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Yr 2 - EMS > Ischaemia, Infarction and Shock > Flashcards

Ischaemia, Infarction and Shock Flashcards

1
Q

How do hypoxia and ischaemia differ?

A

Hypoxia: when the oxygen supply to the tissues is impaired but other metabolites (e.g. glucose) are still available Ischaemia: the interruption/disturbance of blood flow to cells and tissues which reduces O2 supply AND metabolites Ischaemia ALWAYS results in hypoxia but hypoxia can occur without ischaemia (e.g. anaemia)

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2
Q

In ischaemia, does glycolytic anaerobic respiration occur?

A

No - it fails due to lack of glucose

Build up of metabolites impairs anaerobic respiration further

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3
Q

Does ischaemia or hypoxia injure tissues faster/more severely?

A

Ischaemia - failure of glycolytic anaerobic respiration

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4
Q

What happens if ischaemia is prolonged?

A

Cell death

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5
Q

What is individual cell death in ischaemic injury called?

A

Necrosis

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6
Q

What is tissue necrosis caused by ischaemia called?

A

Infarction I.e. infarction is ischaemia (inadequate blood supply) leading to cell death (necrosis) Ischaemia = cause Infarction = effect

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7
Q

Mechanisms of ischaemic cell injury:

A
  1. ↓Oxidative phosphorylation
  2. Switch to anaerobic respiration
  3. Failure of Na pump
  4. Membrane damage
  5. Failure of Ca pump
  6. ↓Protein synthesis
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8
Q

What does decreased oxidative phosphorylation due to ischaemia result in?

A

Reduced ATP

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9
Q

What does a switch to anaerobic respiration due to ischaemia result in?

A
  • Increased lactate - Glycogen stores eventually depleted: even anaerobic eventually fails
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10
Q

What does a failure of the Na pump due to ischaemia result in?

A

Accumulation of Na

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11
Q

What does membrane damage due to ischaemia result in?

A
  • Leakage of intracellular proteins out of cell - Enzymic digestion of cell
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12
Q

What does failure of Ca pump due to ischaemia result in?

A

Influx of Ca

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13
Q

What does increased lactate indicate?

A

Non-specific marker of ischaemia –> lactate rises as damage increases

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14
Q

What are clinical markers of ischaemia?

A
  • Lactate - Creatine Kinase, Troponins - Transaminases, Alk phosphate
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15
Q

What does a rise in Creatine Kinase and Troponins indicate?

A

Ischaemic cardiac muscle damage

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16
Q

What does a rise in Transaminases and Alk phosphate indicate?

A

Ischaemic liver damage

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17
Q

What is the biggest cause of ischaemia?

A

Vascular occlusion seen in: - (Severe) atherosclerosis - Thrombosis - Embolism - Hyperviscosity (rare)

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18
Q

Other causes of ischaemia:

A
  • Vasospasm - Vascular damage - Extrinsic compression - Mechanical interruption - Hypoperfusion
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19
Q

What is a vasospasm?

A

The narrowing of the arteries caused by a persistent contraction of the blood vessels - reduces blood flow

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20
Q

Who might you see vasopasms present in?

A

In the setting of cocaine use: cocaine induces spasms of coronary arteries so there is reduction of blood supply to myocardial tissue

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21
Q

What are examples of vascular damage that may trigger ischaemia?

A
  • Vasculitis - Rupture; AAA
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22
Q

What can cause extrinsic compression that may trigger ischaemia?

A

Tumour

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23
Q

What can cause mechanical interruption that may trigger ischaemia?

A
  • Volvulus - Intussusception - Torsion
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24
Q

What are potential causes for hypoperfusion?

A
  • Cardiac failure
  • Cardiac malformation
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25
Q

What are the variables that the outcome in ischaemia depends on?

A
  1. The nature of blood supply
  2. The duration of ischaemia
  3. The rate of vascular occlusion
  4. Tissue vulnerability
  5. The blood oxygen content
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26
Q

How would an alternative blood supply affect the outcome of ischaemia?

A

An alternative blood supply means less damage –> tissues with a dual vascular supply are generally resistant to infarction of a single vessel

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27
Q

Example of dual vascular supply in lungs?

A

Pulmonary and bronchial arteries

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28
Q

Example of dual vascular supply in the liver?

A

Hepatic artery and portal vein

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29
Q

Example of dual vascular supply in the hand?

A

Radial and ulnar artery

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30
Q

Why are the kidney, spleen and testes more vulnerable to infarction?

