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EMS MOD > ischaemia, infarction and shock > Flashcards

ischaemia, infarction and shock Flashcards

1
Q

what is hypoxia?

A

when the oxygen saturation of the tissue falls

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2
Q

what is ischaemia?

A

the disturbance or interruption of blood flow to the tissues or cells

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3
Q

what is the difference between ischaemia and hypoxia?

A

ischaemia always results in hypoxia but hypoxia can occur without ischaemia
hypoxia is lack of oxygen only
ischaemia is oxygen and metabolites - glycolytic anaerobic respiration fails, build up of metabolites impairs anaerobic respiration further
ischaemic injury is faster and more severe

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4
Q

what are the causes of ischaemia?

A

vascular occlusion - embolus, thrombus or severe atherosclerosis - arterial or venous

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5
Q

what are rarer causes of ischaemia?

A

cardiac failure, twisting of vessel roots, rupture of vascular supply, vasculitis, vasospasm and extrinsic compression

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6
Q

when is cell injury reversible?

A

when damage is limited or of short duration through the therapeutic rapid restoration of blood flow

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7
Q

when does cell death occur?

A

when there is prolonged ischaemia meaning there is irreversible cell damage

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8
Q

what is an example of rapid restoration where the cells can be salvaged?

A

primary percutaneous coronary intervention for myocardial ischaemia / infarction

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9
Q

why does cell death occur?

A

there is prolonged or sustained injury resulting in irreversible cell damage

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10
Q

what type of cell death is ischaemic injury?

A

necrosis

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11
Q

what is tissue necrosis called when it is caused by ischaemia?

A

infarction

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12
Q

what is ischaemia?

A

localised tissue hypoxia that is due to decreased blood flow to an organ or tissue

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13
Q

what is infarction?

A

tissue necrosis as a result of ischaemia

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14
Q

vascular occlusion effects are variable and depend on four factors. what are these?

A

the nature of blood supply
the rate of occlusion
the tissue vulnerability to hypoxia
the blood oxygen content

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15
Q

what is the most important factor in determining whether vascular occlusion causes damage and why?

A

the nature of the blood supply and alternative supplies - if there are alternative supplies then severe ischaemia will be needed for infarction - tissues with a dual blood supply are generally resistant to infarction of a single vessel

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16
Q

what are examples of organs with a dual blood supply?

A

hands - ulnar and radial
lungs - pulmonary and bronchial
liver - hepatic artery and portal vein

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17
Q

what organs are susceptible to arterial infarction?

A

spleen the kidneys and the testis - the have an end arterial circulation and therefore artery only blood supply

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18
Q

what organs are susceptible to venous infarction?

A

the ovaries and testis, as they have only a single venous outflow

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19
Q

why is a slower rate of occlusion less likely to cause infarction?

A

there is time for an alternative blood supply to develop - collateral supply

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20
Q

why is the heart adapted to slower occlusion?

A

small anastamoses connect the major branches in the coronary artery system and they usually have minimal flow. With slow occlusions there is time to direct flow through these branches so infarction can be avoided.

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21
Q

how long until there is irreversible cell damage in a neurone?

A

3-4 minutes

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22
Q

which is more resistant to hypoxia, the brain or the heart?

A

brain - 3/4 minutes
heart - cardiac myocytes can survive for around 20-30 minutes
cardiac fibroblasts for hours as they are not as metabolically active as muscle cells
therefore the heart is more resistant

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23
Q

what does lower oxygen saturations of the blood result in?

A

more vulnerable to infarction and congestive heart failure

24
Q

what is the result in congestive heart failure?

A

poor pulmonary ventilation and cardiac output

infarct in normally inconsequential narrowing of the vessels due to impaired oxygenation of the tissues

25
Q

what will a morpholgy describe?

A

location, colour, shape, type of necrosis and histological changes

26
Q

what are watershed regions and give three examples?

A

they are the point of anastamoses between two vascular supplies - the myocardium, the brain and the splenic flexure of the colon

27
Q

what are the two types of infarction?

A

red (haemorrhage) and white (anaemic)

28
Q

what is a red infarction?

A

where there is a dual blood supply or venous infarction

29
Q

what is a white infarction?

A

it is a single blood supply and therefore totally cut off

30
Q

what happens if the obstruction is at an upstream point of the vessel?

A

the tissue deeper will infarct as the branches go deeper downstream

31
Q

what is a typical shape of an infarct?

A

wedge shaped with the vessel upstream or proximal

32
Q

what type of necrosis is seen in infarction?

A

coagulative or colliquative in brain

33
Q

over the duration of injury, when are changes visible?

