Haemodynamic abnormalities and shock Flashcards
1
Q
What is an oedema?
A
- accumulation of excess interstitial fluid
2
Q
What are the 5 mechanisms of oedema formation?
A
- increased vascular permeability
- increased vascular hydrostatic pressure
- decreased vascular oncotic pressure
- decreased lymohatic drainage
- neurogenic pulmonary oedema
3
Q
What is this showing?
A
- gross apearance of oedema
- clear to yellow coloured fluid
- small amount of protein (transudate)
- fluid may be forced into the body cavities/ open spaces
4
Q
What is pulmonary oedema?
A
- fluid in alveoli
5
Q
What is hydrothorax
A
- fluid in thorax
6
Q
What is hydropericardium?
A
- fluid in pericardium
7
Q
What is ascites (hydroperitoneum)?
A
- fluid in abdominal cavity
8
Q
What is Anasarca?
A
- generalised oedema
9
Q
What is this showing?
A
- severe pulmonary oedema
- quite a bit of protein (pink)
- air spaces in alveolar
10
Q
Describe the mechanism of increased vascular permeability
A
- associated with inflammation/ immunological stimuli
- release of mediators which cause endothelial cell contraction and widening of interendothelial spaces
- histamine, bradykini, substance P
- movement of fluid from the vascular lumen into the interstitium through these gaps causes oedema
- localised/ general
- E.g.
- viruses, bacteria
- immune mediated
- toxins
- neovascularisation
11
Q
Describe the mechanism of increased vascular hydrostatic pressure
A
- increased pressure in vessels
- due to increased blood vol in the microvasculature
- hyperaemia (increased blood flow in inflammation)
- forces fluid out of vessel (increased filtration through vessel wall) and reduced reabsorption leading to oedema
- localised/ generalised
- E.g.
- heart failure
- portal hypertension
- pulmonary hypertension
- localised venus obstruction
- fluid overload
- hyperaemia
12
Q
Describe the mechanism of decreased vascular oncotic pressure
A
- low levels of plasma proteins (albumin)
- results in reduced reabsorption of interstitial fluid back into the vessel by osmosis
- typically generalised oedema
- hypoalbuminaemia can be caused by decreased production of albumin or increased loss of albumin from plasma
- decreased production of albumin
- malnutrition: inadequate protein in diet/ failure to absorb
- sever liver disease: inadequate albumin production
- increased loss of albumin (GI disease)
- water intoxication (haemodilution)
13
Q
Describe the mechanism of decreased lymphatic drainage
A
- lymphatic vessels: contribute to balance of interstitial fluid by draining the slight excess of fluid which has not been reabsorbed by blood vessels
- reduced ability of lymphatic vessels to drain excess interstitial fluid results in oedema
- Causes:
- lymphatic compression or obstruction e.g. neoplasia, inflam
- lymphangitis
- congenital lymohatic aplasia/ hypoplasia
- intestinal lymohangiectasia
14
Q
Describe the mechanism of neurogenic pulmonary oedema
A
- thought to be due to catecholamine release following CNS injuries resulting in increased intracranial pressure
- leads to pulmonary oedema
15
Q
What is Hyperaemia (erythema)?
A
- INCREASED blood flow
- active engorgment of vascular beds caused by increased inflow of blood with a normal or decreased outflow of blood
- increased metabolic activity
- heat dissipation
- inflam
- hyperaemic tissues appear bright red and warm
16
Q
What is congestion and what is the appearance of congested tissues?
A
- DECREASED blood flow
- Passive engorgement of vascular beds caused by decreased outflow of blood with normal or increased inflow of blood
- passive congestion can happen acutely or chronically
- appear enlarged, dark red, swollen (oedema) and cooler
17
Q
What does this show and why?
A
- ACUTE congestion
- occurs in liver and lungs in acute heart failure
- after euthanasia by barbiturate overdose
- tissue appears enlarged and dark red, oozing blood from cut surface
18
Q
When would localised chronic congestion occur?
A
- due to obstruction of venous outflow e.g. neoplasia, inflam
19
Q
When would generalised chronic congestion occur?
A
- due to reduced blood flow through the heart/ lungs
- most commonly heart failure or conditions which limit blood flow in lungs e.g. pulmonary fibrosis
- may be fibrosis caused by hypoxia and cell injury that accompanies congestion
20
Q
How does decreased tissue perfusion occur?
A
- decreased cardiac output results in decreased inflow of blood to tissues
- local congestion results in decreased outflow of blood from tissues
- obstruction to a vessel supplying/ draining a tissue results in decreased inflow or outflow of blood
21
Q
When does ischaemia occur?
