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Cardiographer > Pathology of the Cardiovascular System 2 > Flashcards

Pathology of the Cardiovascular System 2 Flashcards

1
Q

Coarctation of the aorta

A

defined as a constricted aortic segment (congenital)|

The localized constriction may form a shelf-like structure with an eccentric opening or maybe a membranous structure with a central or eccentric opening.

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2
Q

The classic coarctation of the aorta is located in the…

A

thoracic aorta distal to the origin of the left subclavian artery at about the level of the ductal structure.

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3
Q

Coarctation of the aorta can cause…

A

can increase blood pressure in your arms and head, reduce pressure in your legs and seriously strain your heart leading to LVH and possibly heart failure.

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4
Q

Treatment of coarctation of the aorta

A

Surgery may be needed to correct the defect, depending on the severity of the coarctation, and the presence of other congenital defects.

Another option may be a balloon angioplasty or implantation of a stent using cardiac catheterization.

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5
Q

Cyanotic heart disease

A

refers to a group of many different structural heart defects that are present at birth (congenital).

They result in a low blood oxygen level as deoxygenated blood enters the systemic circulation.

Cyanosis refers to a bluish colour of the skin and mucous membranes.

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6
Q

Types of Cyanotic heart disease:

A

Coarctation or complete interruption of the aorta

Ebstein anomaly = The tricuspid valve sits lower than normal in the right ventricle and the tricuspid valve’s leaflets are abnormally formed

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7
Q

Hypoplastic left heart syndrome

A

The left side of the heart (LA, LV and Aorta) are small and underdeveloped and the mitral valve and aortic valve is atretic (unformed and fails to open).

The heart can’t pump enough blood to the body.

The right ventricle, which is only supposed to pump blood to the lungs, pumps blood to the lungs and the body through a connection called a patent ductus arteriosis (PDA).

Babies with HLHS are almost always born with an atrial septal defect (ASD)

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8
Q

Patent ductus arteriosis (PDA)

A

Lets blood reach the aorta and go out to the body from the right ventricle.

Usually, babies don’t need this connection after they’re born so it closes. But a baby with hypoplastic left heart syndrome needs this connection to get blood to the body. Because the right ventricle is pumping blood to the lungs and the body, it is doing extra work.

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9
Q

Atrial septal defect (ASD)

A

This is a hole between the atria that lets blood with oxygen mix with blood low on oxygen.

This way, the blood that the right ventricle pumps out to the body has some oxygen in it.

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10
Q

Treatment for HLHS involves…

A

Give medicine called prostaglandin to keep the ductus open so the right ventricle can continue pumping blood out to the body.

Connecting the superior vena cava and inferior vena cava directly to the pulmonary arteries.

The main pulmonary artery is connected to the aorta and becomes a systemic vessel from a systemic right ventricle.

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11
Q

What Causes Hypoplastic Left Heart Syndrome?

A

HLHS is a birth defect that happens when a baby is growing in the womb. No one knows exactly what causes it, but it could have a mix of causes, including a baby’s genes

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12
Q

A baby born with hypoplastic left heart syndrome may have:

A

fast breathing

blue or grayish coloring of the skin and nails

trouble feeding

low energy and activity

fewer than normal wet diapers

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13
Q

Tetralogy of Fallot

A

combination of 4 heart defects present at birth, includes:

  • ventricular septal defect (VSD)
  • narrow pulmonary valve
  • thickening of the right ventricle
  • misplaced aortic valve

Causes oxygen-poor blood to flow out of the heart and to the rest of the body

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14
Q

Treatment of Tetralogy of Fallot involves…

A

patching the VSD and either bypassing the narrowed pulmonary valve with a conduit or ballooning the valve

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15
Q

symptoms of Tetralogy of Fallot:

A

A bluish coloration of the skin caused by low blood oxygen levels (cyanosis)

Tet spells = develop deep blue skin, nails and lips after crying or feeding, or when agitated due to drop in O2 in blood

Shortness of breath and rapid breathing

Poor weight gain

Heart murmur

An abnormal, rounded shape of the nail bed in the fingers and toes (clubbing)

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16
Q

Tetralogy of Fallot defect: pulmonary valve stenosis

A

Narrowing of the valve that separates the lower right chamber of the heart (right ventricle) from the main blood vessel leading to the lungs (pulmonary artery) reduces blood flow to the lungs. The narrowing might also affect the muscle beneath the pulmonary valve. Sometimes, the pulmonary valve doesn’t form properly (pulmonary atresia).

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17
Q

Tetralogy of Fallot defect: ventricular septal defect

A

A hole in the wall (septum) that separates the two lower chambers of the heart (left and right ventricles). The hole causes oxygen-poor blood in the right ventricle to mix with oxygen-rich blood in the left ventricle. This causes inefficient blood flow and reduces the supply of oxygen-rich blood to the body. The defect eventually can weaken the heart.

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18
Q

Tetralogy of Fallot defect: misplaced aortic valve

A

Normally the aorta branches off the left ventricle. In tetralogy of Fallot, the aorta is in the wrong position. It’s shifted to the right and lies directly above the hole in the heart wall (ventricular septal defect). As a result, the aorta receives a mix of oxygen-rich and oxygen-poor blood from both the right and left ventricles.

