L3 - Physiology of the Heart II Flashcards
When the atria contract how much of its blood volume does it eject?
60%
- Continuous supply of blood from circulation
If the heart doesn’t eject correctly it doesn’t have time to catch up
What is the equation for cardiac output?
Cardiac Output = Heart Rate x Stroke Volume
4.9 litres/min = 70 beats/min x 70mls
Blood volume = 5 litres – entire blood volume pumped every minute
What is the cardiac output during exercise?
35 litres /min
7 fold increase in blood circulation compared to rest
What is the ejection fraction?
Refers to the percentage volume of blood ejected with each cardiac contraction
Normally 55-60% at rest
What % is the ejection fraction?
60%
What bpm is the heart rate?
70bpm
What l/min is cardiac output?
5 l/min
What ml is stroke volume?
70ml
What 4 factors affect heart rate?
Sympathetic nervous system
Parasympathetic nervous system –> through vagus nerve
Circulating catecholamines
Drugs
How do circulating catecholamines affect the heart rate?
Extension of the sympathetic nervous system Circulate in bloodstream so slower to act
Come from the adrenaline gland
- Sympathetic nervous system through noradrenaline acts instantaneously
What 4 factors affect stroke volume?
Intrinsic contractility Extrinsic factors - preload - afterload - sympathetic activity
How does intrinsic contractility affect stroke volume?
The heart tissue needs to be in good condition with the correct conditions
- Intracellular calcium
- Oxygen, free fatty acids, ATP
How does preload affect stroke volume?
Filling pressure
Venous return - how much blood volume is coming back to the heart immediately before it contracts
How does after load affect stroke volume?
Resistance to ejection
Blood vessels can restrict and contract
What are the two supplies of Ca for muscle contraction?
One from inside SR
One from outside SR
One Ca pathway at cell membrane, one at SR membrane
What are the two Ca channel receptors involved in muscle contraction?
L-type
Ryanodine
What are L-type calcium channels?
Small amount of Ca enters the cell - not enough to trigger contraction itself
What are Ryanodine receptors?
Activated by small amount of Ca entering through L-type calcium channels
Triggers an all or nothing response - large Ca influx
How does Ca affect actin and myosin?
- Actin is a filamentous molecule wrapped in troponin and tropomyosin
- Tropomyosin and troponin cover myosin binding sites on actin
- Ca bind to troponin
- Conformational change
- Binding sites are now free so myosin binds
- Physical movement of the two molecules - requires ATP
What is the structure of cardiac muscle?
Cross linking
What is the importance of cross linking in cardiac muscle?
Help to transmit depolarisation across the heart quickly
When the heart contracts it help it contract as one functional unit
What is the Frank-Starling mechanism?
Heart muscle cells – how much they contract depends on their basal state
before the stimulus
The more you stretch the ventricles the more they contract
The more it fills the more it pumps - depends on pre-load
- Intrinsic property of the heart
Where do healthy people lie on the Frank Starling curve?
Steep part of the curve
Small increases in filling pressure dramatically increase cardiac output
How do increases in filling pressure affect stroke volume and cardiac output?
Increases in volume of blood returning to the heart during diastole - preload
Increases LV end-diastolic pressure –> myocardial fibre stretching
Increases force of contraction –> increased stroke volume and cardiac output
Frank-Starling - changes in preload (venous return)
If venous return increases –> end diastolic pressure increases –> stroke
volume increases –> will eventually equilibrate
Frank-Starling - changes in afterload and contractility
If contractility decreases / afterload increases –> heart starts failing –> curve flattens –> decrease in cardiac output –> large preload needed to get same cardiac output
Healthier to be on steep curve at top left
Frank-Starling - effect of sympathetic stimulation
Small stimulation
Small increase in Ca
Small contraction
Frank-Starling - effect of sympathetic stimulation - Isoprenaline
Sympathetic catecholamine
Give isoprenaline and small stimulation
- Stimulus gives greater Ca influx
- Enhanced contraction
Frank-Starling - effect of sympathetic stimulation - noradrenaline
Infuse fluid –> for a smaller change in pressure –> greater change in stroke volume
In a heart failure patient what leads to them operating on high pressure hearts?
Can increase filling pressure but cannot change cardiac output
Cannot survive on normally filling pressures
What can a high end diastolic pressure in a heart failure patient lead to?
High end diastolic pressure –> high pulmonary venous pressure –> breathless
If pressure increases further –> fluid leaks into lung tissue –> pulmonary oedema
How does a diuretic change preload?
Lowers preload –> filling pressure decreases In heart failure patient –> filling pressure decreases without little impact on cardiac output
What happens if cardiac output drops too much?
Start to feel unwell
Don’t want to be in bottom left of curve
What happens if ventricular pressure increases too much?
Breathlessness, pulmonary tension
Don’t want to be too far to the right on the curve
In a heart failure patient how do you change their high filling pressure?
Diuretics
Can do it without dropping cardiac output too much
In a heart failure patient how do you change their high after load?
ACE inhibitor
What is an example of a cardiac glycoside?
Digoxin
How does digoxin impact the heart?
Causes increase in heart contractility
Greater Ca influx –> greater contraction (compared to control)
Increases ionotropic effects of the muscle
Moves curve
- May be enough to get you out of low cardiac state
- Puts you on a curve where you can now use diuretics to avoid high pulmonary venous congestion
When the heart starts to fail why does it dilate?
Because pressure increases –> volume increases –> stroke volume increases –> heart equilibrates
Tends to be
- Large volumes
- Increased pressures
Overall, what do heart failure drugs tend to do?
Decrease after load
Decrease preload –> diuretics
Decrease sympathetic drive on the heart
These are only used for chronic heart failure not acute
Why is thrashing the heart not a good idea?
Oxygen demand of the heart increases more than its output does
