cardiovascular mechanics 2 Flashcards
Phases in the cardiac cycle
diastole - relax
systole - contractile
diastole
2/3 of heart beat
ventricular relaxation - ventricles fill with blood
4 phases
systole
1/3 heart beat ventricles generate pressure overcome afterload in pulmonary and systemic system eject blood into arteries 3 phases
end-diastolic volume
vol in ventricle just before ventricle contracts
end systolic vol
volume in the ventricle when it has expelled all that it is going to expel
stroke volume
the volume pushed out in heartbeat
ejection fraction
(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%
phases of the cardiac cycle
atrial systole isovolumetric contraction rapid ejection reduced ejection isovolumetric relaxation rapid passive filling reduced passive filling
describe atrial systole
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
describe isovolumetric contraction
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
describe rapid ejection
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
describe reduced ejection
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
describe isovolumetric relaxation
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
describe rapid passive filling
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
describe reduced passive filling
longest phase called diastasis ventricle fill slowly, but a lot no electrical activity aortic pressure decrease how much ventricle fills - preload
describe pulmonary circuit pressures
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
how do you measue pressure in th heart
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
what is a pressure volume loop
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
effect of preload and afterload on the pressure volume loop
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
calculation for cardiac output
cardiac output = hart rate * SV
components of SV
preload, afterload, contractility
contractility
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
contractility and Frank-sterling law
increase in contractility = more contraction - higher pressure
makes a family of end systolic pressure volume relations
describe extrinsic stimulation
parasympathetic at rest - slows SAN rate from 110 - 70bpm
sympathetic increase rate through hormone - adrenaline, nerves - noradrenaline - change vol and intrinsic contractility
affect of hardened artery
higher afterload, more pressure needed to overcome backpressure
affect of acute blood loss
decrease venous return to heart, and so ventricular filling - smaller preload - decrease SV
effect of exercise
higher Bp and adrenaline - increase contractility, more powerful contraction
higher preload - higher venous return
higher BP in aorta = higher afterload
overcome by increased contraction
