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Semester 2 - CVS > 20. Haemodynamic Shock > Flashcards

20. Haemodynamic Shock Flashcards

1
Q

Give the equation for:

  1. Mean arterial BP
  2. Cardiac output
A
  • Mean arterial BP = CO x TPR
  • Mean arterial BP = SV x HR x TPR

• CO = SV x HR

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2
Q

How can MABP be measured?

A

maBP = diastolic pressure + 1/3 pulse pressure

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3
Q

What is haemodynamic shock and what causes it?

A
  • Acute condition of inadequate blood flow throughout the body
  • A catastrophic fall in arterial blood pressure
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4
Q

What are the 2 ways shock can occur?

A
  • Shock can be due to fall in CO

* Or fall in TPR beyond capacity of the heart to cope

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5
Q

List and explain the 3 types of shock that can occur 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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6
Q

List and explain the 2 types of shock that can occur due to a fall in TPR

A

Distributive shock:

  • toxic/septic shock
  • anaphylactic shock
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7
Q

What is cardiogenic shock?

A

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

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8
Q

What are possible causes of cardiogenic shock?

A
  • following myocardial infarction: damage to left ventricle
  • due to serious arrhythmias
  • acute worsening of heart failure
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9
Q

Give the pathophysiology of 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
– coronary arteries may be poorly perfused
–> exacerbates problem
– Kidneys may be poorly perfused
–> reduced urine production - oliguria

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10
Q

What is mechanical shock?

A

Shock due to ventricles unable to fill properly

- obstructive

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11
Q

Give 2 causes of mechanical shock?

A
  • cardiac tamponade

- PE

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12
Q

What is cardiac tamponade?

A

compression of the heart by an accumulation of fluid or blood in the pericardial sac.
This puts pressure on the heart and restricts filling.

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13
Q

How does cardiac tamponade affect filling of the heart and which side of the heart does it affect?

A
  • restricts filling of the heart, limits end diastolic volume
  • affects left and right sides of heart
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14
Q

How does cardiac tamponade affect arterial and central venous pressure?

A
  • High central venous pressure
  • Low arterial blood pressure

(Note: raised pulmonary arterial pressure due to back pressure from the raised left atrial pressure)

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15
Q

Give the pathophysiology of mechanical shock

A

The outer layer of the heart is made up of fibrous tissue which has poor stretch abilities. The accumulation of fluid in the pericardial cavity causes an increase in pressure.
As the pressure increases you get a restriction on the filling of the heart, less blood will enter into the ventricles.
This’ll limit end diastolic volume.

The decrease in stroke volume will result in a decrease in cardiac output and can lead to mechanical shock.

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16
Q

What is a pulmonary embolism?

A

A pulmonary embolism is a a blockage of an artery in the lungs by an embolus. This is a substance that has moved from somewhere else in the body throughout the bloodstream.`

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17
Q

Explain the pathophysiology of mechanical shock as a result of a pulmonary embolism

A

• Embolus occludes a large pulmonary artery
– Pulmonary artery pressure is high
– Right ventricle cannot empty - reduction in output.
– 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
– Also chest pain, dyspnoea
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18
Q

Give signs associated with mechanical shock, cardiac tamponade and pulmonary embolism respectively

A

CT:
Distended neck veins and a raised JVP.

PE:
Chest pain and dyspnoea

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19
Q

Where is it most likely for a pulmonary embolus to emerge from? How might the 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
20
Q

What is hypovolaemic shock?

A

Hypovolaemic shock is caused by reduced blood volume. The reduction in blood volume means that organs are less well perfused.

21
Q

What is severity of shock related to in hypovolaemic shock?

A

Related to amount and speed of blood loss

22
Q

In hypovalaemic shock, What percentage of blood loss causes symptoms?

A
  • < 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
23
Q

Give the 3 factors that can cause hypovolaemic shock

A
  1. Haemorrhage with 30-40% blood loss
  2. Severe burns
    The body’s response to injury is acute inflammation, part of this response is to make the capillaries leakier.
    However as the skin is burnt off the fluid leaking out isn’t contained and is lost from the body.
  3. Extremely severe diarrhoea or vomiting
  4. Loss of sodium
    Water follows sodium, so if there’s reduced sodium there’s less water, therefore a reduced blood volume.
24
Q

How does haemorrhage cause hypovolaemic shock (how does it reduce CO)?

A

– venous pressure falls
– cardiac output falls (Starling’s Law)
– arterial pressure falls
– detected by baroreceptors

25
Q

What is the compensatory response to hypovolaemic shock due to hemorrhage?

A 
– increased sympathetic stimulation
– tachycardia
– increased force of contraction
– peripheral vasoconstriction
– venoconstriction
26
Q

How does the hypovolaemic shock and its compensatory response affect filtration at the capillaries?

A

(Normally: net movement out of the capillaries)

During hypovolaemic shock you get a degree of internal transfusion occurring at the capillaries.

The increased peripheral resistance as a result of blood loss results in a reduction in capillary hydrostatic pressure.
However you still have a constant oncotic pressure between the capillary and tissue fluid.

This leads to a net movement of fluid into the capillary from the tissue fluid causing a small increase in circulating volume helping to slightly recover blood pressure.

