BS2014: Cardiovascular Physiology

Stroke volume

volume of blood ejected from the heart during each cycle

If a ventricle contains 100ml of blood at the end of filling, and 40 ml at the end of contraction, what is the stroke volume?

60 ml

Cardiac output

total volume of blood pumped by the ventricle per minute

Cardiac output equation

cardiac output = stroke volume x heart rate

What is the cardiac output at rest

5 L/min

Roughly what % of cardiac output is dedicated to the muscles during rest and during exercise

• during rest — 15-20%

• during heavy exercise — 70-85%

Roughly what % of cardiac output is dedicated to the GI tract during rest and during exercise

• during rest — 20-25%

• during heavy exercise — 3-5%

Why may cardiac output to the skin increase from rest to exercise

thermoregulation

What is the cardiac output during exercise

25 L/min

What does ECG stand for

electrocardiogram

What does the P wave represent in an ECG

atrial systole

What does the QRS wave represent in an ECG

ventricular systole

What does the T wave represent in an ECG

ventricular diastole

What does the R-R interval of an ECG represent

the heart beat duration

What does the Q-T interval represent in an ECG

the time taken for ventricles to depolarise and then repolarise

Significance of LONG QT intervals

• they are arrhythmogenic

• these long QT intervals can cause sudden death in athletes unaware of their condition

What does the P-R interval represent in an ECG

conduction time between atria and ventricles

Where is the P-R interval measured from (despite its name)

from the beginning of the upslope of the P wave to the beginning of the QRS wave

What does the P-R interval represent in an ECG

length of time for electrical conduction to pass from the atria to ventricles

Why is atrial repolarisation not visible on an ECG

because it is masked by ventricular systole (QRS wave)

What changes to the ECG occur during exercise

• shortening of R-R interval

• slight increase in P wave amplitude

• shortening of P-R interval

• shortening of Q-T interval

• S-T segment depression

• T-wave amplitude may flatten

Why does the P-R interval shorten during exercise

shorter conduction time between atria and ventricles

Why does the Q-T interval shorten during exercise

faster depolarisation of ventricles

What are the 2 main centres of the control of heart rate

• central command in the motor cortex of the brain

• cardiovascular control centre in the medulla in the brainstem

What are 2 nerves associated with controlling the heart rate + their effect on HR

• Accelerator nerve (sympathetic NS) — increases HR

• Vagus nerve (parasympathetic NS) — decreases HR

How do sympathetic nerves increase heart rate at the SAN

• accelerator nerves release noradrenaline at the SAN

• noradrenaline binds to β₁ adrenergic receptors on the SAN

• this activates G-proteins, stimulating adenyl cyclase to produce cAMP

• increased cAMP causes faster depolarisation, increasing the heart rate

How do parasympathetic nerves decrease heart rate at the SAN

• Vagus nerves release acetylcholine at the SAN

• acetylcholine binds to M₂ muscarinic receptors on the SAN

• opening K⁺ channels leading to hyperpolarisation of the cell membrane

• inhibiting adenylyl cyclase, reducing cAMP, and decreasing intracellular concentrations of Ca²⁺ and Na⁺

• decreasing heart rate

What is the intrinsic heart rate

100 BPM

What is the normal resting heart rate

60-70 BPM

What is vagal tone

the continuous parasympathetic activity of the vagus nerve to lower the intrinsic heart rate from 100 BPM to 60-70 BPM at rest

What is the first thing that happens (in terms of the nervous system) when we start to exercise

Inhibition of vagal tone (to stop releasing acetylcholine, allowing the HR is drift back up to 100 BPM)

What is the maximum heart rate?

220 - age

Chronotropic effect

changes in heart rate

Inotropic effect

the force of muscle contraction

Which catecholamines have a positive chronotropic and inotropic effect

adrenaline and noradrenaline

Which catecholamine has a negative chronotropic and inotropic effect

acetylcholine

What does stroke volume depend on

• end diastolic volume (due to an increase in venous return)

• aortic or pulmonary arterial pressure (pressure against which ventricles contract)

• circulating adrenaline and noradrenaline (increases contractility)

How does a heart transplant affect heart rate

• takes longer for heart rate to increase during exercise and decrease following exercise

• a higher resting heart rate (90-110 bpm)

Why does a heart transplant cause changes in heart rate

• nerves to the heart are cut so heart is denervated

• removing vagal tone and allowing the heart to beat at its intrinsic, faster rate

• heart rate is regulated by circulating catecholamines rather than nervous system

What peripheral receptors are involved in control of heart rate

baroreceptors and chemoreceptors in the blood vessels, joints and muscles

What do baroreceptors detect

changes in pressure

What do chemoreceptors detect

changes in metabolites

What are the 2 main baroreceptors controlling heart function located

• carotid sinus (in the neck)

• aortic arch (in the heart)

