Common Cardiovascular Conditions Flashcards

1
Q

Define congenital heart conditions.

A

‘A range of developmental defects that affect heart function’

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2
Q

What are the aetiologies of congenital heart conditions?

A

Genetic linkage
Environmental factors
Maternal illness
Exposure to toxins

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3
Q

What are the categories of clinical presentation of congenital heart conditions?

A

Apparent at or before birth

Weeks to months before detection

Can present years after or even in adulthood

No clinically relevant issues

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4
Q

What is the sinus venosus?

A

Becomes coronary sinus / part of the right atrial wall during early development

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5
Q

What is the ductus arteriosus?

A

Connects pulmonary trunk to the aorta before birth

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6
Q

What is the foramen ovale?

A

Connects both atria together before birth

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7
Q

What is a common congenital heart lesion?

A

Atrial Septal defects

Left to right shunt.
Oxygenated blood from systemic enters pulmonary circulation.
Usually acyanotic

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8
Q

How does pulmonary hypotension affect blood flow?

A

Pulmonary hypotension can reverse the flow of the blood so it is no longer a shunt from left to right.

However, a shunt from right to left can possibly cause cyanotic issues

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9
Q

What is a ventricular septal defect?

A

An opening in the interventricular septum. Usually a left to right shunt.

Oxygenated blood from systemic enters pulmonary circulation. Usually acyanotic.

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10
Q

What is a large defect?

A

If the defect is more severe (i.e. larger hole) more blood can be shunted left to right and can cause volume overload.

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11
Q

What is a patent ductus arteriosus (PDA)?

A

A defect that is less relevant before birth, but after birth can cause a problem.

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12
Q

When does a patent ductus arteriosus (PDA) occur?

A

PDA results when the ductus fails to close. Left to right shunt can occur.

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13
Q

What can happen when the ductus arteriosus doesn’t close and the shunt is maintained?

A

At birth, smooth muscle in the walls of the ductus arteriosus will contract and close off, but when approaching adulthood, this will become fibrosed and permanently close off.

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14
Q

What is a congenital valve stenosis?

A

Creates key problems with the left ventricle and reduced flow through the systemic circulation.

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15
Q

What are some symptoms of a congenital valve stenosis?

A

Reduced Blood flow

LV hypertrophy

Fatigue

Tachycardia and Tachypnoea.

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16
Q

What is stenosis?

A

Narrowing of a gap or opening of a valve

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17
Q

What are the 4 main congenital heart defects?

A
  1. Atrial septal defects
  2. Ventricular septal defect
  3. Patent ductus arteriosus
  4. Congenital valve stenosis
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18
Q

What is dilated cardiomyopathy?

A

When there is a dilation of the left and right ventricle.

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19
Q

What are the symptoms of cardiomyopathy?

A

Reduced pumping efficiency.

Tachycardia.

Arrhythmia.

Leads to lung congestion and heart failure.

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20
Q

What is endocarditis?

A

An infection of the heart valves - usually bacterial. It is more common in congenital heart disease or valve conditions.

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21
Q

What does bacteria do to the heart valves in endocarditis?

A

Bacterial damage eats away the tissue and damages/removes the tissue.

This interferes with the function of the heart.

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22
Q

What is myocarditis?

A

Myocarditis is the necrosis and inflammation of the myocardium.

Usually linked to viral infections.

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23
Q

What are the symptoms of myocarditis?

A

Decrease in myocardinal function.

Enlargement of the heart.

Pulmonary oedma and congestive heart failure.

24
Q

What is pericarditis?

A

An infection of the pericardium - fluid accumulation in the pericardial space.

25
Q

What are the characteristics of fluid in pericarditis?

A

Fluid builds up between the visceral and parietal layers of the ‘sac’ that the heart is protected by.

The membranes are tough and heavy weight so are not as flexible. If fluid builds up in the pericardial space, it creates cardiac tamponade.

26
Q

What is cardiac temponade?

A

Restricted space for the heart to operate and move.

27
Q

What are the symptoms of pericarditis?

A

Severe limitation to venous return and cardiac ouput.

Severe hypotension.

Cerebral hypoperfusion - syncope

Cardiac arrest.

28
Q

What is atherosclerosis?

A

Atherosclerosis is the thickening or hardening of the arteries.
It is caused by a build-up of plaque in the inner lining of an artery.
As plaque builds up in the arteries, the artery wall becomes thickened and stiff.

29
Q

What are some risk factors of atherosclerosis?

A

Hyperlipidaemia (LDL, HDL)

Hypotension

Diabetes

Smoking

Obesity

Advanced age

30
Q

What is a low density lipoprotein?

A

A small molecule.

Crosses endothelium more easily.

Facilitates carrying lipids into the arterial wall.

Positive risk factor.

31
Q

What level of LDL and HDL puts someone at a higher risk of developing atherosclerosis?

