Sepsis and Shock Flashcards
What is sepsis?
An overwhelming global response to infection
What haemodynamic changes are there in sepsis and what sort of clinical signs do these lead to?
- In sepsis there is peripheral vasodilation and maldistribution of flow
- This leads to HYPOTENSION
- this activates baroreceptors which increase HR in response TACHYCARDIA
What other key clinical signs are there in sepsis beyond haemodynamics?
- Elevated respiratory rate
- TEMPERATURE (usually of >38 but can also be <36)
- WCC >12 or <4
- Altered mental state (drowsy, confused etc.)
- Not passed urine in a while (12-18h)
- They might have CLINICAL SIGNS OF SHOCK (mottled, low CRT)
What is septic shock?
What type of shock is septic shock and how does this occur?
- Septic shock is defined as sepsis with refractory hypotension <90
- lack of blood flow to peripheral organs and other structures DISTRIBUTIVE SHOCK
How should we initially manage sepsis when it is first identified?
Initiate the SEPSIS6 or BUFALO (within 3 HOURS)
- Blood cultures (FBC, UE, glucose, VBG,)
- Urine output (catheter if necessary)
- Fluids- fluid challenges (500mL 0.9% NaCl over 10-15mins).
- Antibiotics - attempt to identify a source of infection and treat with the right abx according to trust guidelines. If no source identified then go broad spectrum
- Lactate - good measurement of the level of tissue hypo perfusion - get this with a blood gas. CONCERNING IF >3
- Oxygen - Resp rate will usually be high and they might be hypoxic. Correct this with O2 therapy
What would make you consider elevating to a senior after your initial management? How might they then be managed?
Concerning features include:
- Only TRANSIENTLY RESPONDING TO FLUID CHALLENGES (their BP is peaking after each challenge but then dropping again)
- PERSISTENTLY HIGH LACTATE - this suggests ongoing tissue hypoxia
***will need ICU input - consider central venous catheterisation and arterial line insertion - they might need to be managed with IV ADRENALINE to maintain their mean arterial pressure
What are the criteria for SIRS?
Must have 2 of the following:
- Temp >38 or <36
- HR >96
- WCC <4 or >12
- Resp rate >20
- Blood glucose >7.7 (in non-diabetic). An early response to infection is to release sugars into the blood
SIRS is the same as sepsis however SIRS can be caused by things other than infection (Trauma, burns)
What is the difference between SIRS and SEPSIS?
Technically SEPSIS is just SIRS secondary to an identified source of infection.
both caused by the large and overwhelming release of cytokines and inflammatory mediators
What is shock?
-The life-threatening hypo perfusion and resulting hypoxia of organs
What mnemonic can be used to identify the clinical signs of shock?
HEP B
Hands - Cool, clammy, reduced CRT, sweating
End-organ perfusion - Low consciousness, poor urine output
Pulses - weak, thready
Blood Pressure - low due to vasodilation
What are the different types of shock?
Distributive (inc septic, anaphylactic, neurogenic)
Cardiogenic
Hypovolaemic
Obstructive
What is meant by preload and afterload?
These are important terms in shock.
- Preload is the amount of the blood in the heart at the end of diastole (how much blood the hearts primed with before contraction)
- Afterload is the pressure the heart must work in systole (the systemic vascular resistance)
In the early stages of shock how does the body attempt to compensate and what effect does this have?
- Poor tissue perfusion causes VASOCONSTRICTION to try and preserve blood flow (increase after load)
- As the shock process becomes overwhelming the constriction will not be enough and the blood pressure will fall once more
What is pathophysiology of hypovolemic shock?
What are some causes of hypovolaemic shock?
What is the treatment?
- Major loss decreases preload, afterload is increased to compensate but ultimately oxygen delivery is decreased
- LOSSES - major haemorrhage, D+V, burns or pancreatitis, bowel obstruction
- TREAT CAUSE AND REPLACE FLUIDS
What is cardiogenic shock?
What are some causes?
Treatment?
- The heart stops pumping effectively and doesn’t empty its contents and so preload increases, afterload increases as response
- Reduced cardiac output (CO) leads to decreased oxygen delivery
PostMI/myocarditis/overdose/arrythmias/fluid overload (CCB, BB, digoxin)
Treatment: optimise pump performance
(if ACS: treat -not GTN if shocked. If overload: furosemide)
What are some examples of obstructive shock and what is the process?
- Obstruction to cardiac filling or emptying (preload might be increased or decreased) - RAISED JVP
- Afterload is increased due to body’s vasoconstriction
- Decreased CO leads to decreased oxygen delivery (similar to cardiogenic)
What are some examples of distributive shock? What is unique about this type?
-Anaphylactic, septic and neurogenic are all types of distributive shock
- The difference is that in distributive the preload and AFTERLOAD are DECREASED (CO increases)
- overwhelming vasodilation is the cause of poor perfusion rather than poor cardiac circulation
Causes of obstructive shock? (within vs outside circulation)
Treatment?
Obstruction within circulation (blockage)
- Massive PE
- Air/amniotic fluid embolism
- LVOT obstruction (HOCM)
Obstruction outside circulation (pressure)
- tension pneumothorax
- cardiac tamponade
- fatal asthma
Treatment: remove obstruction
What are the classes of haemorrhagic shock?
(this is a type of hypovolaemic shock)
I - up to 750mL blood loss- 15% blood loss
II - 750-1500mL - 15-30% blood loss. (no BP loss yet)
III -1500-2000mL -30-40% - only now does BP drop- when 30% drops!!!
IV - >2000mL - >40%
Resp rate and Heart rate increase with each stage
Describe the Pathophysiology of neurogenic shock
What are common causes?
- There is a loss of sympathetic tone (AUTONOMIC BLOCKADE) meaning there is global vasodilation with no compensation!!
- Also causes BRADYCARDIA (reduces CO)
- Hence why it is a form of distributive shock
- Most commonly due to anaesthetic incident or spinal cord trauma (above T1-T4)
What is the treatment for spinal shock?
-IV fluids to address relative hypovolaemia (refractory shock in trauma?>think spinal!)
- Inotropes and vasopressors to ↑sympathetic tone
e. g. Noradrenaline
What is an Addisonian crisis?
- Someone with Addison’s has destruction of adrenal cortex and so they have reduced amounts of mineralocorticoids and glucocorticoids.
- As a result they cannot activate the renin-angiotensin aldosterone response pathway meaning there is no water and sodium retention and there can be very low BP - SHOCK (hypovoleamic)
How should we treat shock?
ABCDE ASSESSMENT (Always remember signs like BP, HR, CRT, urine output, RR, O2 sats
IV ACCESS - two wide bore cannula (14G orange or 16G grey) into each of the ACFs
Get some bloods (FBC, U+E, Glucose, VBG, Crossmatch, CRP)
FLUID CHALLENGE (500mL NaCl 0.9% over 10-15mins or as short a time as possible). Giving too much fluid to a patient with cardiogenic shock can make situation worse BLOOD PRODUCTS IF HAEMORRHAGIC
DRUGS - consider ADRENALINE 1mg of 1 in 10,000 (100 micrograms/ml solution)
What is a complication of systemic inflammation?
What is it?
Disseminated intravascular coagulation
- The inflammatory markers can activate the clotting cascade
- Leading to widespread platelet aggregation and microvascular thrombosis formation
- DIC uses up many platelets> concurrent bruising and bleeding elsewhere - can be life-threatening
