3-Cardiac Output Flashcards
cardiac output =
stroke volume x heart rate
vol of blood ejected by heart per min (L/min) FLOW
regulation of stroke vol
- myocyte contractility
- afterload
- preload
regulation of heart rate
- speed of diastolic depolarization
-parasymp and symp nervous sys
length-tension relationship
inc length of muscle fiber changes overlap of thick/thin filaments (resting tension) for contraction (active tension)
-aka inc length/stretch inc tension
titin important for this
preload affect on length-tension
preload/filling of vents = stretch on ventricle prior to contraction
volume of ventricle
pressure-volume loop
- isovol contraction, pressure builds
- aortic valve opens, pressure peaks as muscle contracts and systolic ejection, vol dec
- aortic valve closes, pressure high volume low
- isovol relaxation, vol stays same pressure dec until mitral valve opens
- diastolic filling to phase 0 (LV end-diastolic pressure) then restart
width of loop = stroke volume
just look at power point chart
increasing HR = ? CO
cardiac output
generally will inc CO up to a point then dec bc stroke volume is down, lose ventricle filling
end diastolic volume
amount of blood in heart at end of filling
end systolic volume
amount blood leftover in heart at end of ejection
determinants of stroke vol
- preload- vent filling, stretch of myocytes
- afterload- tension needed to oepn aortic valve (after contraction), systemic resistance, aortic valve resist
- contractility- inotropic agents
inc afterload = ? stroke vol
stroke vol dec with inc afterload
inc contractility = ? stroke vol
increases at any given point with pre and afterload bc calcium cycling
inc preload = ? stroke volume
increases up to maximal stroke vol then dec
frank-starling law of heart- if more comes in then more goes out
preload changes from
venous return into vena cava
-venous pressure needs to be higher than atrial (central) for blood to enter RA so if inc CVP then dec venous return
mean systemic filling pressure changes
- inc blood vol = inc preload, higher venous return
- dec blood vol = dec venous return, from bleeding out or dehydration
arteriolar tone on venous return
inc tone aka vasoconstriction = venous return slowed, blood vol stays the same just takes longer to return to heart
dec tone aka vasodilation = venous return inc bc returns quicker
why afterload dec stroke vol
inc afterload = more effort to eject blood/harder bc inc tension required to open aortic valve = less blood gets ejected
-work harder to open the valve than eject blood
positive inotropes = ? stroke vol
inc peak tension during contraction + inc amount blood ejected so lower end systolic vol = inc SV
norepinephrine
disease states on contraction
reduce ability of heart muscle to contract + less tension produced = dec stroke vol
i.e. heart failure, MI, arrhythmias (change how electric signal moves thru tissue)
regulation cardiac output
balance b/t stroke volume and HR so change CO by those two
-changes based on tissue demand
venous pressure and CO
must be equal/matched
inflow = outflow
if not then congestion and volume acc somewhere not supposed to
sympathetic stim = ? CO
cardiac output inc with symp stimulatin
-pos inotropy (contract) + pos chronotropy (HR)
moderate heart failure and CO
- reduced contractility
- fluid retention > shift venous return bc inc volume to compensate for heart failure
CO stays at same level as normal bc of compensation
short term
severe heart failure and CO
continued deterioration of contractility = inc venous pressure + dec CO
-decompensated
how to assess CO
mainly
- fick method
- indicator dilution technique
both rely on conservation of mass
fick method
relies on oxygen into lungs
-oxy leaving lungs = oxy entering for steady state so
oxy consumption / (arterial-venous oxygen difference) = cardiac output
indicator dilution method
indicator injected upstream then measured downstream until gone
thermal dilution uses cold saline
