Cardiac output

Question 1

Learning outcomes

Answer 1

• To introduce the concept of cardiac output and define it
• To show that cardiac output widely varies
depending on the metabolic demands made by
the body
• To explain how cardiac output may be
controlled by alterations in either heart rate or stroke volume
• To show how cardiac sympathetic and
parasympathetic input affect heart rate.
• To describe how stroke volume may be altered
by mechanisms, some dependent on initial
muscle fibre length (heterometric
autoregulation) and others independent of it
(homeometric autoregulation)
• To explain several ways by which cardiac
output may be measured

Question 2

What is cardiac output defined as?

Answer 2

• Cardiac ouput is the volume of blood pumped by the left ventricle in one minute.
• In health, left ventricular output = right ventricular output (circulations in series)
• Calculated by multiplying heart rate by stroke volume
• Altered by varying either one
• HR, biggest changes, SV less.

Question 3

How is heart rate altered?

Answer 3

Except during periods of high demand, most changes in CO are made through alterations in heartrate.
-Achieved through autonomic innervation of the heart by the 2 branches of the autonomic NS, the sympathetic NS and the parasympathetic nervous system. The sympathetic nervous system increases cardiac output and the parasympathetic nervous system acts to decrease cardiac output.
Sympathetic- FF
Parasympathetic- RD

Question 4

How is heart rate altered?

Answer 4

Except during periods of high demand, most changes in cardiac output are made through alterations in heartrate.

• Achieved through the autonomic innervation of the heart by the 2 branches of the autonomic nervous system, the sympathetic (Fight or flight) nervous system and the parasympathetic (rest and digest) nervous system.
• Using this logic, the sympathetic nervous system increases cardiac output and the parasympathetic nervous system acts to decrease cardiac output.

Question 5

Sympathetic effects on heart rate

Answer 5

• Speeds up heart (+ve chronotropic effect)
• B1 receptor opens Ca++ L channels
• Increases slope of prepotential, making it reach firing
level quicker, more rapid SA firing.
• Speeds AV conduction
• R symps to SA node, L to AV node

Question 6

Parasympathetic effects on heart rate

Answer 6

• Slows down heart (-ve chronotropic effect)
• M2 receptor opens K+ channels, slows opening of Ca++ channels
• Hyperpolarises cell, decreases slope of prepotential, making it reach firing level more slowly, slower SA firing.
• Slow AV conduction
• R vagus to SA node, L vagus to AV node

Question 7

Altering cardiac output

Answer 7

• Cardiac output can also be influenced by alterations in stroke volume
• These changes may depend on the intrinsic properties of cardiac muscle, on autonomic stimulation and on hormones
• Heterometric regulation; changes in C.O. dependent on initial length of cardiac muscle fibre
-homeometric regulation; changes in C.O. independent of such changes

Question 8

The Frank-Starling relationship

Answer 8

This relationship was originally characterised separately by Otto Frank in 1895 and by Ernest Henry Starling in 1914

• “Experiments carried out in this laboratory have shown that in an isolated heart, the greater the diastolic volume, the greater is its energy of contraction.” Put more succinctly, stroke volume and therefore cardiac output is dependent on the degree of stretch on the ventricular walls.
• Increases in stroke volume due to enhanced venous return stretch the ventricular walls, increasing stroke volume. Effectively cardiac output increases as venous return increases or MORE IN = MORE OUT.
• Happens in absence of neural or hormonal input and is a result of the intrinsic length tension relationship of cardiac muscle.
• Originally this was thought to be due to actin/myosin overlap (see previous lecture), but latterly research has focused on the effect that initial length has on calcium influx into, and calcium sensitivity of cardiac myocytes

Question 9

What happens in overstretching of the cardiac myocytes?

Answer 9

Often you’ll see the degree of initial stretch of cardiac myocytes referred to as preload in medical texts, with the pressure against which the heart pumps (blood pressure) being afterload.
-The Frank-Starling relationship only works to a point. At this point, cardiac muscle becomes excessively stretched, and any further increases in end diastolic volume actually lead to a decrease in stroke volume . –This sometimes happens in cardiac failure and is known as decompensation.

Question 10

Contractility and the sympathetic/parasympathetic nervous system

Answer 10

• Sympathetic stimulation
•-Shifts Starling up and to the left
- Affect on B1 adrenergic receptors
- Positive inotropic effect of sympathetic stimulation
• Parasympathetic stimulation
- Negative inotropic effect on atria but no effect on ventricles

Question 11

Other factors that influence contractility

Answer 11

• Catecholamines (noradrenaline and
adrenaline)
- Amplify B effects

• Force-frequency relation
-Post-extrasystolic potentiation
-Paired stimuli
- Fast heart rates
• Last 2 screens are examples of
homeometric regulation

Question 12

Clinical- cardiac output measurement

Answer 12

• Amount of a substance taken up per unit time by an organ (or the whole body) equals arterial content – venous content (A – V difference) times the blood flow through the organ (or body). (THE
FICK PRINCIPLE). This principle can be used to determine CO, with oxygen being the substance.
• VO2 is easy to measure using expired gases. We can determine arterial content of oxygen from any arterial sample (arterial content doesn’t vary from artery to artery). Mixed venous content is sampled from a catheter inserted into a forearm and guided up to the
pulmonary artery. Do a worked example using these values in the space provided. VO2 = 250 ml.min, arterial oxygen content = 190ml.l-1, venous oxygen content = 140 ml.l-1
• If VO2 = (arterial – venous difference in oxygen content ) X C.O., then by simple algebra, C.O. = VO2
/ (arterial – venous difference in oxygen content). = 250/50 = 5L min
Dont worry about too much, nor the method- be aware

Question 13

The indicator-dye method

Answer 13

-A small known quantity of dye is injected into the right hand side of the heart and arterial blood sampled thereafter with dye concentration monitored over the next 30 – 60 seconds, using a spectrophotometer. The greater the flow, the quicker the dye is distributed, and the quicker the fall in dye concentration.
-This may be done with cold saline instead of a dye.
Cold saline is injected into the right atria, and temperature in the pulmonary artery is measured using a thermistor. The quicker the blood flow, the more dissipated the cold becomes and the smaller the temperature change.

Question 14

In the hospital- cardiac failure

Answer 14

• A situation where there is “insufficient peripheral perfusion despite normal blood volume, a sufficient filling pressure and intact intrinsic and extrinsic compensatory mechanisms”- heart isnt pumping well
• Causes include cardiac tamponade (fluid in pericardium) and valvular problems, but the most common cause is coronary artery disease.
• Systemic effects- if right heart valves/ muscles are damaged, less blood goes out of the heart than in- blood backs up, it swells up (pulmonary capillary pressure increases, alveoli fill with fluid)
Left heart failure- backed up venous circulation, oedema in liver/ jugular veins
• Treatment.