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Y1&2 Medicine Zoe Veary > CVS 146 Aortic Stenosis > Flashcards

CVS 146 Aortic Stenosis Flashcards

1
Q

Describe what happens to the heart during diastole

A

Ventricles are rapidly relaxing

AV valves remain closed until the pressure drops sufficiently

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2
Q

Describe what happens during atrial systole

A

Atrial depolarisation causing atrial contraction which fills the ventricles with blood

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3
Q

What waves on the JVP tracing and ECG account for atrial systole?

A

a wave and P wave

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4
Q

What is the End Diastolic Volume and what is its normal value?

A

Volume of blood inside the ventricles once they have been filled
Normally 120-140mls

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5
Q

What is the end diastolic pressure and what is its normal value?

A

Pressure inside the ventricles after filling and is normally 10mmHg

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6
Q

Why is the EDP in the left ventricle slightly higher than the right?

A

It is larger with increased wall thickness and stiffness

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7
Q

Why is EDV important?

A

It is an important determinant of the strength of the subsequent contraction - Starlings Law of the Heart

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8
Q

Describe what happens during ventricular systole?

A

Ventricles contract - sharp rise in pressure
the AV valves close
Once pressure inside the ventricles exceed that of the outflow vessels the pulmonary and aortic valves open

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9
Q

What waves on ECG and JVP tracing are seen in ventricular systole

A

QRS complex
c wave = the wave when the pressure inside the ventricles rises but not sufficiently for outflow valves to open but causes the mitral valve to bulge into the atria

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10
Q

What is the difference in pressure between the pulmonary artery and the aorta?

A

Aorta is ~80mmHg and the pulmonary artery = ~15mmHg

these are pressures in diastole

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11
Q

What wave on ECG accounts for muscle repolarisation during the second half of ventricular systole?

A

T wave

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12
Q

What makes the first and second heart sounds?

A 
1st = AV valves closing (mitral and tricuspid) at beginning of ventricular systole
2nd = Closure of pulmonary and aortic valves at end of ventricular systole
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13
Q

In the normal heart what is stroke volume? And therefore what usually is the end-diastolic volume?

A

~70mmHg

EDV ~ 50mmHg

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14
Q

What is the ejection fraction of the heart?

A

The proportion of the blood in the heart that is ejected = stroke volume/ end diastolic volume

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15
Q

What accounts for the v wave on JVP tracing?

A

An increased in atrial pressure as the veins fill the atria

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16
Q

What proportionately to systole is the length of diastole at rest?

A

Double the length of systole

17
Q

What accounts or the y descent on JVP tracing?

A

As ventricular pressure decreased the AV valves open causing a decrease in atrial pressure

18
Q

What is the JVP tracing a measure of?

A

Right atrial pressure

19
Q

What accounts for the x descent on JVP tracing?

A

Downward motion of the heart in ventricular systole

20
Q

What is the pressure volume loop?

A

Ventricular pressure plotted against volume - generates a loop

21
Q

What is the shape of the pressure volume loop affected by?

A

Contractility, compliance of the ventricles and factors affecting refilling or ejection

22
Q

What does the volume inside of the pressure volume loop account for?

A

measure of the work done during a heart beat - an indicator of cardiac function

23
Q

What may be seen on JVP tracing in atrial hypertrophy? What is a common cause behind this?

A

Large a wave - pulmonary hypertension

24
Q

What may be seen on JVP tracing in tricuspid regurgitation?

A

Giant v wave

25
Q

What are the three main pathologies of aortic stenosis?

A

Acquired calcification
Rheumatic fever
Congenital - biscuspid valve

26
Q

What is the pathophysiological mechanism behind Aortic Stenosis?

A

There is a chronic inflammatory response to epithelial damage = inflammation, lipid plaques and leukocyte infiltration
leukocytes cause insterstitial cells to differentiate into osteoblasts = bone nodule synthesis and calcification

= stenosis due to decreased compliance of leaflets
= reduced aortic vave area

27
Q

Why is there LVH in aortic stenosis?

A

The increased pressure required in the LV to maintain stroke volume and the pressure difference causes increased recruitment of myocytes and hypertrophy

28
Q

When do symptoms tend to develop in AS?

A

When valve surface area is down to about 1-1.5 cm^2

= late presentation

29
Q

Why does angina develop in AS?

A

Increased demand for oxygen but decreased supply

Increased demand: increased work due to greater pressures needed and increased number of myocytes

Decreased supply: shortened diastole ( increased systole as LV takes longer to eject same SV); lower aortic pressures ( pressure required to fill CA’s); reduced capilliary density ( hypertrophy squashes CA’s = reduced myocardial perfusion)

30
Q

What are the possible mechanisms behind development of syncope in AS?

A

Failure to meet O2 demand - mostly during exertion
Aortic hypotension - vasodilation in exercise but can’t overcome low BP
High ventricular pressure stimulates mechanoreceptors = bradycardia
Ventricular arrhythmias

31
Q

What does dyspnoea develop in AS?

A

Due to LVH - decreased filling pressure = higher left atrium pressure = higher pulmonary BP due to back pressure into veins = left sided heart failure

32
Q

Why may there be GI bleeding in AS?

A

Angiodysplasia in GI tract, denatured clotting factors, platelets disturbed by turbulent flow

33
Q

What are some of the signs of AS?

A

Heaving apex beat (due to LVH)
Slow rising pulse with reduced pulse pressure (slow passage of blood through stenosis and blood loss to arterioles)
Ejection systolic murmur

34
Q

What are the 3rd and 4th heart sounds?

A

Not usually heard:

3: blood passively rushing into ventricles in diastole
4: turbulent blood flow during atrial systole

35
Q

When does an ejection systolic murmur occur? And why in AS?

A

between 1st and 2nd heart sounds and due to turbulent blood flow through stenosed AV

Y1&2 Medicine Zoe Veary (60 decks)

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