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HAEMATOLOGY > Shock > Flashcards

Shock Flashcards

1
Q

What definitions can be used to describe shock?

A
  • tissue perfusion inadequate for tissue’s metabolic requirement
  • cellular and tissue hypoxia due to:
    => reduced O2 delivery, increased O2 consumption, inadequate O2 utilisation (or a combination)
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2
Q

What 3 components are required for normal tissue perfusion?

A
  • Cardiac Function (heart as pump)
  • Capacity of vascular bed (blood vessels
  • Circulating blood volume
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3
Q

Why can normal perfusion not be measured and what is used as a surrogate marker?

A
  • perfusion is different in every part of body

- BP is used instead (not perfect)

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4
Q

How is the mean arterial pressure calculated?

A

Mean Arterial Pressure =

C.O. (pump) x Systemic Vascular Resistance (vessels)

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5
Q

What are the main classifications of shock?

A

Hypovolaemic

Cardiogenic

Distributive - septic, anaphylactic

Obstructive - cardiac tamponade, tension pneumo, PE,

(Endocrine)

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6
Q

Explain the physiological problem in hypovolaemic shock

A

Loss of blood/plasma
=> not enough fluid in circuit
=> decreased systemic vascular resistance
=> decreased blood returning to heart (preload)
=> C.O. reduced
=> tissues cant be perfused

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7
Q

What would cause loss of plasma that may result in hypovolaemic shock?

A

Dehydration e.g. due to vomiting

extensive burns

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8
Q

Explain how pump failure results in cardiogenic shock

A
  • decreased C.O. as pump not able to perfuse body
  • usually caused by ischaemia from MI
  • may also be due to cardiomyopathy/ valve defect
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9
Q

What can cause obstructive shock?

A 
- mechanical obstruction
=> heart function is normal but pumping against something
- PE, air embolus
- Cardiac tamponade
- Tension pneumothorax
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10
Q

What can cause distributive shock and what is the underlying pathophysiology of this subtype?

A

“hot” shock
- caused by sepsis, anaphylaxis, neuro etc
- Vasodilation occurs => circuit TOO BIG for circulating volume
=> SVR decreases, Preload decreases, C.O decreases

O2 extraction also impaired

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11
Q

What can precipitate endocrine shock?

A
  • severe uncorrect hypothyroidism OR Addisonian Crisis

- causes decreased C.O and vasodilatation

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12
Q

How does the body attempt to compensate when in shock?

A

sympatho-adrenal response
=> aims to preserve CO and BP
- activates chemo and baroreceptors in vasomotor centre to increase sympathetics

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13
Q

How do neuroendocrine hormones help us to compensate when in shock?

A

Release of pituitary hormones – ACTH, ADH and endogenous opioids

=> Cortisol release – fluid retention, antagonises insulin
=> Glugagon release

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14
Q

Mixed pictures of shock are common (i.e. shock can be caused by multiple different things at the same time). TRUE/FALSE?

A

TRUE

these causes may come under different categories

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15
Q

Describe what happens during the inflammatory response in shocked patients?

A
  • COMPLEMENT cascade (attracts leucocytes)
  • CYTOKINES release – Interleukins, TNF-alpha
  • Platelet activating factor – Increased vascular permeability, platelet aggregation
  • Lysosomal enzymes – Myocardial depression, coronary vasoconstriction.
  • Adhesion molecules – damage to vessel walls, leucocyte attraction
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16
Q

What haemodynamic changes can occur during shock?

A
  • Vasodilatation/Constriction
  • Maldistribution of blood flow
  • Microcirculatory abnormalities – AV shunting, leaky capillaries
  • Inappropriate coagulation (e.g. DIC)
  • Reperfusion injuries
17
Q

What is released in shock that causes blood vessels to lose their reactivity?

A
  • Nitric oxide release (X1000) from endothelium => vessels fail to constrict
18
Q

Myocardial dysfunction in shock occurs due to reduced coronary blood flow. TRUE/FALSE?

A

FALSE

  • reversible biventricular systolic and diastolic dysfunction
  • Cytokines have direct myocardial effect
  • Beta-receptors down regulated
  • Decreased cardiomyofilament calcium sensitivity
19
Q

What are the main clinical features of shock?

