Ischaemia, infarction and shock Flashcards Preview

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Flashcards in Ischaemia, infarction and shock Deck (34):
1

What is hypoxia?

–Any state of reduced tissue oxygen availability

•Generalised - whole body e.g. altitude, anaemia

•Regional - specific tissues affected

2

What is ischaemia and why is it worse than hypoxia alone?

–Pathological reduction in blood flow to tissues

–Usually as a result of obstruction to arterial flow

  commonly as a result of thrombosis / embolism

–Ischaemia results in tissue hypoxia

 

Worse as there's no removal of waste products in addition to hypoxia.

3

What is PCI for MI?

Percutaneous intervention for myocardial infarction.  Only suitable for reversible ischaemia.

4

What is reperfusion injury?

Generation of ROS by inflammatory cells causes further cell damage.

5

What is infarction?

–Ischaemic necrosis caused by occlusion of the arterial supply or venous drainage 

6

What causes the majority of infarctions?

Thrombosis and emobolisms.  Most common within arteries.

7

What are the other causes of infarction?

Vasospasm, atheroma, extrinsic compression (eg tumour), twisiting of vessel roots, rupture of vascular supply (eg AAA)

8

Why do lung infarctions look red?

Dual blood supply.  One supply blocked, the vessels for the other are damaged and leak blood into the infarcted area.

9

What is the difference between coagulative necrosis and liquefactive necrosis?

In coagulative necrosis the tissue retains it's basic arcitecture,  Tissue arcitecture lost in liquefactive as there is no collagen (brain).

10

What factors influence the severity of the ischaemic damage?

1.Nature of the blood supply

2.Rate of occlusion

3.Tissue vulnerability to hypoxia

4.Blood oxygen content

11

How does the nature of the blood supply influence the severity of the ischaemic damage?

•An alternative blood supply will mean less damage hence severe ischaemia required for infarction

–Lungs (pulmonary and bronchial arteries)

–Liver (hepatic artery and portal vein)

–Hand (radial and ulnar artery)

•Kidneys, spleen, testis etc. have single supplies hence are vulnerable to infarction

12

How does the rate of occlusion effect the severity of ischaemic damage?

•Slow developing occlusions are less likely to infarct tissues

•Allows time for the development of alternative (collateral) perfusion pathways

•Coronary arteries

–Small anastomoses connect major branches 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

13

How does the tissue vulnerabilty to hypoxia influence the severity of ischaemic damage?

•The brain

–If a neurone is deprived of oxygen irreversible cell damage occurs in 3 to 4 minutes

–Brain is 1 to 2% of total body weight but requires 15% of cardiac output and 20% of body oxygen consumption

–Therefore very vulnerable to injury

•The heart

–Slightly more resistant with cardiac myocyte death taking 20 to 30 minutes

14

How does the blood oxygen content influence the severity of ischaemia?

•Reduced oxygen in the blood (anaemia etc.) increases the chances of infarction

•Congestive cardiac failure

–Poor cardiac output and impaired pulmonary ventilation

–May develop an infarct with a normally inconsequential narrowing of the vessels!

•Watershed regions occur at the point of anastomosis between two vascular supplies

–E.g. Splenic flexure and brain

15

What are the most common causes of an ischaemic stroke?

–Thrombosis secondary to atherosclerosis
–Embolism (e.g. mural thrombus)

16

What are the most common causes of a haemmorhagic stroke?

–Intracerebral haemorrhage (hypertensive)
–Ruptured aneurysm in the circle of Willis (subarachnoid)

17

What is the usual cause of ischaemic bowel disease?

•Usually caused by thrombosis or embolism in the superior or inferior mesenteric arteries
•Presents with abdominal pain

18

What are the different types of gangrene?

•Gangrene
–Infarction of entire portion of limb (or organ)
•Dry gangrene
–Ischaemic coagulative necrosis only
•Wet gangrene
–Superimposed infection
•Gas gangrene
–Superimposed infection with gas producing organism                     

e.g. clostridium perfringens

19

What is the definition of shock?

•A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased oxygen delivery to the tissues.

•Shock results in a critical imbalance between oxygen delivery and oxygen consumption.

•Impaired tissue perfusion and ultimately prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at first cellular and eventually systemic levels.  Initially reversible but rapdly becomes irreversible.

