Haemodynanic Shock Flashcards

1
Q

What is Haemodynamic shock?

A

• Acute condition of inadequate blood flow throughout the body

• A catastrophic fall in arterial blood pressure leads to
circulatory shock

  • Mean arterial BP = CO x TPR
  • Shock can be due to fall in CO
  • Or fall in TPR beyond capacity of the heart to cope
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2
Q

Shock can be divided into a fall in cardiac output and a fall in peripheral resistance. What is the result of this?

A

Fall in CO:

  • Causes mechanical problems where the pump cannot fill
  • Pump failure
  • Loss of blood volume

Fall in peripheral resistance:
- Excessive vasodilation

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3
Q

What are the different types of shock that are due to a fall in cardiac output?

A

• Cardiogenic shock (pump failure)
– ventricle cannot empty properly

• Mechanical shock (obstructive)
– ventricle cannot fill properly

• Hypovolaemic shock
– reduced blood volume leads to poor venous return

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4
Q

What is cardiogenic shock?

A

Acute failure of the heart to maintain cardiac output - pump failure

Potential causes:

• following myocardial infarction
– damage to left ventricle

  • due to serious arrhythmias - Tachycardia and bradycardia
  • acute worsening of heart failure
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5
Q

What happens in cardiogenic shock?

A
  • Heart fills, but fails to pump effectively
  • Central venous pressure (CVP) may be normal or raised
  • Dramatic drop in arterial BP

• Tissues poorly perfused
- Brain needs contestant perfusion, neurones die quickly in absence of oxygen
– coronary arteries may be poorly perfused, this exacerbates problem

– Kidneys may be poorly perfused

• reduced urine production - oliguria

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6
Q

What is cardiac arrest?

A

When heart stops

Not related to Haemodynamic shock

Defined as: Unresponsiveness associated with lack of pulse

  • Heart has stopped or has ceased to pump effectively
  • Asystole (loss of electrical and mechanical activity)
  • Pulseless Electrical Activity (PEA)

• Ventricular fibrillation (uncoordinated electrical activity)
– most common form of cardiac arrest
– often following MI because depolarisation sets off electrical activity in an uncontrolled way
– or electrolyte imbalance
– or some arrhythmias (eg long QT and Torsades de Pointes)

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7
Q

What is Asystole?

A

When you lose electrical activity of the heart so you cannot get any mechanical activity of the heart

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8
Q

How would you treat or manage cardÏact arrest?

A

• Basic life support
– chest compression and external ventilation

• Advanced life support
– defibrillation
– electric current delivered to the heart
– depolarises all the cells – puts them into refractory period
– allows coordinated electrical activity to restart

• Adrenaline
– enhances myocardial function
– increases peripheral resistance and increases blood pressure and maintains increased BP

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9
Q

What is an example of mechanical shock?

A

Mechanical shock – cardiac tamponade

• Cardiac tamponade
– blood or fluid build up in pericardial space (this is a fibrous and rigid space)
– restricts filling of the heart 
– limits end diastolic volume 
– affects left and right sides of heart

• High central venous pressure
- blood is returning to the heart but the heart can’t be filled

• Low arterial blood pressure
- heart isn’t filling in diastole so can’t get good CO in systole

• Heart attempts to beat
– continued electrical activity
- this increase in heart rate but can’t increase the CO because stroke volum is too low

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10
Q

What is another thing that can cause a mechanical shock?

A

• Massive pulmonary embolism (PE)

• Embolus occludes a large pulmonary artery
– Pulmonary artery pressure is high
– Right ventricle cannot empty
– Central venous pressure high
– Reduced return of blood to left heart – Limits filling of left heart
– Left atrial pressure is low
– Arterial blood pressure low
– Shock
- blocking the filling of right side of heart
– Also chest pain, dyspnoea

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11
Q

How might an embolus reach the lungs?

A
  • Typically due to deep vein thrombosis
  • Portion of thrombus breaks off
  • Travels in venous system to right side of the heart
  • Pumped out via pulmonary artery to lungs
  • The effect of this will depend on the size of the embolus and size of artery that is blocked
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12
Q

How does hypovolaemic shock reduce CO?

A
  • Reduced blood volume
  • Most commonly due to haemorrhage
  • < 20% blood loss unlikely to cause shock
  • 20-30% some signs of shock response
  • 30-40% substantial decrease in mean aBP and serious shock response
  • Severity of shock is related to amount and speed of blood loss
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13
Q

How does your body respond to hypovolaemic shock?

