Cardiovascular Physiology - Pressure Waveforms and Cardiac Output

Question 1

What is the cardiac cycle?

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Answer 1

Everything that happens in the heart within a single heart beat, this involves the process of relaxation and filling of the heart with blood (diastole), and ejection of the blood into the great vessels (systole).

Question 2

What happens during diastole in the cardiac cycle?

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Answer 2

1. Isovolumetric (ventricular) relaxation
The start of isovolumetric relaxation is marked by the second heart sound (closure of the AV and PV). The closure of the AV gives a brief rise in aortic pressure known as the dicrotic notch. The v wave on a CVP trace is due to the atria filling with closed TV and MV.
2. Rapid relaxation and filling
The pressure gradient between the atria and now-relaxed ventricles leads to the atrioventricular valves opening, with blood flowing rapidly into the ventricles, causing the y descent on a JVP trace
3. Slow relaxation and filling
The AV and PV remain closed, and the MV remains open, but the pressure gradient is reducing, with slow blood flow. CVP continues to rise, filling the atria further.
4. Atrial contraction
Once the atria fill, the p wave of an ECG triggers atrial contraction. At rest, this only accounts for 10-15% of ventricular filling, but during tachycardia can be up to 30-40%. This is why patients with AF decompensate when they develop a significant tachycardia.

Question 3

What happens during systole in the cardiac cycle?

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Answer 3

1. Isovolumetric contraction
Ventricles contract and generate higher pressure than the atria, forcing closure of the atrioventricular valves, heard as the first heart sound (LUB)
The pressure continues to increase, and the atrioventricular valves bulge back into the atria, accounting for the c wave on a CVP waveform
When pressure reaches and exceeds aortic pressure, the AV suddenly opens, ejecting blood into the aorta
2. Rapid ejection
The initially large pressure gradient between the LV and aorta results in fast flow. The RV also contracts, pulling the RA down, and reducing CVP x descent
3. Reduced ejection
As the ventricle empties, the pressure rise slows, then plateaus and begins to drop off when the ventricle relaxes. When the pressure in the ventricle falls below aortic pressure, the AV slams shut, heard as the second heart sound (DUB)

Question 4

Draw and explain the left ventricular pressure-volume loop

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Answer 4

Rapid & Slow Relaxation and Filling
Starting at point A, the MV opens, and the LV fills passively during diastole.

Atrial contraction
Volume increases further, with an uptick in pressure. When the ventricles begin to contract and LV pressure exceeds that of the LA, the MV closes, marking point B. This is LVEDF (Left Ventricular End Diastolic Volume)

Isovolumetric contraction
The ventricles contract against a closed MV and AV, increasing pressure while volume remains unchanged, until point C where ventricular pressure exceeds aortic pressure (about 90mmHg), and the AV opens, causing a drop in volume. Pressure continues to rise initially, but then falters, and when below aortic pressure, the AV closes at point D

Isovolumetric relaxation
With both valves closed, the LV relaxes, resulting in no change in volume, but a large drop in pressure, until lower than LA pressure, and the MV opens at point A again

Question 5

How can work done and stroke volume be demonstrated on the left ventricular pressure volume loop?

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Answer 5

Work done is the area within the loop
Work done = force x distance, in this case, is pressure x volume (hence the area within the graph)

Stroke volume is the difference between the volume at the end of diastole (LVEDV) and the end of systole

SV = LVEDV - LVESV

This would be a horizontal measurement between the two vertical sections of the graph, in the example:

120ml - 50ml = 70ml

Question 6

How does preload affect stroke volume?

Answer 6

Preload is the length of the sarcomere in the myocardium immediately prior to contraction, and reflects the volume of blood which the ventricle can pump.

Preload can either be approximated from end-diastolic volume (often using echo), or by end-diastolic pressure (Using a CVC and PA catheter and pressure transducer). CVP is approximately RV end-diastolic pressure, and pulmonary capillary wedge pressure is approximately LV end-diastolic pressure.

Question 6

What factors affect stroke volume?

Answer 6

Preload, contractility and afterload

Question 7

What factors determine preload?

Answer 7

1. Venous return
   Reduced venous return impairs filling, and thus sarcomere distension. Possible pathologies include (hypovolaemia and raised intrathoracic pressure)
2. Myocardial compliance
   A stiffer ventricule will be less distensible (HOCM or diastolic heart failure)
3. Pericardial compliance
   Preventing ventricular filling (pericarditis or tamponade)
4. Valve pathology
   If the MV or TV valves have reduced flow, then there will be reduced ventricular filling
   If the AV or PV have reduced flow, then there will be increased end-systolic volume, and thus increased ventricular filling
5. Atrial function
   Reduced atrial function, such as AF, will reduce the atrial kick during diastole, resulting in reduced ventricular filling

Question 8

How does contractility (inotropy) affect stroke volume?

