Shock Flashcards by Zoe Doak

What definitions can be used to describe shock?

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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What 3 components are required for normal tissue perfusion?

Cardiac Function (heart as pump)
Capacity of vascular bed (blood vessels
Circulating blood volume

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

perfusion is different in every part of body

- BP is used instead (not perfect)

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How is the mean arterial pressure calculated?

Mean Arterial Pressure =

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

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What are the main classifications of shock?

Hypovolaemic

Cardiogenic

Distributive - septic, anaphylactic

Obstructive - cardiac tamponade, tension pneumo, PE,

(Endocrine)

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Explain the physiological problem in hypovolaemic shock

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

Dehydration e.g. due to vomiting

extensive burns

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Explain how pump failure results in cardiogenic shock

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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What can cause obstructive shock?

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

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

“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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What can precipitate endocrine shock?

severe uncorrect hypothyroidism OR Addisonian Crisis

- causes decreased C.O and vasodilatation

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How does the body attempt to compensate when in shock?

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

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

Release of pituitary hormones – ACTH, ADH and endogenous opioids

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

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

TRUE

these causes may come under different categories

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Describe what happens during the inflammatory response in shocked patients?

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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What haemodynamic changes can occur during shock?

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

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

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Nitric oxide release (X1000) from endothelium => vessels fail to constrict

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

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FALSE

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

What are the main clinical features of shock?

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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

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

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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

What should be monitored in patients with potential shock?

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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

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

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Pulmonary capillary wedge pressures (surrogate for LA pressure)

C.O = Thermodilution with a PA catheter

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

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Establish wide bore IV access

resuscitate while investigating

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

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70-80 mmHg

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

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

Invasive = arterial line Non-invasive = standard BP cuff

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

Aim to increase MAP to look for urine response | - if no response consider other cause of not urinating

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

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

What is the mainstay of management for shock?

fluids

How do fluids help in shocked patients?

Increase pre-load | => Increase C.O. and decrease SVR

What is the risk of giving fluids in shock?

Fluids are given rapidly => patient may be fluid overloaded - Shocked patients more susceptible to pulmonary oedema (microvasc. dysfunction)

What is a fluid challenge?

300-500ml over 10-20 mins then reassess Aims to: Increased MAP, Decreased HR, increase urine output

A fluid challenge cannot be repeated. TRUE/FALSE?

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?

What different types of fluids can be given?

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

When are drugs given in shock?

If shock is severe OR fluids dont work | usually given in HDU

What drugs can be used in shock?

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

What mechanical procedures can be used to treat shock?

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

How is hypovolaemic shock managed prior to fluids/drugs?

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

What are the main side effects of fluid resuscitation?

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

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

- 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

Shock Flashcards

(39 cards)