CVD Flashcards
Risk Factors for stroke
- Hypertension
- Atherosclerosis
- Age
- Diabetes
What is a stroke
- Rapid onset of focal disturbance in cerebral function of vascular origin of >24h duration (or leading to death)
Types of Stroke
- Ischaemic: caused by thrombosis or embolus
2. Haemorrhagic: bleeding caused by a ruptured artery
Penumbra
‘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
Reperfusion Injury
- 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
Ischaemic Stroke Complications
- 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
Cerebral Oedema and Elevated ICP
- Leading cause of death within one wk of stroke
- Predictor of poor outcome
- Mortality rate of malignant cerebral oedema is in excess 60-80%
Ischaemic Stroke: Treatment
- Thrombolysis with tPA within 4.5hrs of symptom onset
- Surgical removal of clot (thrombectomy)
- Stenting of artery
- Management of complications (haemorrhage, cerebral oedema)
Ischaemic Stroke: Prevention
- Prevent recurrent stroke: antiplatelet (asprin) or anticoagulant (warfarin)
- Manage risk factors: HT, poor diet, inactivity
tPA Mechanism of Action
- Catalyses the breakdown of fibrin into small fragments -> lyses the clot
- Plasminogen activated -> plasmin formed -> acts on fibrin to break it down
SAH: Clinical Features
- severe headache
- Nausea
- vomiting
- Photophobia
- loss of consciousness
- seizure
Intracranial Contents
- Brain tissue = 70%
- CSF = 15%
- Blood 15%
ICP
- Normally 5-15mmHg
CPP
CPP = MABP - ICP
When ICP > MABP, CPP is 0 -> no cerebral blood flow, death ensues
BBB
- Comprised of endothelial cells, glial cells, tight junctions, basement membrane
Vasogenic Oedema
- 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
Cytotoxic Oedema
- 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
Monro-Kellie Doctrine
- 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
ICP Compensation
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
Elevated ICP
- Compresses BVs -> ischaemia
- Reduces perfusion -> ischaemia
- Loss of function for brain tissue
- Displaces brain tissue = herniation
- Brain stem compression -> intermittent resp/HR -> death
Herniation Types
- Subfalcine/cingulate: most common
- Uncal/transtentorial: compresses third cranial nerve -> effects input to eye on affected side -> fixed/dilated pupil
- Tonsillar: life threatening
Mannitol
- 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
Symptoms/Clinical Presentation of Stroke
- Abrupt onset
- Loss of function based on part of the brain that is ischaemic/compressed by accumulation of blood
