Gus suffered a rugby injury that required an examination of cardiovascular and respiratory responses to exercise. The document provides definitions and explanations of terms related to: - The differences between dynamic and isometric exercise - Factors affecting oxygen consumption and delivery during exercise - Cardiovascular and respiratory changes that occur with increasing exercise intensity - Effects of posture on venous circulation and blood pressure regulation - Causes and physiology of hemorrhage and shock

1. Gus’s Rugby Injury
Cardiovascular and Respiratory Responses to Exercise
1. What is the difference between dynamic exercise and isometric exercise?1
2. What causes vasodilatation in vascular smooth muscle during exercise?2
3. What type of graph/curve would describe the relationship between oxygen
consumption and work during exercise?3
4.What is the equation used to calculate O2
consumption?4
5.How are (i) arterial O2 content (ii) venous O2 content
(iii) cardiac output affected by exercise and why?5
6.What is the main reason someone would be able to
raise their level of work and O2 consumption to a higher
level than someone else?6
7.The graphs show changes blood pressure, stroke
volume, cardiac output, total peripheral resistance, blood
O2 content and heart rate, with overall O2 consumption
on the x-axis, label which graph shows which7
1 Isometric exercise = muscle contraction without muscle shortening, sustained contraction (e.g. some
circuits exercises like planking, pilates, holding a weight without moving). Dynamic exercise = muscles
shorten, rhythmic contraction and relaxation (e.g. skeletal muscle).
2 Local metabolites, sympathetic stimulation of B2 receptors, nitric oxide, decreased PO2, increased PCO2,
increased H+, increased adenosine all contribute.
3 The relationship would be linear with work and O2 consumption both increasing proportionately up to a
point, which would be the maximum work output, after which VO2max and max. work output is reached and
cannot be exceeded.
4 O2 consumption (mls/min) = cardiac output (mls/min) (arterial - mixed venous O2 content). This is
dependent on the amount of oxygen delivered (ventilation/perfusion) to the tissues and the extraction of that
by the tissues.
5 (i) Arterial O2 content is unaffected by exercise (ii) venous O2 content falls progressively as exercise
intensity increases, because more of the blood O2 is taken up by the tissues, it may fall slightly with training
(iii) Cardiac output increases with increasing exercise intensity, the maximum CO is the main factor
determining VO2 max.
6 Able to raise CO more than another
7 A = cardiac output, B = stroke volume, C = heart rate, D = Blood pressure (top to bottom: systolic, mean,
diastolic), E = Total peripheral resistance, F = overall O2 consumption shown by the gap between arterial
and venous oxygen levels

2. 8. What is the main factor affecting (i) maximum heart rate (ii) resting heart rate8
9. If O2 consumption at rest is 250ml/min what might this be during maximum
exercise?9
10.What is the main variable in heavy exercise that increases cardiac output?10
11.How do you work out mean BP from cardiac output and TPR?11
12.How does HR change during isometric exercise compared to dynamic exercise?12
13.How does isometric exercise affect systolic and diastolic in comparison to
dynamic exercise and what accounts for this?13
14.What factors increase increase oxygen consumption by the tissues?14
15.X andY refer to rest and exercise in the following statement, but which is which?
“In conditions of X, the oxygen saturation (%) of haemoglobin is lower for any
given pO2 than conditions ofY”15
16.The inflection point on a curve comparing oxygen consumption with ventilation is
higher in the trained individual than in someone who is unfit, why is this?16
8 maximum heart rate = decreases with age (220-age) so is fastest in a child, resting heart rate = decrease
with increasing physical fitness
9 Increases by about 10x to 2800ml/min
10 Consistent linear increase in heart rate up to max, more modest increase in stroke volume due to
increased filling pressure of the heart and increased contractility despite reduced time for heart to fill.
11 cardiac output x total peripheral resistance
12 HR increases steadily with length of contraction in isometric exercise, but the increase is not as steep and
high as that seen in dynamic exercise.
13 Systolic and diastolic BP both increase whereas the effect of dynamic exercise on diastolic blood pressure
is negligible. The greater rise in BP in isometric exercise is a result of compression of blood vessels in
contracting muscle.
14 Increased blood flow (vasodilation and re-routing from splanchnic circulation), increased removal of
oxygen owed to low tissue PO2 (so increased release of O2 from Hb), decreased affinity of Hb. Increased
PCO2 and reduced pH in exercising tissues also contribute to greater O2 unloading from Hb.
15 X = exercise, Y = rest, remember O2 sats donʼt change for arterial blood in healthy individuals, but they
decrease in venous blood for increasing exercise level, so decreases overall.
16 The anaerobic threshold of a trained person is higher. More oxygen is offloaded to the tissues in the
trained person so haemoglobin effectively more efficient. Lungs have better perfusion because of increased
capillaries.

