CVR Ischaemic heart disease & hypoxia Flashcards

1
Q

WHat is IHD?

A

the term given to heart problems caused by narrowed heart arteries that supply its muscle

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2
Q

signs of IHD

A
  • angina (syncope, aching, radiation in arms, high or low BP)
  • Heart rhythm problems (palpitations, heart murmurs, tachycardia, atrial fibrillation, S4, S3 gallop from non-compliant ventricle)
  • general important symptoms (nausea, sweating, fatigue, shortness of breath diaphoresis, leg swelling)
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3
Q

what is the leading cause of death in the world?

A

IHD

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4
Q

where is IHD most prevalent?

A

eastern europe

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5
Q

who is IHD most prevalent amongst?

A

older people (65+)

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6
Q

who is IHD most prevalent amongst?

A

older people (65+)

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7
Q

risk factors types of IHD (2)

A

modifiable

non modifiable

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8
Q

non-modifiable risk factors types of IHD

A

age, gender. family history CVD. ethnicity. genetic evidence, previous history of CVD

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9
Q

modifiable risk factors types of IHD

A

high BP, cholesterol, smoking, blood sugar/diabetes/LVH, BMI, diet, stress, low socioeconomic state, alcohol, income, certain meds, social deprivation environment

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10
Q

causes of IHD

A

obstruction cause by atheroma. spasms, embolus

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11
Q

what is involved in artherosclerosis? (3)

What is the process called?

A

lipids,
macrophages
smooth muscle cells
-> process is called artherogenesis

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12
Q

how do smooth muscle cells interact with plaques?

A

proliferate and cover plaque. Contains the plaque (lumen of blood vessel reduced)

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13
Q

TGF B and T-reg cells and macrophages do what to fibrous cap of stable plaque?

A

stabilise and protect it

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14
Q

when does a plaque become vulnerable?

A

when the fibrous cap thins

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15
Q

when does a plaque become vulnerable?

A

when the fibrous cap thins

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16
Q

presentations of IHD (3)

A
  • asymptomatic
  • chronic stable angina (stable fixed plaque)
  • unstable angina, non-ST elevation MI, ST elevation MI (unstable plaques)
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17
Q

how does an occlusion occur in IHD?

A
  • direct contact with the flowing blood
  • blood platelets adhere to it, fibrin deposited, RBC entrapped to form a clot
  • clot grows until artery occlude
  • can break away e.g. PE
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18
Q

what happens to collaterals in sudden event?

A

doubling by the second/third day

- achieve normal flow within 1 month

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19
Q

what happens to collaterals in chronic atherosclerotic patients??

A
  • slow occlusion vessels can develop at the same time while the atherosclerosis become more severe-
  • these collaterals can also get damaged
  • sometimes hypoxic area is too large
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20
Q

soon stages after MI (2)

A
  • small amount of collaterals open
  • local blood vessels dilate and cause overfilling with stagnant blood,
    muscle fibres use all remainign O2 -> bloof turns blue brown
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21
Q

later stages after MI

A

vessel wall permeability increases, fluid leak and local tissue oedematous
- cardiac muscle cells swell and no blood supply means they die within a few hours

22
Q

causes of death after MI (4)

A
  • decreased CO (systolic stretch from muscle death and cardiac shock)
  • damming of blood in body’s venous system
  • ventricular fibrillation
  • rupture of infarcted area (Early little danger after few days infarcted area begin to degenerate heart walls become very thin stretched until finally rupture)
23
Q

x

A

x

24
Q

recovery after an acute MI

A
  • when large area of ischemia:
  • > some of centre dies
  • > immediate surrounding can recover
25
Q

can CO stay the same after MI?

A

cardiac resolve means it can

26
Q

how to diagnose IHD?

A

clinical history, clinical examination, Lab tests, bio markers (b types natiuretic peptide)

27
Q

ECG in stable angina

A

looks normal

28
Q

ECG in unstable angina

A

NSTEM - ST depression, T wave inbversion

29
Q

ECG in acute MI/STEMI

A

ST segment elevation

T wave inversion

30
Q

what does transthoracic eco assess?

