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Haematology > Shock > Flashcards

Shock Flashcards

1
Q

How common is shock?

A

Affects 1/3 of patients in critical care at any given time

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2
Q

What is shock?

A

Syndrome in which tissue perfusion is inadequate for the tissue’s metabolic requirement

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3
Q

What is the underlying cause of shock?

A

State of cellular and tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilisation or a combination of all three

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4
Q

What does normal tissue perfusion rely on?

A

Cardiac function, capacity of vascular bed and circulating blood volume

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5
Q

How is normal perfusion measured?

A

Difficult to measure clinically = blood pressure most commonly used surrogate

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6
Q

What are the classifications of shock?

A

Hypovolaemic, cardiogenic, distributive, obstructive, endocrine

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7
Q

What are the causes of hypovolaemic shock?

A

Most commonly acute haemorrhage

Also severe dehydration and burns

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8
Q

What is the pathophysiology of hypovolaemic shock?

A

Volume depletion causes reduced SVR and subsequent vasoconstriction = reduced pre-load reduces cardiac output

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9
Q

What occurs in cardiogenic shock?

A

Pump failure = reduced cardiac output

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10
Q

What are the causes of cardiogenic shock?

A

Primarily due to ischaemia induced by an MI

Cardiomyopathies, valvular problems and dysrhythmias

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11
Q

What does cardiogenic shock occurring due to an MI suggest?

A

Suggests that >40% of left ventricle is involved

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12
Q

What is the mortality of cardiogenic shock?

A

> 75% unless due to a reversible cause

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13
Q

What is obstructive shock?

A

Mechanical obstruction to normal cardiac output in an otherwise normal heart

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14
Q

What are the causes of obstructive shock?

A

Direct obstruction to cardiac output = PE, air embolism

Restriction of cardiac filling = tamponade, tension pneumothorax

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15
Q

What are the causes of distributive shock?

A

Hot shock = sepsis, anaphylaxis, acute liver failure, spinal cord injuries

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16
Q

What is the mechanism of distributive shock?

A

Due to disruption of normal vascular autoregulation and profound vasodilation

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17
Q

What are the features of distributive shock?

A

Poor perfusion despite increased cardiac output
Regional perfusion differences
Alteration of oxygen extraction

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18
Q

What are some causes of endocrine shock?

A

Severe uncorrected hypothyroidism and Addisonian crisis = reduce cardiac output and cause vasodilation
Thyrotoxicosis causes shock paradoxically

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19
Q

What is the most common class of shock?

A

Distributive shock

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20
Q

Is it common for patients to have a mixed picture of different types of shock?

A

Yes

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21
Q

What is the sympatho-adrenal response?

A

Pathways to preserve normal cardiac output and hence blood pressure

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22
Q

To what extent do organs have their own autoregulatory sympatho-adrenal response?

A

Organs have degree of autoregulation between MAP of 50 or 60 through to 150

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23
Q

How does the sympathetic system respond to decreased blood pressure?

A

Sensed by baroreceptors and chemoreceptors = information travels to vasomotor centre to increase sympathetic activity to heart

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24
Q

How do the adrenals respond to decreased blood volume?

A

Adrenal medulla increases NA and adrenaline secretion and activates RAAS to increase salt and water = increases circulating volume

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25
Q

What does the neuroendocrine response involve?

A

Release of pituitary hormones = ACTH, ADH, endogenous opiates
Release of cortisol = fluid retention, insulin antagonism
Release of glucagon

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26
Q

What type of shock blunts the ACTH response?

A

Septic shock

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27
Q

What is the pathophysiology of shock?

A

Cascade of inflammatory mediators as a consequence of cellular ischaemia = causes cycle of vasoconstriction and oedema which worsens cellular ischaemia

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28
Q

What does cellular hypoxia cause?

A

Local vasoconstriction, thrombosis, regional variations in perfusion, release of free radicals and direct cellular trauma

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29
Q

What does neutrophil activation due to cellular hypoxia cause?

A

Release of pro-inflammatory cytokines

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30
Q

What processes can the inflammatory response be a part of?

A

Can be part of a pathological process or occur as a consequence of a disease process

31
Q

How does the inflammatory response predispose to infection?

A

It is often followed by secondary immune suppression

32
Q

What are some features of the inflammatory response?

A

Activation of complement cascade
Cytokine release = interleukins and TNF-a
Endothelium derived mediators = nitric oxide
Imbalance between anti-oxidants and oxidants

33
Q

What is the purpose of the activation of the complement cascade by the inflammatory response?

A

Attraction and activation of leucocytes

34
Q

What is the effect of the platelet activating factor produced by the inflammatory response?

A

Increased vascular permeability and platelet aggregation

35
Q

What are the effects of the lysosomal enzymes involved in the inflammatory response?

A

Myocardial depression and coronary vasoconstriction

36
Q

What is the purpose of the adhesion molecules involved in the inflammatory response?

A

Further leucocyte attraction due to the damage they cause to the vessel wall

37
Q

What are the haemodynamic changes associated with shock?

A

Vascular abnormalities = vasodilation/constriction
Maldistribution of blood flow and reperfusion injuries
Microcirculatory abnormalities
Inappropriate activation of coagulation system and DIC

38
Q

What are some microcirculatory abnormalities caused by shock?

A

AV shunting, “stop flow” or “no flow” capillary beds, failure of capillary recruitment, increased capillary permeability

39
Q

What causes loss of vascular reactivity?

A

Failure of vascular smooth muscle constriction

40
Q

What are the functions of nitric oxide?

A

Helps regulate blood flow, coagulation, neural activity and immune function

41
Q

Where is nitric oxide produced?

