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1B Cardiorespiratory > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

what is ischemic heart disease?

A

heart problems caused by narrowed heart (coronary) arteries that supply blood to heart muscle

creates a mismatch between supply and demand

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2
Q

how can IHD manifest clinically

A

as MI and ischemic cardiomyopathy

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3
Q

how can death occur from IHD?

A

some suddenly due to acute coronary occlusion

some slowly over weeks to years due to progressive weakening of heart pumping process

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4
Q

what are the symptoms of IHD?

A
  1. angina
  2. heart rhythm problems
  3. Nausea, sweating, fatigue or shortness of breath, weakness or dizziness
  4. Reduced exertional capacity
  5. Leg swelling (when left ventricular dysfunction is present)
  6. Diaphoresis
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5
Q

what can angina from IHD be mistaken as?

A

indigestion or heart burn

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6
Q

what are the angina associated symptoms of IHD?

A
  1. Aching, burning, fullness, heaviness, numbness, pressure, squeezing
  2. Radiation in arms, back, jaw, neck, shoulder
  3. High or low BP
  4. Syncope
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7
Q

what heart rhythm problems may be caused by IHD?

A
  1. Palpitations (irregular heartbeats or skipped beats)
  2. Heart murmurs
  3. Tachycardia (Acute coronary syndrome ACS, Acute myocardial infarction AMI)
  4. Atrial fibrillation
  5. Ventricular tachycardia or ventricular fibrillation
  6. S4 gallop: A common early finding of diastolic dysfunction
  7. S3 gallop: An indication of reduced left ventricular function and a poor prognostic sign
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8
Q

what are the non-modifiable risk factors of IHD?

A

age

gender

family history of CVD

ethnicity

genetic evidence

previous history of CVD

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9
Q

what are the modifiable risk factors of IHD?

A

high BP

total cholesterol/ HDL cholesterol/ Lipoprotein a

smoking/ diet/ exercise/ alcohol

blood sugar/ diabetes/LVH

BMI

stress/ mental health

low socioeconomic state/ socail deprivation/ income

environment

centain medication

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10
Q

what are the most important risk factors to prevent over non-modifiable risk factors for IHD?

A

diet

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11
Q

who are the highest risk in high-income countries for IHD?

A

hypertension

cholesterol

tobacco use

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12
Q

what are the highest risk for IHD in low-income countries?

A

poor diet

low education

air pollution

low strenght

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13
Q

when does myocardial ischaemia occur?

A

imbalance between supply of oxygen (and other nutrient) and the myocardial demand

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14
Q

what might coronary blood flow be obstructed by?

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

what might cause a general decrease of oxygenated blood flow to myocardium?

A

anemia

carboxyhaemoglobulinaemia

hypotension causing decreased coronary perfusion pressure

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16
Q

what is atherosclerosis?

A

complex inflammatory process

plaques in the intima in large and medium-sized coronary arteries

also called atherogenesis

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17
Q

what triggers 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)
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18
Q

what are the features of athersclerotic plaques?

A

fibrous tissues

necrotic lipid rich core

foam cells

FC + infl cells

calcium

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19
Q

what occurs during the fatty steak phase?

A

dysfunctional endothelial cells + retention of lipoproteins (LDL,VLDL)

This causes:

increased expression of monocyte interaction(migration into intimal space)

Other immune cells that mediate the internalization of LDL to form foam cells

this is reversible!!

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20
Q

how does the plaque progress to form fibrous fatty lesions?

A

infiltration and proliferation of tunica media smooth muscle cells

various growth factors e.g TGF-B, FGF) create more inflammation

SMCs are recruited to luminal side of lesion to form a barrier between lesional prothrombotic factors

fibrous fatty lesions are less likely to regress than fatty streaks

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21
Q

what is the composition of a stable plaque?