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19
Q

Tetralogy of Fallot defect: right ventricular hypertrophy

A

When the heart’s pumping action is overworked, the muscular wall of the right ventricle becomes thick. Over time this might cause the heart to stiffen, become weak and eventually fail.

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20
Q

Total anomalous pulmonary venous return:

A

the veins bringing blood back from the lungs (pulmonary veins) don’t connect to the left atrium like usual. Instead they go to the heart by way of an abnormal (anomalous) connection.

oxygen-rich blood does not return from the lungs to the left atrium. Instead, the oxygen-rich blood returns to the right side of the heart. Here, oxygen-rich blood mixes with oxygen-poor blood. This causes the baby to get less oxygen than is needed to the body. To survive with this defect, babies with TAPVR usually have a hole between the right atrium and the left atrium (an atrial septal defect) that allows the mixed blood to get to the left side of the heart and pumped out to the rest of the body.

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21
Q

Transposition of the great arteries

A

The great vessels are transposed so that the aorta arises from RV and the pulmonary valve arises from the LV. A septal defect (ASD/ VSD) or patent ductus arteriosus must be present for survival. Treatment involves surgically switching the arteries.

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22
Q

Symptoms of Cyanotic Heart Disease

A
  • blue lips, fingers and toes
  • Breathing problems
  • Tiredness
  • Sweating
  • Poor weight gain
  • Fainting and chest pain may occur
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23
Q

cyanotic defects:

A

tetralogy of fallot

transposition of the great arteries

result in mixing of blood, obstructed pulmonary blood flow

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24
Q

hypothermia

A

core body temperature of less than 35 degrees centigrade

25
Q

Hypothermia changes seen on the ECG:

A

Bradycardias, including:
- Sinus bradycardia (may be marked)
- Atrial fibrillation with slow ventricular response
- Slow junctional rhythms
- Varying degrees of AV block

Osborn wave (J wave)

Long QT interval

26
Q

Osborn wave (J wave)

A

a positive deflection at the J point (negative in aVR and V1). It is usually most prominent in the precordial leads. The height of the Osborn wave is roughly proportional to the degree of hypothermia.

27
Q

Dextrocardia

A

heart condition characterized by abnormal positioning of the heart.

The apex is positioned on the right side of the chest

may be associated with the condition situs inversus where other organs are in a mirror image

28
Q

In the more common types of dextrocardia, other heart defects are also present…

A
  • Double outlet right ventricle
  • Endocardial cushion defect
  • Pulmonary stenosis or atresia
  • Single ventricle
  • Transposition of the great vessels
  • Ventricular septal defect
29
Q

ECG findings of dexocardia include:

A
  1. Predominantly negative P wave, QRS complex, and T wave in lead I
  2. Low voltage in leads V3-V6 (since these leads are placed on the left side of the chest)
30
Q

Modified ECG Procedure for dexocardia:

A

A standard 12 lead ECG should be performed followed by a second ECG with right sided chest electrodes applied. Limb electrodes should not be reversed.

The resultant modified ECG will show normalised R wave progression but with a negative lead I.

31
Q

Aortic valve stenosis

A

Valve leaflets of not open completely. The area through which blood moves out of the heart to the aorta is narrowed (stenosis)

heart must work harder to pump enough blood into the aorta and to the rest of the body

extra work of the heart can cause the left ventricle to thicken and enlarge

Eventually the strain can cause a weakened heart muscle and can ultimately lead to heart failure and other serious problems

may require valve replacement

32
Q

Aortic valve stenosis symptoms

A

Some people with aortic valve stenosis may not have symptoms for many years.

Symptoms generally occur when narrowing of the valve is severe.

  • An irregular heart sound (heart murmur)
  • Chest pain (angina) or tightness with activity
  • Feeling faint
  • Shortness of breath
  • Fatigue
  • palpitations
33
Q

causes of aortic valve stenosis

A

Congenital heart defect e.g. bicuspid aortic valve

aortic valve calcification (calcium deposits can build up on the heart valves)

Rheumatic fever (complication of untreated strep throat which can cause scar tissue to form on valve)

34
Q

Aortic valve regurgitation

A

condition that occurs when your heart’s aortic valve doesn’t close tightly

some of the blood pumped out leaks backward

The leakage may prevent your heart from efficiently pumping blood to the rest of your body

the left ventricle holds more blood, possibly causing it to enlarge and thicken

at first, the larger left ventricle helps maintain good blood flow with more force. But eventually these changes weaken the left ventricle

can lead to heart failure and arrhythmias

35
Q

symptoms of aortic valve regurgitation

A

Shortness of breath

Fatigue

Heart murmur

arrhythmia

fainting

Chest pain

palpitations

Swollen ankles and feet

36
Q

causes of aortic valve regurgitation

A

Congenital heart defect e.g. bicuspid aortic valve

aortic stenosis due to calcification

aortic valve calcification (calcium deposits can build up on the heart valves)

endocarditis (Inflammation of the lining of the heart’s chambers and valves)