A

• Haemorrhage
– venous pressure falls (filling pressure)
– Therefore stroke volume reduces and then cardiac output falls and then so does blood pressure(Starling’s Law)
– arterial pressure falls
– detected by baroreceptors

• Compensatory response
– increased sympathetic stimulation
–-> tachycardia
–-> increased force of contraction

– peripheral vasoconstriction because you get sympathetic outflow to arterioles which releases noradrenaline to alpha 1 receptors leading to increase in peripheral resistance

– venoconstriction
—> can help maintain venous pressure and so maintain filling of the heart

This system doesn’t cope well in high volume of blood loss

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14
Q

How do the capillaries cope with hypovolaemic shock?

A

• Normally at the capillaries you get a small movement of fluid out to the tissues
- the hydrostatic pressure of the blood in the capillaries pushes fluid out of the capillaries

  • pressure of the proteins inside forces fluid into capillaries

• This then returns to the venous system via the lymphatic drainage

• In hypovolaemic shock this reverses
- get some ‘internal transfusion’

• Increased peripheral resistance reduces the capillary hydrostatic
pressure

• Net movement of fluid into capillaries because we have reduced capillary hydrostatic pressure

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15
Q

What are the symptoms of hypovolaemic shock?

A
• Patient has:
– Tachycardia 
– Weak pulse 
– Pale skin 
– Cold, clammy extremities
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16
Q

What else can hypovolaemic shock result from?

A

– Severe burns

– Severe diarrhoea or vomiting and loss of Na+

17
Q

Explain the concept of “Danger of decompensation” in hypovolaemic shock

A
• Danger of Decompensation 
• Peripheral vasoconstriction (shutdown) impairs tissue perfusion
– Tissue damage due to hypoxia
– Release of chemical mediators 
– vasodilators
– TPR falls
– Blood pressure falls dramatically
– Vital organs can no longer be perfused
– Multi system failure
18
Q

Outline ways the longer term responses to restore blood volume

A
  • Renin-angiotensin-aldosterone system
  • Anti-diuretic hormone

But they do take time (about 3 days) so the acute response with baroreceptors are used

• 20% blood volume loss
– Restoration of body fluid volumes in about 3 days

• If salt and water intake are adequate

19
Q

We also get a type of shock that is due to a reduction in total peripheral resistance. What is this called? How does it work?

A

Distributive shock

• Low resistance shock (normovolaemic)

  • Increase in volume of tube circulation

• Profound peripheral vasodilation - decrease in TPR

– blood volume constant, but volume of the circulation has increased

  • Toxic (Septic) shock
  • Anaphylactic shock
20
Q

What is toxic (septic) shock?

A

Type of shock caused by sepsis

• Sepsis
– Serious life-threatening response to infection

  • Can lead to septic shock
  • Endotoxins released by circulating bacteria

– Profound inflammatory response (excessive)

– Causes profound vasodilation

– Dramatic fall in TPR

– Fall in arterial pressure

– If this is substantial will lead to impaired perfusion of vital organs

– also - capillaries become leaky this leads to reduced blood volume

– Increased coagulation, leading to peripheral vasoconstriction and thus localised hypo-prefusion

21
Q

By describing the effects of septic shock, outline the symptoms seen on patients

A

Septic shock

• Persisting hypotension requiring treatment to maintain
blood pressure despite fluid resuscitation

• Decreased arterial pressure
– Detected by baroreceptors
– increased sympathetic output
– Vasoconstrictor effect overridden by mediators of vasodilation
– Heart rate and stroke volume increased to try an maintain BP

• Patient has
– Tachycardia
– Warm, red extremities initially BUT

• Later stages of sepsis
– vasoconstriction
– localised hypo-perfusion

22
Q

What is anaphylactic shock?

A

• severe allergic reaction (anaphylaxis)
– release of histamine from mast cells

• other mediators

– powerful vasodilator effect
– fall in TPR
– dramatic drop in arterial pressure

• increased sympathetic response 
- Increase in CO, but the CO can't be increased enough so can’t
overcome vasodilation 
- thus can't maintain blood pressure
– impaired perfusion of vital organs

– mediators also cause bronchoconstriction and laryngeal
oedema

• difficulty breathing

23
Q

What are the symptoms of anaphylactic shock?

How is it treated?

A
• Patient will have
– Difficulty breathing 
– Collapsed 
– Rapid heart rate 
– Red, warm extremities

• Acutely life threatening

• Adrenaline
– Vasoconstriction via action at α1
adrenoceptors
- at high doses only

EPIPEN - contains adrenaline, administered intramuscularly

24
Q

What is the common effect of shock?

A

Initially, shock an cause a decrease in Total peripheral resistance or Cardiac output

However they all ultimately lead to a reduction in blood pressure

This causes a decrease in tissue perfusion and there are some vital organs that require constant blood supply - brain, heart and kidneys

This eventually leads to multi organ failure