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Cardiorespiratory > Ischaemic Heart Disease and Hypoxia > Flashcards

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
Q

blood clots in coronary arteries can grow to cause?

A

acute coronary occlusion

26
Q

collaterals in an acute episode

A

dilate within seconds, doubling by every 2nd or 3rd day usually reaching normal coronary flow in 1 month

27
Q

what are coronary collaterals?

A

“natural bypasses,” anastomotic connections w/o an intervening capillary bed between portions of the same coronary artery and between different coronary arteries

28
Q

collaterals in chronic atherosclerotic patients

A

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

29
Q

with the presence of collaterals, why do patients still get issue?

A

collaterals can also get atherosclerosis or damage is so extensive that even collaterals can’t help > can cause weakening of the heart > HF

30
Q

after acute occlusion > ischaemia > ?

A

infarction

31
Q

pathogenesis of myocardial infarction (soon after)

A

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
Q

pathogenesis of myocardial infarction (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

33
Q

causes of death following a myocardial infarction

A

decreased cardiac output - systolic stretch and cardiac shock, damming of blood in venous system, ventricle fibrillation, rupture of infarcted area

34
Q

effects of small area of ischaemia

A

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

35
Q

effects of 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

36
Q

risk assessment tools for cardiovascular

A

JBS3

QRISK

37
Q

clinical history for IHD

A

symptoms: chest pain type, associated symptoms and signs, age, sex, ethnicity, smoking, FH

38
Q

clinical examination for IHD

A

heart auscultation
BP
BMI
GPE

39
Q

lab tests for IHD (lipid profile)

A 
LDL
HDL
triglycerides
lipoprotein A
C reactive proteins
40
Q

Serum markers in patients with suspected acute cardiac events (ACS, MI)

A

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

41
Q

Biomarkers for predicting death were the following:

A 
B-type natriuretic peptide
CRP
Homocysteine
Renin
Urinary albumin-to-creatinine ratio
42
Q

what would you see on ECG with 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

43
Q

what would you see on ECG with unstable angina/NSTEMI?

A

ST depression and T wave inversion

44
Q

what would you see on ECG with acute MI/STEMI?

A

ST elevation with T wave inversion

Q waves

45
Q

transthoracic echocardiography helps to assess?

A

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

46
Q

transoesophageal echocardiography is used for assessing?

A

possible aortic dissection in the setting of AMI

47
Q

stress echocardiography can be used to assess?

A

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

48
Q

coronary angiography procedure

A

iodinated contrast agent injected through catheter placed at ostium of coronaries > contrast visualized through radiographic fluoroscopic heart examination

49
Q

coronary angiography is gold standard for?

A

detecting stenoses that may be revascularized through percutaneous or surgical intervention

50
Q

ultrasonography

A

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
Q

doppler velocity probes

A

for measuring coronary flow in humans

52
Q

pharmacological treatment for IHD

A 
HMG-CoA reductase inhibitors
Bile Acid sequestrants
calcium channel blockers
ACE inhibitors
betablockers
anti-anginal agents
platelet aggregate inhibitors
nitrates
53
Q

revascularisation therapies

A

percutaneous coronary intervention (angiohgraphy + stent)

CABG (vessel from somewhere else used to make a graft)

54
Q

WHO recommendations for prevention

A 
physical activity
avoid smoking
balanced healthy diet
maintain a normal body weight
reduce stress

Cardiorespiratory (20 decks)

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