A & P - Cardiovascular System, The Heart - Cardiac Output

Front 1

What is stroke volume (SV)?

Back 1

The volume of blood pumped out by one ventricle with each beat

Highly correlated with the force of ventricular contraction

Stroke volume = difference between end diastolic volume (EDV) and end systolic volume (ESV)

Front 2

What is cardiac output?

Back 2

Amount of blood pumped out by EACH ventricle in 1 minute

Cardiac output (CO) = stroke volume (SV) x heart rate (hr)

Front 3

What is cardiac reserve?

Back 3

Cardiac reserve is the difference between resting and maximal cardiac output.

Front 4

What two factors determine end diastolic volume (EDV)?

What's the typical EDV?

Back 4

Length of ventricular filling time (longer increases EDV)

Venous pressure (higher venous pressure increases EDV)

Typical EDV = 120 mL

Front 5

What two factors determine end systolic volume (ESV)?

Back 5

Arterial blood pressure (higher = higher ESV)

Force of ventricular contraction (higher = lower ESV)

Front 6

What is the ejection fraction? What is the average ejection fraction?

Back 6

Ejection fraction is SV/EDV (in other words, the amount that came out compared to the amount that was in)

Normal ejection fraction around 67%

Front 7

What is preload?

Back 7

Preload refers to the degree to which cardiac muscle cells are stretched just before they contract.

Front 8

Describe the Frank-Starling law of the heart:

Back 8

There is an optimal length of cardiac muscle fibres at which:

1) The maximum number of active cross bridge attachments is possible between actin and myosin
2) The force of contraction is maximal

In other words, cardiac muscle, like skeletal muscle, exhibits a length-tension relationship. But while resting skeletal muscle is already at its optimal length, resting cardiac muscle fibres are shorter than their optimal length and must be stretched out to a certain degree to reach maximum force of contraction

The Frank-Starling law, therefore, states that stretching cardiac muscle fibres up to a certain point increases the force of contraction, while stretching them past that point decreases the force of contraction. Preload (the degree of stretch) therefore becomes a key determinant of cardiac output

Preload is the strength of the rower (greater stretch = stronger rower)
Contractility is how hard that rower is rowing (strong rower might not be trying that hard, after all)

Front 9

What is venous return?

Back 9

The amount of blood returning to the heart and distending the ventricles

In other words, venous return is the amount of blood returning to the ventricles

Front 10

What effect does a slow heart rate have on venous return?

Back 10

Slow heart rate increases ventricular filling time (diastole), thereby increasing venous return

Front 11

What is contractility?

Back 11

Contractile strength for a given muscle fibre length (independent of muscle stretch and EDV)

Front 12

Name 3 endogenous positive inotropic factors:

Back 12

Adrenaline

Glucagon

Thyroxine

Front 13

What are factors that increase contractility called?

Back 13

Positive inotropic factors

Front 14

What is afterload?

Back 14

Afterload is the pressure that must be overcome for a particular ventricle to eject blood.

For the left ventricle this is the systemic diastolic blood pressure (e.g. 80 mmHg)

For the right ventricle this is the pressure in the pulmonary trunk (e.g. 8 mmHg).

Front 15

What are the three main determinants of stroke volume?

Back 15

1) Preload (degree to which muscle fibres are stretched, determined by venous return)

2) Contractility (how hard the fibres contract at a given length, i.e. how much effort the rower is giving, determined by presence of positive or negative inotropic factors)

3) Afterload - pressure that must be overcome for ventricles to eject blood (80 and 8 mmHg, respectively)

Front 16

What type of adrenergic receptors are found on cardiac myocytes?

Back 16

Beta-1 receptors

Front 17

On an ionic level, how does sympathetic stimulation through the cardiac accelerator nerves and beta-1 receptors lead to increased heart rate?

Back 17

Somehow stimulation of the beta-1 receptors leads to increased probability that the pacemaker channels will be open, so threshold voltage is reached more quickly.

Front 18

How does sympathetic stimulation increase contractility?

Back 18

Stimulation of beta-1 adrenergic receptors by adrenaline or noradrenaline results in the phosphorylation of the L-type Ca++ channel, enhancing Ca++ influx and leading to increased cytosolic Ca++ levels.

These increased levels, through Ca++ induced Ca++ release, result in greater force of contraction.

Front 19

What is the major determinant of the force of cardiac contraction with each heartbeat?

Back 19

The concentration of cytosolic Ca++. Mechanisms that increase cytosolic Ca++ increase contractility. Mechanisms that reduce Ca++ reduce contractility.