A
  • left ventricular function
  • wall motion abnormalities in the setting of ACS or AMI
  • mechanical complications of AMI
31
Q

best way to assess coronary arteries

A

coronary angiography

32
Q

x

A

x

33
Q

treatment - pharmacological

A
  • HMG-CoA reductase inhibitors e.g. atorvastatin - bile acid sequestrants (increased fecal loss of cholesterol)
  • calcium channel blockers
  • ACE inhibitors (esp important for hypertension)
  • beta blockers for angina to decrease demand of MI O2
  • antianginal agent e.g. ranolazine by reducing myocardial cellular and Ca overload. Inhibition of the later Na current of the cardiac action potential
  • platelet aggregation inhibitors
  • nitrates
34
Q

treatment - revascularisation therapies

A
  • percutaneous coronary intervention involving stent placement
  • CABG - vessel from another part of body for blood to bypass blocked artery (when not possible to put stents in)
35
Q

causes of reduced blood flow to a region in IHD

A
  1. Atheroma
  2. Thrombosis
  3. Spasm
  4. Embolus
  5. Coronary ostial stenosis
  6. Coronary arteritis
36
Q

causes of decreased O2 blood flow to myocardium (3)

A
  • Anaemia
  • Carboxyhaemoglobulinaemia
  • Hypotension causing decreased coronary perfusion pressure
37
Q

What triggers artherogenesis? (6)

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

38
Q

serum markers in patients with suspected acute cardiac events

A
  1. Troponins(I or T)
  2. Creatine kinasewith MB isozymes
  3. Lactate dehydrogenase and lactate dehydrogenase isozymes
  4. Serumaspartate aminotransferase
39
Q

biomarkers for predicting death in IHD (5)

A
  1. B-type natriuretic peptide
  2. CRP
  3. Homocysteine
  4. Renin
  5. Urinary albumin-to-creatinine ratio
40
Q

what is Transoesophageal echocardiography use for?

A

assessing possible aortic dissection in the setting of AMI.

41
Q

what can Stress echocardiography be used to evaluate

A

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

42
Q

procedure of coronary angiography

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.
  • Coronary angiography remains gold standard for detecting stenoses that may be revascularized through percutaneous or surgical intervention
43
Q

What is coronary CT angiography an important tool in?

A

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

44
Q

Pros of performing ultrasonography on the common and internal carotid arteries

A
  • a noninvasive measure of arterial wall anatomy

- may be performed repeatedly and reliably in asymptomatic individuals.

45
Q

what is the most widely applied technqiue for measuring coronary flow in humans

A

Doppler Velocity probes
- It helps evaluating whether normal blood flow has been restored after percutaneous transluminal coronary angioplasty (PTCA).

46
Q

How does Doppler Velocity probes work?

A

Doppler guidewire measures phasic flow velocity patterns and tracks linearly with flow rates in small, straight coronary arteries.

47
Q

Example of bile acid sequestrants

A

Cholestyramine (Questran, LoCholest, Prevalite)

48
Q

how do Ca channel blockers work?

A

amlodipine (Norvasc) relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery.
Amlodipine (Norvasc)

49
Q

examples of ACE inhibitors

A

Captopril (Capoten), enalapril (Vasotec), and lisinopril (Zestril).

50
Q

what does percutaneous coronary intervention involve?

A

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

51
Q

What does CABG involve?

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.

52
Q

Recommendations from WHO for reducing risk of CHD

A
- Take moderate physical activity for a total
of 30 minutes on most days of the week.
-  Avoid tobacco use and exposure to
environmental smoke; make plans to quit if
you already smoke.
-  Choose a diet rich in fruits, vegetables and
potassium, and avoid saturated fats and
calorie-dense meals.
- Maintain a normal body weight; if you
are overweight, lose weight by
increasing physical activity and
reducing calorie intake.
- Reduce stress at home and at work.