Shock Flashcards
Define clinical shock
Acute circulatory failure with poorly distributed tissue perfusion leading to cellular hypoxia
What is normal MAP
100mmHg
What is MAP is a person with clinical shock
60mmHg
Describe how cellular hypoxia leads to cel death
- Cells switch from aerobic to anaerobic
- Lactic acid is produced
- Cell function ceases, swells
- Membrane becomes more permeable
- Electrolytes and fluids move in and out
- Na+/K+ pump damage
- Mitochondria damage
- Cell death
What 2 things control heart rate
Baroceptors in carotid sinus activate/ inhibit ANS
Concious threat perception
What 2 things control stroke volume
Preload
Myocardial contractability
Is it usually heart rate or stroke volume
Stroke volume
When is it heart rate impaired
Drugs/ CNS involved
Define preload
Amount of blood in heart before it contracts
The greater the preload…
Greater force of contraction
Greater the stroke volume
3 ways that increase myocardial contractility
Sympathic nervous system
Circulating catecholamines
Inotrope drug (b1 agonists)
3 ways that myocardial contractility can decrease
Cardiac disease
Hypoxia
pH/ electrolyte disturbance
Drugs (bb, ccb)
What mainly regulates systemic venous resistance
Arteriolar constriction at end organs
4 ways that arteriolar constriction is regulated
- Sympathetic nervous system releasing noradrenaline
- Circulating hormones like angiotensin 2
- Endothelin released from lining enodthelium constricts arterioles and NO
- Prostacyclin is vasodilator
Where is noradrenaline released from
Outside the nerve terminal
What receptors does noradrenaline act on and where are these located?
Catecholamine alpha receptors in the tunica media
What receptors does angiotensin act on
AT1 receptors lining the lumen
Another name for prostaglandin
PG12
Where is prostglandin produced and from what
Endothelial cells from arachiodonic acid
2 functions of prostaglandin
Prevents formation of platelet plug by inhibiting platelet activation
Local vasodilator that acts by reducing calcium entry