A

LDL >190mg/dl

HDL <40mg/dl

32
Q

What is a high density lipoprotein?

A

Larger Molecule.

Much less able to cross endothelium.

Poor transport of cholesterol into arterial wall.

Captures cholesterol and carriers it back to the liver.

33
Q

Why does the heart walls thicken in atherosclerosis?

A

Atheromas thicken and stiffen the artery wall leading to hypotension or blockage (loss of elasticity)

34
Q

What are the 4 developmental stages of atherosclerosis?

A

Injury to the endothelium of the blood vessel.

Accumulation of oxidised lipids.

Proliferation of smooth muscle and fibrous cap formation.

Complicated plaque.

35
Q

What causes injury to the endothelium of a blood vessel

A

Haemodynamic stresses.

Cholesterol build-up

Pathogenic chemicals.

Hypertension.

Infective agents (bacteria/virus)

36
Q

How do oxidised lipids accumulate in the endothelium of the tunica intima?

A

Endothelial damage triggers inflammatory response.

LDL carries lipids into tunica intima. The lipid then oxidises.

This damage surrounding tissue/attracts macrophages.

Macrophages take-up LDLs to become foam cells.

37
Q

How does smooth muscle proliferation eventually lead to the formation of fibrous cap?

A

Smooth muscle cells proliferate.
Lymphocytes are attracted to the area.
Elastic and collagen fibres accumulate
Some foam cells die and release their lipid content.
Core of dead and dying foam cells develop.
Fibrous cap develops.
Plaque can become pro-thrombotic due to the inflammatory chemicals exposing the plaque to blood.

38
Q

How does plaque damage the heart?

A

A fragile blood vessels invade the plaque. These can bleed into the mass.

Smooth muscle cells differentiate and produce calcified regions.

Hydrodynamic forces can lead to erosion or rupture of the unstable plaque.

Circulating blood may even undermine and life the plaque.

Haemorrhage and thrombosis combine to obstruct the vessel.

39
Q

What are some complications of plaque build up?

A

Arterial stiffening and hypertension.

Vessel constriction leading to chronic ischemia.

Thrombus formation.

Acute occlusion with risk of ischemic necrosis.

Aneurysm formation resulting from invasion of tunica media.

40
Q

What does the lumen look like if you have stable angina?

A

Lumen is narrowed by plaque.
Inappropriate vasodilation.
Reduced blood flow.

41
Q

What does the lumen look like if you have unstable angina?

A

Plaque rupture.
Platelet aggregation.
Thrombus formation.
Unopposed vasoconstriction.

42
Q

What does the lumen look like if you have variant angina?

A

No overt plaques.
Intense vasospasm.
Reduced blood flow due to vasospasm only.
No clear evidence of atherosclerosis

43
Q

What is ischemia?

A

An inadequate blood supply leading to a shortage of oxygen.

44
Q

If you experience ischemia what could potentially happen?

A

If you have inadequate blood supply:

Waste metabolites are not being flushed out causing a build up.
Lactate build up.
Tissue is deprived of nutrients.

45
Q

What are the three main outcomes of ischemia?

A
  1. Can be transient without lasting damage.
  2. Protracted dysfunction with no necrosis.
  3. Or results in irreversible myocardial necrosis.
46
Q

What is coronary heart disease?

A

When the coronary arteries cannot deliver enough oxygen-rich blood to the heart.

47
Q

What is acute coronary syndromes usually linked to?

A

atherosclerosis

48
Q

What is the pathology of a blood clot in the heart?

A

Disruption of atherosclerotic plaque .

Platelet aggregation and thrombus formation.

Risk of embolus formation.

Thrombus/embolus blocking blood flow to myocardium.

49
Q

What are three causes of thrombus formation.

A
  1. plaque rupture (fibrous cap weakening by immune cells or turbulent blood flow)
  2. Erosion of fibrous cap
  3. Dysfunctional endothelium
50
Q

True or false, all Myocardial infarctions are linked to coronary heart disease?

A

False

51
Q

What is the P wave in an ECG?

A

Atrial depolarisation

52
Q

What is the QRS complex in an ECG

A

Ventricular depolarisation

53
Q

What is the T wave in an ECG?

A

Ventricular repolarization

54
Q

What does an ST elevation in an ECG indicate?

A

Abnormal currents in damaged cardiomyocytes.

55
Q

What are some complications of a myocardial infarction?

A
Arrhythmias.
Embolism.
Pericarditis.
Cardiac tamponade.
Congestive heart failure.
Cardiogenic shock.
56
Q

What are arrhythmias?

A

Abnormalites of the electric rhythm.

Associated with a wide range of common clinical problems

57
Q

True or false, there is a spectrum of arrhythmias?

A

True.

Common benign palpitations, we could live our whole lives with these and not know and have a normal life.