Flashcards in 28. Shock Deck (27):
What is clinical shock?
This is an acute circulatory failure - with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia
How can tissue perfusion be adequately maintained?
Via maintenance of cardiac output and blood pressure
CO - 5l/min
Systolic BP - 120mmHg
MAP - 10mmHg
What can cause a drop in blood pressure sufficient to cause shock?
BP = CO x systemic vascular resistance
SO a drop in blood pressure leading to shock can be caused by a low cardiac output or a low vascular resistance
Why might there be a low CO?
CO = HR x SV
A low heart rate may be due to inhibition of autonomic system (perception of threat)
A low stroke volume (more common) due to reduced preload or due to reduced myocardial contractility
What factors can lead to a reduced myocardial contractility?
pH or electrolyte disturbance
Drugs e.g. beta blockers, calcium channel blockers
Why is it important to maintain systemic vascular resistance?
Need to maintain adequate resistance to ensure an adequate distribution of the blood
If the resistance to just one organ falls then the blood will take this route i.e. the path of less resistance
SO the blood supply to all the other organs will fall
SO must maintain the level of resistance and pressure in all the systemic arteries i.e. the systemic vascular resistance
Which hormones act to maintain systemic vascular resistance?
Angiotensin 2 - acts on receptors of the endothelium to mediate constriction of the vascular muscle
Noradrenaline released from the nerves that innervate the smooth muscle to cause their constriction
SO angiotensin works on the lumen and noradrenalin works on the outside
What happens when the body goes into shock (moderate and severe)?
When in moderate shock, compensation will occur (compensated shock) and the circulation will return back to normal
BUT if the shock is too severe, the body cannot compensate and will move into decompensated shock
This means that no matter what you do, you cannot raise the blood pressure enough to maintain tissue and organ perfusion and the person will most likely die
What are the four classifications of shock?
Give the most common examples of each
Obstructive shock - physical obstruction causing failure of cardiac output e.g. pulmonary embolism
Distributive shock - loss of vasoconstriction leading to a failure of vascular resistance maintenance e.g. sepsis
Hypovolemic shock - where you have bled and lost too much blood so there is not enough circulating blood so that even if you were to increase the heart rate, preload cannot increase e.g. haemorrhage
Cardiogenic shock - failure of the heart to pump efficiently and supply blood to the body e.g. myocardial infarction/heart failure
How does hypovolemic shock present?
SO generally due to haemorrhage - major blood loss
Body tries to compensate for this by shutting down circulation to the skin - greyish pallor to the skin, cold and clammy skin, slow capillary refill
Low blood pressure
Oliguria - there will be a massive release of ADH as don't want to lose any more water through the urine (already lost so much from the bleed)
How does cardiogenic shock present?
Most of these patients have an AMI so present with chest pain, shortness of breath, nausea, vomiting
How does distributive shock present?
How does obstructive shock present?
Generally due to tension pneumothorax
Breath sounds are absent on affected hemiothorax
Trachea deviates away from affected side
How much blood loss is life threatening?
Total body water is 45 litres
Total blood volume is 4.5-5 litres
Acute loss of greater than 40% of blood volume i.e. greater than 2 litres is immediately life threatening
Describe and explain the immediate compensatory response to haemorrhage
Works within seconds to minutes
The loss of blood results in a drop in blood pressure which is detected by baroreceptors
These then compensate by increasing sympathetic output to increase heart rate and contractility
The vasomotor centre in the medulla also signals to the hypothalamus to release ADH to reduce urine flow and sodium excretion
Does a loss of blood always immediately lead to a reduced blood pressure? Explain this
Loss in arterial blood leads to a reduced blood pressure
Loss in venous blood causes a reduced venous return i.e. a reduced preload - this then reduces stroke volume and so reduces cardiac output
THIS leads to a reduced blood pressure
What is the longterm compensatory response to haemorrhage?
This works between hours to days
Increased release of renin from the kidney and release of aldosterone from the adrenal cortex by angiotensin II - causes increased sodium retention
Thirst is stimulated by angiotensin II receptors in the brain to increase water intake
Stimulation of albumin and plasma proteins in the liver
What are the four classes of hypovolemic shock?
Class 1 - loss of <15% of blood volume - will always be full compensation - this is what happens when you donate blood - urine output decreased and thirst increased
Class 2 - loss of 15-30% - some clinical symptoms of tachycardia, tachypnoea, cool clammy skin, delayed capillary refill
Class 3 - greater than 30% loss of blood - leads to drop in blood pressure - moving close to stage of decompensation - requires blood transfusion but at this point, most important thing is maintenance of fluid in general so any fluid transfusion is sufficient
Class 4 - greater than 40% loss in blood - immediately life threatening and requires immediate blood transfusion
What is outlined by Starling's law of the heart?
The greater the preload, the greater the force of contraction and therefore, the greater the stroke volume
The end diastolic volume - the end volume of blood that will be pumped to the body by the left ventricle
How is the SVR maintained throughout the body?
Via constriction of blood vessels
Which hormones are responsible for the maintenance of the systemic constriction of blood vessels and what receptors do these act on?
Noradrenaline via the sympathetic NS - alpha receptors on the outside of the arterioles
Angiotensin 2 - angiotensin receptors (AT1) of the endothelium - within the lumen
What local factors can alter the SVR/size of the lumen of blood vessels?
Endothelin - vasoconstrictor
NO - vasodilator
Prostacyclin - vasodilator
When is endothelin normally released?
When damage has occurred to the blood vessel
What is the function of prostacyclin?
Local vasodilator - reduce calcium entry into smooth muscle
Inhibits platelet activation in primary haemostasis
What is prostacyclin produced from?