7. Haemodynamics Flashcards Preview

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Flashcards in 7. Haemodynamics Deck (18)
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What is normal BP?

What are the guidelines for hypertension for systolic and diastolic e.g. when should you intervene?


120/80 mmHg

 >140/>90 = marginal hypertension; >160/>100 = intervention threshold




How do you calculate MAP?

MAP: diastolic + 1/3(pulse pressure)

(pulse pressure = systolic - diastolic)


So normal = 90 + 1/3(120-90) = 100mmHg


What is compliance, is it good or bad, and why?

What happens to this as people age?

Arteriolar stretchiness, due to elastin fibres in arterial walls, GOOD b/c it smooths out pulse pressure and the stretchiness reduces the work of the heart in pumping blood b/c some blood stored in large arteries by them stretching and inc. their vol.

Age: elastin replaced by collagen, systolic pressure increases b/c aorta can't stretch to accomodate stroke vol, can decrease C.O. as isovolumetric contraction phase is longer


Describe the Windkessel effect.

Compliance of small elastic arteries: walls of aorta and elastic arteries distend when BP rises during systole and recoil when BP falls during diastole. Thus there's a net storage of blood during systole which discharges during disatole.


What is pre-hypertension?

120-139/80-89 mmHg


What is Poiseuille's Law and how does this relate to arterial flow?

Flow of liquid through a tube depends on 4th power of radius of tube.  Thus small changes in arterial diameter produce large changes in flow. Arteriole SM only has to constrict SLIGHTY to effect a sig. flow reduction.


What is the formula for cardiac output?

How would you measure each parameter?

What is normal C.O in healthy resting man?

Give another less-used may of measuring C.O.

C.O. = HR x stroke volume

HR directly/ECG, SV via echocardiography (ultrasound)


Doppler ultrasound/transoesophageal doppler


What factors affect

a) HR

b) stroke volume

What is the formula for stroke volume?

a) ANS, hormones, fitness levels, age

b) heart size, fitness levels, gender, contractility, contraction duration, preload (EDV)




C.O. is 5L/min at rest. How is this distributed?

Kidneys = 25%, Brain= 14%, Heart = 4%

2.7-3L/min remain for the rest of the body and where it goes depends on digestive state. After a meal 1.5L/min to gut leaving 1.2-1.5/min for muscles and skin. Rest and digest = 1L/min to muscles. Skin v. variable.


What mechanisms increase C.O. during exercise, and how much does C.O increase by?

During exercise, diastolic filling time decreases but ventricular filling/stroke vol is maintained - how?

What other changes occur during exercise?

Increasing HR or sroke volume, C.O can increase to nearly 4x (3.75 times).

MAINTAINED due to contraction of atria and increased ventricular contractility (= decreased ESV).

Increased O2 uptake, respiration rate and depth which increases pulmonary pO2 -> pulmonary arteries relax -> small increase in pulmonary arterial pressure = improves perfusion of lung esp. apices


What 2 things does the work of the heart depend on?

1) viscosity of blood (depends mainly on haematocrit, normally abour 45%, and on deformability of RBC)   2) arteriole diameter (5um or less)

(NB. haematocrit too high - heart has to work harder, if too low, not enough O2)(RBC = 7um)


RBC interact with capillaries. How, and what does this cause?

Edges of RBC interact with polypeptide chain protruding into lumen of capillary, which are connected to proteins embedded in endothelium of capillary walls.

AS RBC move along -> deflect chains -> allows Ca2+ to enter endothelium -> formation of NO which causes vasodilation and is a local anticoagulant.


What are the 4 primary determinants of blood viscosity?

1) haematocrit (strongest influence)

2) RBC deformability

3) RBC aggregation

4) plasma viscosity


What is polycythemia? What are the 2 types?

Haematocrit increases. Blood viscosity increases. Reduced flow through BVs. May cause organ failure.

Can be 1) Absolute (excessive production of RBC) or 2) relative (decrease in volume of plasma)


What is Laplace's Law?

What does this mean?

How does this relate to aneurysm formation?

The smaller the vessel radius, the greater the pressure the wall strength can withstand.

Small diameter arterioles only need thin walls to withstand normal arterial pressures.

If artery call weakens/tears, its radius increases and so balancing pressure (Laplace's law) that elastic  tissue generates is less. Wall balloons out = reduces effectiveness of wall to withstand pressure. Aneurysm may occur. Common site = aorta.


Where do aneurysms most commonly occur?

Why do aneurysms occur?

Just before points where BVs branch. Cerebral arteries (more convoluted. Berry aneurysms)


Due to pulsatile blood flow, eddies or vortices at branch points from turbulent flow in artery (which is in turn associated with atheroma formation). Narrowed artery lumen in atheroma plus turbulent flow produces local 'spikes' of high BP. Hypertension and artery disease = major risk factors for aueurysm formation. Often local inflammatory reaction in atheroma destroys elastin fibres in wall making it more prone to stretch where there is a BP spike.


What 3 ways can aneurysms present in?

1. MRI/angiography

2. Rupture -> subatachnoid brain hemorrhage

3. Symptoms of mass effect on neural structures


How can aneurysms be treated?


Coiling (wire pushed into swollen artery to form a coil, blood clots around it which takes pressure off wall and forms a stable structure)

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