Physiology and Treatment of Shock Flashcards

1
Q

How is “shock” defined?

A

Inadequate perfusion to sustain normal organ function

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2
Q

What are the 5 main categories of Shock?

A

Hypovolaemic - loss of circulating volume
Cardiogenic - inefficient pump
Obstructive - physical blockage to heart filling/outflow
Distributive - circuit too big (vasodilation)
Cytotoxic - reduced oxygen delivery/ uptake

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3
Q

Loss of what components can cause hypovolaemic shock?

A

blood
interstitial fluid
RARE = pure water deficit

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4
Q

Why should we be aware of young patients who may go into hypovolaemic shock?

A

They compensate incredibly well before crashing

- BP can be maintained for longer than in older patients

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5
Q

How do our bodies attempt to compensate in hypovolaemic shock?

A
  • Baroreceptor reflex => detects less stretch and inhibits parasympathetic outflow => HR increases
  • Sympathetic neurohormonal => releases vasoconstrcitors => redirects blood away from peripheries to the heart
  • Capillaries absorb interstital fluid
  • Hypothalamo-Pituitary Response => vasoconstriction and ADH secretion to retain Na and water
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6
Q

When do our bodies begin to decompensate?

A

When circulating vasodilators increase

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7
Q

How can the heart increase its cardiac output?

A
  • Increase rate
  • Increase Stroke Vol. (children cant do this)
  • Increase both
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8
Q

How do we attempt to increase cardiac output in a patient who is hypovolaemic?

A

Fluid challenge

- Frank Starling curve shows this will have large effect on stroke volume and increase BP

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9
Q

Why should excess fluid be carefully monitored in patients with heart failure?

A

Can result in pulmonary congestion

  • if the heart cant pump as well, it increases its end diastolic volume to increase the stroke volume
  • this causes back pressure => pulmonary congestion
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10
Q

What are the principles of prescribing fluids to patients in shock?

A
  1. Fluids are a drug => do you know what’s in it? Dose?
  2. Consider individual patient (e.g. small/elderly dont need 3 litres maintenance saline)
  3. Consider the fluid AND electrolyte requirements
  4. Consider the difference between resuscitation and
    maintenance
    (i.e. dont give 500ml fluid challenge as maintenance)
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11
Q

What is the most common cause of cardiogenic shock?

A
  • acute MI

but may also follow acute valve dysfunction (e.g. if papillary muscles are ruptured during MI)

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12
Q

WHat are the clinical signs of cardiogenic shock?

A

Poor forward flow
=> Hypotension/shock
=> fatigue
=> syncope

Backpressure
=> Pulmonary oedema
=> elevated JVP
=> hepatic congestion

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13
Q

If the main issue of cardiogenic shock is an inefficient pump, how can this be treated pharmacologically?

A
  • drugs given to improve contractility of pump i.e. INOTROPES

=> β and dopaminergic stimulation
– Dobutamine, adrenaline
– Dopamine, Dopexamine

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14
Q

What can be inserted to help treat cardiogenic shock?

A
  • Intra aortic balloon pump
  • Inflates during ventricular diastole (allows coronary arteries to perfuse heart better)
  • Deflation during ventricular systole (reduced afterload => reduces pressure that heart needs to pump against)
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15
Q

Causes of obstructive shock usually cause a problem with the heart filling rather than emptying. Give examples of this and how we treat it

A

– Pulmonary embolism – Anticoag. +/- thrombolysis
– Cardiac tamponade – Pericardial drainage
– Tension pneumothorax – Decompression/ chest drainage

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16
Q

How can a PE be identified on an ECHO?

A

– Dilated RV - not much movement
– Bowing of interventicular septum into LV
– RV apex is moving lots

17
Q

What are the 3 main subtypes of distributove shock and how do they make the circuit “too big”?

A

Septic – Bacterial toxins mediate vasodilation
Anaphylactic – Mast cell release of histamine = vasodilation
Neurogenic – Loss of thoracic sympathetic outflow following spinal injury = unopposed vasodilatation from parasympathetics

18
Q

What treatments should be given early in septic shock?

A

Early use of antibiotics and vasopressors

19
Q

What treatment is given in anaphylactic shock and why?

A

Adrenaline

- Acts as both a vasoconstrictor and a mast cell stabiliser

20
Q

What test can be done to check if a patient is in anaphylactic shock?

A

Serum mast cell tryptase levels

Tryptase is released from mast cells when they degranulate

21
Q

Why do patients in neurogenic shock normally experience BRADYcardia?

A

Occurs due to unopposed vagal tone

  • if thoracic sympathetic outflow is compromised, this will not oppose parasympathetics

=> bradycardia

22
Q

What should clinicians be aware of if they think a patient is in neurogenic shock?

A
  • dont perform any examinations/procedures which increase vagal tone (e.g. PR exam, suction)
  • this could exacerbate bradycardia, making patient less likely to survive
23
Q

HOw is neurogenic shock normally treated?

A

Dopamine and vasopressors (to squeeze dilated vessels)

24
Q

What are the 8 reversible causes of cardiac arrest?

A
4Hs
Hypovolaemia
Hypoxia
Hypothermia
Hypo/Hyper- kalaemia (OR other metabolic causes)
4Ts
Thrombosis
Tamponade
Tension Pneumothorax
Toxins
25
Q

What is the importance of allowing the chest to recoil during CPR?

A

decreases the intra-thoracic pressure

=> allows more venous return to the heart

26
Q

What Cardiac Arrest Rhythms are Shockable?

A
Ventricular Fibrillation (VF)
Pulseless Ventricular Tachycardia (pVT)
27
Q

What cardiac arrest rhythms are NON-shockable?

A

Pulseless Electrical Activity

Asystole