Rheumatic fever (complication of untreated strep throat which can cause scar tissue to form on valve)

37
Q

With hypothermia, the ECG can first show…

A

artefact due to shivering (uncommon below 32°C )

38
Q

Hypothermia results in a decline in…

Hypothermia leads to ECG with…

A

heart rate and conduction velocity = bradycardia, heart block

prolongation of PR, QRS and QT intervals

39
Q

Below 32°C

A

atrial activation becomes slow and irregular

40
Q

Below 28°C

A

junctional bradycardia may be seen

41
Q

most specific ECG finding in hypothermia

A

J wave (Osborn wave)

a dome/hump elevation in the terminal portion of the QRS deflection, best seen in left chest leads (the size of the J wave corresponds with severity of hypothermia)

42
Q

ECG features of hypothermia:

A

Tremor artefact from shivering

AF with slow ventricular rate

J wave (Osborn wave)

Bradycardias, especially junctional

Prolonged PR, QRS and QT interval

Premature ventricular beats, ventricular tachycardia, ventricular fibrillation (ventricular arrhythmias are most common cause of death in hypothermia)

Asystole = absence of cardaic activity (almost flat line)

43
Q

ECG changes of pericarditis:

A

Saddle shaped ST elevation (concaves upwards) throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6)

PR segment depression can be in these leads due to atrial inflammation

Reciprocal ST depression and PR elevation in lead aVR (± V1)

Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion

44
Q

Pericarditis

A

Inflammation of the pericardium secondary to infection, localised injury or systemic disorders producing characteristic chest pain, dyspnoea and serial ECG changes.

Pericarditis is a common cause of chest pain, and may mimic the signs and symptoms of myocardial infarction. It is a result of inflammation of the pericardium.

45
Q

dyspnoea

A

Shortness of breath

46
Q

chest pain associated with pericarditis is…

A

often retrosternal in nature, pleuritic, and positional (relieved by sitting forward, worse lying flat)

47
Q

in pericarditis widespread ST segment changes occur due to

A

involvement of the underlying epicardium (myopericarditis)

48
Q

Echo is useful in the early assessment of patients with suspected pericarditis to look for complications such as

A

pericardial effusion and cardiac tamponade

49
Q

In pericarditis the degree of ST elevation is typically…

A

modest (0.5 – 1mm)

50
Q

Pericarditis is classically associated with ECG changes that evolve through four stages:

A

Stage 1 – widespread ST elevation and PR depression with reciprocal changes in aVR (occurs during the first two weeks)

Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks)

Stage 3 – flattened T waves become inverted (3 to several weeks)

Stage 4 – ECG returns to normal (several weeks onwards)

51
Q

Causes of Pericarditis:

A

Infectious – mainly viral (coxsackie virus); occasionally bacterial, fungal, TB.

Immunological – SLE, rheumatic fever

Uraemia

Post-myocardial infarction or following cardiac surgery (Dressler’s syndrome)

Trauma

Paraneoplastic syndromes

Drug-induced (isoniazid, cyclosporin)

Post-radiotherapy

52
Q

Pericardial effusion

A

collection of fluid within the pericardial sac.

most commonly occurs with pericarditis.

When the pericardial sac fills, this puts pressure on the ventricles, and compromises their pumping function. This causes problems with circulation.

When this occurs, it is known as cardiac tamponade.

Tamponade generally comes on very quickly – it is acute heart failure due to compression.

53
Q

ECG features of pericardial effusion

A

low voltage QRS complexes

54
Q

treatment of pericardial effusion

A

most pericardial effusions resolve spontaneously

In cases of a rapid forming effusion, then tamponade will probably result; and acute treatment would involve pericardiocentesis, and perhaps a drain, just to allow the fluid to escape.

55
Q

Cardiac Tamponade

A

heart become compressed by excess fluid in the pericardium. Compression causes reduced diastolic filling of the heart, which can cause cardiac arrest.

56
Q

Atrial septal defects

A

results from incomplete closure of the atrial septum in utero

ECG may appear relatively normal

PR interval prolonga- tion and first degree heart block may occur in up to 20% of cases

QRS complexes may show some right ventricular conduction delay denoted by an rsR1 in V1

Associated mitral valve clefts can occur, leading to mitral regurgita- tion and, if severe, left ventricular hypertrophy

57
Q

Ventricular septal defects

A

small ventricular septal defects close spontaneously in 50-70% of cases during childhood

Generally these are not asso- ciated with any ECG abnormalities - degree of the ECG abnormality is directly proportional to the haemodynamic effect on ventricular function

A medium sized ventricular septal defect can exhibit left ventricular hypertrophy and left atrial enlargement

A large ventricular septal defect results in biventricular hypertrophy and equiphasic QRS complexes in the mid-precordium known as the Katz-Wachtel phenomenon

58
Q

Coarctation of the aorta

A

results in left ventricular hypertrophy in 50-60% of asymptomatic children and adults (deep S wave seen in V1)

The strain pattern of lateral T wave inversions is seen in about only 20% of asymptomatic children and adults.

Cardiographer (5 decks)

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