27
Q

Give the clinical signs and symptoms associated with hypovolaemic shock

A

The patient will have:

  1. Tachycardia
  2. A weak pulse (Due to a reduction in SV in response to the fall in blood volume)
  3. Pale skin (due to increased peripheral vasoconstriction)
  4. Cold, clammy extremities (due to increased peripheral vasoconstriction)
  5. Low CVP
28
Q

What is the danger in hypovolaemic shock?

A

Danger of decompensation:

  • Arterial vasoconstriction
  • Tissue damage due to hypoxia
  • Release of chemical mediators - vasodilators
  • vasodilators build up and overcome sympathetic vasoconstriction
  • TPR falls
  • Blood pressure falls dramatically
  • Vital organs can no longer be perfused
  • Multi system failure
29
Q

What are the long term responses to hypovolaemia to restore blood volume?

A

Initially as a response to hypovolaemia you get the activation of the sympathetic nervous system. However this is only a short term response.

There are longer term response working to restore blood volume.
1. Activation of the Renin-angiotensin-aldosterone system:
This is done to promote salt and water retention by the kidneys to increase plasma volume.

  1. The release of the Anti-diuretic hormone:
    To promote the retention of sodium at kidneys and to restore blood volume.
30
Q

How long does it take to restore blood volume from 20% blood volume loss?

A

Restoration of body fluid volumes in about 3 days

• If salt and water intake are adequate

31
Q

How is cardiac arrest defined?

A
  • Unresponsiveness associated with lack of pulse

* Heart has stopped or has ceased to pump effectively

32
Q

What are 3 different forms of cardiac arrest?

A
  1. Asystole
    There’s a loss of electrical and mechanical activity.
  2. Pulseless electrical activity (PEA)
    This refers to cardiac arrest in which the electrocardiograph shows a heart that should produce a pulse, but does not. So there’s electrical activity, but the heart either doesn’t contract or there are other mechanisms resulting in an insufficient cardiac output to generate a pulse and supply to the organs.
  3. Ventricular fibrillation
    This is when the heart quivers instead of pumping due to disorganised electrical activity in the ventricles.
    This means that cardiac output is non-existent resulting in cardiac arrest.
33
Q

Which form of cardiac arrest is the most common and what causes it?

A

• Ventricular fibrillation

  • often following MI
  • or electrolyte imbalance
  • or some arrhythmias (eg long QT and Torsades de Pointes)
34
Q

What life support treatment is given to a patient in cardiac arrest?

A

• Basic life support
- chest compression and external ventilation

• Advanced life support
- defibrillation

35
Q

How does defibrillation work?

A
  • electric current delivered to the heart
  • depolarises all the cells - puts them into refractory period
  • allows coordinated electrical activity to restart
36
Q

What may be given in cardiac arrest and why?

A

Adrenaline

  • enhances myocardial function
  • increases peripheral resistance
37
Q

What is distributive shock?

A

Distributive shock is shock caused by reduced total peripheral resistance as a result of profound peripheral vasodilation.
This results in a reduction in BP.

This means that the blood volume is constant (normovolaemic), but volume of the circulation has increased.

38
Q

What are 2 types of distributive shock?

A
  • Toxic (spetic) shock

* Anaphylactic shock

39
Q

What is the pathophysiology in toxic (septic) shock?

A

Endotoxins released by circulating bacteria and chemical mediators by inflammatory cells:

  • Profound inflammatory response (excessive)
  • Causes profound vasodilation
  • Dramatic fall in TPR
  • Fall in arterial pressure
  • Impaired perfusion of vital organs
  • also capillaries become leaky: reduced blood volume
  • Increased coagulation and localised hypo-perfusion
40
Q

How does the body respond to the effects of toxic (septic) shock?

A

The decrease in arterial pressure is detected by baroreceptors resulting in an increase in sympathetic activity.
This tries to increase vasoconstriction, heart rate and stroke volume

However the attempted vasoconstrictor effect is overridden by mediators of vasodilation.
Overall the action of the sympathetic system isn’t enough to overcome the septic shock.

41
Q

How does a patient with toxic shock present?

A
  • Tachycardia
  • Warm, red extremities initially BUT
    • Later stages of sepsis - vasoconstriction - localised hypo-perfusion
42
Q

What is anaphylactic shock?

A

Severe allergic reaction

43
Q

What is the pathophysiology in anaphylactic shock?

A

Release of large amount of histamine, as well as other mediators, from mast cells.

Histamine has a powerful vasodilatory effect causing a fall in TPR which then decreases arterial pressure.
This causes impaired perfusion of vital organs.

There’s increased sympathetic response in attempt to increase cardiac output however this can’t overcome vasodilation.

In addition of this the other mediators released also cause bronchoconstriction and laryngeal
oedema. This causes difficulty breathing.

44
Q

How does a patient with anaphylactic shock present?

A
  • Difficulty breathing
  • Collapsed
  • Rapid heart rate
  • Red, warm extremities
45
Q

How is anaphylactic shock treated?

A

Adrenaline

- vasoconstriction via alpha 1 receptors (due to higher than physiological concentrations)

Semester 2 - CVS (20 decks)

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