Control of cardiac output Flashcards
Cardiac output
Amount of blood ejected from the heart per minute.
CO = HR x SV
- Heart rate = how often the heart beats per minute.
- Stroke volume = how much blood (ml) is ejected per beat.
- Cardiac output affects blood pressure and blood flow.
- CO = BP / TPR (Total peripheral area)
Preload and afterload, important in stroke volume
- Preload = stretching of heart at rest, increases stroke volume (Starling’s law)
- Afterload = Opposes ejection, reduces stroke volume (Laplace’s law)
Preload - Starling’s law
- ‘Energy of contraction of cardiac muscle is relative to the muscle fibre length at rest’
- Greater stretch of ventricle in diastole (blood entering) –> the greater the energy of contraction and greater stroke volume achieved in systole.
- More blood in = more blood out (intrinsic property of heart, no nerves/hormones involved)
Preload - molecular basis of Starling’s law
- Un-stretched fibre - overlapping actin/myosin, Mechanical interference, Less cross-bridge formation available for contraction.
- Stretches fibre - Less overlapping actin/myosin, Less mechanical interference, Potential for more cross-bridge formation, Increased sensitivity to Ca2+.
Preload - roles and effects of Starling’s law
- Balances outputs of the right and left ventricles.
- Responsible for fall in cardiac output during a drop in blood volume or vasodilation (haemorrhage, sepsis etc)
- Restores cardiac output in response to intravenous fluid transfusions.
- Fall in cardiac output during orthostasis –> leading to postural hypotension and dizzines as blood pools in legs.
- Contributes to increased stroke volume and cardiac output during upright exercise.
Afterload - Laplace’s law
Afterload opposes the contraction that ejects blood from the heart and is determined by wall stress directed through the heart wall. Stress prevents muscle contraction.
- More energy of contraction is needed to overcome this wall stress to produce cell shortening and ejection.
- Laplace’s law describes parameters that determine afterload:
- Wall tension (T), pressure (P), radius (r)
- T ∝ Pr
- Wall stess (S) is made of tension (T) and wall thickness. S=T/W so S=Pr/2w
Afterload - wall stress
Small ventricle radius:
* Greater wall curvature.
* More wall stress directed towards centre of chamber.
* less afterload.
* Better ejection
Larger ventricle radius:
* Less wall curvature.
* More wall stress directed through heart wall.
* More afterload.
* Less ejection.
Huge theoretical radius:
* negligible wall curvature.
* Virtually all stress directed through wall.
Importance of Laplace’s law
- Opposes Starling’s law at rest:
* Increased preload = increased stretch of chamber = increased chamber radius (decreased curvature) = Increased afterload.
* In a healthy heart, Starling’s law overcomes Laplace’s law, so ejection is ok. - Facilitates ejection during contraction:
* Contraction reduces chamber radius, so less afterload as the chamber empties.
* This helps expulsion of last blood portion and increases SV. - Contributes to a failing heart at rest and during contraction:
* In a failing heart, chambers anre dilated and with large radius, so increased afterload opposes ejection.
SUMMARY: Laplace’s law means good ejection with small radius but BAD with large radius.
Afterload - arterial blood pressure and stroke volume
Laplace’s law states that increased blood pressure (P) will increase wall stress
which will increase afterload & reduce ejection. S=Pr/2w
- Acute rises in blood pressure offset by:
* Starling’s law - increased stretch gives increased contraction and increased stroke volume.
* Local positive inotropes - noradrenaline.
* Baroreflex - decreased sympathetic tone which decreased blood pressure. - Chronic increase in arterial blood pressure:
* Increased energy expenditure attempts to maintain stroke volume but ultimately stroke volume will gradually decrease.
* Decrease in blood pressure would increase efficiency of the heart.
* This is why blood pressure needs to be kept constant during excercise, high blood pressure will reduce cardiac output.
Laplace’s law and hypertrophy in heart failure
- Inreased radius (r) - Heart failure = where heart doesn’t contract properly so blood left in ventricle leads to volume overload.
- Increased pressure (P) - Pressure-overload = heart failure due to increased pressure/afterload in chamber (hypertension,aortic stenosis).
S=Pr/2w –>increases in radius or pressure will increase wall stress/afterload which oposes ejection.
The heart compensates with ventrivular hypertrophy - Greater myocyte size and more sarcomeres, which increases wall thickness, which decreases wall stress per sarcomere and therefore afterload, so maintains SV and CO.
However, this requires more energy since more sarcomeres are used - more 02. The amount of energy needed increases so contractility will decrease –> leading to heart failure.
Energy of contraction
Energy of contraction = amout of work required to generte stroke volume - depends on Starling’s law and contractility.
Functions of stroke work:
* Contracts until chamber pressure > aortic pressure (isovolumetric contraction.)
* Ejection from ventricle.
Preload increases stroke volume and afterload opposes the stroke volume.
Higher energy used in isovolumetric contraction
reduces energy available for ejection
Preload and ventricular pressure-volume loop
Excercise - Increased venous return = increased preload = higher end diastolic volume (EDV).
Thr ventricle will eject blood to the same end systolic volume (ESV) –> increase in SV (shown by increased width of the PV loop.)
Afterload and ventricular pressure-volume loop
Hypertension - increased afterload = Longer time spent in isovolumetric contraction to increase pressure in the chamber above that in the aorta to open the valve.
Uses more energy and lowers forcce of contraction reducing SV and increasing end systolic volume (ESV).
