk of MI + stroke
51
doppler velocity probes
for measuring coronary flow in humans
52
pharmacological treatment for IHD
``` HMG-CoA reductase inhibitors Bile Acid sequestrants calcium channel blockers ACE inhibitors betablockers anti-anginal agents platelet aggregate inhibitors nitrates ```
53
revascularisation therapies
percutaneous coronary intervention (angiohgraphy + stent) | CABG (vessel from somewhere else used to make a graft)
54
WHO recommendations for prevention
``` physical activity avoid smoking balanced healthy diet maintain a normal body weight reduce stress ```