A

Have end-arterial circulations (one artery supplies one region)

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31
Q

If ischaemia is limited/short duration, can the cell injury be reversed?

A

Yes - initial 30 mins tends to be reversible

Rapid restoration of blood flow is critical

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32
Q

What is the ‘golden hour’?

A

Period of time in which intervention for ischaemia is critical

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33
Q

Are slow developing vascular occlusions more or less likely to infarct tissues? Why?

A

Less likely - as allows time for development of alternative perfusion pathways (collateral supply)

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34
Q

How can infarction in the heart be avoided due to collateral supply?

A

◦ Small anastomoses normally connect the major branches of the coronary artery system and have minimal flow

◦ If a coronary arterial branch is slowly occluded flow can be directed through these channels.

◦ Infarction can be avoided even if the main arterial branch is totally occluded.

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35
Q

In the brain, if a neurone is deprived of its blood supply, how long does it take to undergo irreversible cell damage ?

A

3-4 minutes –> very vulnerable

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36
Q

In the heart, if a cardiac myocyte is deprived of its blood supply, how long does it take to undergo irreversible cell damage?

A

20-30 minutes

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37
Q

In the heart, if a cardiac fibroblast is deprived of its blood supply, how long does it take to undergo irreversible cell damage ?

A

Hours –> less vulnerable

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38
Q

What is the vulnerability of a cell determined by?

A

How metabolically active the cell is

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39
Q

How can the blood oxygen content affect the outcome of ischaemia?

A

Reduced O2 in the blood (e.g. anaemia) leaves you more vulnerable to infarction

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40
Q

What are the 2 types of necrosis seen in ischaemia?

A
  1. Coagulative necrosis
  2. Liquefactive/colliquative necrosis
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41
Q

Which type of necrosis is the most common?

A

Coagulative

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42
Q

What characterises coagulative necrosis?

A

A type of accidental cell death mainly caused by ischaemia

  • Leads to protein denaturation (includes enzymes), so they are unable to break down the cell structure
  • Basis of dead cells are preserved for at least a couple of days –> eosinophilic ‘ghost cells’
  • Tissue remains firm
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43
Q

What are the dead cells in coagulative necrosis referred to as?

A

Eosinophilic ‘ghost’ cells

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44
Q

What characterises liquefactive necrosis?

A
  • Mainly occurs in brain
  • Invovles enzyme digestion
    • ​Cells are completely digested and broken down
    • Tissue is essentially liquefied
      • This creates a cavity or a cyst within the brain (when it heals) not dense scar tissue
45
Q

What can the morphology of infarcts be divided into?

A

White vs red infarcts

46
Q

Where does white infarction occur?

A

Organs with a single blood supply e.g.

47
Q

Where does red infarction occur?

A
  • Organs with a dual blood supply
  • Venous infarction (obstruction to venous supply of organ)
48
Q

Why are most infacts wedge-shaped?

A

◦ Vascular supply is “up-steam” or “proximal” in the tissue.

◦ Deeper into the tissue the vascular branches expand into wedge shape

◦ If obstruction occurs at an upstream point, the entire down-stream area will be infarcted

49
Q

What would be the first indicator of ischaemia?

A

Biochemical alterations (e.g. lactate) –> as the changes begin to be seen macroscopically, then ischaemia is more severe

50
Q

Morphology of myocardial infarction

A

Helps during post mortems

51
Q

When is the myocardial infarction at risk of rupturing?

A

3-7 days: when yellow centre becomes soft

Yellow centre may rupture and perforate –> cardiac tamponade

52
Q

What is cardiac tamponade?

A

When fluid in the pericardium (the sac around the heart) builds up, resulting in compression of the heart.

53
Q

Diagram of 1-2 days of myocardial infarction

A

Can see dark mottling

54
Q

Diagram of 3-4 days of myocardial infarction

A

Yellowing of lesion with haemorrhagic edge

55
Q

Diagram of 2-8 weeks of myocardial infarction

A

White fibrous scar

56
Q

What is reperfusion injury?

A

The tissue damage caused when blood supply returns to tissue after a period of ischemia

57
Q

How does reperfusion injury occur?

A

◦ Generation of reactive oxygen species by sudden reperfusion of ischaemic tissues

◦ Cytokines recruitment of inflammatory cells during ischaemic process

◦ Activation of complement pathway

58
Q

What are reactive oxygen species?

A
  • Normally formed in cells as a byproduct of metabolic anaerobic respiration processes
  • Are free radicals –> can cause damage if build up
59
Q

How are cells normally protected against reactive oxygen species?