A

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

it provides an effective barrier preventing plaque rupture

stable plaques have a small necrotic core

the production of TGF-B by t-reg cells and macrophages maintains fibrous cap quality by being potent stimulator of collagen production in smooth muscle cells

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22
Q

what makes a plaque vulnerable

A

unresolved inflammation causes thinning of fibrous cap

thin areas are prone to rupture exposing prothrombotic components to platelets and pro-coagulation factors

leading to thrombus formation

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23
Q

what happens when atherosclerotic plaque breaks through the endothelium?

A
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24
Q

what are the possible stages of presentation of coronary/ ischemic heart disease?

A

asymptomatic

chronic stable angina

acute coronary syndrome (unstable angina, non ST-elevation MI, ST-elevation MI)

heart failure

sudden death

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25
Q

what happens to the collateral vessels during acute episode hypoxia?

A

dilate

double by the day and reach normal coronary flow within 1 month

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26
Q

what happens to the collateral vessels in hypoxia for chronic atherosclerotic patients?

A

slow occlusion- collateral vessels can develop at same time while the atherosclerosis becomes more severe

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27
Q

how can an ACS occur with collaterals?

A

collaterals get atherosclerosis or damage is so extensive the collaterals cannot help

this can cause weaking of the heart and heart failure

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28
Q

what happens to the heart after an acute occlusion?

A

area of muscle that has either zero flow or so little that it cannot sustain cardiac muscle function= myocardial infarction

29
Q

what happens do the affected areas of muscle soon after an MI with hypoxia?

A

small amounts of collaterals open and blood seeps into infarcted area

local blood vessels dilate and area becomes overfilled with stagnant blood

muscle fibres use all remaining oxygen

haemoglobin becomes deoxygenated giving blueish brown hue

blood vessels appear engorged despite lack blood flow

30
Q

what happens to the area of affected tissue after an MI with hypoxia in the later stages?

A

vessel wall permeability increases, fluid leak and local tissue oedmatous

cardiac muscle cells swell and due to no blood supply die within hours

31
Q

what percentage of blood supply is required to keep the muscle alive?

A

15-30%- muscle will not die accept in the central portion of a large infarct with no collaterals

32
Q

what are the causes of death after an MI?

A

decreased cardiac output- systolic stretch and cardiac shock

damming of blood in venous supply

ventricle fibrillation

rupture of infarcted area

33
Q

how can ventricle fibrilation occur after an MI?

A

can happen in first 10 mins to 1 hour

due to low cardiac flow -> low blood flow to kidneys -> fail excrete, add to blood volume -> pulmonary oedema -> die after few hours of symptoms

34
Q

how does rupture of infarcted area occur?

A

early little danger

after few days infarcted area begin to degenerate, heart walls become very thin stretched

finally rupture

35
Q

what is the recovery after an MI with a small area of ischemia?

A

little or no death muscle

might become non-functional temporarily due to lack of nutrients

36
Q

what is the recovery after an MI with large area ischemia?

A

some centre die rapidly within 1-3 hours due to loss blood supply

immediately around is non-functional

area- failure of contraction and impulse conduction

surrounding non- functional still contracting but weak dye to mild ischemia

37
Q

in a recovered patient from an MI when can symptoms restart?

A

after exercise

increases load on the heart

not enough resolve to compensate as usually does

38
Q

what is the risk assessment done for IHD?

A

heath check program

10 year risk assessed every 5 years using QRISK- except for people with CVD or high risk or >85yrs

39
Q

what biomarkers are used to predict death from IHD?

A

B-type natriuretic peptide

CRP

homocysteine

renin

urinary albumin to creatinine ratio

40
Q

what is seen on an ECG for stable angina?

A

normal ECG- need an exercise stress test

during stress might see ST depressions

41
Q

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

A

ST depressions and T wave inversion

42
Q

what is seen on an ECG for acute MI/ STEMI

A

ST-segment elevation with T wave inversion

Q waves

43
Q

what can transthoracic echocardiography be used to assess in IHD?

