Heart as a pump Flashcards
which valves are open in late diastole
mitral and R AV
explain what happens in late diastole
blood will flow from SVC to R atrium to R ventricle
blood from pulmonary veins into L atrium to L ventricle
phase of atria nd ventricle filling
late diastole
explain the percentages of blood nd how it travels from atria to venticles
70% - passively bc of low psi in ventri
30% - atrial systole
why is the remaining 30% need to be pumped in atrial systole
bc ventricles are 70% filled - not low psi anymore - needs force
why is there regurgitation during atrial systole
as atria contracts - strong - no valves present in great veins - most to ventricle some to veins - normal
when does AV valve close
during ventricular systole; towards close pa lng sa late dias and atrial sys to prople remaining 30%
explain why isovolume ventricular contraction is needed
ventricle has low psi compared to pulmo artery nd aorta - need to be high psi to overcome pulmo and aortic valves
explain the ventricular systole
1st part - isovlome contract - ventr contracts but no ejection - only to build up psi
2nd part - ventri ejection - aortic nd pulmo valces open - rapid ejection slows as systole progress
if psi declines in vent sys why does blood continue to flow in late systole
bc of momentum built up is ivc
how do AV valves close in vent sys
strentch of ventricles pull down AV valves
explain the volumes of blood in vent during dias and sys
dias 130 ml - sys 50 ml tira - 65% ejection fraction (should be pumped) - not all is pumped - 80 ml pumped
significance of ejection frac
if <65% ok for operation bc heart is strong
what valves close in early dias
aortic nd pulmonic
why does aortic nd pumonic close in early dias
psi in vent drops - high psi aorta nd pulmo art - closes to avoid backflow
explain the sig of IVR
dec in vent psi - prep for opening of mitral nd AV valves - for vent filling - dapat lower than atrial psi end when it is
signifies close of AV valve
C prime
what is the signifcance of the pericardium
Separates it from thoracic viscera
- Pericardial sac has 5 - 30 ml clear fluid
- Lubricates the heart
- Permits it to contract with minimal friction
which atrial systole happens first
right before left - bc of SA node on R atrium
which ventric contraction happens first
LV before RV - L has thiccker muscle - more force to overcome in IVC so need to contract first
which ventric eject begins first
RV before LV - 10 mmHg on RV - 80 mmHG on LV
explain the timing of closing of pulmo nd aortic valves in respiration
expire - simultaneous
inspurt - aortic muna
why aortic valve closes slightly before pulmonic valve in inspire
- psi in thorax creates suction effect that causes backflow in aorta kaya need to close first
co of both vent are
=
what is arterial pulse
waves of blood along arteries; what we palpate
speeds of arterial pulse in diff arteries
4 m/s in aorta; 8 m/s in large arteries; 16 m/s in small arteries of young adults
when is radial pulse felt
0.1 sec after peak of systolic ejection in aorta
why hsould hr nd pr be =
not equal - TAO - masks out pulse
why is pr faster in older pt
Aging produces rigid vessels thus makes waves travel faster
give causes of pounding heart
palpitations - aortic insufficiency - allergic reax
what is dicrotic notch
Small oscillation on the falling pulse wave cause by aortic valves snaps shut
pulse is thready in
shock - hemmorhage
explain rising atrial pressure
Atrial systole - atria has to pump the remaining blood to the heart
Isovolumetric contraction o AV valves bulge into the atria; because the pressure is building up in the ventricles
- Blood flows in the atria until AV valves open
- Seen in atrial systole, isovolumetric ventricular contraction and before AV valves are open
what is A wave
Due to atrial systole; Blood regurgitation o Venous inflow stops = rise in venous pressure
C wave
Rise in atrial pressure due to bulging of the AV valves during isovolumetric contraction
V wave
Rise in atrial pressure before AV valves open in diastole.
s1 vs s2
s1 - close AV
s2 - close aortic nd pulmo valves
what are the patholig cheart sounds
s3 - 1/3 dias; rapid filling of vent
s4- before s1; in stiff vent - psi of atria to high - vent hypertophy
stenosis vs insufficiency
stenosed - valve not open maayos - narrow
insuff - valve does not close properly - backflow
timing of murmurs of aortic/pulmo valves
sten - sys
induff - dias
timing of murmurs of mitral/tricusp
sten - dia
insuff - sys
explain ficks principle
o Amount of substance taken up by an organ per unit time is equal to the arterial level of the substance minus the venous level (A-V difference) times the blood flow o Substance is oxygen
normal CO
5L/min
cardiac index
an organ recieves 3.2 L of blood
factors that control CO
hr, myocardial contractility, preload, afterload
CO in diff situations
no change - sleep, moderate temp change
inc - anxiety - excite - 700% - hogh temp - pregy - epi
dec - sitting to stand rapid - arrythmias - heart disease
what is + chronotrpic effect
inc co - ne and e
what is + inotropic action
inc co - in qual of contract - ne and e
relate frank starlings law to CO
Extent of the preload o More venous return, the better the stroke volume would be and multiply that with the heart rate, cardiac output will also increase
- Is proportionate to the end-diastolic volume
Preload, venous return, contractility of the heart will affect myocardial fiber shortening according to FrankStarling Law
- If Frank-Starling Law is good, then the stroke volume will also be good
- Stroke volume x heart rate = cardiac output
factors affecting end dia vol
- Increase
o Stronger atrial contractions o Increased total blood volume o Increased venous tone o Increased pumping action of skeletal muscles o Increased negative intrathoracic pressure - Decrease
o Standing o Increased intrapericardial pressure o Decreased ventricular compliance
exp sympathetic stim in myocardial contractility
Sympathetic stimulation
Shift upward & to the left of the curve
Positive chronotropic and inotropic effect
exp force-frequenct in myocardial contractility
Ventricular extrasystoles condition the myocardium that the next contraction is stronger
Postextrasystolic potentiation ▪ Increased Ca++ availability
oxygen consumptions
2 ml/100g/min –heart stoppage
- 9 ml/100g/min – beating heart at rest
what determines o2 consumption
Intramyocardial tension
Contractile state of the myocardium
Heart rate
why does o2 consumtion inc when SV inc
25% increase in SV without a change in arterial pressure produces the same increase in O2 consumption & vice versa.
If there is 25% increase in stroke volume, then that 25% correlates to 7x the work of left ventricle than that of right ventricle * Pressure work produces > O2 consumption
