Hemorrhage, Fainting, Exercise Flashcards
What is hypovolaemia ?
A reduction in blood volume?
What are the two types of shock?
Compensatory/non progressive shock
Progressive shock
What blood pressure value is associated with compensatory shock?
Bp remains greater than 45mmHg
What bp value is associated with progressive shock?
Bp falls below 45mmHg
What is the difference in the outcome for a patient with progressive shock vs non progressive shock?
Progressive shock - patient will get worse without therapy
Non progressive - the body’s own compensatory mechanisms will cause recovery
What are the main compensatory mechanisms for shock?
- Baroreceptor reflex
- Chemoreceptor reflex
- Central nervous system response to cerebral ischaemia
- Reabsorption of tissue fluids
- Hormonal vasoconstrictors
- ADH release from pituitary
- Angiotensin II and aldosterone release from adrenal cortex
What happens in the initial response to hemorrhage, a resonse caused by the baroreceptors ?
- General arteriolar constriction = TPR ↑
- Venous constriction = venous return ↑
- HR increases from ≈60bpm to ≈180bpm
Why are other compensatory mechanisms needed, apart from the baroreceptor reflex?
Once MAP drops below 60mmHg, baroreceptor intensity doesn’t increase - plateau
Below ___ mmHg of MAP, baroreceptor reflexes plateau
60mmHg
What stimulates chemoreceptors?
PO2 ↓
What does stimulation of chemoreceptors cause?
- Peripheral vasoconstriction
- Increased venous return as an increased rate and depth of perspiration reduces intrathoracic pressure
What is the respiratory pump?
When venous return is increased due to a reduction in intrathoracic pressure caused by increases respiratory rate
Why is cerebral ischamia a compensatory reflex?
When PO2 ↓ and PCO2 ↑ in the brain
Causes extreme activation of SNS
More vasoconstriction and contractility of heart
What causes the plateau at 50mmHg?
The compensatory mechanism caused by cerebral ischaemia
How does the reabsorption of tissue fluids happen during shock?
- Reduced MAP, increased TPR and increased venous return - capillary hydrostatic pressure ↓
More tissue fluid reabsorbed
why does the oncotic pressure of plasma decrease during hemorrhage?
More tissue fluid = more dilution of blood = lower protein conc
How much tissue fluid can be reabsorbed per hour during hemorrhage ?
1 litre per hour
What increases adrenaline release?
When MAP drops to 40mmHg, adrenal medulla increases adrenaline output by 50 fold
What causes the pituitary to release ADH?
Sensory input from baroreceptors and other vascular stretch receptors
How is salt and water conserved in the kidney?
- Reduction in MAP means less filtration occurs
- Increased production of angiotensin II causes release of aldosterone
- ADH causes water reabsorption
What is Angiotensin II ?
A vasoconstrictor released by the kidneys
What is aldosterone?
A sodium retaining hormone, whos release is stimulated by angiotensin II
How long does it take for sympathetic reflexes to become active after hemmorhage?
30-60 sec
How long does it take for angiotensin and vasopressin mechanisms to respond completely after hemmorhage?
10-60 mins
How long does it take for reabsorption of tissue fluid to become effective after hemmorhage?
1 to 48 hrs
What causes progressive shock?
Decompensatory mechanisms
What determines the outcome of a shock patient?
The relative strength of the compensatory and decompensatory mechanisms
List the decompensatory mechanisms
- Cardiac failure
- Increased tissue hypoxia
- Acidosis
- CNS depression
- Sludged blood
- Endotoxin release
Why is cardiac failure a decompensatory mechanism?
Ventricular function ↓ - cardiac output ↓ - coronary blood flow ↓ - ventricular function ↓
Why is increased tissue hypoxia a decompensatory mechanism ?
Tissue blood supply ↓ - tissue hypoxia ↑ - vasodilatory metabolites ↑ - TPR ↓ - MAP ↓
How does acidosis cause decompensation in a shock patient?
O2 delivery ↓ - acidic metabolites produced in cells so [H+] increases - acidosis then depresses cardiac function and reduces vasoconstriction by decreasing sensitivity to noradrenaline
How does CNS depression cause decompensation in a shock patient?
Reduction in cerebral perfusion depresses the activity of cardiovascular control centres
This reduces sympathetic outflow
How does slugged blood cause decompensation in a shock patient?
- acidosis causes agglutination in small blood vessels
- small blood clots
- further acidosis causes cells to release thromboxane A which causes further platelet aggregation
How does endotoxin release cause decompensation in a shock patient?
- macrophages in liver detoxify endotoxins released into circulation by intestinal bacteria
- shock depresses their phagocytise activity
- increased endotoxin levels causes widespread vasodilation and impairs cardiac function
SEPTIC SHOCK
What is syncope/fainting?
Sudden, usually temporary loss of consciousness caused by insufficient supply of O2 to neuronal cells in the brain
What causes most fainting episodes?
hypoxia or rapid hypotension
Where to triggers for fainting originate and how do they cause fainting?
