P: Haemorrhage, fainting & exercise

Question 1

What is hypovolaemia?

Answer 1

Severe blood loss reduces blood volume

Question 2

Effects of hypovolaemia?

Answer 2

Reduction in venous return, cardiac output, mean arterial pressure and perfusion of regional circulations.

Question 3

Nonprogressive/ compensatory shock:

Answer 3

• > 45mmHg
  Bodily compensatory mechanisms can cause full recovery

Question 4

Progressive shock:

Answer 4

• <45mmHg
  Without therapy, shock steadily worsens until death

Question 5

Chemoreceptor reflexes: when is it stimulated and what does it cause?

Answer 5

• When MAP < 60mmHg, baroreceptor reflex intensity does not increase –> decreased pO2 will stimulate peripheral chemoreceptors
• Enhances peripheral vasoconstriction

Question 6

Cerebral ischaemia

Answer 6

• Caused by activation of CAN ischaemic response resulting from decreased PO2 and increase pCO2 in brain
• Causes extreme stimulation of SNS
• Increased vasoconstriction and cardiac contractility

Question 7

Vasopressin

Answer 7

• Antidiuretic hormone (ADH)
• Secreted by pituitary in response to haemorrhage
• Potent vasoconstrictor

Question 8

Renal salt + water conservation mechanisms:

Answer 8

• Reduction in MAP reduces renal glomerular filtration rate + increases renal sympathetic nerve activity
• Increases production of angiotensin II stimulates release of aldosterone from adrenal cortex
• Increases salt & water reabsorption in nephrons
• ADH also promotes renal water reabsorption.

Question 9

Acidosis

Answer 9

• Reduced O2 delivery increases cellular production of acidic metabolites and impaired kidney function slows excretion of H+
• Resultant metabolic acidosis further depresses cardiac functiob and reduces vasoconstriction by decreasing sensitivity to noradrenaline

Question 10

What causes CNS depression

Answer 10

• Reduction in cerebral perfusion depresses activity of cardiovascular control centres
• Further reduction in sympathetic outflow

Question 11

What causes sludged blood/ blood agglutination?

Answer 11

• In small blood vessels, acidosis causes blood agglutination
• Causes minute blood clots which plug vessels
• Further acidosis causes thromboxane A which promotes further platelet aggregation

Question 12

Endotoxin release due to progressive shock?

Answer 12

• Macrophages in liver detoxify endotoxins released into circulation by intestinal bacteria
• Shock depresses their phagocytic activity and increased levels of endotoxins result in widespread vasodilation (septic shock) and depress cardiac function

Question 13

What is vasovagal syncope?

Answer 13

• Fainting caused by triggers that stimulate NTS and results in:
• Activation of vagal centre of medulla that reduces heart rate
• Inhibition of spinal sympathetic nerves, reducing vasoconstrictor tone
• Rapid fall in MAP, reducing blood flow to brain and loss of consciousness

Question 14

Triggers of vasovagal syncope?

Answer 14

• Heat exposure
• Sight of blood/ having blood drawn
• Intense fear/ emotional shock

Question 15

Orthostatic hypotension:

Answer 15

• Drop in MAP caused by rapid movement
• Gravity causes rapid movement of venous blood into legs
• Decreased venous return –> decreased cardiac output –> decreased MAP
• Baroreceptor reflex rapidly restores normal MAP

Question 16

Cardiovascular/ respiratory control centres receive input from:

Answer 16

• Muscular mechanoreceptors
• Baroreceptors
  -Vascular & muscular chemoreceptor

Question 17

Cardiovascular nervous responses to exercise:

Answer 17

• Inhibits vagal impulses to heart and increases sympathetic discharge
• Immediate increase in myocardial contractility + tachycardia
• Increased CO
• SN stimulation causes vasoconstriction of skin, splanchnic & inactive muscle circulations
• Increase in circulating catecholamines released by adrenal medulla enhances effects of SN stimulation

Question 18

3 factors that increase venous return:

Answer 18

• SNS-induced vasoconstriction of venules in tissues/muscles moves additional blood towards heart
• Contracting skeletal and respiratory muscles pump venous blood back into heart
• Increased depth/ rate of ventilation decreases intrathoracic pressure, increasing blood flow into thoracic cavity.

Question 19

Effect on TPR during intense exercise using a few muscles:

Answer 19

• Vasodilation in active muscles, vasoconstriction in inactive muscles
• Large increase in TPR, MAP can increase to 170mmHg

Question 20

Effect on TPR during whole-body exercise

Answer 20

• Vasodilation in large masses of active muscle
• TPR decreases during exercise
• Slight rise in MAP as effect of increased CO
• Vasoconstriction in inactive muscles will prevent major drop in TPR

Question 21

On cessation of exercise:

Answer 21

• HR and CO quickly reduced
• Accumulation of vasodilatory metabolites keeps TPR low
• MAP may fall briefly until corrected by baroreceptor reflex

Question 22

Vo2 equation

Answer 22

HR x SV x (PaO2 - PxO2)

Question 23

2 serious side effects of progressive shock:

Answer 23

• Sludged/ agglutinated blood
• Endotoxin release –> causes widespread vasodilation (septic shock) and depresses cardiac function