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Block 15 > Shock > Flashcards

Shock Flashcards

1
Q

What is the

  1. Lay definition
  2. Medical definition

Of shock

A
  1. a psychological condition in response to a terrifying event
  2. failure of the circulation that results in inadequate tissue perfusion
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2
Q

What is involved in the autoregulation of blood flow?

A

Humoral control

Neural control

Blood flow local mechanism e.g. kidney constricts efferent arterioles to maintain same blood flow

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3
Q

What is involved in humoral autoregulation

A

Renin/angiotensin

Aldosterone

ADH

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4
Q

What is involved in neural regulation?

A

Baroreceptor response

Increase BP-> increase baroreceptor stretch->signal to inhibit sympathetic tone

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5
Q

What is the Valsalva manoeuvre to test autoregulation?

A

Forcible exhalation with closed glottis

Increased intra-thoracic pressure, reduces venous return, BP drops

Baroreceptors detect decreased BP and causes increased sympathetic outflow causing tachycardia and vasoconstriction

Hence blood pressure starts to increase with tachycardia

Sudden release of Valsalva manoeuvre causes sudden increase in BP, which is detected by baroreceptors which increase vagus activity (i.e. slows HR) and decreases sympathetic activity to lower BP

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6
Q

Describe blood flow autoregulation?

A

Local mechanism e.g. kidney constricts efferent arterioles to maintain same blood flow at a range of different BPs

BP fluctuates (e.g. stand up, sit down, lie down, exercise), but local action (at kidneys, brain etc.) maintain the same blood flow at different BP

Note: if someone has had a head injury, they tend to lose the autoregulation, hence it is even more important to maintain their BP

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7
Q
  1. Cardiac output=
  2. Pressure=
  3. Mean arterial pressure=
A
  1. CO=SV x HR
  2. Pressure=flow x resistance
  3. MAP= CO X SVR (CO=MAP/SVR)
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8
Q

What is starlings law

A

the force of contraction of the cardiac muscle is proportional to its initial
length – the greater the preload, the greater the pumping action

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9
Q

What is the definition of hypotension and what are the pitfalls?

A 
Accepted definitions
o SBP (systolic BP) < 90 mmHg
o SBP 20 mmHg below patients normal

Pitfalls
o May not know patient’s normal BP o Young and previously fit
o Elderly
o Drugs

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10
Q

What are the causes of shock?

A

Anaphylaxis – allergic reaction

Hypovolaemic – blood loss

Cardiogenic – MI

Neurogenic – damage to spinal cord

Septic

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11
Q

Describe the pathophysiology of shock?

A

Body is autoregulated to maintain perfusion (flow)
For each type of shock there exists
o A prime problem
o Compensatory changes o Clinical consequences

MAP = CO x SVR
MAP = (HR x SV) x SVR
o C = inadequate circulating volume
o P = failure of the pump
o R = damage to the control of resistance
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12
Q

What is CPR of shock

A

Circulating problem
Pump problem
Resistance control damaged

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13
Q

In hypovolaemia what is

  1. prime problem
  2. Compensation
  3. Clinical consequence
A
  1. Inadequate volume (C)/ Fall in cardiac output (P)
  2. Increased resistance (R)/ Tachycardia but cardiac output falls/Hypotension
  3. Cold, clammy peripheries/ Tachycardia/ Prolonged cap refill time/ Empty veins
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14
Q

What are the
1. Intravascular
2. Extravascular
causes of hypovolaemia

A
  1. Haemorrhage – visible or concealed

2. Evaporation/GI losses /Polyuria

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15
Q

In pump failure what is the

  1. Prime problem
  2. Compensation
  3. Clinical consequence
A
  1. Fall in cardiac output (P)
  2. Increased resistance (R) / Tachycardia / Further problem /Increased capacitance (C) / Failure of Starling’s law
  3. Cold, clammy peripheries / Tachycardia / Prolonged cap refill time /Raised JVP
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16
Q

What are the
1. Intrinsic
2. Extrinsic
Causes of pump failure

A
  1. Muscle / Conduction tissue / Valves

2. Obstruction – e.g. pulmonary embolus / Compression – e.g. tamponade / Blood supply

17
Q

For vasodilation what is

  1. Prime problem
  2. Compensation
  3. Clinical consequences
A
  1. Vasodilation (R)
  2. Tachycardia / Cardiac output rises / Autoregulation
  3. Warm, dry peripheries / Tachycardia / Short cap refill time / Bounding pulse
18
Q

What are the causes of vasodilation

A

Sepsis – SIRS/septic shock

Anaphylaxis

Neurogenic

Other

19
Q

What is systemic inflammatory response syndrome (SIRS)

A 
How the body responds to stress/ infection/insult 
2 or more of the following 
Heart rate >90
Fever >38 or >36
WCC >12000 or < 4000
Respiratory rate >20 or PCO2 <32
20
Q

What is septic shock?