A

to start with there are only biochemical alternations and cell death, as time goes on first you can see ultrastructural changes, then light microscopic changes and the gross morphological changes

34
Q

for gross features, what will you see over time?

A 
nothing for first four hours 
4-12 hours: occasional dark mottling 
12-24: dark mottling 
1-3 days: yellow with haemorrhagic edges 
3-7: yellow core goes soft 
1-2 weeks: red grey colour 
2-8:fibrous scar
35
Q

for microscopic features what will you see over time?

A

for first four hours nothing
4-12: oedema, haemorrhage and start of coagulative necrosis
12-24: ongoing coagulative necrosis
1-3: oedema with neutrophil infiltration
3-7: neutrophil dying and macrophage infiltration
1-2: granulation tissue formation
2-8: colagen deposition increase and fibrous scar formation

36
Q

what is IRPI?

A

ischaemic reperfusion injury - reperfusion of ischaemia leads to generation of reactive oxygen species due to the sudden reperfusion of dysfunctional tissues. These species are produced by inflammatory cells that cause further cell damage

37
Q

how is reperfusion injury related to myocardium?

A

following coronary occlusion the contractile ability is lost after 2 minutes and viability after 20. The sooner perfusion is received the better salvaged the tissues are. However some damage may incur from perfusion - the function may not return for days.

38
Q

what is shock?

A

it is a pathophysiological state of reduced systemic tissue perfusion resulting in a lack of oxygen delivery to tissues. It causes a critical imbalance between the oxygen delivery and requirements of the tissues.

39
Q

what is the result of prolonged shock?

A

impaired tissue perfusion and prolonged oxygen deprivation will lead to cellular hypoxia and derranged cellular biochemistry - end organ dysfunction eventually - rapidly irreversible

40
Q

how can shock result in death?

A

the result is sequential. Cell death due to hypoxia, end organ dysfunction, multi-organ failure and then death

41
Q

what is the same as total peripheral resistance?

A

SVR - systemic vascular resistance

42
Q

what is the equation for mean arterial pressure?

A

MAP = CO x SVR

43
Q

what are the basic causes of shock?

A

anything that makes cardiac output or systemic vascular resistance decrease

44
Q

what are the three types of shock?

A

distributive, cardiogenic and hypovolaemic

45
Q

what is hypovolaemic shock?

A

when there is intra-vascular fluid loss. This results in a decreased venous return to the heart (pre-load), decreased SV and CO, and therefore to compensate the SVR increases by vasoconstriction. This results in a cool and clammy presentation and HR increase.

46
Q

what are the causes of hypovolaemic shock?

A

haemorrhagic or non-haemorrhagic fluid loss

47
Q

what is third spacing?

A

it is a type of non-haemorrhagic fluid loss - it is the acute loss of fluid into body cavities and this is common post operatively and in pancreatitis, cirrhosis and intestinal obstruction

48
Q

what is cardiogenic shock?

A

it is when there is cardiac pump failure - the drop in BP causes SVR to increase through vasoconstriction to compensate and get blood to extremities

49
Q

what are the four categories of causes for cardiogenic shock?

A

arrythmia-related, mechanical, extra-cardiac or myopathic

50
Q

when would you get ‘stunned myocardium’?

A

following a cardiopulmonary bypass

51
Q

what does myopathic mean?

A

heart muscle failure

52
Q

what does arrythmia related mean?

A

abnormal electrical activity - muscle is ok but not beating correctly, atrial or ventricular - impaired ventricular contraction or filling resulting in reduced cardiac output

53
Q

what is mechanical?

A

it is when there is acquired or developmental defects in the blood flow through the heart, it can be valvular or VSD, atrial myxomas or ruptured vetricular free wall aneurysm

54
Q

what is extra-cardiac?

A

obstruction to blood flow - anything outside heart that disrupts filling or ejection of blood. It can be constrictive pericarditis, pericardial tamponade, PE or tension pneumothorax

55
Q

what is disruptive infarction?

A

when there is a reduces SVR due to severe vasodilation -presents with increased CO - bounding heart and flushed, and warm - particularly with septic shock

56
Q

what are the four subtypes of disruptive?

A

neurogenic (loss of sympathetic tone)
anaphylatic - mass cells
sever vasodilation septic shock - cytokines
toxic shock syndrome - cytokines

57
Q

shock subtypes can coexist, how would a patient with septic shock present in a) primary distributive component, b) hypovolaemic component and c) cardiogenic component?

A

PDC - inflammatory and anti-inflammatory cascade - increased vascular permeability and vasodilation

HV - decreased oral intake, vomiting and diarrhoea, insensitive losses

CG - sepsis related myocardial dysfunction

EMS MOD (28 decks)

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