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ACC > Sepsis and Shock > Flashcards

Sepsis and Shock Flashcards

1
Q

What is sepsis?

A

An overwhelming global response to infection

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2
Q

What haemodynamic changes are there in sepsis and what sort of clinical signs do these lead to?

A
  • In sepsis there is peripheral vasodilation and maldistribution of flow
  • This leads to HYPOTENSION
  • this activates baroreceptors which increase HR in response TACHYCARDIA
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3
Q

What other key clinical signs are there in sepsis beyond haemodynamics?

A
  • 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)
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4
Q

What is septic shock?

What type of shock is septic shock and how does this occur?

A
  • Septic shock is defined as sepsis with refractory hypotension <90
  • lack of blood flow to peripheral organs and other structures DISTRIBUTIVE SHOCK
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5
Q

How should we initially manage sepsis when it is first identified?

A

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
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6
Q

What would make you consider elevating to a senior after your initial management? How might they then be managed?

A

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

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7
Q

What are the criteria for SIRS?

A

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)

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8
Q

What is the difference between SIRS and SEPSIS?

A

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

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9
Q

What is shock?

A

-The life-threatening hypo perfusion and resulting hypoxia of organs

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10
Q

What mnemonic can be used to identify the clinical signs of shock?

A

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

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11
Q

What are the different types of shock?

A

Distributive (inc septic, anaphylactic, neurogenic)
Cardiogenic
Hypovolaemic
Obstructive

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12
Q

What is meant by preload and afterload?

A

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)
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13
Q

In the early stages of shock how does the body attempt to compensate and what effect does this have?

A
  • 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
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14
Q

What is pathophysiology of hypovolemic shock?

What are some causes of hypovolaemic shock?

What is the treatment?

A
  • 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
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15
Q

What is cardiogenic shock?

What are some causes?

Treatment?

A
  • 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)

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16
Q

What are some examples of obstructive shock and what is the process?

A
  • 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)
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17
Q

What are some examples of distributive shock? What is unique about this type?

A

-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
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18
Q

Causes of obstructive shock? (within vs outside circulation)

Treatment?

A

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

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19
Q

What are the classes of haemorrhagic shock?

A

(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

20
Q

Describe the Pathophysiology of neurogenic shock

What are common causes?

A
  • 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)
21
Q

What is the treatment for spinal shock?

A

-IV fluids to address relative hypovolaemia (refractory shock in trauma?>think spinal!)

  • Inotropes and vasopressors to ↑sympathetic tone
    e. g. Noradrenaline
22
Q

What is an Addisonian crisis?

A
  • 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)
23
Q

How should we treat shock?

A

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)

24
Q

What is a complication of systemic inflammation?

What is it?

A

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
25
Q

What blood markers would you see in DIC?

What about the clotting times?

A

↓ Platelets (cant clot-bleed)
↓ Fibrinogen (cant clot-bleed)
↑ D dimer (fibrin being degraded)

**prologues PT and APPT

26
Q

What is the anaphylaxis algorithm

A

ORDER OF ANAPHYLAXIS
1. ABCDEG approach and call for help, lie patient down
2. IM ADRENALINE (vasoconstrictor) 1 in 1000 REPEAT THIS EVERY 5 MINS
• Adult or child 12+ GIVE 500 micrograms (0.5ml)
• Child 6-12 GIVE 300 microgramas (0.3ml)
• Child <6 years GIVE 150micrograms (0.15ml)
3. IV fluid challenge crystaloid
a. Adult 500ml-1000ml
b. Child 20ml/kg
4. IV CHLORPHENAMINE 10mg - anti-histamine that will help regulate the inflammatory response and reverse vasodilation
5. IV HYDROCORTISONE (slower acting)

-ONCE RECOVERED MONITOR FOR MINIMUM 6 HOURS
for biphasic reaction
-SEND HOME WITH EPIPEN

27
Q

What primary investigation should you try and get for anaphylaxis?

