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

blank

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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

blank

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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

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

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

25
What are the stages of shock?
Compensatory: neurohormonal responses compensate for decreased CO Progressive: compensatory mechanisms begin to fail Activation: inflammatory and immune responses occur
26
What are the compensatory mechanisms against shock?
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
What is the progressive stage of shock?
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
How does SaVO2 relate to tissue perfusion?
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
What is the irreversible stage of shock?
Cellular and tissue injury severe | Patient exhibits signs of multi organ dysfunction syndrome
30
What is the management for hypovolaemic shock?
``` Restoring intravascular volume Fluids blood Restoring oxygen carriage Resolving the cause ```
31
What is the management for cardiogenic shock?
↑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
What are the pharmacological interventions for shock?
``` 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
What are the types of Central Venous Access Devices?
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
What is the purpose of a Central Venous Access Device?
``` Deliver multiple infusions Deliver multiple medications Measure CVP Deliver TPN Deliver medication that causes phlebitis, e.g. hyperosmolar substances or vancomycin ```
35
What is phlebitis?
Inflammation of the walls of a vein
36
Which lumen on a Central Venous Access Device is used for CVP measurement?
Distal lumen, it is largest
37
Which line on a Central Venous Access Device is used for large volumes of fluid?
Distal line
38
How can you prevent CVAD associated infection?
``` Hand hygiene Aseptic technique Skin antisepsis Catheter site dressing and change Securing catheter Face mask ```
39
What equipment is used to remove a CVAD?
``` Suture cutter Dressing pack Sterile gauze Sterile glove Chlorhexidine 2% (preferred) Occlusive dressing Goggles/face shield ```
40
What is the procedure for removing a CVAD?
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