Lecture 3 Flashcards
how much blood is ejected when the atria contract?
60%
what is the equation for cardiac output?
Cardiac Output = Heart Rate x Stroke Volume
what is the ejection faction ?
Refers to the percentage volume of blood ejected with each cardiac contraction – normally ~55-60% at rest
what factors affect heart rate?
o Sympathetic nervous system – increases HR
o Parasympathetic nervous system – decreases HR via vagus nerve
o Circulating catecholamines- sympathetic nervous system – response isn’t instant as constantly circulating in blood.
o Drugs
what intrinsic factors affect stroke vol?
o Intrinsic contractility – heart muscle:
Intracellular calcium – AP and contractility
Oxygen, free fatty acids, ATP
what extrinsic factors affect stroke vol?
Preload (filling pressure) – how much blood vol is coming back to the heart – venous return – filling before contraction.
Afterload (resistance to ejection) – can be easily changed
Sympathetic activity
what is the role of calcium in cardiac muscle?
• Platau phase is supported by Ca entering cell.
• L-type Ca channels
• Small amount of Ca enters cell – not enough to trigger contraction
• Ca – cell membrane and sarcoplasmic reticulum
• Small influx binds to Ryanodine receptors – bigger release of Ca from sarcoplasmic reticulum – causes contraction.
• Actin and myosin need to bind to cause contraction – covered by troponin in absence of Ca
• Ca binds to tropomyosin – actin and myosin can bind to cause contraction.
• Cross branches between muscle cells
o Help to transmit depol across heart
o When heart contracts – hold together – all contract together
what are the steps in the frank-starling mechanism?
- Increases in filling pressure (LV end-diastolic pressure/myocardial fibre stretching)
o when stretch cells they will contract more and greater – pump more – more it fills the more it contracts. Blood vol increases = preload will increase.
o LV-EDP – stretch before contraction
o More stretch – more cardiac output – until a point - Increased force of contraction
- Increased stroke volume and cardiac output
what is the effect of changes in venous return (preload)?
- LVEDP = preload
- If venous return increases – EDP increases - stroke vol go up
- Venous return decreases – pressure fall – cardiac output fall
what are the effects of changes in afterload and contractility (inotropy)?
- The ventricle operates on a family of curves determines by afterload and contractility.
- Red dotted line – if you don’t do anything to the heart
- Decreased contractility – curve flattens – need a high increase in preload to increase cardiac output.
- Increased afterload – high resistance – need to fill heart more to get cardiac output that they require.
- Increased contractility – steeper curve
- Decreased afterload – easier to eject
what are the effects of sympathetic stimulation?
• Stimulus – Ca releases – tension in muscle
• Isoprenaline – stimulus – increased Ca released – bigger contraction
o Basically like the sympathetic nervous system acting
o Enhanced cardiac contraction – move curve
• If you infuse fluid – pressure goes up in the heart – stroke vol goes up
• Noradrenaline – curve moves left – smaller change in pressure – greater change in cardiac output.
What does the curve show for failing heart?
o Increased filling pressure but no change in cardiac output.
o If filling pressure begins to come down to normal levels, cardiac output starts fall – need more filling pressure to push failing heart harder to give more cardiac output – operate on high pressure heart
o More pressure needed to get cardiac output
o If pressure in ventricles at end of diastole is increased significantly, that transmits back to left atrium, no valve, so this transmits back to lungs – pulmonary venous congestion
o High pulmonary venous pressure in lungs – breathlessness – if pressure goes up even more it can become pulmonary oedema – fills lung space with fluid.
what effect does the diuretic have on a curve?
lowers preload – filling pressure decreases
o Can lower high filling pressure down to something reasonable without fall in cardiac output – if u stay in flat part of curve – only in heart failing patient
o Couldn’t do in non-failing heart as it would cause too much of a decrease in cardiac output
what is the effect of cardiac glycosides such as digoxin?
- slows down AV node – slows down heart rate
- Positively ionotropic effect on the heart - increase in contractile function
- takes you out of low cardiac output
- Bigger influx of Ca -> Bigger contraction
- Increases ionotropic effect – positively
why does the heart dilate when it starts to fail?
• Thin walls, muscle scarred, contractility is impaired
• Operate with large volumes and with higher pressures
• Pressure increases – volume increases – stroke vol increase – heart dilates further
• Heart becomes more inefficient the more you thrash it
o Want to decrease afterload, decrease preload, decrease sympathetic drive
• If you stimulate the heart – the oxygen consumption goes up substantially – does so greater than the amount of work you get out of the heart
