CO = Heart rate (HR) × stroke volume (SV)
HR is primarily determined by CNS.
CO is directly related to HR.
SV is therefore is determined by
Preload - amount of blood present in the heart chamber, the end-diastolic stretch of the heart muscle fiber
Afterload - the pressure against which the heart must work, the forces that impede the flow of blood out of the heart
Contractility - the strength of the cardiac contraction
Preload essentially equals venous return.
The greater the stretch, the stronger the contraction
Frank-Starling Law relates the stretch of the muscle fiber to its strength of contraction
Normal EDV is approximately 110 -120 ml
Normal SV is approximately 70 ml
Ejection fraction (EF) = SV/EDV expressed as a percentage
(You will see patients in ICU who have EF's of less than 50%)
Contractility is the amount of force the myocardium produces at any EDV.
Increased contractility results in greater EF for any EDV.
Called positive inotropism.
If both afterload and contractility increase together, SV is maintained.
Afterload is the resistance against which the ventricles pump, so more afterload makes it harder for the ventricles to eject the SV.
RV afterload is equal to PVR.
LV afterload is equal to SVR.
All else constant, an increase in vascular resistance would decrease SV.
Usually this does not occur as contractility increases to maintain SV and thus CO.
Increased EDV will increase contraction (Starling's Law) to a point, then the heart muscle fails, resulting in ventricular or heart failure, which causes a back up in the system. LV failure backs up into pulmonary circulation, increases PVR, increases RV afterload and leads to RV failure.
The sum of all opposing forces to blood flow through the systemic circulation is systemic vascular resistance (SVR)
SVR = Change (Δ) in pressure from beginning to end of system, divided by flow
SVR = (MAP – RAP)/CO
Where: MAP = mean aortic pressure
RAP = right atrial pressure or CVP
CO = cardiac output
Δ delta - indicates the sum of change
Normal SVR 17.2 mm Hg / L / min
PVR is sum of all opposing forces to blood flow through the pulmonary circulation
PVR then calculated as is SVR (ΔP/flow)
PVR = (MPAP – LAP)/CO
Where: MPAP = mean pulmonary artery pressure
LAP = left atrial pressure or wedge pressure
CO = cardiac output
PVR is normally much lower than SVR as the pulmonary system is low pressure, low resistance
MPAP (Mean Pulmonary Artery Pressure)
Normal PVR = 1.6 mm Hg / L / min
PVR increases with decreased PAO2, increased pH (usually a result of increased PCO2)
Conditions that can also increase PVR include emboli, sclerosis, destruction of capillary bed, and compression of the lung
Baroreceptors respond to pressure changes:
First set: Arch of aorta and carotid sinus
Monitor arterial pressures generated by left ventricle.
Second set: Atrial walls, large thoracic and pulmonary veins¾low-pressure monitors
Respond to volume changes
Baroreceptor output is directly proportional to vessel stretch
Negative feedback system, so greater stretch causes venodilation and decreased heart rate and contractility.
Located in aortic arch and carotid sinus
Respond to changes in blood chemistry.
Decreased PaO2 provides strong stimulus
Low pH and high PaCO2
Major CV response to their increased output is vasoconstriction and increased heart rate.
Occur only when CV system is overtaxed, so generally will have little affect.
Best noted under abnormal conditions
Hemorrhage sets up this sequelae.
10% blood volume loss decreases CVP.
50% decrease in baroreceptor discharge
⇑ Sympathetic discharge increases HR.
ADH begins to rise.
Normal BP is maintained.
Blood loss approaches 30%, BP starts to fall
Aortic barorecptors now increase output.
IF no further blood loss, BP still maintained.