Preload

Question 1

What are the Major Determinants of Cardiac Output?

Answer 1

Preload, After Load, Heart Rate and Myocardial Contractility

Question 2

What is the Equation of Cardiac Output?

Answer 2

Cardiac Output = Stroke Volume x Heart Rate

Question 3

What is Heart Failure?

Answer 3

Inability of the heart to maintain normal cardiac output

Question 4

What does a Reduced Cardiac Output result in?

Answer 4

Under filling of the arterial circulation

Question 5

What is Preload?

Answer 5

The volume of blood in the ventricle at the end of diastole (end diastolic pressure)

Question 6

What is Venous Return?

Answer 6

Volume of blood that comes back to the RA per unit time

Question 7

What is the Frank-Starling Mechanism?

Answer 7

An intrinsic cardiac autoregulatory mechanism (reflex)

Question 8

What happens in the Frank-Starling Mechanism?

Answer 8

It ensures that stroke volume changes in proportion to the change in end diastolic volume

Question 9

When does Cardiac Output Vary?

Answer 9

In response to physiological and pathological factors

Question 10

What does the parasympathetic innervation effect in relation to the Major Determinants of Variation?

Answer 10

Decreases Heart Rate which increases Cardiac Output

Question 11

What does the sympathetic innervation effect in relation to the Major Determinants of Variation?

Answer 11

Increases contractility which leads to a increased stroke volume

Question 12

How Is Stroke Volume Regulated?

Answer 12

Mechanical Means: Increased Preload
Neuronal: Increases sympathetic innervation
Hormonal: Increased plasma epinephrine
All = Increased Stroke Volume

Question 13

How do we work out Mean Arterial Pressure?

Answer 13

Mean Arterial Pressure = Cardiac Output x Total Peripheral Resistance

Question 14

What is Starlings Law of the Heart?

Answer 14

The energy of contraction of a cardiac muscle fibre is proportional to the initial fibre length at rest. Ensures that the right ventricular output equals left ventricular output.

Question 15

What Governs Central Venous Pressure? (and therefore preload?)

Answer 15

Volume of blood, distribution of blood, sympathetic nerve activity, gravity and movement

Question 16

What are the Determinants of Preload?

Answer 16

Circulating fluid volume, venous return, venous tone, heart rate, myocardial compliance

Question 17

What does excessive preload cause?

Answer 17

Increased atrial pressure, increased venous pressure , signs of congestion

Question 18

What do baroreceptors detect?

Answer 18

High pressure. Increased/Decreased blood volume causes an increase or decrease in arterial pressure which is sensed by the baroreceptors which either fire more or less depending on whether the arterial pressure has increased or decreased.

Question 19

What do baroreceptors cause?

Answer 19

Higher/Lower sympathetic outflow to arterioles, veins and heart or the depressor reflex (reduce volume and pressure) or the opposite pressor reflex by increasing or decreasing the parasympathetic outflow to the heart

Question 20

What receptors also contribute to CVRS homeostasis?

Answer 20

Atrial Receptors

Question 21

What is the role of Atrial Receptors?

Answer 21

They are low pressure stretch receptors in the walls of the atria that act as volume receptors. Increased blood volume = stimulation of atrial volume receptors

Question 22

What do atrial receptors do when increased blood volume is detected?

Answer 22

Inhibit ADH secretion and sympathetic vasoconstrictor pathways to kidneys leading to diuresis

Question 23

What receptors contribute to restring blood volume following haemorrhage?

Answer 23

Both baroreceptors and atrial volume receptors

Question 24

What are Natriuretic Peptides?

Answer 24

Peptides released into the blood when blood volume in the atria is increased

Question 25

What is the role of Natriuretic Peptides?

Answer 25

Atrial Natriuretic Peptide and Brain NP reduce blood volume by stimulating excretion of salt and water by the kidney. Relax vascular smooth muscle/vasodilation so reduces TPR and inhibits RAAS.