Ischaemia, Infarction & Shock (14) Flashcards Preview

EMS - Mechanisms of Disease > Ischaemia, Infarction & Shock (14) > Flashcards

Flashcards in Ischaemia, Infarction & Shock (14) Deck (58):
1

Hypoxia

Any state of reduced tissue oxygen availability (generalised - whole body/regional - specific tissues)

2

Ischaemia

Pathological reduction in blood flow to tissues, result of obstruction usually due to thrombosis/embolism > tissue hypoxia

3

If ischaemic for short duration

Cell injury reversible

4

If prolonged/sustained ischamia

Irreversible cel damage/cell death occurs by necrosis/infarction

5

Therapeutic reperfusion

Good if reversible

6

Examples of therapeutic reperfusion

PCI for MI or thrombolysis for stroke

7

Reperfusion injury

Generation of reactive oxygen species by inflammatory cells causes further cell damage

8

Infarction

Ischaemic necrosis caused by occlusion of arterial supply/venous daring

9

Infarct

Area of infarction in tissues

10

Causes of infarction

Thrombosis, embolism, vasopasms (narrow), atheroma expansion, extrinsic compression (tumour), twisting of vessel roots (volvulus), rupture of vascular supply (AAA), venous occlusion

11

Red infarction

Haemorrhagic, dual blood supply/venous infarction (blood supply damaged so leaks)

12

White infarction

Anaemic, single blood supply hence totally cut off

13

What shape are most infarcts?

Wedge-shaped, obstruction usually occurs upstream, entire down-stream will be infarcted

14

Histological characteristic of infarction

Usually coagulative necrosis (in brain - colliquative)

15

Effects of vascular occlusion vary on..

1. Nature of blood supply
2. Rate of occlusion
3. Tissue vulnerability to hypoxia
4. Blood oxygen content

16

Nature of blood supply

Lung (pulmonary and bronchial arteries), liver (hepatic artery, portal vein), hand (radial and ulnar artery), severe ischameia for infarction

17

Which organs are more vulnerable to infarction due to the nature of their blood supply?

Kidneys, spleen, testis (single supplies)

18

Heart hypoxia

Cardiac myocyte death takes 20-30mins

19

Brain hypoxia

Neurone deprived of oxygen irreversible cell damage occurs 3-4 mins, brain is 1-2% of total body weight but requires 20% body oxygen consumption and 15% cardiac output

20

Clinical manifestations

Heart - IHD/stable angina/MI

Brain - cerebrovascular disease (TIA/CVA)

Intestines - ischaemic bowel

Extremities - peripheral vascular disease/gangrene

21

Cerebrovascular disease

Any abnormality of the brain caused by pathological process involving blood vessels

22

Causes of ischaemic stroke

Thrombosis secondary to atherosclerosis, embolism

23

Causes of haemorrhagic stroke

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

24

Causes of ischaemic bowel disease

Thrombosis/embolism in superior/inferior mesenteric arteries

25

What does IBD present with?

Abdominal pain

26

Gangrene

Infarction of entire portion of limb/organ

27

Dry gangrene

Ischaemic coagulative necrosis only

28

Wet gangrene

Superimposed infection

29

Gas gangrene

Superimposed infection with gas producing organism e.g. clostridium perfringens

30

What is shock?

Physiological state, significant reduction of systemic tissue perfusion (severe hypotension) > decreased oxygen delivery to tissues

31

Shock results in a critical imbalance between

Oxygen delivery and oxygen consumption

32

Cellular effects of shock

Membrane ion pump dysfunction, intracellular swelling, leakage of intracellular contents into extracellular space, inadequate regulation of intracellular pH, anaerobic respiration > lactic acid

33

Systemic effects of shock

Alteration in the serum pH (academia), endothelial dysfunction > vascular leakage, stimulation of inflammatory and anti-inflammatory cascades, end-organ damage (ischaemia)

34

Results of prolonged shock

Cell death, end-organ damage, multi-organ failure, death

35

Hypovolaemic shock

Intra-vascular fluid loss (blood, plasma etc)

36

Mechanism of hypovolaemic shock

Decrease venous return to heart (pre-load), decrease stroke volume > decrease cardiac output, decrease mean arterial blood pressure. Need vasoconstriction increase SVR

37

Haemorrhagic causes of hypovolaemic shock

Trauma, GI bleed, ruptured haematoma, haemorrhagic pancreatitis, fractures, ruptured aortic, abdominal/left ventricular free wall aneurysm

38

Non-haemorrhagic causes of hypovolaemic shock

Diarrhoea, vomiting, heat stroke, burns, third spacing

39

Third spacing

Acute loss of fluid into internal body cavities, common postoperatively and in intestinal obstruction, pancreatitis/cirrhosis (draws in fluid)

40

Cardiogenic shock

Cardiac pump failure, decreased CO and arterial pressure

41

Causes of cardiogenic shock

1. Myopathic (muscle failure)
2. Arrhythmia-Related
3. Mechanical
4. Extra-cardiac (obstruction to blood outflow)

42

Myopathic shock causes

MI (>40% LV myocardium), RV infarction/dilated cardiomyopathies, 'stunned myocardium' - following prolonged ischaemic/cardiopulmonary bypass

43

Arrhythmia-related cardiogenic shock causes

Atrial and ventricular arrhythmias

44

Atrial fibrillation and shock

Flutter > decrease CO by impairment of co-ordinated atrial filling of ventricles

45

Ventricular tachycardia, bradyarrhythmias and complete heart block and shock

While ventricular fibrillation, abolishes CO

46

Mechanical cardiogenic shock

Valvular defects (prolapse), ventricular septal defects, atrial myxomas (non-cancerous tumour - often grows on atrial septum), rupture ventricular free wall aneurysm

47

Extra-cardiogenic shock causes

P.E, tension pneumothorax, severe constrictive pericarditis, pericardial tamponade (impairs cardiac filling/ejection of blood from heart)

48

Pericardial tamponade

Blood filling pericardial sac usually aids dilation

49

Distributive shock sub-types

Septic, anaphylactic, neurogenic shock, toxic shock syndrome

50

Distributive shock

Decrease SVR due to severe vasodilation, compensate by increasing CO > flushed/bounding heart

51

Septic shock

Severe systemic infections - gram +ve/-ve bacteria/fungi

52

Who gets septic shock?

Immunocompromised, elderly, very young

53

What happens in septic shock

Increase in cytokines/mediators > vasodilation > pro coagulation (DIC) > ischaemia > wide spread clotting and thrombosis > use of all clotting factors > haemorrhage > death

54

Anaphylactic shock

Severe type 1 hypersensitivity reaction, small doses of allergy > IgE cross-linking, mast cell degranulation > vasodilation > respiratory distress/laryngeal oedema/circulatory collapse

55

Who gets anaphylactic shock?

Sensitised individuals

56

Neurogenic shock

Spinal injury/anaesthetic accidents, loss of sympathetic vascular tone, vasodilation > shock

57

Toxic shock syndrome

NOT SAME AS SEPTIC SHOCK, S.aureus/S.pyogenes produce exotoxins 'superantigens' non-specific binding of class 2 MHC to T cell receptors (up to 20% of T cells activated at once), widespread release of cytokines, decrease SVR

58

Treatment of shock

O2, fluid, antibiotics