A

CARDIOGENIC
- signs of myocardial failure
=> patient pale, clammy, cold peripheries

HYPOVOLAEMIC
- hypotension

OBSTRUCTIVE

  • Raised JVP,
  • Pulsus paradoxus

SEPTIC

  • Pyrexia
  • rapid cap refill
  • hypotension

ANAPHYLACTIC

  • vasodilatation => erythema
  • bronchospasm
  • oedema
20
Q

Class 1 and 2 of hypovolaemic shock involves patients who are decompensated. TRUE/FALSE?

A

FALSE
- patients observations can be variable but often are compensating in this stage

e.g. the BP may be normal but this doesn’t tell you if all vessels are vasoconstricted in an attempt to maintain pressure

21
Q

What should be monitored in patients with potential shock?

A

Examination – Pale, cold skin, prolonged capillary refill.

Urine output – Indicator of renal perfusion

Neurological – Disturbed consciousness a good indicator of cerebral hypoperfusion

Biochemical – Acidosis, lactate levels

22
Q

How can pressures and cardiac output be measured in specialist centres?

A

Pulmonary capillary wedge pressures (surrogate for LA pressure)

C.O = Thermodilution with a PA catheter

23
Q

What should be done whilst investigating for the cause of shock?

A

Establish wide bore IV access

resuscitate while investigating

24
Q

What would be considered a minimal acceptable BP if the patient is alert?

A

70-80 mmHg

however be aware that patient is probably compensating and can’t be left like this for long

25
Q

HOw can BP be measured both invasively and non-invasively?

A

Invasive = arterial line

Non-invasive = standard BP cuff

26
Q

If a patient’s MAP is 65-70 but they have not produced any urine what should be done?

A

Aim to increase MAP to look for urine response

- if no response consider other cause of not urinating

27
Q

What must be optimised for patients to gain adequate O2 delivery?

A

Hb (=> fix anaemia)
SpO2 (=> fix their sats)
Cardiac output

28
Q

What is the mainstay of management for shock?

A

fluids

29
Q

How do fluids help in shocked patients?

A

Increase pre-load

=> Increase C.O. and decrease SVR

30
Q

What is the risk of giving fluids in shock?

A

Fluids are given rapidly => patient may be fluid overloaded

  • Shocked patients more susceptible to pulmonary oedema (microvasc. dysfunction)
31
Q

What is a fluid challenge?

A

300-500ml over 10-20 mins then reassess

Aims to: Increased MAP, Decreased HR, increase urine output

32
Q

A fluid challenge cannot be repeated. TRUE/FALSE?

A

FALSE - can be repeated if patient has shown a small response and you think they may just require a larger fluid volume

STOP if non-responsive and consider causes of this

  • too little fluid given?
  • losing as much as is being given?
  • got enough fluid on board already?
33
Q

What different types of fluids can be given?

A

Crystalloids - saline, Hartmann’s
=> these are rapidly lost from circ. to extravascular space

Colloids - more expensive but reduced volume req’d.
=> these may cause anaphylaxis

Blood transfusion -higher O2 carrying capacity, stays in circulation
=> scarce, and has risks

34
Q

When are drugs given in shock?

A

If shock is severe OR fluids dont work

usually given in HDU

35
Q

What drugs can be used in shock?

A

adrenaline - alpha and beta agonist (beta at low dose)
=> increases HR and contractility

noradrenaline - alpha agonist
=> vasoconstriction

Others:
Vasopressin (ADH) - useful in cardiogenic shock (not in septic!)
Dopamine
Dobutamine/Dopexamine

36
Q

What mechanical procedures can be used to treat shock?

A
  • balloon pump
  • Left/ Right Ventricular assist device (LVAD/RVAD)
  • Venous-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) [heart and lung support]
37
Q

How is hypovolaemic shock managed prior to fluids/drugs?

A
  • Establish source
  • estimate volume and speed of blood loss
  • Direct pressure on area / use tourniquet’s
  • Damage limitation resuscitation and surgery
38
Q

What are the main side effects of fluid resuscitation?

A
  • positive fluid balance
    => Extra-vascular overload BUT intra-vascularly “dry”
  • Sub-cutaneous oedema
  • Less obvious oedema – “wet” lungs/ARDS, bowel oedema, etc
39
Q

What is de-resuscitation and how can this be achieved?

A
  • removing extra fluid from a patient once shock has resolved.
  • reduces mortality by getting patients “dry” as early as possible
  • can happen Spontaneously in patient
  • OR can be achieved through Diuretics OR Dialysis

HAEMATOLOGY (24 decks)

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