Control of cardiac output

Question 1

What is cardiac output?

Answer 1

Volume of blood pumped by each ventricle per minute

Stroke volume x Heart rate (measured in L/ min)

Question 2

What is preload?

Answer 2

Initial stretching of the cardiac myocytes prior to contraction related to the filling of the ventricles before contraction.

[direct measure = sarcomere length but normally measured using end diastolic volume - the higher the EDV, the higher the preload]

Question 3

What is afterload?

Answer 3

Force/ load against which the heart has to contract to eject blood.

[Measured in terms of arterial pressure]

Question 4

What is stroke volume?

Answer 4

Volume of blood ejected from each ventricle during each ventricular contraction

Stroke Volume = End Diastolic Volume - End Systolic Volume

Question 5

What is total peripheral resistance?

Answer 5

Resistance to flow provided by systemic circulation (e.g. due to diameter of arterioles/ viscosity)

Question 6

What nerve provides parasympathetic input to the heart?

Answer 6

Vagus (CN X)

Question 7

What is Starling’s Law?

Answer 7

Stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles before contraction (when all other factors remain constant)

Question 8

What increases as a result of increased cardiac preload?

Answer 8

Atrial contractility 
Aortic pressure
Thoracic venous blood volume 
Central venous pressure 
Ventricular compliance

Question 9

What is End Systolic Volume (ESV)?

Answer 9

The volume of blood in a ventricle at the end of a contraction (systole) and at the beginning of filling (diastole).
Lowest volume of blood in the ventricle at any point during the cardiac cycle.

Question 10

What is End Diastolic Volume (EDV)?

Answer 10

The volume of blood in a ventricle at the end of filling (diastole).

Question 11

What factors affect heart rate?

Answer 11

Hormones

Atrial/ Bainbridge reflex (caused by increased venous pressure) - reflex alters ANS innervation

Question 12

What factors affect the end diastolic volume (EDV)?

Answer 12

Preload (influenced by venous return and filling time)

Question 13

What factors affect end systolic volume (ESV)?

Answer 13

Contractility (influenced by ANS innervation and hormones)

Afterload (influenced by vasodilation or vasoconstriction)

Question 14

What is the baroreceptor reflex?

Answer 14

Response to increased blood pressure
Increased firing of vagal nerve and glossopharyngeal nerve
Decreased firing of sympathetic nerves

Question 15

What nerves provide sympathetic input to the heart?

Answer 15

Sympathetic cardiac nerves

Question 16

What is the chemoreceptor reflex?

Answer 16

Response to low pO2 / high pCO2
Increased firing of sympathetic nerves
Decreased firing of vagal nerve

Question 17

How do inotropic agents affect contractility?

Answer 17

Positive inotropic agents increase contractility.

Negative inotropic agents decrease contractility.

Question 18

What decreases as a result of increased cardiac preload?

Answer 18

Venous compliance

Heart rate

Question 19

What factors affect stroke volume?

Answer 19

Preload (determined by venous return and filling time)
Contractility (regulated by hormones and ANS)
Afterload (determined by vasoconstriction/ dilation)

Question 20

How does an increased heart rate impact cardiac output?

Answer 20

An increased HR reduces cardiac output as it reduces filling time during ventricular diastole

[Exacerbated by mitral stenosis or atrial fibrillation due to loss of atrial contractility]

Question 21

How does the ANS impact heart rate?

Answer 21

Sympathetic stimulation increases heart rate by reducing repolarisation time and increasing speed of depolarisation and also increases contractility

Parasympathetic stimulation decreases heart rate by slowing depolarisation. APs also hyperpolarise

Question 22

How does the baroreceptor reflex respond to increased BP?

Answer 22

Baroreceptors in the carotid sinus and aortic arch detect raise in BP and increase firing of glossopharyngeal and vagal nerves to the cardiac and vasomotor centres in the medulla. This increases firing of efferent vagal fibres (to decrease HR) and decreases firing of sympathetic nerves to the heart (negative inotropy and chronotropy) and blood vessels (vasodilation).

[+ causes release of noradrenaline and inhibition of RAAS]

Question 23

What is the Bainbridge (atrial) reflex?

Answer 23

Increased venous pressure detected by stretch receptors at the venoatrial junctions of both atria which increases firing of vagal afferents to the cardiac and vasomotor centres in the medulla. This decreases parasympathetic efferent firing and increases sympathetic efferent firing thus increasing heart rate.

[Prevents pooling of blood in venous system]

Question 24

What is the chemoreceptor reflex?

Answer 24

Chemoreceptors in the carotid sinus and aortic arch detect changes in arterial gas concentrations. Increased pCO2 +/- decreased pO2 causes increased firing of afferent glossopharyngeal and vagal fibres to chemoreceptors in the medulla. This then causes cardiac and vasomotor centres to decrease efferent vagal stimulation and increases sympathetic stimulation to the heart and blood vessels

Question 25

What is contractility?

Answer 25

Force of contraction of the myocardium

[directly controls stroke volume - the greater the contractility, the greater the stroke volume]

Question 26

How do inotropic agents alter contractility?

Answer 26

Positive inotropic agents increase contractility

Negative inotropic agents decrease contractility