A 
Evidence of infection
End organ failure 
Refractory hypotension 
Sepsis with refractor hypertension 
Mortality 43-54%
21
Q

What is

  1. Sepsis
  2. Severe sepsis
A
  1. SRIS + confirmed or presumed infections / Mortality: 10-15%
  2. sepsis with end organ dysfunction / Mortality: 17-20%
22
Q

What are the clinical signs of shock?

A

Poor tissue perfusion (skin/gut/liver/kidneys/brain/heart)

Oliguria

Altered conscious level

23
Q

What are clinical signs of compensation

A

Fright
Fight
Flight response

24
Q

What are clinical signs of correction of acidsosis?

A

Acidosis occurs if your tissues aren’t being perfused due to anaerobic respiration producing lactic acid
Tachypnoea

25
Q

What is the initial assessment/management of shock?

A

A: Airway with oxygen therapy (Airway compromise, Give high flow oxygen)

B: Breathing with ventilatory assessment/assistance (Respiratory rate, Inspect, palpate, percuss, auscultate)

C: Circulation with fluid resuscitation (Peripheral perfusion – cool and clammy v warm and dry, Pulse: volume/rate, IV access (blood for investigations, which tests?), Fluid challenge is nearly the always the first ‘C’ treatment – crystalloids v colloids, indications for blood transfusion, In younger patients especially, hypotension is not required for shock to exist because the body is good at autoregulation, hence it is frequently a sign of de-compensation)

D: disability (Conscious level: AVPU v GCS (Glasgow coma score), Pupils)

E: exposure, environment and other examinations (Causes: revealed bleeding, concealed bleeding, peripheral oedema)

26
Q

Describe perfusion pulse and veins for

  1. C (hypovolaemia)
  2. P (pump failure)
  3. R (vasodilation)
A
  1. Perfusion=cold and clammy, pulse weak and veins empty
  2. Perfusion=cold and clammy, pulse weak and full veins with JVP)
  3. Perfusion=warm and dry, bounding pulse and full veins
27
Q

What is the role of the following CVS receptors?

  1. Alpha
  2. Beta 1
  3. Beta 2
A
  1. vessels (Peripheral vasoconstriction)
  2. heart (Inotropic, Chronotropic, Peripheral vasodilatation)
  3. lungs and arteries of skeletal muscles (Arteriolar vasodilation)
28
Q

What is the treatment of sepsis?

A

Antibiotics - for bacterial infection

Crystalloids - to replace blood volume

Vasopressors - to try and maintain BP

29
Q

What is the sepsis 6

A 
Give O2 – saturation above 94%
Take blood cultures
Give IV antibiotics
Give a fluid challenge
Measure lactate
Measure urine output
30
Q

Adrenaline

  1. Receptors
  2. actions
A 
Beta 1 and 2 
Alpha 
Increases HR and SV 
Vasoconstrictor 
Increase BP
31
Q

Dobutamine

  1. Receptors
  2. Actions
A
  1. Beta 1 and 2
  2. Increases HR and SV
    Vasodilation (decreases BP)
32
Q

Dopexamine

  1. Receptors
  2. Actions
A
  1. Beta 2, dopamine

2. Increase HR, splanchnic vasodilator

33
Q

Noreadrenaline

  1. Receptor
  2. Actions
A

1, alpha

2. Vasoconstrictor

34
Q

For reduced capacitance what is

  1. compesation
  2. Principle management
A
  1. Increase HR and SVR (falls in CO)

2. Fluids (vasopressors)

35
Q

For pump failure what is

  1. Compensation
  2. Principle management
A
  1. Increase SVR

2. Inotropes (venodilators)

36
Q

For reduced resistance what is

  1. Compensation
  2. Principle management
A
  1. Increase SV and HR (SV more than HR)

2. Vasopressors (fluids)

Block 15 (11 decks)

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