cardiovascular mechanics 2

Question 1

Phases in the cardiac cycle

Answer 1

diastole - relax

systole - contractile

Question 2

diastole

Answer 2

2/3 of heart beat
ventricular relaxation - ventricles fill with blood
4 phases

Question 3

systole

Answer 3

1/3 heart beat
ventricles generate pressure 
overcome afterload in pulmonary and systemic system 
eject blood into arteries 
3 phases

Question 4

end-diastolic volume

Answer 4

vol in ventricle just before ventricle contracts

Question 5

end systolic vol

Answer 5

volume in the ventricle when it has expelled all that it is going to expel

Question 6

stroke volume

Answer 6

the volume pushed out in heartbeat

Question 7

ejection fraction

Answer 7

(100*SV)/end-diastolic volume = ejection fraction
amount of blood that leaves the heart in relation to the amount of blood that enters the heart
clinical sign of vitality of the heart - how well it is contracting
normal = 16% heart failure = 40%

Question 8

phases of the cardiac cycle

Answer 8

atrial systole 
isovolumetric contraction 
rapid ejection 
reduced ejection 
isovolumetric relaxation 
rapid passive filling 
reduced passive filling

Question 9

describe atrial systole

Answer 9

contraction of atria caused by pacemaker signal - the rate at which this fires AP can be modulated
atria almost full from passive filling
p wave signify muscle contraction - rise in vol of blood in ventricle, start of systole
can have 4th heart sound - abnormal: congestive heart failure, pul embolism or tricuspid incompetence - valve doesn’t close properly

Question 10

describe isovolumetric contraction

Answer 10

wave of depolarisation conducted to ventricle – AP – contraction
QRS - start of ventricular depolarisation
all valves shut - muscle fibres can’t shorten - blood has no where to go - no change in volume (isovolumic)
1st hart sound - lub - closure of AV valves at start f this phase

Question 11

describe rapid ejection

Answer 11

open of aortic and pulmonary valves
pressure in ventricles exceeds the afterload (ie pressure in arteries and aorta)
semi-lunar valves open, fibres shorten blood ejected, isotonic contraction - ventricular volume decrease
aortic pressure mirror increase in ventricular pressure
no heart sounds

Question 12

describe reduced ejection

Answer 12

end of systole
more blood laves ventricle - slower
less pressure in vessels
reduced pressure gradient - valves close
pressure in ventricles reduce lower than arteries - backflow - semilunar valves close
ventricle repolarise - denoted by T wave

Question 13

describe isovolumetric relaxation

Answer 13

volume of ventricle doesn’t change
aortic and pul valves shut - 2nd hart sound ‘dub’
AV valves shut until vent pressure lower than atrial pressure
dichrotic notch caused by rebound pressure against aortic valve as distended wall relaxes
2nd heart sound- close of semilunar valves

Question 14

describe rapid passive filling

Answer 14

blood from atria to ventricle - increase ventricular volume
in isoelectric (flat) parts ECG
AV valves open
abnormality = 3rd heart sound - AV valves wrong eg calcified so hardened so don’t close properly - blood more turbulent through them - ventricular galloping

Question 15

describe reduced passive filling

Answer 15

longest phase 
called diastasis 
ventricle fill slowly, but a lot
no electrical activity 
aortic pressure decrease 
how much ventricle fills - preload

Question 16

describe pulmonary circuit pressures

Answer 16

R ventricle same changes in pressure as L - has to pump same amount of blood
R has a lower absolute pressure than L
peak BP is 25mmHg in pul artery
in both the pressures decay through arterioles and capillaries

Question 17

how do you measue pressure in th heart

Answer 17

enter catheter in vena cava
has pig tail to tuck into right atria and ventricle
pigtail with pressufe transducer - measure pressue in atria, vent and pulmonary tree
pump up balloon and assess the back pressure in lungs
see if anything going wrong in left side of heart
called capillary pulmonary presser

Question 18

what is a pressure volume loop

Answer 18

y axis - L ventricular pressure
x axis - L ventricular vol
end diastolic vol (low p)
isovolumetric contraction (high pressure, high vol)
end-systolic volume (low vol, high pressure)
isovolumeric relaxation (low vol and pressure)
see how well the heart is contracting, give idea of ventricular filling pressure

Question 19

effect of preload and afterload on the pressure volume loop

Answer 19

end diastolic pressure affected by preload - cause stretch infibre
pressures in great vessel determine after load
high preload = larger SV, move up active force load - more force
higher afterload= more pressure needed, PV line move up, less shortening = smaleer SV

Question 20

calculation for cardiac output

Answer 20

cardiac output = hart rate * SV

Question 21

components of SV

Answer 21

preload, afterload, contractility

Question 22

contractility

Answer 22

contractile capability (strength of contraction) of the heart 
measure of change of contraction the muscle can produce 
measured by ejection fraction 
increased by sympathetic stimulation - eg adrenaline/noradrenaline - bind to muscle cell - change phosphorylation, change ca delivery, force of contraction increases

Question 23

contractility and Frank-sterling law

Answer 23

increase in contractility = more contraction - higher pressure
makes a family of end systolic pressure volume relations

Question 24

describe extrinsic stimulation

Answer 24

parasympathetic at rest - slows SAN rate from 110 - 70bpm

sympathetic increase rate through hormone - adrenaline, nerves - noradrenaline - change vol and intrinsic contractility

Question 25

affect of hardened artery

Answer 25

higher afterload, more pressure needed to overcome backpressure

Question 26

affect of acute blood loss

Answer 26

decrease venous return to heart, and so ventricular filling - smaller preload - decrease SV

Question 27

effect of exercise

Answer 27

higher Bp and adrenaline - increase contractility, more powerful contraction
higher preload - higher venous return
higher BP in aorta = higher afterload
overcome by increased contraction