Control of Cardiac Output Flashcards
What is the equation for blood flow?
Blood flow (CO) = BP / TPR • BP = blood pressure • TPR = total peripheral resistance
What 2 things does Cardiac output effect?
- blood pressure
- blood flow
What controls the heart rate?
SA node pacemaker also sympathetic and parasympathetic nerves control heart rate (beats per minute, autonomic nervous system).
What controls the contractility of the heart (strength of contraction)?
– Strength of contraction (contractility) due to sympathetic nerves and circulating adrenaline increasing intracellular calcium
What is the energy of contraction?
The amount of work requied to generate stroke volume.
Where in the heart is most of the energy used?
in the left ventricle
What does energy of contraction depend on?
Starling’s law and contractility.
What happens after the ejection phase?
• After the ejection there is some more squeezing to get more blood out.
What functions does stroke work carry out?
- Contracts until chamber pressure is greater than aortic pressure (isovolumetric contraction).
- Ejection from ventricle
What happens the more we contract isovolumetrically?
The more we contract isovolumetrically, the more energy we store and the easier the ejection.
What happens when in certain types of heart diseases where the heart may have to do too much work?
• In certain types of heart disease, the heart may have to do too much work, and cannot get enough oxygen to maintain that work. – and so, tries to increase its muscle mass to work harder, but this also requires oxygen and etc…
Effect on stroke volume by preload and afterload.
Preload increases the stroke volume and afterload opposes the stroke volume.
Starling’s law
- Starling’s law states that the greater stretch of ventricle in diastole (blood entering), then greater energy of contraction, and greater stroke volume achieved in systole.
- When more blood comes back to the heart (e.g. during exercise), the heart automatically increases stroke volume. – This is an intrinsic property of cardiac muscle (nerves, hormones etc. are not involved).
Stroke volume equation in Starling’s law.
Stroke volume = end diastolic volume – end systolic volume
How does bolus fluid affect Stroke volume?
o Bolus of fluid increases the amount of blood in venous return, which increases the amount of blood in end diastolic volume, which increases the strength of contraction and this increases the stroke volume.
How does removing fluid haemorrhage affect the stroke volume?
removing fluid haemorrhage (escape of blood from a ruptured blood vessel)– the venous return was decreased, the end diastolic volume decreased, strength of contraction decreased and the stroke volume decreased.
Preload in an un-stretched fibre (molecular basis).
• In an un-stretched fibre – There is overlapping actin meaning there is a lot of mechanical interference in forming cross-bridge between the actin and myosin for muscle contraction, and so less cross-bridges are formed.
Preload in a stretched fibre (molecular basis).
• In a stretched fibre – There is less overlapping between the actin, and so less mechanical interference, and so potential for more cross-bridge formation, leading to increased sensitivity to Ca2+ ions – which is a signal for contraction and so better force of contraction.
Roles and efect of Starling’s law.
1) Importantly; it balances outputs of the right and left ventricles within a few heart beats.
2) Its responsible for fall in CO (Cardiac Output) during a drop-in bloods volume or vasodilation (e.g. haemorrhage, sepsis).
3) Restores CO in response to intravenous fluid transfusions.
4) Responsible for fall in CO during Orthostasis (standing up for a long time) leading to postural hypotension and dizziness as blood pools in legs – as there’s less blood going back to the heart, from the legs, and the heart as a results pumps less strongly. – If this goes on for too long then you will faint.
5) Contributes to increased SV and CO during upright exercise – as more blood comes back to the heart and so the heart pumps harder and equalises the blood in the heart.
What does Laplace’s law state?
- Laplace’s law is for afterload!
- States that if you are overstretching the muscle, then you are opposing ejection of blood from the heart. – Function of the heart muscle itself (not the blood vessels).
- More heart wall stress, prevents muscle contraction.
- More energy of contraction is needed to overcome the wall stress to produce cell shortening and ejection.
What is the equation for Laplace’s law?
T = (Pr)/2
• Wall tension (T), pressure (P) and radius (r) in a chamber (ventricle)
• The wall tension (T) is made up of wall stress (S) x wall thickness (w).