Originate in cerebral cortex
Stimulate vagal centre via anterior hypothalamus
Explain mechanism behind vasovagal syncope
Trigger happens - could be blood, heat, fear etc
Vagal centre of brain stimulated
HR reduced, sympathetic nerves inhibited, leading to rapid fall in MAP and then fainting
Explain orthostatic hypotension
Sitting -> standing
Drop in MAP since blood in veins moves to legs
Venous return ↓ CO ↓ MAP ↓
Baroreceptor reflex normally restores normal MAP fast
Fainting can occur in people with chronic hypotension, hypovolaemia or on α1 blockers
Why can people on α1 blockers faint after standing up?
Vasoconstriction can’t occur
What mediates cardiovascular/respiratory responses during exercise?
Neural stimulation and local metabolic factors
What to cardiovascular/respiratory control centres recieve input from ?
- Chemoreceptors (vascular and muscular)
- Mechanoreceptors in muscle
- Baroreceptors
What triggers muscular mechanoreceptors?
Muscle contraction
What are vascular and muscle chemoreceptors sensitive to ?
PO2, PCO2, pH, metabolic products
What cardiovascular responses happen upon initiation of exercise?
- Vagal impulses inhibited, sympathetic discharge ↑.
This causes HR ↑ and contractility ↑ - Vasoconstriction of skin, splanchnic and inactive muscle circulations
Why prevents blood being diverted away from cerebral or coronary circulations and towards active muscles during exercise?
Functional sympatholysis
How much extra blood is diverted to the active muscles and the heart during exercise?
Up to 2L/min extra
Sympathetic nerves cause vasoconstriction of some circulations and also increase in HR and contractility during exercise. What enhances these effects?
Release of adrenaline from adrenal medulla
How do the active muscles cause blood to be diverted towards them during exercise?
Production of metabolic vasodilators - active hyperaemia
How much does blood flow to muscles increase by during exercise?
20-50 fold
What happens as body temperature rises during exercise ?
Vasodilation of skin circulation assisted by stimulation of sweat production
This promotes heat loss.
Sweat production = increase in bradykinin (a vasodilator) = bradykinin also causes increase in NO
What causes the increase in CO during exercise?
Tachycardia mainly, HR can increase to 180bpm during exercise
Why is SV only increased by a small amount, if there is a large increase in contractility of the heart during exercise?
Tachycardia reduces filling time and decreases EDV
How is EDV increased during exercise?
Venous return increased due to
1. Muscle pump
2. Vasoconstriction of venules
3. Intrathoracic pressure decreasing due to increased depth and rate of breathing
What determines the effect on TPR during exercise?
The type of exercise occurring - weightlifting has a different effect to long distance running
What will happen to TPR and MAP during exercise which only uses a few muscles, e.g weightlifting ?
- vasodilation in working muscles, vasoconstriction in inactive muscles
- lots of vasoconstriction causes TPR ↑
- MAP can increase to 170mmHg
What will happen to TPR and MAP during exercise which uses many muscles, e.g running or swimming?
- vasodilation in large masses if active muscle
- TPR decreases
- only a slight rise in MAP, to about 140mmHg (due to CO still increasing)
- vasoconstriction in inactive muscles prevents TPR from dropping too low
Does exercise cause a greater increase in systolic or diastolic pressure?
Systolic. Increased SV = increased pulse pressure.
What happens when you stop exercising?
- HR and CO quickly reduce
- accumulation of vasodilatory metabolites keeps TPR low
- MAP falls briefly until corrected by baroreceptor reflex
What is VO2?
The volume of O2 consumed by the body per min
What is the equation for VO2?
VO2 = HR x SV x (PaO2 - PvO2)
(PaO2 - PvO2) is the arteriovenous O2 difference
What is the value of resting VO2?
3.5ml/min/kg of body mass
Why does VO2 increase during exercise?
More O2 needed to synthesise more ATP
What does the value of VO2 during exercise depend on?
Fitness level and genetics
What is VO2 max?
The O2 consumption at maximum exercise intensity
What is anaerobic threshold ?
When anaerobic respiration increases and arterial pH falls
What does anaerobic threshold stimulate?
High rate of ventilation via chemoreceptors
What determines your exercise tolerance (Muscle pain and feeling of exhaustion)?
The reduction in tissue pH beyond anaerobic threshold
What can regular exercise result in?
- improved capacity to deliver O2 to active muscles
- improved utilisation of O2 by muscles
- progressive increase in VO2 max
What causes fitness?
- lower HR means increased ventricular filling (more vagal tone on heart than unfit people)
- decreased TPR caused by angiogenesis (more capillaries means more NO production means more vasodilation in active muscles)
- biochemical changes in muscle cells results in improved extraction of O2 from blood (size and no. of mitochondria increase)
What does stroke volume increase by during exercise ? %
10-30%
