Hemodynamics of Valvular Heart Disease (Tillisch)

Question 1

How does the heart respond to acute loading?

Answer 1

Increase HR

Increase contractility

Increase Frank-Starling effect

Question 2

What causes chronic loading?

Answer 2

1) High output state, so increased demand for cardiac work (anemia, pregnancy, cirrhosis (excessive vasodilation), hyperthyroidism)
2) Damaged ventricle with normal demands (MI)
3) Impedance to ejection causing increased pressure work (aortic stenosis, hypertension)
4) Valvular regurgitation or intra/extra cardiac shunting causing increased volume work

Question 3

Conditions leading to increased pressure work

Answer 3

Valvular stenosis

Arterial hypertension

Increased wall tension (increased chamber radius)

Question 4

Excessive pressure work causes hypertrophy, what are the consequences of hypertrophy?

Answer 4

1) Increased myofilament production within myocardial cell
2) Abnormal myosin with just one head
3) Decreased Ca2+ entry and decreased Ca2+ channels per weight

Question 5

Different forms of hypertrophy

Answer 5

Concentric: Sarcomeres added in parallel (each cell is fatter); pressure overload

Eccentric: Sarcomeres added in series (each cell is longer); volume overload

Note: hypertrophy causes tall QRS because lots of mass depolarizing (also get high QRS if you’re skinny, no insulation of electricity)

Question 6

Limits of myocardial adaptation for pressure loading

Answer 6

Limited capacity for protein production and replication

Concentric hypertrophy limits ventricular filling and increases LVEDP

Increased myocardial cell mass requires more coronary blood flow

Question 7

Decompensation (failure of heart to maintain pressure work)

Answer 7

Decreased compliance (increased LV stiffness and difficulty filling LV) –> lung venous congestion (congestive heart failure)

Decreased ejection –> ventricular dilation –> mitral valve dilatation/mitral valve insufficiency –> less forward flow and more backward flow

Question 8

Conditions increasing volume work

Answer 8

Mitral regurgitation

Aortic regurgitation

Shunts: hole between LV/RV or LA/RA (have to generate 10L just to get 5 L to body)

Question 9

Consequences of excessive volume work

Answer 9

Eccentric hypertrophy (increased myocyte length, so increased chamber size/radius) actually DECREASES efficiency

Question 10

Heart compensating for decreased efficiency due to eccentric hypertrophy

Answer 10

1) Preload increase increases force of contraction (Starling) but this is small and used up quickly
2) Increase in volume of ventricle means more volume ejected with each beat
3) Volume work cheaper than pressure work because of LaPlace (note: easier to get blood out because low afterload; as ventricle ejects, it is shortening its radius thus reducing work (T))

Question 11

Limits of adaptation for volume loading

Answer 11

Limited capacity for protein production

Increase in LV diastolic pressure caused by increasing volume (complicance)

Question 12

Treating volume loading

Answer 12

Want to decrease radius and make ventricle contract more fully

Reduce afterload (vasodilate, reduce volume with diuretics)

Question 13

Why do you get hypertrophy in the first place?

Answer 13

Trying to reduce wall tension!

If wall tension increases, you can increase wall thickness (hypertrophy) to decrease wall tension (LaPlace)

Question 14

Isn’t an increase in volume good because you’re increasing preload?

Answer 14

Yes, but you’re also increasing afterload, meaning the heart will need to work harder to pump out that volume