T = Sw
so..
wall stress is
S = (Pr)/2w
How is afterload increased and decreased?
• Afterload is increased by increasing pressure and radius (increases wall tension) and reduced by increasing wall thickness.
What is the difference between stress and tension?
The difference between stress and tension – wall stress is the wall tension spread across a bigger area (the width is included in stress but not in tension).
Why does radius determine wall stress/afterload?
- Small ventricle radius – Leads to greater wall curvature – Leads to more wall stress directed towards centre of chamber – less afterload – less resistance to contraction – Better ejection.
- Larger ventricle radius – leads to less wall curvature – leads to more wall stress directed through heart wall (not towards the centre as much) – More afterload – More resistance to contraction – Less ejection.
importance of Laplace’s law.
• Starling’s law and Laplace’s law are opposing each other at rest.
- Increased preload gives increased stretch of chamber (Starling’s law). This increases chamber radius (decreases curvature), Increasing afterload.
- In a healthy heart, Starling’s law overcomes Laplace’s – So good ejection.
• Facilitates ejection during contraction.
- Contraction reduces chamber radius so less afterload in ‘emptying’ chamber. – This aids expulsion and increases stoke volume.
- (During ‘emptying’ chamber after contraction, the heart wall doesn’t stretch, so Starling’s law is less dominant).
• Contributes to failing heart at rest and during contraction.
- In a failing heart, the chambers are often dilated – so increased afterload which opposes ejection. – SV is low and CO will be low.
• Laplace’s law is good ejection with small radius, bad with large radius.
What happens during acute rises in BP?
• Acute rises in blood pressure offset (counterbalanced) by, e.g. exercise.
- Starling’s law is dominant in healthy hearts. – Increased stretch gives increased contraction and increased SV. Local positive inotropes (noradrenaline) or Anep effect (accumulation of Ca2+), Baroreflex receptors– decreased sympathetic tone, decreasing blood pressure.
What happens during chronic rises in BP?
• Chronic increase in arterial blood pressure
- Increased energy expenditure to maintain SV, and ultimately decrease in SV.
- Decreasing BP will increase efficiency of the heart.
Why does CP need to be kept fairly constant during exercise?
High BP will reduce CO.
Effect of increase venous return during exercise, on cardiac contraction
During exercise increased venous return leads to an increase in EDV (end diastolic volume) causing increased preload and more stretch. This causes a shorter (and stronger) isovolumetric contraction phase, and increase in SV due to Starling’s law. More blood back to the heart, more blood ejected from the heart.
Effect of high blood pressure and greater afterload
With high blood pressure, there is greater afterload and it’s difficult to eject as there is more wall stress. This means a longer time spent in isovolumetric contraction to increase pressure in the chamber above that in the aorta, to open the valve. This uses more energy, and so there’s less energy for contraction, lowering the force of contraction, reducing SV (end systolic volume increases), and having more blood in the heart left after ejection.
Why is the Pr divided by 2?
• The Pr is divided by 2 because a chamber has 2 directions of curvature (the degree to which something is curved) - side to side, or up and down.
What is preload?
Stretching of the heart’s left ventricle (on filling) at rest
What is afterload?
Opposes ejection (resistance to ejection)
Example of increased radius of the heart
• Increased radius (r) – increased stress – e.g. Heart failure where heart does not conduct properly (MI, cardiomyopathies, mitral valve re-gurgitation – valve doesn’t close properly as its been damaged) blood left in ventricle leading to eventual volume overload.
Example of increased pressure
• Increased pressure (P) – e.g. Pressure-overload heart failure due to increased pressure/afterload in chamber (this is seen in hypertension, aortic stenosis – blockage of the aorta and narrowing of aorta).
Effect of increased pressure and radius
• Increases in either radius or pressure will increase wall stress (afterload), which opposes ejection.
• The heart compensates with ventricular hypertrophy (greater myocyte size and more sarcomeres), increasing wall thickness. This decreases wall stress per sarcomere and therefore afterload, so maintains SV and CO. – good for short term.
But this requires more energy (more sarcomeres used) – greater O2. The amount of energy required contributes to increase, so ultimately contractility will decrease and produce more heart failure – it’s a vicious circle.
