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Assessing and Managing the Deteriorating Patient > Week 4: Shock > Flashcards

Week 4: Shock Flashcards

1
Q

What is shock?

A

Shock is a syndrome characterised by decreased tissue perfusion and impaired cellular metabolism
Cell demand for oxygen exceeds supply

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2
Q

What conditions are required for tissue oxygenation and perfusion?

A

Ability of lungs to oxygenate blood
Ability of heart to pump blood to tissues
Adequate haemoglobin and blood volume
Effective vasculature

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3
Q

What is stroke volume?

A

Amount of blood pumped into the aorta with each contraction of the left ventricle

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4
Q

What is cardiac output?

A

Amount of blood pumped per minute into the aorta by the left ventricle
CO = SV X HR

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5
Q

What is mean arterial pressure?

A

Is a product of CO and systemic vascular resistance

DP + (SP –DP)/3

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6
Q

What are the consequences of shock?

A 
Tissue hypoperfusion
Activation of the sympathetic nervous system
Activation of neurohormonal responses
Systemic Inflammatory response
Multi organ dysfunction
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7
Q

What are the classifications of shock?

A 
Hypovolaemic
Cardiogenic
Circulatory or distributive
Anaphylactic
Neurogenic
Septic
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8
Q

What are the classifications for hypovolaemic shock?

A

Absolute fluid loss
Haemorrhage
Gastrointestinal losses -vomiting and/or diarrhoea
Water loss e.g. diabetes insipidus
Relative fluid loss
Fluid volume moves out of the intravascular space into the extravascular spaces (e.g. burns fluid leaks into the interstitial space)

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9
Q

Include pathophysiology and S + S hypovolaemic shock

A

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10
Q

What is cardiogenic shock?

A

Results from either diastolic or systolic dysfunction and there is reduced cardiac output

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11
Q

What is systolic dysfunction?

A

Inability of the heart to pump blood forward

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12
Q

What is the main cause of systolic dysfunction?

A

Myocardial infarction

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13
Q

Include pathophysiology and S + S cardiogenic shock

A

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14
Q

What are the types of distributive shock?

A

Anaphylactic
Neurogenic
Septic

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15
Q

What is the pathophysiology of distributive shock?

A

Massive peripheral vasodilation –> reduced preload –> reduced SV –> reduced CO

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16
Q

What is neurogenic shock?

A

Can occur within 30 minutes of spinal cord injury above T5

Loss of sympathetic tone causes unopposed parasympathetic tone (results in vasodilation)

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17
Q

Include S + S of neurogenic shock

A

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18
Q

What is the difference between spinal shock and neurogenic shock?

A

Spinal:
decreased reflexes
loss of sensation
flaccid paralysis

Neurogenic:
loss of vasomotor tone
vasodilation
hypotension
bradycardia
19
Q

What is anaphylactic shock?

A

Chemical cascade from immune system causes vasodilation and increased capillary permeability

20
Q

What is the pathophysiology of anaphylactic shock?

A

Vasodilation –> blood flow to peripheries –> decreased preload –> decreased SV –> decreased CO
Increased capillary permeability –> fluid leaking into interstitial space (third spacing)

21
Q

Include S + S anaphylactic shock

A

blank

22
Q

What is septic shock?

A

Chemical cascade from infection causes vasodilation and increased capillary permeability

23
Q

What is the pathophysiology of septic shock?

A

Vasodilation –> blood flow to peripheries –> decreased preload –> decreased SV –> decreased CO
Increased capillary permeability –> fluid leaking into interstitial space (third spacing)
Myocardial depression
Decreased circulation to micro-circulation –> tissue hypoxia

24
Q

Include S + S septic shock

A

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25
Q

What are the stages of shock?

A

Compensatory: neurohormonal responses compensate for decreased CO
Progressive: compensatory mechanisms begin to fail
Activation: inflammatory and immune responses occur

26
Q

What are the compensatory mechanisms against shock?

A

Increased RR and depth of breathing

SNS:
Increased CO
Increased HR (B1)
Increased myocardial contractility (B1)
Increased systemic vascular resistance - afterload 
Venoconstriction --> increased preload

Hormonal activation:
Aldosterone and ADH to increase preload
Angiotensin 2 for vasoconstriction

27
Q

What is the progressive stage of shock?