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Answer 8

Largely dependent on calcium concentration within the myocyte.
Higher contractility results in a higher fraction of the blood in the ventricle being expelled during systole.

Question 9

What factors determine contractility (inotropy)?

Answer 9

1. Heart disease
Ischaemia, acidosis and heart failure
2. Drugs
Negatively inotropic drugs, particularly beta blockers
3. Autonomic innervation
Increased sympathetic innervation increases contractility
4. Bowditch effect
Increasing HR will increase contractility (less time to sequester calcium from myocyte, leading to higher intracellular calcium concentrations)
5. Anrep effect
Contractility increases with afterload. Tension-dependent Na/H+ exhange pumps are activated, causing sodium to enter the myocyte, reducing the sodium gradient, which is used by the Na/Ca pumps which remove calcium from the cell, thus resulting in higher intracellular calcium concentrations

Question 10

How does afterload affect stroke volume?

IMAGE - Laplace’s law

DEFINE AFTERLOAD

Answer 10

Afterload is defined as

It is calculated with the equation
T = (rP)/(2u)
Tension = (Radius x transmural pressure) / (2 x wall thickness)

Question 11

What factors determine afterload?

Answer 11

1. Systemic vacular resistance
Vasoconstriction, haematocrit, and arterial stiffness. The Windkessel effect refers to the ability of arteries to stretch in systole (reducing SVR), then recoil and maintain arterial blood pressure during diastole. Calcified arteries cannot do this, and is one of the many reasons that elderly patients are prone to crashing their blood pressure on induction
2. Ventricular outflow obstruction
Higher pressures are generated to overcome the obstruction (HOCM/Aortic Stenosis)
3. Intrathoracic pressure
Lower intrathoracic pressure results in higher trans-mural pressure and thus afterload, worsening CCF and pulmonary oedema. CPAP reverses this mechanism, and can therefore reduce afterload (although it also reduces venous return)
4. Increased LVEDV
Increased end diastolic volume causes ventricular distension, increasing the radius, as well as relative thinning of the myocardium
5. Myocardial thickness
Reduced myocardial thickness increases tension, as fewer myocytes bear the load of contraction. The opposite is seen in ventricular hypertrophy, which reduces afterload

Question 12

How is ejection fraction calculated?

Answer 12

Normal ejection fraction is around 60-65% at rest

It is the amount of blood ejected from the ventricule, expressed as a percentage of the end-diastolic volume

Ejection fraction = (Stroke volume/end diastolic volume) x 100

EF = SV/EDV x 100

Question 13

What is the significance of the increase in gradient between A and B in the LV pressure-volume loop?

IMAGE in the question

Answer 13

It demonstrates that as the ventricle fills, the pressure required to add more volume increases exponentially, preventing overdistension of the ventricle

It reflects the elastance of the ventricle (change in pressure per unit change in volume), and is the reciprocal of compliance (volume change per unit change in pressure)

Question 14

What effect would an increase in preload have on the LV pressure-volume loop?

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Answer 14

Higher preload increases LDEDV, which shifts point B to the right. This also results in a higher end-diastolic pressure, shifting it upwards too

Provided the heart can cope with the added demand, the Frank-Starling mechanism generates a more powerful contraction, resulting in point C and the apex of the curve being higher, before returning to a similar ESV, widening the loop rightwards to reflect the increased work (area within the curve), and stroke volume

Question 15

What effect would aortic stenosis have on the LV pressure-volume loop?

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Answer 15

The stiff, narrow aortic valve slows the rate at which blood can leave the LV

The loop becomes steeper and taller, with a narrower profile, reflecting the resultant reduced stroke volume

Question 16

What effect would dilated cardiomyopathy have on the LV pressure-volume loop?

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Answer 16

The distended ventricle results in overall higher volumes at all times, shifting the entirety of the loop to the right

There is a higher end-diastolic pressure point B (reflecting the higher volume), and the** B-C section ** is non-vertical, reflecting an element of valvular failure secondary to the distorted anatomy

A lower overall pressure is obtained, and the ejection fraction is lower, as the Frank-Starling mechanism is unable to respond to the increase in volume

Question 17

What is heterometric autoregulation?

