Venous Return & Cardiac Output
What is stroke volume?
Stroke volume is the amount of blood ejected by the left ventricle in one contraction. Although stroke volume can refer to either left or right side of the heart, it is most associated with the left side.
What is preload relevant to?
The filling of the ventricle
Molecular Basis of Starling's Law
The increased force of contraction produced by stretching the muscle fibres is thought to result from the actin and myosin strands being drawn closer together rather like fibres in a piece of wool which is stretched (this is compensation) If the muscle fibre is stretched too much the ability to form cross bridges is reduced because of the reduced overlap of actin and myosin fibrils and the force of contraction starts to diminish (this is decompensation)
How can we measure left ventricular pressure?
The left atrial pressure (LAP) can be taken as a measure of the preload of the left ventricle but it is difficult to measure and we often use "pulmonary artery wedge pressure" instead to estimate it or left ventricular end diastolic pressure (LVEDP) is measured directly using an arterial catheter passed into the left ventricle
How can you measure right ventricular pressure?
The right atrial pressure (RAP) can be taken as a measure of the preload of the right ventricle (and very indirectly as a measure of left ventricular preload)
Starling's Law of the Heart
The work done by the heart in systole is related to the resting (end diastolic) length of the ventricular muscle fibres (if you stretch the heart when you fill it, t does more work e.g. inc cardiac output)
Heart Failure
- Heart failure is defined as the inability to maintain a normal cardiac output at a normal filling pressure (preload) - On the previous slide we saw that left heart failure will result in raised pulmonary blood pressure and thus breathlessness (the lungs become "stiff") and possibly pulmonary oedema - This increased right heart afterload may eventually cause right heart failure - This will cause a fall in cardiac output and a fall in kidney perfusion. By mechanisms which you will learn about later, the body retains salt and water which increases blood volume - The resulting increased central venous pressure helps to restore right heart output but may also cause peripheral oedema (e.g. swollen ankles) and raised jugular venous pressure. Combined right and left heart failure is congestive heart failure
Venous Return & Cardiac Output
- In some circumstances an increased venous return can produce an increase in cardiac output but there are many factors which control cardiac output - However the venous return will always limit the cardiac output. If the cardiac output is to increase there must be an increase in venous return
The muscle pump
- Large veins pass between muscle blocks especially in the limbs - The veins are compressed when the muscle contracts - The veins have valves which only permit blood to move towards the heart - The pump is activity related - increased activity causes increased venous return
The thoracic pump
- On inspiration the diaphragm flattens, abdominal pressure is raised and thoracic pressure falls, blood moves from the abdomen into the thorax and pools in the legs - On expiration the diaphragm becomes dome shaped, abdominal pressure falls, blood moves from the legs into the abdomen - A useful feature of the thoracic pump is that it is activity related and thus venous return increases with increased activity
Left Heart Failure
- People with left heart failure often suffer from "orthopnoea" they become breathless when they lie flat. - This is because the increased venous return increases right heart preload and thus right heart output and pulmonary blood pressure rise since the left heart is inefficient at increasing its output - In severe cases there may be PND - paroxysmal nocturnal dyspnoea - where the subject wakes with very severe breathlessness and coughing up fluid - (The nocturnal attacks of severe breathlessness seen in some asthmatics may be mistaken for PND caused by heart failure)
Starling's Experiments
- Starling worked on an isolated heart lung preparation in dogs - He replaced the systemic circulation by an artificial "Starling resistor" - Thus he was able to vary peripheral resistance - He could vary preload (RAP) by raising or lowering a reservoir connected to the right atrium - First experiment - he increased preload (RAP) while he kept the arterial pressure constant - Second experiment - he increased afterload (arterial pressure) - He measured ventricular volume and thus output (diastolic volume - systolic volume = stroke volume) - In both cases the heart was paced so the rate was unchanged
Contractility
- Stimulation of the sympathetic nervous system or the administration of positive inotropic drugs is said to cause an increase in contractility - An increase in contractility is an increase in the force of contraction which does not result from stretching the muscle in diastole - i.e. is not a result of Starling's law. It permits the ventricle to contract to a smaller end systolic volume. - An increase in contractility results from an increase in intracellular [Ca++] - Acidosis reduces contractility
