Shock and Hypotension *** Flashcards
Define circulatory shock
- Generalised loss of blood flow to organs - causing necrosis and death
Link the following equations to shock:
- π=Ξπ/π
- π΅π=πΆπ π₯ πππ
- πΆπ=π»π
π₯ ππ
Describe hypovolaemic shock.
- Arises from loss of blood or blood fluid
- BP affected by reduction in SV (due to loss of fluid)
How does blood pressure become reduced by hypovolaemic shock?
- Reduction in blood volume
- Decreased venous return
- Decreased preload
- Decreased SV and CO
- Decreased BP
Give examples of factors that can cause hypovolaemic shock.
- Trauma
- Postpartum haemorrhage
- Burns
- Vomiting
- Diarrhoea
(ANYTHING CAUSING A LOSS OF FLUID FROM CVS)
What are the long- and short-term responses to hypovolaemic shock?
- SHORT-TERM: Vasoconstrictor activity by sympathetic NS and catecholamines - increase TPR
- LONG-TERM: RAAS
- Heart rate increases - causes rise in CO to compensate for decrease in SV
Why donβt the compensatory effects of hypovolaemic shock, last for significant periods of time?
- Increased vascular resistance
- Reduced blood flow to organs
- Can progress to tissue ischaemia
Describe cases that can lead to cardiogenic shock.
- CHF - leading to cardiac hypertrophy - reduced pumping ability and space for ventricular filling. Reduced SV
- MI - damage to myocardium. Reduction in pumping ability and ability to contract quickly
- Myocarditis
- Congenital heart defects
Describe cardiogenic shock.
- Reduced perfusion due to problems with heart
- Caused by any condition affecting pumping of heart
Describe the steps by which myocardial failure can lead to cardiogenic shock. PART 1
- Increased ESV
- Increased preload and LV diastolic filling pressure
- Raised pressure in LA
- Congestion of blood in pulmonary circulation
Describe the steps by which myocardial failure can lead to cardiogenic shock. PART 2
- Raised hydrostatic pressure of blood in lungs
- Fluid pushed out of pulmonary circulation into lungs - causes pulmonary oedema
- Reduced ability for lungs to absorb O2 and deliver it to circulation
- Exacerbates myocardial failure
Why might S3 be heard during myocardial failure?
- Raised ESV
- LV overfilling
SLIDE 8 ***
Describe septic shock. PART 1
- Entry of bacteria or fungi into bloodstream and release toxins. Gram-negative release endotoxins. Opposite for gram-positive
- Toxins travel in bloodstream - direct cell damage.
- Activate mast cells to release pro-inflammatory mediators
Describe septic shock. PART 2
- Mediators cause widespread vasodilation - reduced TPR
- Increased permeability of blood vessels and leakage into tissues
- Reduced CO
Describe anaphylactic shock.
- Response to allergic reaction
- Inhalation of allergen activates basophils and mast cells - release histamines
- Cause vasodilation and raised permeability of capillaries
- Reduced TPR and CO
What would patients with septic and anaphylactic shock present with?
- Raised temperature - due to increase in systemic vasodilation
- Pyretic response by toxins in septic shock
Describe neurogenic shock.
- Occurs in patients with SCI, concussion or under anaesthesia
- Occurs in absence of any loss of blood volume
- Increased vascular capacity - loss of sympathetic tone
- Loss of vascular resistance
- Reduced BP and venous return
What are the 3 stages of circulatory shock?
- NON-PROGRESSIVE - where normal physiological mechanisms can overcome loss of flow/pressure
- PROGRESSIVE - shock becomes worse without treatment
- IRREVERSIBLE - tissue/organ damage so severe no current treatments can save patient from dying
When is a patient considered truly in clinical circulatory shock and how will they present?
- On reaching progressive stage
- KEY FEATURE - Hypotension
- Donβt respond to IV fluid administration
What are baroreceptors and what is their role in shock?
- Baroreceptors in aortic arch, carotid sinus and RA detect decreases in BP and blood volume
- Reduced venous return leads to reduced CO in all cases of shock
- Decreased BP - detected by baroreceptors
What are the responses caused by baroreceptors?
- Signal to vasomotor regions of medulla
- Peripheral vasoconstriction by catecholamines, sympathetic NS activation and raised RAAS activity by raised renal sympathetic nerve activity
- BP and blood volume raised back to normal
What is a downside of the baroreceptor-induced compensatory mechanisms in cardiogenic shock?
- Increased blood volume
- Increased preload
- Raised burden on heart
