The Cardiovascular Response to Stress

Question 1

What is the equation for Cardiac Output?

Answer 1

CO=HR x SV

Question 2

What is the equation for stroke volume?

Answer 2

SV=EDV-ESV

Question 3

Normal Cardiac Output:

Answer 3

5 Litres per minute

• HR is 70
• SV is 70ml (140 EDV- 70ESV) (Ejection fraction is normally 50-60%)

Question 4

How is cardiac output in an athlete different?

Answer 4

The body requires a lot more oxygen and so cardiac output can increase as much as 5 fold

• So cardiac output can increase to 25 litres per minute
• Heart rate increases (MAX=220-age)
• Stroke volume increases because diastolic volumes increase due to increased venous return due to muscle pumps and systolic volumes decreases because inotropy increases so ejection fraction increases slightly

Question 5

What is sudden cardiac death?

Answer 5

When the heart seizes functioning and death ensues with no apparent warning

Question 6

Why does sudden cardiac death occur in athletes?

Answer 6

During chronic, intensive exercise, adaptations to the heart associated with the exercise allow cardiomyopathies that usually would have gone un-noticed become apparent. For example Hypertrophic Cardiomyopathy
-These myopathies are generally caused by genetic faults and black african americans are generally at greater risk

Question 7

What is one of the main factors that cardiac output depends on?

Answer 7

The return of blood from the peripheral system, otherwise known as the PRELOAD. If preload doesn’t increase, then the heart rate increases without extra blood so there will eventually be nothing left to pump around the body

Question 8

Which mechanisms decrease venous return?

Answer 8

Gravity/Standing-blood pools in the legs rather than be returned to the heart because there is very little venous blood pressure. Without muscle action, the blood does not return

Question 9

What mechanisms increase venous return?

Answer 9

1. Skeletal Muscle Pumps
   - the muscles of the legs, especially the calves squeeze the blood forcing it back to the heart. During exercise, the muscles contract even more than usual so venous return increases
2. Abdomino-thoracic pump

Question 10

How does the abdomino-thoracic pump increase venous return on the right side of the heart?

Answer 10

as we breathe in, thoracic volume increases but pressure decreases which creates a negative thoracic pressure. (pressures in the right atrium and thoracic vena cava are very dependent on intrapleural pressure so it is the decrease in pleural pressure during inspiration that affects venous return)
Negative thoracic pressure causes the right atrium to dilate resulting in reduced atrial pressure
The reduced atrial pressure creates an intracardiac pressure gradient which pulls blood in from the veins where pressure is higher and thus increases venous return

Question 11

How does the left side of the heart respond to the abdomino-thoracic pump?

Answer 11

The left side of the heart responds in an opposite way to the right.
Inspiration causes pulmonary volume to increase which transiently decreases the flow of blood from the lungs to the left atrium because of resistance.
During expiration, this process is reversed because lung deflation reduces the resistance and allows blood to flow from the lungs to the left atrium

Question 12

Is slow or fast breathing in exercise better?

Answer 12

SLOW AND DEEP IS BETTER IN EXERCISE
-this reduces ‘dead space’ and increases the efficiency of the abdomino-thoracic pump i.e slow and deep breathing maximises the changes in pressure gradients and so can increase venous return more efficiently

Question 13

What type of heart rate is the most effective in exercise?

Answer 13

Similar to breathing, a slow heart rate with greater force of contraction is more effective in exercise. This is why athletes exhibit bradycardia.
If the heart rate is slower, there is more time for diastolic filling, and if the heart fills more it will contract harder (frank starling law) so the cardiac output will be maintained

Question 14

Why are quick heart rates not so useful in exercise or during stress?

Answer 14

at very high heart rates, the heart begins to exceed diastolic filling and so cardiac output begins to drop

Question 15

What happens to the heart during mild exercise?

Answer 15

Both heart rate and stroke volume increase

Question 16

What happens to the heart during moderate exercise?

Answer 16

Stroke volume becomes a limiting factor because the heart cannot eject anymore

Question 17

What happens during heavy exercise?

Answer 17

The heart rate rises too much and diastolic filling is reduced

Question 18

How is heart rate influenced at rest?

Answer 18

During rest, the parasympathetic nervous system predominates
-The intrinsic heart rate of the SA Node is 100bpm, but the parasympathetic system reduces heart rate by 30% so normal resting heart rate is 70bpm

Question 19

What point decides if the parasympathetic or sympathetic predominates?

