Cardiac Output and its Regulation

CO = Heart rate (HR) × stroke volume (SV)

HR is primarily determined by CNS.

CO is directly related to HR.

HR > 160 -180 is exception; too little time for filling results in decreased EDV, EF, SV, and thus CO

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



pre and afterload.jpg


frank starling curve.jpg


Stroke Volume and Preload

Preload essentially equals venous return.

Amount of volume and pressure at end diastole (EDV, EDP) that stretches myocardium.

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

Normal EF is approximately 65%

(You will see patients in ICU who have EF's of less than 50%)


Stroke Volume and Contractility

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.

Stroke Volume and Afterload

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.

Vascular Resistance

Systemic Vascular Resistance

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




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


Pulmonary Vascular Resistance (PVR)

PVR is sum of all opposing forces to blood flow through the pulmonary circulation

PVR then calculated as is SVR (ΔP/flow)




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


Peripheral Receptors


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.

Response to Changes in Volume

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.