A

left ventricular function

mechanical complications of AMI

44
Q

when are left ventricular wall motion abnormalities seen on echocardiography?

A

ACS or AMI

45
Q

what can stress echocardiography evaluate in IHD?

A

haemodynamically significant stenoses in stable patients who are thought to have CAD

46
Q

when is transoesophageal echocardiography used?

A

assessing possible aortic dissection in setting of AMI

47
Q

what is the gold standard for IHD diagnosis?

A

coronary angiography - detect stenoses that may be revascularized through percutaneous or surgical intervention

important in detecting presence and extend CAD

independent predictors of significant coronary stenosis and other CV events

48
Q

how does coronary angiography work?

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.

49
Q

what does a Doppler ultrasound look at?

A

common and internal carotid arteries in a non-invasive m3easure of arterial wall anatomy

50
Q

what are the benefits of doppler ultrasound?

A

non-invasive

performed repeatedly

reliable in asymptomatic individuals

51
Q

what can be predicted through a doppler ultrasound?

A

risk of cardiovascular disease and MI/stroke

combined thickness of intima and media of carotid artery is associated with the prevalence of cardiovascular risk factors

52
Q

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

A

doppler velocity probes

53
Q

what does doppler velocity probe measure?

A

doppler guidewire measure phasic flow velocity patterns and trachs linearly with flow rates in small, straight coronary arteries

54
Q

what are the indications for doppler velocity probe?

A

determining severity of intermediate stenosis (40-60%(

55
Q

what does a doppler velocity probe help evaluate?

A

whether normal blood flow has been restored after percutaneous transluminal coronary angioplasty (PTCA).

56
Q

what are the medicinial treatments for IHD?

A

HMG-CoA reductase inhibitors

Bile acid sequestrants

CCBs

ACEi

B-Blockers

antianginal agents

platelet aggregate inhibitors

nitrates

57
Q

what are HMG-CoA reductase inhibitors?

A

These agents lower LDL-C levels. They also lower triglyceride levels and raise serum HDL levels.

Atorvastatin (Lipitor)

58
Q

what are bile acid sequestrants?

A
  • The bile acid sequestrants block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol.
  • Cholestyramine (Questran, LoCholest, Prevalite)
59
Q

what are CCBs?

A
  • The calcium-channel blocker amlodipine (Norvasc) relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery.
  • Amlodipine (Norvasc)
60
Q

what do ACEi do?

A
  • Hypertension and atherosclerosis may be intimately linked through their effects on vascular endothelial dysfunction
  • Captopril (Capoten), enalapril (Vasotec), and lisinopril (Zestril)
61
Q

what do beta blockers do?

A
  • Beta-blockers 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.
62
Q

what do antianginal agents do?

A

Ranolazine is a novel antianginal agent

believed to relieve ischemia by reducing myocardial cellular sodium

reduces calcium overload via inhibition of the late sodium current of the cardiac action potential.

63
Q

what do platelet aggregate inhibitors do?

A

May exert protection against atherosclerosis through inhibition of platelet function and through changes in the hemorrhagic profile.

Clopidogrel

Aspirin

64
Q

what are nitrates effective for?

A
  • Nitrates are effective in the treatment of acute anginal symptoms.
  • In this situation, they are usually given sublingually.
  • The primary anti-ischemic effect of nitrates is to decrease myocardial oxygen demand by producing systemic vasodilation
65
Q

what revascularisation therapies can be used to treat IHD?

A

percutaneous coronary intervention

coronary artery bypass grafting

66
Q

what is involved with percutaneous coronary intervention?

A
  • Involves angiography and stent placement:
  • Common to treat stable CAD
  • Improves blood flow by placing a stent and compressing the plaque
67
Q

what is involved 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. (cant put stents in every place)
68
Q

what are the prevention recommendations for IHD?

A
  • moderate physical activity- 30 minutes/day
  • Avoid tobacco use and exposure to
  • 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
  • Reduce stress

1B Cardiorespiratory (15 decks)

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