20

What is hypovolaemic shock?

•Intra-vascular fluid loss (blood, plasma etc)

•↓ venous return to heart AKA “pre-load”

•↓ stroke volume à ↓ cardiac output

•How could you compensate for this? - increase systemic vascular resistence by increasing HR and arterial muscle tone (sympathetic - clammy, olgouria).

 

Patient will be very pale, cool, tachy, clammy and have long cap refill

21

What is third spacing?

Where you loose your blood volume into internal body cavities (eg bowel)

22

What are the causes of hypovolaemic shock?

•Haemorrhage

–Trauma, gastrointestinal bleeding, ruptured haematoma,

–Haemorrhagic pancreatitis, fractures

–Ruptured aortic, abdominal, or left ventricular free wall aneurysm

 

•Non-haemorrhagic fluid loss

–Diarrhoea, vomiting, heat stroke, burns, third spacing

23

What is cardiogenic shock?

•Cardiac pump failure

•↓ CO

•How could you compensate for this?

•↑ SVR

24

What are the causes/categories of cardiogenic shock?

–Myopathic (heart muscle failure)

–Arrythmia-related (abnormal electrical activity)

–Mechanical

–Extra-cardiac (obstruction to blood outflow)

25

What are the causes of myopathic shock?

•Any causes of myopathic cardiogenic shock??

–Myocardial infarction (> 40% left ventricular myocardium)

–Right ventricular infarction, dilated cardiomyopathies

–“Stunned myocardium” following prolonged ischemia or cardiopulmonary bypass.

26

What are the causes of arrthymia-related shock?

•Arrhythmia-related cardiogenic shock

–Atrial and ventricular arrhythmias

–Atrial fibrillation / flutter à ↓CO by impairment of co-ordinated atrial filling of the ventricles.

–Ventricular tachycardia, bradyarrhythmias, and complete heart block ↓ CO, while ventricular fibrillation abolishes CO.

27

What are the causes of mechanical cardiogenic shock?

•Mechanical cardiogenic shock

–Valvular defects (e.g. prolapse), ventricular septal defects

–Atrial myxomas, ruptured ventricular free wall aneurysm.

28

What are the causes of extra-cardiac cardiogenic shock?

–Anything that impairs cardiac filling or ejection of blood from heart

–Massive pulmonary embolism, tension pneumothorax, Severe constrictive pericarditis, pericardial tamponade

29

What is distributive shock and what are the different types?

•↓ SVR due to severe vasodilation

•How could you compensate for this?

•↑ CO Flushed / bounding heart

 

•SEPTIC SHOCK

•ANAPHYLACTIC SHOCK

•NEUROGENIC SHOCK

•TOXIC SHOCK SYNDROME

30

What are the features of septic shock?

•Severe, over-whelming systemic infections with...

–Gram+ve, gram-ve bacteria or fungi

•Immunocompromised, elderly, very young etc.

•↑ Cytokines / mediators

–VASODILATION

•Pro-coagulation (DIC)

–Ischaemia

31

What are the features of anaphylactic shock?

•Severe type I hypersensitivity reaction

–Sensitized individuals

•Hospital e.g. drugs (penicillin etc)

•Community e.g. peanuts, shellfish, or insect toxins

–Small doses of allergen à IgE cross-linking

–Massive mast cell degranulation à

–Vasodilation

–Contraction of bronchioles / respiratory distress

–Laryngeal oedema

–Circulatory collapse à shock / death

32

What are the features of neurogenic shock?

•Spinal injury / anesthetic accidents
•Loss of sympathetic vascular tone
•Vasodilation -> shock

33

What are the features of toxic shock syndrome?

•NOT the same as septic shock!!!!

•S. aureus / S. pyogenes produce exotoxins “superantigens”

•Do not require processing by antigen-presenting cells

•Non-specific binding of class II MHC to T cell receptors

•Up to 20% of T cells can be activated at one time!!!!!

•Widespread release of massive amounts of cytokines ↓SVR

34

How might different types of shock combine?

–Primary distributive component

•Inflammatory and anti-inflammatory cascades ↑ vascular permeability / vasodilation

–Hypovolemic component

•Decreased oral intake

•Insensible losses

•Vomiting, diahorrhea

–Cardiogenic component

•Sepsis-related myocardial dysfunction