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
Name the 4 classifications of shock
Obstructive
Distributive
Hypovolaemic
Cardiogenic
2 stages of shock
- Stage 1= compensated shock
- Stage 2= decompensated shock
Define obstructive shock
Physical obstruction to vessels leaving and entering the heart
Causes of obstructive shock
Pulmonary embolism
Pneumothorax
Cardiac tamonade
Signs and symptoms of obstructive shock if its tension pneumothorax
- Tachycardia
- Chest pain
- Absent pulse
- Breath signs
Signs and symptoms of obstructive shock if its pulmonary embolism
- Hypoxia
- Sudden onset chest pain
- Shortness of breath
Define cardiogenic shock
Failure of the heart to pump efficiently
Name some causes of cardiogenic shock
- mi
- heart failure
- valvular disease
What do people with cardiogenic shock always present with
Chest pain, shortness of breath, nausea and vomiting
What do people with cardiogenic shock sometimes present with
Pulmonary oedema
Acute circulatory collapse
Define distributive shock
Loss of vasoconstriction at one end organ leading to excess blood flow at this organ but lack of blood flow at other organs
Define sepsis
Systemic response to presence of pathogens in blood or other organs
Define septic shock
Sepsis with hypotension
Temperature in somebody with sepsis
36 degrees
Heart rate in somebody with sepsis
90bpm
Resp rate in somebody with sepsis
> 20 breaths per min
White blood cell count in somebody with sepsis
> 12x10^9/L
Descibe process by which bacterial infection to shock
- Excessive host response
- Micro-vascular damage
- Lower systemic vascular resistance
- Low BP
- Shock
How do lipoproteins in bacterial wall lead to prevention of constriction
- Stimulates neutrophils and monocytes to release cytokines
- Affects endothelium preventing constriction
- Lowers SVR
Signs of hypovolaemic shock
Confusion, cold and clammy skin, high BP and HR, slow capillary refill time
How much blood loss is acutely life threatening
> 40%
What are the immediate compensatory responses of shock
- BP fall detected by baroceptors and these increase sympathetic outflow
- Increased HR
- Large vein constriction to restore preload
- Medullary vasomotor signals to hypothalamus to release ADH and reduces ANP release
- Reduced urine flow
What are the long term compensatory responses of shock
- Increases renin and aldosterone
- Thirst stimulated by angiotensin 2 receptors in brain
- Peritubular cells sensitive to hypoxia and increase release of erythropoietin
What is class 1 shock (blood loss, pulse, BP, compensated?)
- 15% blood volume lost
- Pulse <100
- Normal BP and PP
- Fully compensated by immediate compensatory effects
What is class 2 shock (blood loss, heart rate and resp rate, pulse pressure? signs and symptoms?)
- Loss of 15-30% blood volume
- Tachycardia and tachypnoea
- Low pulse pressure
- Clammy skin, delayed capillary refill
What is class 3 shock (how much blood lost, BP? Treatment required)
- > 30% blood loss
- Persistent BP drop
- Patients require blood transfusion, plasma volume
- May have end organ damage
What is class 4 shock (how much blood lost, signs and symptoms
- > 40% blood loss
- Confused/ unconcious
- No urine output
- Severly decreased systolic pressure
- immediate transfusion required
What are the goals of shock treatment
Central venous pressure 8-12mmHg
MAP> 65mmHg
urine output 0.5ml/kg
SVC>70%
How can circulating blood volume be restored
- IV colloids or crystalloids to restore preload
What drugs are used to treat shock
- Noradrenaline
- Phenylephrine
- ADH