3. 17.What factors (in terms of equations) do (i) ventilation, (ii) alveolar ventilation
depend on?17
18.What effect does increasing ventilation (up toVO2max) with dynamic exercise
have on: pH, PvO2, PvCO2 PaO2, PaCO2?18
Venous Circulation and Posture
1. What would typical pressures be in mmHg in a vein and a venule?19
2. At any one time, at rest, what proportion of the blood is in the venous system and
what in the arterial?20
3. What cardiovascular problems, can be caused by upright posture?21
4. How could you work out approximate blood pressure in the feet or head for a
healthy individual with normal blood pressure?22
5. What is the equation for flow?23
6. What effects do valves have on venous pressure in the legs?24
17 Ventilation = tidal volume x respiratory frequency, Alveolar ventilation = (tidal - dead space volume) x
respiratory frequency
18 pH = although acid is being produced, this remains roughly constant because of buffering, decreases
sharply once you approach VO2max.
PvO2 = venous oxygen pressure decreases sharply with the difference between rest and moderate activity,
then continue to decrease at a slower rate as intensity increases,
PvCO2 = Venous PCO2 rises with exercise intensity (roughly proportional to the fall in venous O2)
PaO2 = arterial PO2 levels generally remain constant by increase at high ventilation/heavy exercise
PaCO2 = remains constant but may decrease in high ventilation/heavy exercise
19 Vein = 10mmHg, venule = 12-18mmHg
20 40% arterial, 60% venous
21 Lack of cerebral perfusion, syncope (fainting), edema in feet and ankles. All due to gravitational force
affecting blood flow.
22 Distance from heart in cm x 0.77 (mmHg change per cm away from heart), if above the heart then -ve
figures and if below +ve.
23 Flow = pressure gradient from start to finish / resistance (TPR), (pressure differential = e.g. the difference
between veins and arteries in the foot is 186mmHg (arteries) ---> flow across capillaries ---> 100 (veins)
24 Skeletal muscle pumping in conjunction with the valve system decreases venous pressure in the
extremities.