A

Compensatory mechanisms begin to fail
Activation of inflammatory and immune responses occur
Biochemical mediators case myocardial depressions
Microcirculation fails leading to increase capillarity permeability and further compromising tissue oxygenation
Development of interstitial oedema
Activation of the coagulation system

28
Q

How does SaVO2 relate to tissue perfusion?

A

The ability to provide oxygen to the cells is called oxygen delivery ( DaO2)
Cell use about 25% of the available oxygen (VO2)
When cells need more oxygen they can extract more oxygen
When demand is greater than supply cells switch to anaerobic metabolism leading to lactic acidosis causing a metabolic acidosis

29
Q

What is the irreversible stage of shock?

A

Cellular and tissue injury severe

Patient exhibits signs of multi organ dysfunction syndrome

30
Q

What is the management for hypovolaemic shock?

A 
Restoring intravascular volume
Fluids
blood
Restoring oxygen carriage
Resolving the cause
31
Q

What is the management for cardiogenic shock?

A

↑myocardial oxygen delivery (↑FiO2)
Maximising cardiac output
Decreasing ventricular workload
Fluids to provide adequate filling without ventricular overdistention
Diuretics to reduce preload
Nitrates for veno and vasodilation
Narcotics and sedatives to ↓myocardial oxygen consumption

32
Q

What are the pharmacological interventions for shock?

A 
Sympathomimetics:
Vasopressors cause peripheral vasoconstriction
Noradrenaline
Adrenaline
Vasopressin (not for cardiogenic shock)
Vasodilators for cardiogenic shock to decrease afterload
sodium nitroprusside
Venodilatorsto reduce preload
Glyceryltrinitrate
Sodium nitroprusside

Drugs to increase myocardial contractility ( inotropes)
adrenaline
dopamine
dobutamine

33
Q

What are the types of Central Venous Access Devices?

A

Hickmans: surgically implanted in chest, tunnelled
Peripheral inserted central catheters: peripherally inserted into anticubital fossa. Power PICC can withdraw blood and infuse CT contrast
Port a Cath: implantable CVAD, accessed by a Huber needle. Power port can infuse CT contrast
Central venous catheters: centrally inserted into subclavian, intrajugular or femoral vein

34
Q

What is the purpose of a Central Venous Access Device?

A 
Deliver multiple infusions
Deliver multiple medications
Measure CVP
Deliver TPN
Deliver medication that causes phlebitis, e.g. hyperosmolar substances or vancomycin
35
Q

What is phlebitis?

A

Inflammation of the walls of a vein

36
Q

Which lumen on a Central Venous Access Device is used for CVP measurement?

A

Distal lumen, it is largest

37
Q

Which line on a Central Venous Access Device is used for large volumes of fluid?

A

Distal line

38
Q

How can you prevent CVAD associated infection?

A 
Hand hygiene
Aseptic technique
Skin antisepsis
Catheter site dressing and change
Securing catheter
Face mask
39
Q

What equipment is used to remove a CVAD?

A 
Suture cutter
Dressing pack
Sterile gauze
Sterile glove
Chlorhexidine 2% (preferred)
Occlusive dressing
Goggles/face shield
40
Q

What is the procedure for removing a CVAD?

A

Explain procedure to patient
Lie patient flat
Remove non-sterile dressing
Wash hands
Set-up sterile field
Wash hands – sterile gloves
Clean site as per dressing technique
Remove sutures or device holding CVC in place
Instruct patient in valsalva maneuver
Deep breath, bear down on glottis
Prevents air embolism
Remove CVC
Hold CVC near insertion site with one hand
In other hand place sterile gauze over insertion site
Whilst patient is performing valsalva maneuver pull CVC firmly and gently out
Apply pressure to insertion site with other hand as you remove CVC
Maintain pressure until bleeding from insertion site has stopped
Check catheter tip to ensure it is intact
If CVC tip is to be cultured follow protocol
Clean insertion site with chlorhexidine
Allow to dry
Cover insertion site with occlusive dressing
Assess ever 24hours, once epithelialisation has occurred, occlusive dressing may be removed

Assessing and Managing the Deteriorating Patient (9 decks)

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