A
- when the perfusion becomes inadequate to meet the metabolic needs of the tissue (reduced oxygen delivery and waste removal)
22
Q
Give examples of how ischaemia occurs
A
- arterial disease
- incomplete luminal blockage by an embolus or thrombus
- decreased flow of oxygenated blood into an area
- arteriolar vasoconstriction
- if prolonged and result in decreased flow of oxgenated blood into an area
- venous obstruction
- luminal blockage/ extravascular compression
- congestion- reduced oxygen
Heart and brain are most susceptible to ischaemia
23
Q
What is a reperfusion injury and how does it happen?
A
- if blood is returned after brief ischaemia - tissue returns to normal
- if blood is returned after prolonged- reperfusion injury
- reflow into tissue after prolonged =
- oedema
- haemorrhage
- release of TF - thrombus formaton
- ATP degradation to hypoxathine during ischaemia
- further reactive oxygen species are created by superoxide anions
24
Q
What is infarction?
A
- coagulative necrosis due to peracute ischaemia
- caused by same events that cause ischaemia
- secondary to thromosis
- complete arterial blockage = immediate infarction
- venous obstruction = extensive congestion and oedema preceding and promoting infarction
25
Q
What is happening at 1 and 2?
A
- 1 = normal arterial flow
- 2 = thrombus occluding artery
- black area - necrosis
26
Q
What is happening at 1 and 2 and M?
A
- M = mass compressing vein 1
- 2 = normal venous flow
27
Q
What tissues are most prone to infarction?
A
- tissues with a single blood supply
- e.g. brain, heart, kidney, spleen
- occlusion of nearly any sized vessel results in infarction of the dependent tissue
28
Q
How likely is infarction in tissue with parallel blood supply with anastomoses?
A
- less likely than single
- e.g. skeletal muscle, GIT
- occlusion less serious
29
Q
Which tissues are least prone to infarction?
A
- tissues with dual blood supply e.g. liver/ lung
- not susceptible unless concurrent underlying disease compromises whole blood supply
30
Q
What is this showing?
A
- acute renal infarction
- haemorrhage results in dark red discolouration
31
Q
What does this show?
A
- acute cellular swelling causes buldging of infarction
- acute renal infarction
32
Q
What does this show?
A
- acute venous infarction in volvulus of a portion of intestine
- can lead to endotoxic shock - bacteria travel through more permeable gut
33
Q
What is this showing?
A
- acute renal infarction
- central coagulation necrosis bordered by inflammatory cells (blue)
34
Q
What is shown here?
A
- chronic renal infarction
- replacement of necrotic tissue by fibrosis, with contraction- resulting in an indented appearance
35
Q
What is this showing?
A
- chronic myocardial infarction
- replacement of necrotic tissue by fibrosis disrupting myofibre bundles
36
Q
What is shock?
A
- cardiovascular shock
- circulatory dyshomeostasis
- loss of circulating blood vol, reduced CO and/ or inappropriate peripheral resistance
- results in hypotension, reduced tissue perfusion, cellular hypoxia, degeneration and death
37
Q
What are the 3 categories of shock?
A
- cardiogenic
- hypovolaemic
- maldistributive
- septic
- anaphylatic
- neurogenic
38
Q
Describe cardiogenic shock
A
- failure of heart to adequately pump blood e.g. inadequate CO
- caused by cardiac failure:
- myocardial infarction
- ventricular tachycardia
- fibrillation
- cardiomyopathies
- obstruction of outflow of blood from the heart
39
Q
Describe hypovolaemic shock and its causes
A
- reduced circulating blood vol leading to hypotension and hypoperfusion
- caused by:
- haemorrhage
- fluid loss
- vomiting
- diarrhoea
- burns
40
Q
What are the compensation mechanisms of hypovolaemic shock?
A
- peripheral vasoconstriction
- fluid movement into plasma
41
Q
What % of blood volume do you need to lose to cause a dramatic fall in pressure and CO?
A
- 35-45%
42
Q
What is maldistributive shock?
A
- decreased peripheral resistance
- pooling of blood in peripheral tissues
- hypotension and hypoperfusion
43
Q
What is anaphylatic shock?
A
- generalised type I hypersensitivity
- widespread mast cell degranulation leading to systemic vasodilation and increased vascular permeability
44
Q
What is neurogenic shock?
A
- CNS trauma, electrocution, emotional stress
- autonomic discharges leading to systemic vasodilation
45
Q
What is septic shock?
A
- components of microorganisms such as endotoxin
- activates endothelial cells, leukoctres, platelets releasing cytokines
- results in actvation of myriad vascular, proinflam and procoagulant pathways
- systemic vasodilation, hypotension and hypoperfusion
46
Q
How might shock progress?
A
- may be compensated for (non-progressive shock)
- may result in organ failure- due to prolonged hypotension and hypoperfusion
- may progress to disseminated intravascular coagulation (DIC)
