Ischemic Heart Disease and Hypoxia Flashcards

(65 cards)

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
How does hypoxia arise as a result of atherosclerosis?
Once the atherosclerotic plaque breaks through the endothelium and forms a clot, the clot can occlude a vessel
26
What is a coronary embolus?
When the clot formed by a ruptures atherosclerotic plaque breaks away and blocks a more distal artery
27
What is a collateral?
When small arteries anastomose together
28
What happens to collaterals in an acute episode?
They dilate within seconds and can double by the second or third day
29
How do collaterals develop in chronic atherosclerotic patients?
Slowly as the atherosclerosis gets worse
30
Why does ACS still occur even though collaterals exist?
Extensive atherosclerosis can damage the collaterals themselves, also if they get too big they may not be able to maintain blood supply
31
Is full recovery post MI possible?
Yes, in about a month its possible
32
How does infraction occur?
After occlusion there is no flow or very little flow to the muscle so function cannot be sustained
33
What occurs to muscle after infraction?
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
How much oxygen do cardiac muscle cells need?
1.3ml of oxygen per 100ml of tissue
35
How much blood supply is required to stop cardiac muscle from dying?
15-30%
36
What are causes of death after MI?
Decreased cardiac output Ventricular fibrillations Rupture of infarcted area Damming of blood in the venous system
37
What is systolic stretch?
When there is dead muscle after MI, it is pulled on in systole and when it stretched it can become balloon shaped
38
How may the heart be damaged further after MI?
If there is excess exertion damage may occur as the heart has reduced reserve
39
How is risk of MI calculated?
JBS3 is used in GPs | Q risk is used in hospitals
40
What clinical examinations are done when diagnosing MI?
Heart auscultations BP BMI GPE
41
What lab tests are done when diagnosing MI?
``` LDL HDL Triglycerides Lipoprotein A C reactive protein ```
42
What are the serum markers in patients with suspected acute cardiac events?
Troponins (I or T) Creatine kinase with MB isozymes Lactate dehydrogenase and lactate dehydrogenase isozymes Serum aspartate aminotransferase
43
What are biomarkers for predicting death?
``` B-type natriuretic peptide CRP Homocysteine Renin Urinary albumin-to-creatinine ratio ```
44
What is seen on an ECG for stable angina?
Pretty much normal | If you want to see the changes do an exercise stress test, during stress test might see ST depressions indicating
45
What is seen on an ECG for unstable/NSTEMI angina?
ST depressions and T wave inversion
46
What is seen on an ECG for acute MI/STEMI angina?
ST segment elevation with T wave inversion, Q waves
47
What is transthoracic ECG used for?
Assess left ventricular function Wall-motion abnormalities in ACS or AMI Mechanical complications of AMI
48
What is transoesophageal ECG used for?
Assessing possible aortic dissection in the setting of AMI
49
What is stress ECG used for?
To evaluate hemodynamically significant stenosis in stable patients who are thought to have CAD
50
What is coronary angiography used for?
In vivo assessment of coronary arteries
51
How do HMG CoA reductase inhibitors work?
They lower LDL-C levels and triglyceride levels Raise serum HDL levels
52
How do bile acid sequestrates work?
Block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol
53
How do CCBs work?
Relaxes coronary smooth muscle and produces coronary vasodilation to increase oxygen delivery to the heart
54
How do ACE inhibitors work?
Hypertension and atherosclerosis may be intimately linked through their effects on vascular endothelial dysfunction so they can help
55
How do beta blockers work?
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
How do antianginal agents work?
Reduces myocardial cellular sodium and calcium overload via inhibition of the late sodium current of the cardiac action potential
57
How do platelet aggregate inhibitors work?
Exert protection against atherosclerosis through inhibition of platelet function and through changes in the hemorrhagic profile
58
How do nitrates work?
They decrease myocardial oxygen demand by producing systemic vasodilation
59
What are the 2 main revascularisation therapies?
Percutaneous coronary intervention | CABG
60
How does percutaneous coronary intervention work?
Angiography and stent placement helps improve blood flow
61
When is percutaneous coronary intervention used?
To treat stable CAD
62
How does CABG work?
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
When is CABG performed?
In people who have several narrowed coronary arteries
64
What are some preventative measures for IHD and MI
``` Do physical activity Stop smoking Healthy diet Reduce weight if overweight Reduce stress at home and work ```
65
What do Q risk and JBS3 show?
Risk of MI in the next 10 years