Haemorrhage and shock Flashcards
Define shock.
Acute circulatory failure with inadequate/inappropriate distributed tissue perfusion leading to cellular hypoxia
What are the signs of hypoperfusion? How does hypoperfusion occur?
Signs:
- pallor
- confusion
- tachypnoea
- tachycardia
Occurs when cardiac output and BP are not maintained
How is BP calculated?
BP = CO x SVR
How can cardiac output decline?
- reduced HR
- feedback from baroreceptors
- will activate or inhibit medullary vasomotor centre
- this will activate or inhibit the ANS - reduced stroke volume
- determined by preload/EDV and inotropy
- Starling’s Law: when inotropy increases, EDV increases
- inotropy can decrease due to: cardiac disease, hypoxia, hypercapnia, pH, electrolyte disturbance, BBs, CCBs
What are the vasoconstricting factors that determine SVR?
- Noradrenaline:
- act on alpha receptors outside arterioles - Angiotensin II
- acts on AT1 receptors (on the endothelium of arterioles)
- cause contract of SMCs - Endothelin/Serotonin
What are the vasodilating factors that determine SVR?
- Prostacyclin (PGI2)
- produced by endothelial cells from arachidonic acid
- reduced Ca2+ entry into SMCs
- reduces contractility of muscle - NO
- produced by endothelial cells from arginine
- stimulates cAMP formation in SMCs
- reduces Ca2+ and relaxes msucles - Adenosine
- released from endothelial cells and SMCs
What happens in shock (i.e. early and late stage)?
- SVR is not maintained (no arteriolar constriction)
- OR preload is reduced –> reduces stroke volume and thus reduced cardiac output
Initial stage: Compensation
- Increased HR –> increased CO –> increased BP
Later stage: Decompensation
- arterioles cannot maintain constriction or preload reduction is too great
- end organs are not perfused with oxygenated blood and fail
- -> can be FATAL
What are the different types of shock?
- Obstructive
- Distributive (loss of vasoconstriction/poor perfusion)
- Cardiogenic
- Hypovolaemic
What can cause obstructive shock? What are the signs?
Causes:
- PE
- Pneumothorax
- Cardiac tamponade
Signs:
- Tachycardia
- SOB (PE)
- Trachea deviates AWAY from affected side (PT)
- Absent breath sounds (PT)
- Chest pain, if pleuritic = PE
What can cause distributive shock? What are the signs?
Causes:
- sepsis
- anaphylaxis
- neurogenic
Signs:
- low BP
- tachycardia
- fever + chills
- nausea and vomiting
- difficulty breathing
- anxiety/confusion
- inflammation
What can cause cardiogenic shock? What are the signs?
Causes:
- MI
- heart failure
- arrhythmias
- ventricular septal rupture
- ischaemic cardiomyopathy
- valvular disease
Signs:
- chest pain
- SOB
- nausea + vomiting
- diaphoresis (excessive sweating)
- pulmonary oedema
- acute circulatory collapse
What can cause hypovolaemic shock? What are the signs?
Causes:
- Haemorrhage
- burns
- surgery/trauma
- loss of fluid + electrolytes from the gut
Signs:
- cold
- low BP
- clammy skin
- slow capillary reflex
- greyish pallor
- increased HR
- oliguria
- absent bowel sounds
- confusion/anxiety
What are the different physiological responses to hypovolaemic shock?
CV system:
- activates SNS
- increased HR, inotropy, peripheral vasoconstriction
Haematologic system:
- Platelets activated (via TXA2) = immature clot forms
- -> coagulation cascade + vasoconstriction activated via TXA2
Renal system:
- increase in aldosterone = increased Na+ and water reabsorption = oliguria
- increase in renin, therefore, increase in angiotensin II = peripheral vasoconstriction and stimulates aldosterone secretion
Neuroendocrine system:
- increased reabsorption of water and NaCl
- release of ADH (post. pituitary) = increase BP and reduced Na+ in plasma
What is the compensatory response to hypovolaemic shock?
- Immediate:
a. arterial:
- reduced BP (detected by baroreceptors)
- reduced preload and ANP
- release of ADH
- reduce urine flow and Na+ excretion
b. venous:
- reduced BP causes reduced preload, SV and CO
- increase sympathetic drive
- increase HR and inotropy
- constriction of large veins = more blood out of reservoir –> restore preload - Long-term (hours - days)
- increased renin release = increased angiotensin II = increased aldosterone
- thirst stimulated = increased water intake
- water and Na+ retention increased = restored blood volume
- stimulation of albumin and other plasma protein synthesis in liver
- fibroblasts in peritubular cells are sensitive to hypoxia = increased EPO = increased RBC production
How much blood loss is considered life-threatening?
Acute loss of >40%/2 litres
–> Sympathetic NS will attempt to maintain O2 supply to the heart and brain