A

Healthy cells have defence mechanisms to stop reactive oxygen species causing any harm –> damaged cells don’t have these defence mechanisms

60
Q

What pathological effects can reactive oxygen species have on a cell?

A
  • DNA damage –> mutations
  • Lipid peroxidation –> membrane damage
  • Protein modificatinos –> breakdown, misfolding
61
Q

What % is reperfusion injury thought to make up of final infarct?

A

Up to 50%

62
Q

What is myocardial stunning?

A

The reversible reduction of function of heart contraction after reperfusion not accounted for by tissue damage or reduced blood flow i.e. heart muscle has been salvaged but is not functioning correctly

May be due to reperfusion injury

63
Q

Clinical Case Scenario:

Baby born with cardiac malformation. Poor gut perfusion. Extensive ischaemic coagulative necrosis (i.e. infarction) of bowel. Died 2 weeks later.

Post Mortem: Disseminated Pseudomonas aeruginosa infection. Bacterial invasion and destruction of vessels. Ischaemic coagulative necrosis (i.e. infarction) of lungs and trachea.

What are the causes of infarction?

A

2 causes:

  • Hypoperfusion –> due to cardiac malformation
  • Vascular damage –> due to infection
64
Q

What is ‘shock’?

A

A pathophysiological state of reduced systemic tissue perfusion (i.e. systemic hypoperfusion) due to cardiovascular collapse.

Impaired tissue perfusion leads to ischaemia … derangement of cellular biochemistry … end organ dysfunction … multi-organ failure … and eventually death.

The final common pathway for a number of conditions and is initially reversible, but rapidly becomes irreversible.

65
Q

What is shock in relation to mean arterial pressure (MAP)?

A

Reduced MAP

66
Q

What is the equation for MAP?

A

Cardiac output x total peripheral resistance

i.e. Anything that causes ↓ cardiac output, ↓ systemic vascular resistance, can lead to shock

67
Q

What is the equation for cardiac output?

A

Heart rate x stroke volume

68
Q

What are the 3 types of shock?

A
  1. Hypovolaemic
  2. Cardiogenic
  3. Distributive
69
Q

What is hypovolaemic shock?

A

State of intravascular fluid loss (blood, plasma) i.e. blood volume is reduced

70
Q

How does hypovolaemic shock affect cardiac output?

A
  • Decreased venous return to the heart (‘preload’)
  • Decreases stroke volume which decreases cardiac output
71
Q

How does the body try and compensate in hypovolaemic shock?

A
  1. Increased heart rate –> to increase cardiac output
  2. Constrict blood vessels via the sympathetic nervous system to try and increase the total peripheral vascular resistance

This overall aims to increase MAP

72
Q

How will a patient present in hypovolaemic shock?

A
  • Cool
  • Peripherally shut down (blood not being sent to extremeties)
  • Normal blood pressure (N.B. blood pressure and heart rate stay close to normal if you lose up to 30% of blood)
73
Q

What are the causes of hypovolaemic shock?

A
  1. Haemorrhage
  2. Non-haemorrhagic fluid loss
  • Diarrhoea / vomiting
  • Heatstroke
  • Burns
  • Third space losses
74
Q

What are third space losses?

A

Acute loss of fluid into internal body cavities

Third-space losses are common postoperatively and in intestinal obstruction, pancreatitis, or cirrhosis.

75
Q

What is cardiogenic shock?

A

Cardiac pump failure (a condition in which your heart suddenly can’t pump enough blood to meet your body’s needs). Causes MAP to drop.

76
Q

How does the body compensate in cardiogenic shock?

A

Increase total peripheral vascular resistance via sympathetic nervous system –> patient will be cool and peripherally ‘shut down’

77
Q

What are the 4 categories of cardiogenic shock?

A

◦Myopathic

◦Arrhythmia-related

◦Mechanical

◦Extra-cardiac

78
Q

What is myopathic cardiogenic shock?

A

Failure of the heart muscle itself

79
Q

What is arrhythmia-related cardiogenic shock?

A

Due to electrical abnormalities. Atrial and ventricular arrhythmias cause impaired ventricular contraction or filling –> ↓ cardiac output

80
Q

What is mechanical cardiogenic shock?

A

Defects relating to blood flow through the heart

81
Q

What is extra-cardiac cardiogenic shock?

A

Anything outside of the heart impairs cardiac filling or ejecting properly

E.g:

  • Massive pulmonary embolism, tension pneumothorax
  • Severe constrictive pericarditis, pericardial tamponade etc.
82
Q

What is distributive shock?