Measurement of cardiac output
- The "Fick Principle" can be used - "In a closed system at equilibrium if a substance X is neither synthesised or broken down then the rate at which X enters the system must equal the rate at which it leaves" - In this case the substance "X" is oxygen and the closed system is the lungs
The role of heart rate
- The SNS increases heart rate and the PNS slows the heart rate - The natural inherent rate of the SAN is about 100 bpm - At rest the heart is under tonic vagal (PNS) inhibition - The heart rate can be increased from 70 to 100 bpm by decreasing PNS activity - An increase above 100 bpm requires increased SNS input - The maximum effective heart rate is about 180 bpm after this there is an encroachment on rapid ventricular filling time and stroke volume falls rapidly - Blood can only flow through the coronary supply when the muscle is relaxed i.e. during diastole. At very high heart rates there is therefore a danger of cardiac ischaemia - Heart rate increases when RAP increases (Bainbridge reflex) - hence heart rate increases on inspiration and falls on expiration (sinus arrhythmia)
Ventricular Failure
- The contractility of the ventricle may be decreased as a result of ischaemia, acidosis or the death of muscle fibres - If this occurs in the left ventricle then ventricular balance will be disturbed - The right ventricle will continue to pump blood into the lungs but it will not be cleared effectively by the left ventricle - Pulmonary blood pressure, left atrial pressure and left ventricular preload will increase - The left ventricle will move up its new, lower "Starling curve" and eventually ventricular balance will be restored but the price will be pulmonary congestion and possible breathlessness and pulmonary oedema
Blood Volume
- The great veins act as capacitance vessels for the storage of blood - Increased blood volume results in increased central venous pressure and hence increased preload - Low blood volume, e.g. after a haemorrhage, will cause reduced central venous pressure and decreased preload
Venomotor Tone
- The great veins have some smooth muscle within their walls - This smooth muscle has similar pharmacology to that in the arterioles i.e. it will contract when α1 receptors are stimulated (sympathetic) - This will increase central venous pressure and increase preload
Role of Starling's Law
- The law implies that an increase in venous return will cause an increase in cardiac output - This may have some role to play early in exercise - The main role of Starling's Law is to ensure ventricular balance
The role of stroke volume
- The stroke volume can be increased by filling the ventricle more or by emptying it more - The effect of increasing ventricular filling (i.e. stretching the ventricle) was investigated by the British physiologist Starling
Co-localisation
- Veins are bound together with arteries and nerves in tight connective tissue sheaths - As the artery pulsates the vein is massaged - The presence of valves means that this movement causes blood to move towards the heart
In Exercise
- Venous return increases if the exercise is isotonic (i.e. the muscles are able to contract and relax) - Cardiac filling is thus increased sending the heart up its Starling curve - Cardiac Contractility is increased by the sympathetic nervous system stimulation so that the heart moves to a new higher curve and less blood is left in the ventricle at the end of systole - Heart rate increases - Maximum cardiac output is about 25 litres per minute in a healthy young adult male
How is oxygen uptake measured?
By collecting expired air in a "Douglas bag" and measuring the oxygen concentration
How is blood oxygen content measured?
By measuring the haemoglobin concentration and the oxygen saturation. One gram of haemoglobin when fully saturated binds 1.33 ml of oxygen
How is pulmonary venous oxygen content measured?
By measuring the oxygen content of the blood in any systemic artery
Cardiac output formula
Cardiac output = Heart Rate x Stroke Volume
Factors which contribute to Preload
Gravity The thoracic pump The muscle pump Co-localisation Venomotor tone Blood volume
Example of Cardiac Output Calculation
In slides
Gravity in the supine position
In the supine position venous return is increased and the resulting lung congestion may contribute to orthopnoea, breathlessness when lying flat (N.B. orthopnoea can also be caused by obesity when an overweight abdomen presses on the diaphragm)
Gravity in the upright position
In the upright posture this is a positive factor from tissues above the heart but a negative factor below the heart. The decreased venous return on standing contributes to postural hypotension especially if blood volume is low or the ANS function is suppressed.
How is pulmonary arterial blood oxygen content measured?
Measured in a sample of right atrial blood obtained by inserting a catheter into an arm vein and pushing it through to the right atrium