A

Produced in tiny amounts (picomolar) concentrations in endothelial and other cells by cNOS

42
Q

What effect do inflammation pathways have on nitric oxide?

A

Activate inducible isoform iNOS in vessel smooth walls = causes 1000x increase in nitric oxide production

43
Q

What is myocardial dysfunction?

A

Reversible biventricular systolic and diastolic dysfunction

44
Q

What is not a cause of myocardial dysfunction?

A

Reduced coronary blood flow

45
Q

What are some causes of myocardial dysfunction?

A

Circulating cytokines with direct myocardial effect
Beta receptor down-regulation
Decreased cardiomyofilament calcium sensitivity

46
Q

What are the clinical features of shock?

A

Depends on underlying cause = hypotension, signs of myocardial failure, raised JVP, pulsus paradoxus, pyrexia, vasodilation, erythema, oedema

47
Q

What is class I hypovolaemia?

A

<15% blood loss and base deficit 0 to -2mEq/l
Heart rate and respiratory rate stay the same
Blood pressure and pulse pressure stay the same
No change in urine output or GCS
Monitor need for blood products

48
Q

What is class II (mild) hypovolaemia?

A

Blood loss 15-30% and base deficit -2 to -6mEq/l
Heart rate stays the same/increases
Blood pressure and respiratory rate stay the same
Pulse pressure decreases
No change in urine output or GCS
Possible need for blood products

49
Q

What is class III (moderate) hypovolaemia?

A

Blood loss 31-40% and base deficit -6 to -10mEq/l
Heart rate increases and pulse pressure decreases
Blood pressure stays the same or decreases
Respiratory rate stays the same or increases
Urine output and GCS decrease
Need for blood products

50
Q

What is class IV (severe) hypovolaemia?

A

Blood loss >40% and base deficit >= -10mEq/l
Blood pressure and pulse pressure decrease
Heart rate increases significantly
Respiratory rate increases and GCS decreases
Urine output decrease significantly
Massive transfusion protocol needed

51
Q

What is the clinical monitoring of a patient with shock?

A

Examination = pale, cold skin, prolonged capillary refill
Urine output = sensitive indicator of renal perfusion
Disturbed consciousness indicates cerebral perfusion
Biochemical = acidosis, lactate levels

52
Q

What pressures are monitored in a patient with shock?

A

Blood pressure = either cuff or invasive arterial line
Central venous pressure = assess fluid responsiveness
Pulmonary artery and pulmonary capillary wedge pressures = rarely used

53
Q

How can cardiac output be measured in a patient with shock?

A

Gold standard is thermodilution with PA catheter = only in specialist units
Pulse contour analysis and doppler ultrasonography

54
Q

What is the management of a patient with shock?

A

Establish bore IV access and resuscitate while investigating
Oxygen delivery and fluids

55
Q

What is the aim of resuscitation?

A

To re-establish sufficient perfusion to allow tissue oxygen delivery

56
Q

What is the target MAP when resuscitating a patient with shock?

A

65-70mmHg unless patient is hypertensive or there is ongoing haemorrhage

57
Q

What is the equation for calculating oxygen dose?

A

Cardiac output x (1.39 x Hb + SpO2) + (PaO2 x 0.003)

Main components are Hb, SpO2 and cardiac output

58
Q

What are the principles for oxygen delivery?

A

Correct anaemia, ensure SpO2 is normal and optimise cardiac output

59
Q

Why is giving fluids beneficial?

A

Increases pre-load

60
Q

How should fluids be delivered?

A

Give rapid fluid replacement = typically 300-500ml given over 10-20mins

61
Q

Why are shocked patients more susceptible to pulmonary oedema?

A

Due to microvascular dysfunction

62
Q

What are some fluids that may be given to resuscitate a shocked patient?

A

Crystalloids, colloids and blood

63
Q

What are the advantages and disadvantages of crystalloids?

A 
Advantages = convenient, cheap, safe 
Disadvantages = rapidly lost from circulation due to extravascular spaces, need significantly larger volumes than loss
64
Q

What are the advantages and disadvantages of colloids?

A 
Advantages = cheap, reduce volumes required
Disadvantages = can cause anaphylaxis, no evidence of their benefit
65
Q

What are the advantages and disadvantages of giving blood?

A 
Advantages = O2 carrying capacity, stays in circulation
Disadvantages = scarce resource, multiple risks
66
Q

When is shock treated pharmacologically?

A

In severe cases when fluids don’t work or stop working = must be given in critical care environment

67
Q

What are some pharmacological agents used to treat shock?

A

Adrenaline = a/b adrenergic agonist (b at low dose)
Noradrenaline = usually first line, mainly alpha agonist
ADH and dobutamine/dopexamine
Dopamine = complex dose dependent effects

68
Q

What are the options for treating shock if drugs fail?

A

Mechanical support = balloon pumps or L/R-VADs for cardiogenic shock, VA-ECMO in severe cases

69
Q

How is hypovolaemic shock managed?

A

Assessment of volume loss and speed of ongoing loss
Establish source and temporisation (e.g tourniquet)
Damage limitation resuscitation until definitive control
Damage limitation surgery

70
Q

What is resuscitation associated with?

A

Significant fluid administration and positive balances

71
Q

Why does resuscitation lead to oedema?

A

Volume delivered never remains intravascular

72
Q

What are some side effects of resuscitation?

A

Sub-cutaneous oedema = obvious

Wet lungs/ARDS and bowel oedema = less obvious

73
Q

What is de-escalation once a patient has been treated for shock?

A

Removal of extra fluid from patient = can be done spontaneously or by using diuretics or dialysis

Haematology (24 decks)

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