A

Systemic vasodilation leads to decreased blood flow to the brain, heart, and kidneys causing damage to vital organs –> inadequate perfusion and decreased MAP

83
Q

How does the body compensate during distributive shock?

A
  • Increased cardiac output: increasing HR and SV
    • Patient would present flushed with a bounding heart
    • Warm (especially with septic shock)
84
Q

What are the subtypes of distributive shock?

A
  1. Septic shock
  2. Anaphylactic shock
  3. Neurogenic shock
  4. Toxic shock syndrome
85
Q

What is mixed shock?

A

Different types of shock co-existing in a patient

86
Q

Mixed shock example: in patients with septic shock

A
  • Primary distributive component
    • Inflammatory and anti-inflammatory cascades ↑ vascular permeability / vasodilation –> this drops peripheral vascular resistance
  • May show a hypovolemic component
    • Decreased oral intake
    • Insensible losses
    • Vomiting etc
  • May also show a cardiogenic component
    • Sepsis-related myocardial dysfunction
87
Q

Clinical Case Scenario:

4m old Down Syndrome. Sudden collapse. At autopsy: haemopericardium, ruptured cardiac diverticulum.

What type of shock is involved?

A
  • Cardiogenic
    • ​Blood within pericardial cavity affected amount of preload in the heart which reduced SV
    • Heart itself unable to pump effectively due to blood

This is extra-cardiac cardiogenic shock

  • Component of hypovolaemic shock
    • Babies don’t have a lot of blood to start with - likely to have reduced blood volume as well
88
Q

What are transaminases?

A

Enzymes that catalyze a transamination reaction between an amino acid and an α-keto acid. They are important in the synthesis of amino acids, which form proteins.

89
Q

How can liver damage lead to elevated transaminases?

A

The liver has transaminases to synthesize and break down amino acids and to convert energy storage molecules. If the liver is damaged, the hepatocyte membrane becomes more permeable and some of the enzymes leak out into the blood circulation.

90
Q

What is ALP? Where in the body is the main source of ALP?

A

ALP is an enzyme found in your bloodstream that helps break down proteins in the body. Main source: liver

91
Q

What is the purpose of peripheral vascular resistance?

A

The resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function.

92
Q

What type of shock is an MI?

A

Cardiogenic - myopathic

93
Q

What type of shock is caused by cardiomyopathies?

A

Cardiogenic - myopathic

94
Q

What type of shock is caused by ‘stunned’ myocardium?

A

Cardiogenic - myopathic

95
Q

What type of shock can be caused by valvular defects (e.g. prolapse)?

A

Cardiogenic - mechanical

96
Q

What type of shock can be caused by ventricular septal defects?

A

Cardiogenic - mechanical

97
Q

What type of shock can be caused by atrial myxomas?

A

Cardiogenic - mechanical

98
Q

What is an atrial myxoma?

A

A noncancerous tumor that most often grows on the atrial septum

99
Q

What type of shock can be caused by a ruptured ventricular free wall aneurysm?

A

Cardiogenic - mechanical

100
Q

What type of shock can be caused by a massive pulmonary embolism?

A

Cardiogenic - extra-cardiac

101
Q

What type of shock can be caused by a tension pneumothorax?

A

Cardiogenic - extra-cardiac

102
Q

What type of shock can be caused by severe constrictive pericarditis?

A

Cardiogenic - extra-cardiac

103
Q

What type of shock cane be caused by pericardial tamponade?

A

Cardiogenic - extracardiac

104
Q

How can sepsis lead to distributive shock?

A

Distributive shock as a result of sepsis occurs due to a dysregulated immune response to infection that leads to systemic cytokine release and resultant vasodilation and fluid leak from capillarie

105
Q

How can anaphylaxis lead to distributive shock?

A

Decreased SVR is due primarily to massive histamine release from mast cells after activation by IgE, as well as increased synthesis and release of prostaglandins.

106
Q

How can neurogenic shock lead to distributive shock?

A

Injury to the spinal cord results in a sudden loss of sympathetic tone

107
Q

How can toxic shock syndrome lead to distributive shock?

A

This disease is caused by Staphylococcus aureus and group A streptococci exotoxins that stimulate systemic cytokine release with resulting vasodilation and capillary leak

108
Q

In what type of shock would you find a flushed patient with a bounding heart?

A

Distributive

Yr 2 - EMS (60 decks)

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