4. 7. What are the cardiovascular effects of ‘venous pooling’?25
8. Where in the body would a fall in blood pressure be physically detected?26
9. What mechanism might supplement the baroreceptor reflex in initiating response
to postural blood pressure changes?27
10.Why would jugular cannulation be performed with the head down when this
could cause increased bleeding?28
11.What does the term vasovagal mean?29
Shock and Hemorrhage
1. What are the most common causes of severe internal bleeding?30
2. How could you detect a gradual blood loss over a long period of time?31
3. What signs and symptoms may be present in severe internal blood loss?32
4. What defines circulatory shock?33
5. What would the approximate total blood volume be in ml/kg for a typical adult
male and female?34
25 Happens when standing still for extended periods. Decreased venous return, decreased CVP, decreased
cardiac output decreased 25%, stroke volume decreased up to 40%, TPR increased around 25%, limb and
splanchnic flow decreased 25%, lower arterial blood pressure (because of stretching of veins) although often
transient because of reflex response, in some cases BP is seen to increase because of reflex.
26 Baroreceptors in the carotid sinus (via carotid sinus and glossopharyngeal nerves) and in the aortic arch
(via aortic nerve and vagus nerve). Responses sent to nucleus tractus solaris.
27 Reflexes from vestibular system, feed forward.
28 Prevents risk of air embolism during inspiration, normally jugular venous pressure is negative.
29 Overwhelming parasympathetic response on vascular system, experienced in fainting (vasodilation and
vagally mediated bradycardia)
30 Ruptured spleen, ruptured ectopic pregnancy, aortic aneurysm, fracture, bleeding peptic ulcer (blood
vomiting).
31 Usually manifest as Fe2+ deficiency or anaemia
32 Pallor, rapid shallow breathing, weak rapid pulse, intense thirst, nausea (reduced splanchnic circulation),
reduced urine output, low BP (may be compensated), anxiety, confusion & aggression, decreased
coagulation time (due to loss of haematocrit)
33 Not simply a low blood pressure but inadequacy of blood flow
34 male 77ml/kg, female 67ml/kg (due to higher proportion of body fat which is less perfused than muscle)

5. 6. In a fit individual, what % blood loss would there have to be to elicit shock?35
7. What is reverse stress relaxation?36
8. What is ‘internal transfusion’?37
9. What happens to levels of atrial naturetic peptide (ANP) in the case of reduced
atrial stretch?38
10.What could cause hypoxia 12-24 hours following hemorrhage even when blood
volume, blood pressure and cardiac output are all normal?39
11.What is oliguria?40
12.How long does it take for haemoglobin levels and blood quality to be restored
after a 20-30% hemorrhage?41
13.What happens to platelets, fibrinogen and coagulation time following
hemorrhage?42
14.Name the hormone released to increase reticulocyte count43
15.Which receptor stimulates an increase in ventilation in response to decreased
blood flow and decreased blood pH?44
35 less than 20%, more than this induces shock and if above 30-50% may be serious consequences
36 Compensatory mechanism for reduced blood volume whereby veins shrink around reduced blood volume.
This maintains venous pressure and venous return despite reduced blood volume and cardiac output.
37 Restoration of blood volume by fluid movement from interstitum to blood caused by fall in BP/hydrostatic
pressure difference. Associated with haemodilution (lower haematocrit as only fluid replaced not cells)
38 This is normally released in response to atrial stretch to reduce blood volume. In the case of decreased
blood volume, decreased levels of ANP are released.
39 As the blood volume is restored by internal transfusion, the red cells become diluted (as their levels
recover slower), as the baroreceptor reflexes are withdrawn (because volume is back to normal) the supply
of red blood cells at any one time is actually decreased because blood has been diluted.
40 Low urine output, may be caused by sudden decrease in blood volume
41 5-6 weeks, although volume is restored much quicker
42 Platelets and fibrinogen decrease as blood is ʻdilutedʼ, clotting time increases
43 erythropoietin released by kidneys
44 Chemoreceptors and baroreceptors in the carotid bodies

6. 16.What is the difference between progressive and non-progressive shock?45
17.Why could some damage from a severe bleed be irreversible even after
transfusion?46
18.What % blood loss would typically have to occur before you saw any change to
BP?47
45 Non-progressive shock gets better without treatment (e.g. less than 20% blood volume loss). Progressive
shock shows an initial recovery in terms of blood pressure and cardiac output but will ultimately lead to death
if left untreated.
46 Damage to myocardium (cardiac muscle is irreplaceable) resulting from ischaemia. An ischemic gut (from
reduced splanchnic circulation) may become ʻleakyʼ and lead to the escape of toxic gut bacteria or factors
such as endotoxin which also perpetuates myocardial damage. Renal failure from significantly reduced GFR.
ARDS from reduced perfusion of the lungs.
47 Around 20%, so it is vital that symptoms are picked up before this point