Answer 19

Heart rate >110 is the sympathetic nervous system

Heart rate <110 is the parasympathetic nervous system

Question 20

What is the heart rate of heart transplant patients and why?

Answer 20

Heart transplant patients have a resting heart rate of 100bpm because they no longer have parasympathetic innervation to reduce it by 30%

Question 21

What is the sympathetic nervous system to the heart?

Answer 21

• It is via the Cervical and Stellate Ganglia and comes MAINLY FROM THE RIGHT side of the body
• Sympathetic nerves innvervate both the atria and ventricles
• Short preganglionic fibres and long post-ganglionic fibres
• The sympathetic nerves come via the SPINAL NERVES
• Pre ganglionic fibres use Acetylcholine (ACh)
• Post ganglionic fibres use Noradrenaline or Adrenaline and act on Adrenergic Receptors e.g Beta

Question 22

What does the sympathetic nervous system do?

Answer 22

Sympathetic innervation increases:

1. Heart rate
2. AVN conduction
3. Irritability

*It does this through activation of Adrenergic receptors which triggers production of cAMP

Question 23

What is the parasympathetic innervation to the heart?

Answer 23

• Involves the left and right branches of the VAGUS nerve
• The right vagus supplies the SA Node
• The left vagus supplies the AV Node
• there is very little parasympathetic innervation to the ventricles
• Long pre-ganglionic fibres using ACh
• Short post-ganglionic fibres using ACh affecting Muscarinic and Nicotinic receptors

Question 24

What does the parasympathetic nervous system do?

Answer 24

It decreases:

1. Heart rate
2. AV conduction
3. Irritability
   * the OPPOSITE to sympathetic

Question 25

What drugs can replicate the actions of the sympathetic nervous system?

Answer 25

Catecholamines such as Adrenaline, Noradrenaline, Dopamine

Question 26

What drugs can replicate the actions of the parasympathetic nervous system?

Answer 26

Atropine

Question 27

What factors increase stroke volume?

Answer 27

1. Increased contractility (squeezes more blood out of the heart so ejection fraction increases)
2. Increased preload because of increased venous return or bigger blood volume i.e fluid bolus

Question 28

What decreases stroke volume?

Answer 28

Increases Afterload.
Afterload is the tension against the ejection of blood so the bigger the afterload, the harder it is to eject blood and the lower the stroke volume

Question 29

Describe Preload:

Answer 29

If their is more blood in the heart, the cardiac muscle has to stretch more
This means that the actin/myosin filaments are brought in to a more optimal position for contraction so the force of contraction is bigger, as stated by the frank starling law.
It is the volume of blood in the heart that is termed the preload, so if the preload increases, so does the inotropy

Question 30

Describe Afterload:

Answer 30

Afterload is the resistance to blood flow

• This resistance can come from the arteries (occurs naturally because the arteries are small but occurs to more of an extensive level if the arteries are stiffened and cannot stretch to accomodate the blood)
• This resistance also occurs if there is a blockage to the flow of blood out of the heart e.g Aortic Stenosis
• The heart has to push against this resistance and so an increased afterload reduces how much blood the heart can squeeze out

Question 31

What is the Frank Starling Law?

Answer 31

‘Energy of Contraction is a Function of the Length of the Muscle Fibre’
i.e the more the muscle fibre is stretched, the harder the force of contraction
It is a bigger preload that determines fibre stretching

Question 32

What may increase preload?

Answer 32

• Increased venous return in exercise due to muscle pumps
• Lying supine because the IVC/SVC flow directly into the RA/RV and gravity does not restrict blood flow
• Giving a bolus of fluid increases preload because the volume of blood in the body increases and there is a bigger volume of blood available to fill the heart in diastole

Question 33

What happens in a failing heart when preload is increased?

Answer 33

Failing hearts are much less able to deal with increased preload
For example, if a fluid bolus is given to a failing heart, the volume of blood returning to the heart increases but the heart cannot function well enough to increase stroke volume to accomadate the extra fluid.
This means that blood becomes backed up and congestion ensues.
Depending on which side of the heart this occurs, either peripheral or pulmonary oedema occurs.
-For this reason we must be very careful when prescribing failing hearts fluid; we don’t want to fluid overload them

Question 34

What are Atrial Natriuretic Peptides?

