P: Haemorrhage, fainting & exercise Flashcards
What is hypovolaemia?
Severe blood loss reduces blood volume
Effects of hypovolaemia?
Reduction in venous return, cardiac output, mean arterial pressure and perfusion of regional circulations.
Nonprogressive/ compensatory shock:
- > 45mmHg
Bodily compensatory mechanisms can cause full recovery
Progressive shock:
- <45mmHg
Without therapy, shock steadily worsens until death
Chemoreceptor reflexes: when is it stimulated and what does it cause?
- When MAP < 60mmHg, baroreceptor reflex intensity does not increase –> decreased pO2 will stimulate peripheral chemoreceptors
- Enhances peripheral vasoconstriction
Cerebral ischaemia
- 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
Vasopressin
- Antidiuretic hormone (ADH)
- Secreted by pituitary in response to haemorrhage
- Potent vasoconstrictor
Renal salt + water conservation mechanisms:
- 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.
Acidosis
- 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
What causes CNS depression
- Reduction in cerebral perfusion depresses activity of cardiovascular control centres
- Further reduction in sympathetic outflow
What causes sludged blood/ blood agglutination?
- 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
Endotoxin release due to progressive shock?
- 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
What is vasovagal syncope?
- 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
Triggers of vasovagal syncope?
- Heat exposure
- Sight of blood/ having blood drawn
- Intense fear/ emotional shock
Orthostatic hypotension:
- 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
Cardiovascular/ respiratory control centres receive input from:
- Muscular mechanoreceptors
- Baroreceptors
-Vascular & muscular chemoreceptor
Cardiovascular nervous responses to exercise:
- 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
3 factors that increase venous return:
- 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.
Effect on TPR during intense exercise using a few muscles:
- Vasodilation in active muscles, vasoconstriction in inactive muscles
- Large increase in TPR, MAP can increase to 170mmHg
Effect on TPR during whole-body exercise
- 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
On cessation of exercise:
- HR and CO quickly reduced
- Accumulation of vasodilatory metabolites keeps TPR low
- MAP may fall briefly until corrected by baroreceptor reflex
Vo2 equation
HR x SV x (PaO2 - PxO2)
2 serious side effects of progressive shock:
- Sludged/ agglutinated blood
- Endotoxin release –> causes widespread vasodilation (septic shock) and depresses cardiac function
