CVD

Question 1

Risk Factors for stroke

Answer 1

• Hypertension
• Atherosclerosis
• Age
• Diabetes

Question 2

What is a stroke

Answer 2

• Rapid onset of focal disturbance in cerebral function of vascular origin of >24h duration (or leading to death)

Question 3

Types of Stroke

Answer 3

1. Ischaemic: caused by thrombosis or embolus

2. Haemorrhagic: bleeding caused by a ruptured artery

Question 4

Penumbra

Answer 4

‘shadow’

• Core of dead tissue (infarct) is surrounded by minimally perfused cells called the penumbra
• Potentially salvageable tissue that cannot function, but not dead
• Can be rescued with timely reperfusion
• If no evidence of penumbra then thrombolysis may do more damage than good = reperfusion injury

Question 5

Reperfusion Injury

Answer 5

• Worsening of injury upon restoration of blood flow
• Ischaemia injures the endothelial cells within the cerebral capillaries and arterioles causing:
• Inflammation -> release of inflam mediators and recruitment of wbc’s -> cellular damage
• Generation of free radicals -> oxidative stress -> activation of destructive enzymes -> cell injury

Question 6

Ischaemic Stroke Complications

Answer 6

• Haemorrhagic transformation of infarct (bleeding into an infarct) - redelivery of blood to ischaemic tissue -> vessels damaged/leaky from ischamia -> blood moves into brain parenchyma
• Cerebral oedema and elevated ICP

Question 7

Cerebral Oedema and Elevated ICP

Answer 7

• Leading cause of death within one wk of stroke
• Predictor of poor outcome
• Mortality rate of malignant cerebral oedema is in excess 60-80%

Question 8

Ischaemic Stroke: Treatment

Answer 8

• Thrombolysis with tPA within 4.5hrs of symptom onset
• Surgical removal of clot (thrombectomy)
• Stenting of artery
• Management of complications (haemorrhage, cerebral oedema)

Question 9

Ischaemic Stroke: Prevention

Answer 9

• Prevent recurrent stroke: antiplatelet (asprin) or anticoagulant (warfarin)
• Manage risk factors: HT, poor diet, inactivity

Question 10

tPA Mechanism of Action

Answer 10

• Catalyses the breakdown of fibrin into small fragments -> lyses the clot
• Plasminogen activated -> plasmin formed -> acts on fibrin to break it down

Question 11

SAH: Clinical Features

Answer 11

• severe headache
• Nausea
• vomiting
• Photophobia
• loss of consciousness
• seizure

Question 12

Intracranial Contents

Answer 12

• Brain tissue = 70%
• CSF = 15%
• Blood 15%

Question 13

ICP

Answer 13

• Normally 5-15mmHg

Question 14

CPP

Answer 14

CPP = MABP - ICP

When ICP > MABP, CPP is 0 -> no cerebral blood flow, death ensues

Question 15

BBB

Answer 15

• Comprised of endothelial cells, glial cells, tight junctions, basement membrane

Question 16

Vasogenic Oedema

Answer 16

• Increased water surrounding the cells of the brain
• Increased BP or increased perm of BVs
• BBB is disrupted allowing plasma proteins enter the extracellular space ‘leaky BVs’
• Plasma proteins increase the osmotic concentration of the brain tissue, causing water to leave the circulation and enter the brain
• Increase in total brain vol
• Responds to treatment

Question 17

Cytotoxic Oedema

Answer 17

• Accum of intracellular fluid
• Na/K ATPase pump normally pumps Na out and K in
• Energy failure -> loss of ATP -> failure/reduced activity of the NA/K pump -> Na accum in cell
• Water enters -> uncontrolled cell swelling -> irreversible cell injury -> death
• No increase in total brain vol
• No treatment

Question 18

Monro-Kellie Doctrine

Answer 18

• Increase in any intracranial component (brain, CSF, blood) must be compensated by a decrease in another otherwsie ICP will increase
• If ICP rises, perfusion and oxygenation becomes difficult

Question 19

ICP Compensation

Answer 19

Spatial Compensation: try to decrease brain vol:
- Shunt off CSF
- Venous vasoconstriction
- Arterial vasoconstriction = BAD (-> brain not getting enough blood -> deprived of vital oxygen and nutrients)
Arterial Vasodilation: improve perfusion of brain tissue
- Occurs in attempt to increase perfusion of brain tissue
- BUT leads to intracranial hypertension -> increases ICP further

Question 20

Elevated ICP

Answer 20

• Compresses BVs -> ischaemia
• Reduces perfusion -> ischaemia
• Loss of function for brain tissue
• Displaces brain tissue = herniation
• Brain stem compression -> intermittent resp/HR -> death

Question 21

Herniation Types

Answer 21

1. Subfalcine/cingulate: most common
2. Uncal/transtentorial: compresses third cranial nerve -> effects input to eye on affected side -> fixed/dilated pupil
3. Tonsillar: life threatening

Question 22

Mannitol

Answer 22

• Osmotherapeutic agent
• Intact BBB is required for osmotic action
• Establishes an osmotic gradient between the plasma and brain paranchyma - draws water from the brain extracellular space into the vasculature thereby reducing the volume of the brain -> decreased ICP
• Decreases blood viscosity -> improves regional microvascular flow and oxygenation
• Peak effect within 30-40 mins; lasts 6hrs
• Rebound ICP may occur - when mannitol gains access to the brain tissue it pull water into the brain

Question 23

Symptoms/Clinical Presentation of Stroke

Answer 23

• Abrupt onset

- Loss of function based on part of the brain that is ischaemic/compressed by accumulation of blood