A

Try and get Mast cell tryptase

  • immediate
  • 1-2 hours
  • 24 hours
28
Q

Long term management of anaphylaxis

A

Long term management anaphylaxis
-ONCE RECOVERED MONITOR FOR MINIMUM 6 HOURS
for biphasic reaction
-SEND HOME WITH EPIPEN
-Outpatients for testing (skin patch-contact/prick-food/ RAST-for specific IGE antigens (penicillin)

29
Q

What are the 2 indications for defibrilator?

A

Defilbrilator

  • Ventriculr tachycardia
  • Ventricular fibrillation
30
Q

What is shock?

A
  • acute circulatory faire
  • inadequate tissue perfusion
  • generalised cellular hypoxia
31
Q

What is the equation for systolic BP?

A

Systolic BP=CO X systemic vascular resistance

32
Q

What is the equation for cardiac output?

A

Cardiac output=HR X SV

33
Q

Pathophysiology of anaphylactic shock?

What is the treatment for adults?

A
  • Type of distributive shock
  • Overwhelming type 1 hypersensitivity
  • IgE mediated mast cell degranulation leading to release of histamine which vasodilates
  • Occurs within 30 mins of exposure and responses can be global
  • Cutaneous
  • GI
  • Respiratory
  • Cardiovascular

-IM 0.5mg of 1 in 1000 adrenaline IM (0.5 ml)

34
Q

What type of shock would you get with priapism?

A

Priapism think neurogenic shock

35
Q

How do you treat haemorrhagic shock?

A 
BATH TUB ANALOGY 
Plug leak 
-direct pressure
-tranexamic acid Ig IV (then 8 hour infusion)
-splinting

Fill the tank
-1:1:1 RBC:FFP:Platelets

36
Q

What sign would make you suspect a tamponade?

A

-Distended neck veins

37
Q

What history would make you suspect tamponade?

A
  • Chest trauma
  • Post MI (ventricular wall rupture>blood)
  • Massive pericardial effusion
38
Q

What is the treatment for tamponade?

A

Treatment:
-paricardiothentisis for effusion

-if blood this wont work.

If shocked: Emergency cardiothoracis surgery

If traumatic: clamshell thoracotomy

39
Q

If someone has had anaphylaxis, what blood test should we do?

A

Serum tryptase

40
Q

What is the QSOFA score for sepsis?

A
  • Altered mental state (GCS<15)
  • Tachypnoea 22+
  • Hypotension (systolic BP<100)

2-3 points is high risk

41
Q

Next steps after refractive shock?

A

Sepsis: Vasopressor
(noradrenaline, phenylephrine/epinephrine)

Cardiac failure: ionotropes
(dobutamine)

**adrenaline does both

42
Q

Treatment of adrenal crisis shock?

A

100mg HYDROCORTISONE IV/IM
(then 200mg/24 hr in Glucose 5% IV)

500ml Na Cl 0.9% bolus
(then general rehydration 3-4L over 24 hours)

43
Q

What is toxic shock syndrome?

What type of shock is it?

A
  • A form of shock caused by EXOTOXINS (usually those produced by strep pyogenes or staph aureus)-SUPERANTIGENS
  • These antigens can activate up to 20% of T cells at any one time and cause a very fast immune response. -Profound vasodilation leads to form of distributive shock
44
Q

What are complications of shock?

A

-DIC (particularly in septic shock)
-Multiple organ dysfunction
•Lungs: ARDS
•Kidneys: AKI (acute tubular necrosis)
•Heart: Cardiac failure
•Brain: Hypoxic encephalopathy
•Liver: necrosis, ↑ liver enzymes, ↓ clotting factors

45
Q

How is hypoxia classified?

A

Hypoxic hypoxia - ↓ O2 supply
Anaemic hypoxia - ↓ haemoglobin function (heamorragic shock)
Stagnant hypoxia – inadequate circulation (PE)
Histotoxic hypoxia – impaired cellular O2 metabolism (cyanide)

ACC (23 decks)

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