Answer 17

The negative feedback mechanism by which the heart matches right and left ventricular ejection volumes despite significant pressure differences

Increased preload means greater power of contraction, and therefore increased stroke volume

This increased stroke volume is delivered to the other side of the heart, and the process repeats

The ejected volume is therefore determined by preload

Question 18

Draw and explain the LV volume/time graph

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Answer 18

Essentially the inverse of the LV pressure/time graph

LV volume increases rapidly at the start of diastole, then slows, followed by the atrial kick providing another 20-30ml.

The maximum volume is the LVEDV, and minimum LVESV

LVEDV - LVESV = Stroke volume Approx 70ml

SV/LVEDV = Ejection fraction Approx 65%

Question 19

What is the equation for venous return?

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Extra info here

Answer 19

Venous return = [(Mean Systolic Filling Pressure - Right Atrial Pressure) / Venous resistance] x 80

=[(MSFP-RAP)/Rven] x 80

The 80 accounts for the different units being used

Question 20

What effect does increasing venous filling have on venous return and cardiac output?

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Extra info here

Answer 20

Mean systolic pressure remains unchanged, but right atrial pressure increases

This leads to improved cardiac output while on the steep area of the curve.

Question 21

What effect does reducing venous resistance have on venous return and cardiac output?

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Answer 21

Reducing venous resistance will improve cardiac funciton, more markedly so when RAP (Right atrial pressure) is low.

Question 22

What is cardiac output?

Answer 22

The rate at which blood is expelled from the heart, expressed in litres per minute.

Cardiac Output = Strove Volume x Heart Rate

CO = SV x HR

Question 23

How does the respiratory cycle affect preload?

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Answer 23

During spontaneous inspiration, intrathoracic pressure drops, reducing right and left atrial pressures (and therefore reducing pulmonary capillary wedge pressures)

This therefore increases preload, end-diastolic volume, and pressure.

This increases the work of the LV, as it increases transmural pressure (difference in the ventricular and thoracic pressures)

Conversely, positive pressure reduces transmural pressures, justifying the use of CPAP in LV failure. In RV failure, the increased thoracic pressures can instead overcome the low-pressure right sided system, and cause haemodynamic collapse.

Question 24

Also known as Starling’s law

Explain the Frank-Starling mechanism in relation to the heart

IMAGE (Frank-Starling Curve)

Answer 24

The ability of the heart to adjust the force of contraction in response to changes in preload.

Increased preload stretches the sarcomeres, and increases the number of overlapping actin and myosin binding sites. It also sensitises the myocardium to calcium.

Positive inotropy shifts the curve leftwards, and vice-versa.

Question 25

What effect does heart failure have on the Frank-Starling curve?

IMAGE - FS curve in HF

Answer 25

The graph is shifted rightwards, reducing the maximal attainable stroke volume.

Rather than plateauing as normal, excessive ventricular filling causes a reduction in stroke volume.

Myocardial sarcomeres become overdistended, reducing the number of overlapping binding sites, and thus the force of contraction

This distension is usually chronic, as the stiff pericardium usually prevents overfilling in the acute setting, but over time, will distend and allow overfilling.

Question 26

What pressure values are normal for each chamber of the heart?

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Might be worth also including the graph you get when advancing a PAFC through the heart, as it explains it quite well.

Answer 26

RA: 2-8mmHg throughout cardiac cycle, identical to CVP
RV: 15-30 systolic, 2-8 diastolic - during systole tricuspid closes and enables pressure to rise
PA: 15-30 systolic (same as RV), 4-12 diastolic - TV closes and keeps diastolic pressure higher
PCW and LA: 2-10mmHg throughout cardiac cycle
LV: 100-140 systolic, 3-12 diastolic - mitral closes and allows pressure to rise during systole
Aorta: 100-140 systole, 60-90 diastole - AV closes and keeps diastolic pressure higher

Question 27

What is the Fick principle, and how is it used clinically?

Answer 27

Input into a system will equal the output if there is no accumulation or depletion of the contents of the system.

If you know the concentration of a marker substance in the blood supplying an organ, and the concentration of blood draining from that organ, as well as knowing the rate of uptake of a marker substance into the organ, then you can calculate the rate of blood flow.

Blood flow ml/min = (rate of uptake mg/min) / (input mg/ml - output mg/ml)

For example:
Cardiac Output = Oxygen Consumption / CaO2 - CvO2

Other specific examples:
Renal blood flow (Para-Aminohippuric acid (PAH)
Kety-Schmidt technique with N2O for calculating cerebral blood flow

Question 28

How can the Fick principle be used to calculate Cardiac output

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Answer 28

Cardiac Output = Oxygen Consumption / CaO2 - CvO2

Through thorough measurement of the inspired oxygen, as well as paired arterial and central venous gases, the CO can be measured.

Conversely, the same measurements for CO2 can be used.