Haemodynamic 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

.Wat can cause a shock

A

Fall in CO - pump cannot full, pump failure, loss of blood volume

Fall in peripheral resistance - excessive vasodilation

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3
Q

What are types of shock due to 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 and what are the potential causes?

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
• acute worsening of heart failure
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5
Q

Describe and explain 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

BP = CO x TPR
CO = HR x SV
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6
Q

What happens in cardiac arrest

A

• 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
– or electrolyte imbalance
– or some arrhythmias (eg long QT and Torsades de Pointes)

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7
Q

Hwo should cardiac arrest be dealt with?

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

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8
Q

Wat are types of mechanical shock?

A

-cardiac tamponade, PE,

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9
Q

What is cardiac tamponade?

A

Mechanical shock • Cardiac tamponade
– blood or fluid build up in pericardial space
– restricts filling of the heart – limits end diastolic volume
– affects left and right sides of heart
• High central venous pressure
• Low arterial blood pressure
• Heart attempts to beat – continued electrical activity

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10
Q

Describe mechanical shock by PE

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 
– Also chest pain, dyspnoea
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11
Q

How much 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 • See Pathological Processes semester 2 • See Respiratory Unit semester 3

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12
Q

What is hypovolaemic shock

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

Describe haemorrhage in hypovolaemic shock and the compensatory response

A
Hypovolaemic shock 
• Haemorrhage
– venous pressure falls 
– cardiac output falls (Starling’s Law) 
– arterial pressure falls 
– detected by baroreceptors
• Compensatory response
– increased sympathetic stimulation 
– tachycardia 
– increased force of contraction 
– peripheral vasoconstriction 
– venoconstriction
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14
Q

Descrie how hypovolaemic shock occurs

A

• Normally at the capillaries you get a small movement of fluid out to the tissues
• 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
See slide

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15
Q

Describe the presentation of hypovolaemic shock

A
• Patient has:
– Tachycardia 
– Weak pulse 
– Pale skin 
– Cold, clammy extremities
• NOTE 
• Hypovolaemic shock can also result from:
– Severe burns
– Severe diarrhoea or vomiting and loss of Na+
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16
Q

Describe the danger of decompensation

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
17
Q

What are the responses to hypovolaemic

A

• Longer term responses to restore blood volume • Renin-angiotensin-aldosterone system • Anti-diuretic hormone
• 20% blood volume loss
– Restoration of body fluid volumes in about 3 days
• If salt and water intake are adequate

18
Q

What is distrubutive shock

A

• Low resistance shock (normovolaemic) • Profound peripheral vasodilation - lowers TPR
– blood volume constant, but volume of the circulation has
increased
• Toxic shock • Anaphylactic shock

19
Q

What is toxic (septic) shock

A

• 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
– Impaired perfusion of vital organs
– also - capillaries become leaky
• reduced blood volume
– Increased coagulation and localised hypo-perfusion

20
Q

Describe the response, treatment, and presentation o septic shock

A

• Persisting hypotension requiring treatment to maintain
blood pressure despite fluid resuscitation (see Infection Unit)
• Decreased arterial pressure
– Detected by baroreceptors – increased sympathetic output – Vasoconstrictor effect overridden by mediators of
vasodilation – Heart rate and stroke volume increased
• Patient has
– Tachycardia
– Warm, red extremities initially BUT
• Later stages of sepsis – vasoconstriction – localised
hypo-perfusion

21
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 - increased CO, but can’t
overcome vasodilation
– impaired perfusion of vital organs
– mediators also cause bronchoconstriction and laryngeal
oedema
• difficulty breathing

22
Q

Describe the presentation of anaphylactic shock

A
• Patient will have
– Difficulty breathing – Collapsed – Rapid heart rate – Red, warm extremities
• Acutely life threatening • Adrenaline
– Vasoconstriction via action at α
adrenoceptors
23
Q

Give an overview of shock

A

See slide