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Immediate Life Support and Critical illness > Circulation > Flashcards

Circulation Flashcards

1
Q

What is shock?

A

“Acute circulatory failure with inadequate or inappropriately diturbed tissue perfusion resulting in generalised cellular hypoxia” - failure to perfuse vital organs

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2
Q

How would you calculate oxygen delivery?

A

Cardiac output x arterial oxygen content

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3
Q

What equation can be used to determine arterial oxygen content?

A

Oxygen saturation x Hb x 1.34

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4
Q

How would you calculate cardiac output?

A

SV x HR

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5
Q

What three factors is SV influenced by?

A
  • Preload
  • Contractility
  • Afterload
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6
Q

What is starling’s law?

A

As the heart muscle is stretched, the force of contraction increases

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7
Q

What is pre-load?

A

The amount of stretch that is exerted on the myocardium during the filling phase

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8
Q

What is the CVP?

A

The pre-load exerted on the right side fo the heart

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9
Q

What is contractility influenced by?

A
  • Pre-load and afterload
  • Other factors - MI, Sepsis, Angina
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10
Q

What is afterload?

A

The load that the heart contracts against during isotonic contraction

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11
Q

What is afterload influenced by?

A
  • Intra-thoracic pressure
  • Valvular disease
  • Vascular resistance - pulmonary or systemic
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12
Q

What will an increase in Systemic Vascular Resistance do to CO?

A

Decrease CO

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13
Q

How do you calculate blood pressure?

A

CO x SVR

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14
Q

What is the difference between CO and BP?

A

Blood pressure refers to the pressure of blood in the systemic circulation, and cardiac output is the flow of blood through the circulation

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15
Q

How does global cellular hypoxia initially manifest?

A

Multi-organ dysfunction - Change in consciousness, oliguria, reduction in myocardial contractility/arrythmias, amound many others

AT THIS POINT EFFECTS ARE REVERSIBLE

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16
Q

What can continuing failure of oxygen delivery lead to?

A

Multi-organ failure - patient very likely to die at this pooint unless aggressively treated

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17
Q

Why is it important to recognise shock early?

A

To avoid reaching the stage of organ failure

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18
Q

What are the main types of shock?

A
  • Cardiogenic
  • Hypovolaemic
  • Obstructive
  • Distributive
  • Neurogenic
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19
Q

What is cardiogenic shock?

A

PUMP FAILURE

A Reduction in CO due to primary reduction in SV or an arrythmia - due to a decrease in contractility

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20
Q

What are typical causes of cardiogenic shock?

A

Don’t always cause cardiogenic shock - only when it fails to perfuse organs and causes clinical syndrome

  • MI
  • Acute mitral regurgitation
  • VT
  • Complete heart block causing severe bradycardia
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21
Q

What is obstructive shock?

A

Mechanical obstruction to cardiac output - may be from within a vessel (PE), compression of a vessel (tension pneumothorax) leading to increased afterload or decreased preloa, or compression of the heart (tamponade)

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22
Q

What is hypovolaemic shock?

A

Reduction of cardiac output due to inadequate circulating volume

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23
Q

What can cause volume loss from circulation?

A
  • Bleeding
  • Third space loss
  • Sepsis
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24
Q

What is distributive shock?

A

Characterised by peripheral vasodilation which causes a reduction in SVR and a fall in BP. This is accompanied by inappropriate distribution of blood flow away from capillary beds, plus capillary leak

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25
Q

What are causes of distributive shock?

A

Sepsis

Anaphylaxis

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26
Q

Are combinations of shock type common?

A

Yes

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27
Q

What types of shock can occur in severe sepsis?

A

Distributive + Cardgiogenic (due to myocardial depression)

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28
Q

In septic shock, what occurs which is indicative of a grave prognosis?

A

Vasoconstriction, reduced contractility and large falls in cardiac output

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29
Q

What are the main compensatory systems involved in shock?

A
  • Sympathetic nervous system
  • RAAS system
30
Q

What is the sympathetic response to hypotension?

A

Signals from baroreceptors and chemoreceptors pass through the brain, which cause sympathetic activation which is augmented by catecholamine release from adrenal medulla

31
Q

What is the response of the RAAS to systemic hypotension?

A

This is a SLOW RESPONSE

Stimulates renin release from juxtaglomerular apparatus. This catalyses conversion of angiotensinogen to angiotensin I, which is converted in the lung to angiotensin II (potent vasoconstrictor).

Aldosterone is also released by adrenal cortex, causing sodium and water retention

32
Q

What are the vital organs?

A
  • Heart
  • Brain
  • Kidneys
  • Gut
33
Q

What can happen to the heart as a result of shock?

A

Any shock state can reduce oxygen supply to the myocardium causing reduced contractility and ischaemia. In septic shock, direct myocardial depression occurs

34
Q

What happens to the brain in shock?

A

Reversible cerebral dysfunction - drowsiness/restlessness/agittion

35
Q

What needs to be ruled out in an anxious or agitated patient?

A

Hypoxia or shock - hypoxaemia can exacerbate any reduction in cerebral perfusion caused by shock

36
Q

What can be one of the earliest indicators of shock?

A

Oliguria

37
Q

What is the cause of oliguria in the initial phases of shock?

A

Pre-renal AKI

38
Q

What occurs in the kidneys if shock is left untreated?

