Sepsis and shock Flashcards
Score system for patinets risk in sepsis
qSOFA
Define SIRS
2 or more of:
- Temperature < 36°C or > 38°C
- Heart rate > 90 beats/min
- Respiratory rate > 20 or PaCO2 less than 4.5 kPa ormechanically ventilated
- White Cell Count < 4 or > 11 or > 10%immature forms
Define sepsis
SIRS plus documented or suspected infection
Define Septic shock
Sepsis with hypotension (Systolic blood pressure <90mmHg or need for vasopressor infusion) despite adequate fluid resuscitation
Name 3 non infective causes of SIRS
- Burns Trauma Pancreatitis Cardiopulmonary bypass - Massive transfusion.
What are Toll like receptors for
recognition of molecules Eg lipopolysaccahride on microorganisms
What happens when toll like receptors activated
Activate transcription factors eg Nuclear factor kappa beta -> secretion of pro/antiinflammatory mediators
Name 2 inflammatory mediators
Interleukins 1,2 and 6
Tumour necrosis factor alpha
What do inflammatory mediators do
Activate leukocytes
activate coagulation cascade
endothelial damage
synthesize NO -> vasodilation and poor perfusion
How much fluid in septic shock
30ml/kg in first 3 hours
Sepsis in ITU hour 1
Measure lactate level*
Obtain blood cultures before administering antibiotics.
Administer broad-spectrum antibiotics.
Begin rapid administration of 30mL/kg crystalloid for hypotension or lactate level ≥ 4 mmol/L.
Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP ≥ 65 mm Hg.
- Remeasure lactate if initial lactate is elevated (> 2 mmol/L)
Additional sepsis considerations
Hydrocortisone 200mg IV once daily if adequate fluid resus / vasopressors and still haemodynamic instability
Keep glucose <10mmol
Define shock
circulatory insufficiency with inadequate oxygen delivery resulting in hypoperfusion and tissue hypoxia
Essentialy DO2
Vasopressor 1st line in shock
For shock of unknown cause ?
For septic shock?
For cardiogenic shock?
For shock of unknown cause use adrenaline.
For septic shock use noradrenaline.
For cardiogenic shock use dobutamine.
Where does the sympathetic autonomic system originate?
Sympathetic autonomic nervous system originates from T1-L2
After originating in T1-L2 where does the sympathetic autonomic system go
- connect through synapses to postganglionic neurons.
- These synapses are located in the two sympathetic chains that lie on either side of the vertebral column
Main parasympathetic nerve? Where are key parasympathetic ganglia?
Which key receptor in parasympathetic system
Vagus
- Parasympathetic ganglia are embedded in the heart, mainly on the SA and AV nodes
- ß2receptors are present on other organs, stimulation causes relaxation e.g. of bronchial and uterine smooth muscle.
Effect of sympathetic systm on heart
- increase chronotropy and ionotrphy
- B1 / B2 receptors
What type of parasympathetic receptors in heart?
What effect when stimulated?
How can you block the parasympathetic effect ?
- acetylcholine receptors located on the SA and AV nodes
- negative chronotropic effect and reduces the speed of conduction through the AV node.
- Constant vagal tone limiting heart rate
- Block this tone by administering atropine
Sympathetic receptor in smooth muscle ? When might it be reduced? effect ?
What happens when stimulated?
- α1 in smooth muscles
- If reduced - e.g. high spinal transection or spinal anaesthesia -> decreased tone
- Increase -> increase in vascular tone and resistance -> increased blood pressure (but a reduction in blood flow)
Blood pressure (BP) =
Blood pressure (BP) = Cardiac output (CO) X systemic vascular resistance (SVR)
CO =
CO = Stroke volume (SV) x Heart rate (HR).
What is hypoperfusion (Low BP) caused by
- low cardiac output (cardiogenic shock, outflow obstruction, hypovolaemic shock)
- low SVR (neurogenic or septic shock) or both (septic shock).
What is the most common cause of low stroke volume in critically unwell pt
low pre-load from either hypovolaemia or relative hypovolaemia is probably the most common cause of a low SV and subsequent low CO and reduced perfusion
Hypovolaemic shock common causes?
What happens?
How does the pt appear?
- fluid loss; haemorrhage, salt and water loss, sepsis, burns,
- decrease the stroke volume and cardiac output - >tachycardia and increased SVR
- Cold and shut down
How does distributive shock present
Peripheral vasodilation Eg Sepsis, anaphylactic and neurogenic shock.
Key features of neurogenic shock
hypotension, bradycardia, warm peripheries, venous pooling and sometimes priapism
Egs of obstructive shock
PE, Aortic stenosis, pericardial effusion and tension pneumothorax.
Why does respiratory rate go up in shock
Tissue hypoxia -> metabolic acidosis -> increase RR as compensatory method
What are the 4 stages of shock ?
1 Initial
2- Compensatory
3 Progressive
- Once compensatory mechanisms fail / can’t keep up
- ->worsening metabolic acidosis + fluid loss into extravascular interstitial places
4 Refactory
- Organs fail -> death
In the initial stage of shock why do you get a metabolic acidoiss
- Hypoperfusion -> hypoxia ->anaerobic metabolism -> lactic acid and metabolic acidosis
In the compensatory stage of shock what happens?
- Hyperventilation - Resp alkalosis to neurtralise acidosis
- Catecholamine response - if hypotensive nor/adrenaline released -> increase SVR and CO
- Renin-angiotensin response -
(Agiotensin II, aldoserone) release -> thirst and vasoconstriction
Vasopressin (ADH) ->fluid retention
Oxygen Delivery =
Oxygen Delivery = CO x Oxygen content (Hb x SpO2x c)
Causes of low oxygen delivery ? Basic management of 3 types
- Low CO - > fluid challenge first line
- Anaemia -> blood
- Hypoxia -> 02
Why do you have to be cautioys with noradrenaline when the patient has low perfusion pressures
- Vasopressor but not not ionotrope.
- > Increases SVR -> creates ‘normal’ BP but increases afterload and reduces CO which reduces DO2
How can you reduce oxygen consumption of septic patient
- May require intubation and ventilation -> reduces WOB and therefore oxygen demand
- Sedation of agitated
Effect of sympatetic stimulation on B2 reptors
Stimulation of ß2 receptors present in some vascular beds eg lungs
vasodilatation
Parasympathetic effects on circulation
none significant
4 main categories of shock
distributative
hypovolaemic
cardiogenic
obstructive
4 causes of cardiogenic shock pathophysiology
filling defect - diastolic HF
contractility defect
arrhythmias - decreased preload / contractility / HR
Structual - valve disease -> backflow / restricted flow
2 causes of contractility defects causing cardiogenic shock
MI
Cardiomyopathy
What causes filling defect in heart
increased growth of muslce -> smaller space
increased stiffness -> less compliant -> less filling
All ends in decreased preload
Name a cardiac support device for cardiogenic shock
Intra aortic baloon pump
ECMO
Impala
Becks triad seen in? what is it?
cardiac tamponade - obstructive shock
Hypotension
muffled heart sounds
raised JVP