Why don’t baroreceptors stop an increase in heart rate

• the baroreflex is RESET to a higher operating point

• allowing for a higher BP before being activated

• while still keeping BP tightly regulated around a new set point

How do baroreceptors respond to high blood pressure

• increased baroreceptor firing

• increased parasympathetic (vagal) output

• decreased sympathetic output

• decrease in heart rate and vessels relax

• blood pressure returns to normal

How do baroceptors respond to low blood pressure

• decreased baroceptor firing

• decreased parasympathetic output

• increased sympathetic output

• increase in heart rate and vasoconstriction

• blood pressure returns to normal

Frank-Stirling Mechanism

stroke volume increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant

Why do we see a plateau in stroke volume in untrained individuals

• tachycardia

• Frank-Starling mechanisms reaches its limit

• reductions in afterload

Why does tachycardia cause stroke volume to plateau (in untrained individuals)

as heart rate increases, diastole shortens disproportionately, reducing ventricular filling time until preload reaches a functional maximum

Why does the Frank-Starling mechanism reaching its limit cause stroke volume to plateau (in untrained individuals)

• ventricular sarcomeres reach their optimal length for force generation

• further increases in length do not produce any further increases in stroke volume

Why do reductions in afterload cause stroke volume to plateau (in untrained individuals)

• during exercise arterial pressure increases

• ventricular afterload decreases

• despite increased contractility, stroke volume reaches a ceiling

Why do trained athletes have a higher stroke volume?

• larger ventricular chamber size

• greater blood volume

• enhanced diastolic filling and compliance

What are the chronic adaptations of the CVS to exercise

• “Athlete’s heart”

• increased end-diastolic volume + increased left heart contractility

• decreased vascular resistance

• bradycardia

• increase in exercise intensity required to reach HRmax

• faster recovery of heart rate after exercise

• larger maximal cardiac output

• increase in VO₂ Max

In trained individuals, why do we mainly see hypertrophy in the left side of the heart

The left side of the heart does the most work as it pumps blood to the rest of the body against high systemic pressure

VO₂ Max

maximum amount of oxygen that can be taken in, transported and utilised in 1 minute (measured in L/min or mL/kg/min)

VO₂ max of UK general public

• 30-40 mL/kg/min for men

• 25-35 mL/kg/min for women

Highest recorded VO₂ max

97.5mL/kg/min (Oskar Svendsen)

What is atrial fibrillation

an irregular heart rhythm, characterized by rapid, irregular electrical signals causing upper chambers of the heart to quiver instead of beating regularly

What is the outcome of atrial fibrillation

blood does not leave the atrium efficiently → blood clots → strokes

Although not fully understood, what are some possibilities for atrial fibrillation in athletes

• increased vagal tone

• cardiac remodelling (enlargement of atrium)

• use of performance enhancing drugs

• energy drinks

• electrolyte abnormalities

Which blood vessel regulates blood flow and pressure

arteriole

How do the arterioles control blood flow and pressure

• they have smooth muscle walls which can control their diameter

• they absorb the greatest drop in pressure to protect the capillaries

What are the 2 intrinsic mechanisms for blood flow regulation

• metabolic regulation

• endothelium derived regulation

Metabolic regulation of blood flow

• blood flow adjusts and is closely coupled to metabolic demand

• metabolic by-products directly affect the smooth muscle and cause vasodilation

Endothelium derived regulation

• increase in cardiac output → increase in blood flow → increase in stress to the vessel walls

• stimulates the endothelium to release very potent vasodilation factors

• which act on the smooth muscle to cause vasodilation

Vasodilators released from the endothelium

• nitric oxide

• prostaglandins

• endothelium-derived hyperpolarizing factor (EDHF)

Role of intrinsic mechanisms for blood flow regulation in exercise

crucial for the robust increase in local blood flow in skeletal muscle

Extrinsic neural regulation of blood flow

• level of vasoconstriction of arteriole is high within skeletal muscle at rest

• exercise increases SNS stimulation and adrenaline is released from the adrenal medulla

• in exercising skeletal muscle SNS activity is opposed by locally released vasoactive substances so that vasoconstriction does not occur

What is functional sympatholysis

release of local vasoactive substances which override the autonomic nervous system and allow for increased blood flow to the muscle

What is blood pressure

the pressure exerted by the blood on the walls of the vasculature

What is systolic blood pressure

pressure in arteries during systole

What is diastolic blood pressure

the pressure exerted onto the walls during diastole (when the heart is relaxed)

How does exercise affect blood pressure

• systolic blood pressure increases

• no change in diastolic blood pressure

Why do we not see changes in the diastolic blood pressure

because it is influenced by our total peripheral resistance

What is total peripheral resistance

the total resistance to blood flow offered by all systemic vasculature

What happens to total peripheral resistance with exercise

it decreases

What does diastolic blood pressure represent

arterial pressure between contractions

Blood distribution in the CVS

• 64% in veins

• 13% in arteries

• 9% pulmonary

• 7% arterioles, capillaries

• 7% heart

Where in the body does most of the blood volume reside

the veins

What 3 factors allow for venous return

• valves in the veins

• muscle pump action

• SNS stimulation

What is the purpose of the valves in the veins

unidirectional blood flow towards the heart

Mechanism of muscle pump in venous return

• before muscle contraction, blood enters vein

• when muscle contracts, upper valve opens further but the lower valve closes

• pushing blood up the vein

• after muscle relaxes, upper valve closes to prevent backflow

• the lower valve then opens to allow vein to be filled again