A

Acute tubular necrosis - difficult to treat once established

39
Q

What is important to rule out if someone is oliguric?

A

Obstruction - catheterise or USS them

40
Q

How does shock affect the gut?

A

Compensatory vasoconstriction of gut vessels leads to transient ischaemia. Prolonged hypoperfusion may lead to loss of mucosal integrity, allowing bacteria to pass into the portal circulation.

This is understood as one of the causes of sepsis and multi-organ failure in severe shock

41
Q

What happens metabolically within cells when they are starved of oxygen?

A

Anaerobic metabolism

42
Q

How does anaerobic metabolism lead to metabolic acidosis?

A

Glucose is metabolised to pyruvate, which instead of entering the krebs cycle, is converted to lactate, generating only 2 atp. The H+ ions released cause a metabolic acidosis

43
Q

How does metabolic acidosis affect the body systemically?

A

Widespread organ dysfunction, particularly in the CVS, which leads to myocardial depression and vasodilatation

44
Q

What are the main components of the inflammatory repsonse?

A
  • Microorganisms and their products
  • Leukocyte activation and migration
  • Endothelial activation
  • Cytokine release
  • Complement cascade
  • Arachadonic acid metabolites
45
Q

What role do leukocytes play in the inflammatory response?

A

Migrate into tissues, degranulating and discharging contents such as protesases and free radicals

46
Q

What does endothelial activation contribute to the inflammatory response?

A

Release mediators such as NO and endothelin-1 - local and systemic effects (vasodilation and increased permeability)

47
Q

What role does arachadonic acid metabolite production have in the inflammatory response?

A

Influence vascular tone and permeability, platelet function, thermoregulation etc.

48
Q

What cirulatory changes occur in systemic inflammation?

A
  • Vasodilation
  • Increased vasular permeability
  • Coagulopathy
  • Arterio-venous shunting and flow maldistribution
49
Q

What are the different syndromes of infection and inflammation?

A
  • SIRS
  • Sepsis
  • Severe Sepsis
  • Septic shock
50
Q

What is SIRS?

A

Combination of tachycardia, tachypnoea, temp disturbance and deranged white cell count in presence of severe illness

51
Q

What is sepsis?

A

SIRS resulting from documented infection

52
Q

What is severe sepsis?

A

Sepsis associated with organ dysfunction, hypoperfusion or hypotension

53
Q

What is septic shock?

A

Severe sepsis with hypotension in the absence of other cause despite adequate fluid resus

54
Q

What would you consider doing as part of your assessment for Circulation?

A

WE PACE JOBS

  • Wide bore cannula + take bloods
  • Examine - Precodium + sites of active bleeding
  • Pulses (central/peripheral) - rate, rhythm, volume, character
  • AVPU
  • CRT/Color
  • ECG
  • JVP
  • Output - urine
  • Blood Pressure
  • Start fluids?
55
Q

How would you assess fluid status in someone who was showing features of shock?

A
  • History - thirst, postural dizziness etc.
  • Exam - BP, JVP/CVP, Pulse, urine output, pulse pressure, CRT
  • Losses estimation - drains, vomiting/diarrhoea, sweating
56
Q

What is a simple yet very sensitive way of measuring fluid status?

A

Lying and standing BP - evidence of postural drop

57
Q

What are signs of hypovolaemia?

A
  • Tachycardia
  • Tachypnoea
  • Oliguria
  • Hypotension
  • Cool peripheries
  • Low CVP/JVP
58
Q

What should you consider as a cause of oliguria in an unwell patient?

A
  • CV compromise
  • Shock
  • Pre-renal/renal/post-renal AKI
59
Q

How would you initially manage shock?

A
  • Two large bore IV cannulas + fluid resuscitation
  • Bloods - consider crossmatch
  • High flow oxygen - maximise oxygen saturation
60
Q

How would you review response to fluids in a shock patient?

A

Review the following

  • HR
  • CRT
  • BP
61
Q

How would you treat someone with hypovolaemia?

A

250-500ml crystalloid, then reassess

62
Q

How would you approach assessing someone with hypervolaemia?

A
  • Consider iatrogenic/cardiogenic cause
  • Investigate (ECG/cardiac enzymes)
63
Q

What are signs of sepsis?

A
  • Tachycardia
  • Pyrexia
  • Tachypnoea
  • Hypotension
  • Lecuocytosis
  • Evidence/suscpicion of infection
64
Q

When should you consider calling a middle grade when treating someone for shock?

A

Failure to respond to fluid

65
Q

What are the 3 main volume statuses?

A
  • Hypovolaemia
  • Normovolaemia
  • Hypervolaemia
66
Q

Why should sepsis always be considered as a cause of hypotension?

A

Sepsis causes a relative hypovolaemia due to increased vascular permeability

67
Q

What should be cultured if there is suspicion of sepsis?

A

Everything - blood, urine, sputum, drain sites, central line tip following removal

68
Q

How much fluid should be given to a shocked patient?

A

Difficult to give exact amount - after 2L with poor response need to seek senior advise and consider level 2 care

69
Q

What is the defining abnormality of hypervolaemia?

A

Raised preload

70
Q

What are features of cardiogenic shock?

A
  • Raised JVP
  • Basal crepitations
  • Hypotension
  • Oliguria
  • Drowsiness
71
Q

What is bradycardia?

A

HR in an adult < 60 BPM

Immediate Life Support and Critical illness (6 decks)

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