Answer 34

A type of peptide/hormone that is released in response to stretching of the atrial muscle fibres.
So when preload is increased and the atria is stretched to accommodate the excess, ANP is released.
-ANP causes the Glomerular Arterioles to dilate which reduces pressures in the kidneys and also triggers diuresis (the removal of water) in order to reduce the blood volumes back to normal
-So ANP has positive effects in offloading fluid from the vasculature and is therefore a REGULATORY mechanisms to maintain normal fluid levels
-ANP is also able to inhibit Aldosterone

Question 35

How does the Renin-Angiotensin System affect the heart?

Answer 35

Renin-angiotensin system is the opposite of ANP.

• This hormone system comes in to effect when cardiac output is LOW whereas ANP works when cardiac output is HIGH
• This system is triggered when a lack of kidney perfusion is noted i.e low blood pressures
• Renin is released which through the conversion of Angiotensin I to II results in the production of Aldosterone
• Aldosterone is a vasoconstrictor and promotes sodium and water retention to increase blood volume

Question 36

How are these hormone mechanisms significant in Heart Failure?

Answer 36

Hormone mechanisms play a significant compensatory role in heart failure

e. g Cardiac output is reduced in heart failure so lowered perfusion of the kidneys triggers the RAAS system to retain sodium and water and boost blood volumes/pressure
- This in the acute setting can be life saving, but chronically is maladaptive because the heart can’t keep up with the boosted blood volumes and so congestion ensues

Question 37

What other factors affect preload?

Answer 37

Venous Vasomotor tone i.e how much the veins constrict or dilate
Residual pressure in the capillaries following systole (usually 25mmHg) - Vis a tergo (from behind)
RV suction in diastole (ventricular pressures fall which pulls blood into the heart from the IVC/SVC - Vis a fronte (from the front)

Question 38

What is the Bainbridge reflex?

Answer 38

This law states that as preload increases, the heart rate increases

Question 39

How does the Bainbridge reflex work?

Answer 39

As preload increases, the muscle fibres in the atria stretch

• Stretching of the atrial fibres causes firing of Vagal afferent B-type fibres which sends signals to the Vasomotor and medullary control centres to modulate sympathetic nerves
• Because of this afferent innervation of control centres, sympathetic innervation is increased and the heart rate is increased too
• This process has been observed in canine models, and human females who have just given birth (blood from the placenta returning to the peripheral circulation causes tachycardia) but apart from that is rarely observed

Question 40

What is the Bowditch effect?

Answer 40

This law states that as heart rate increases, the inotropy increases too

Question 41

How does the bowditch effect work?

Answer 41

As heart rate increases, diastole is shortened so the heart has less time to fill hence inotropy should decrease.
However, the bowditch effect overcomes this.
As HR increases, diastole is shortened and so the Na/Ca ATPase enzymes on the surface of cardiac myocytes have less time to keep up with the rate of Na influx through the Na/Ca Exchanger
-This means that less calcium is able to leave the myocyte during diastole so there is a BUILD UP of calcium
-This build up of calcium means there is more calcium available for contraction so the force of contraction is BIGGER
-So as heart rate increases, to an extent so does inotropy and this overcomes the lack of diastolic filling

Question 42

Which system controls cardiac contractility the most?

Answer 42

The Sympathetic Nervous System has the biggest effect on contractility because it innervates the ventricles whereas the parasympathetic system only innervates the atria.

Question 43

How does acidosis affect cardiac contractility?

Answer 43

Acidosis e.g Diabetic Ketoacidosis, Sepsis, MI (lactic acid induced by ischaemia)

• Acidosis causes REDUCED CONTRACTILITY- it is one of the strongest negative inotropes (Poole-Wilson, 1982)
• The cardiac muscle is VERY sensitive to changes in extracellular pH
• H+ ions bind competitively to cardiac myocytes where calcium would usually bind
• H+ binding therefore means that calcium transients are eliminated
• If calcium cannot enter the cell, cardiac contraction cannot occur because calcium from the SR is insufficient to generate a strong contraction

Question 44

What drugs are positive inotropes?

Answer 44

Digoxin (cardiac glycoside that increases calcium transients), Adrenaline, Noradrenaline, Dopamine, Dobutamine

Question 45

What drugs are negative inotropes?

Answer 45

B-blockers, Diltiazem (calcium channel blocker)

Question 46

What is one of the first features of heart failure compensation?

Answer 46

Tachycardia
Increased inotropy also occurs because the heart beats harder to overcome increased afterload caused by the likes of systemic hypertension (pulse waves return to the heart faster which increases afterload)