Introduction to Stroke and the Stroke Care Unit
-For ischemic stroke, the principal modifiable risk factors include:
Atrial fibrillatio.
Carotid artery stenosis in the neck.
For hemorrhagic stroke, the principal modifiable risk factors include:
Use of anticoagulants (medications that inhibit blood clotting).
Bulging of a cerebral artery (cerebral aneurysm).
Abnormal connections between arteries and veins (arteriovenous malformations).
Hormones: Oral contraceptives or hormone therapies containing estrogen may increase the risk of stroke.
The incidence of stroke has declined in recent decades as public awareness of the importance of controlling hypertension and high cholesterol has increased and smoking-cessation rates have improved. Controlling these factors reduces the risk of atherosclerosis.
Non-modifiable risk factors include:
A previous stroke.
A family history of stroke (genetic factors).
Age: People aged 55 years and older have a higher risk of stroke than younger people.
Sex: Men are more likely to experience stroke than women. However, women are generally older when stroke occurs and are more likely than men to die from stroke.
Pathophysiology of Ischemic Stroke
Stroke results from loss of blood flow to part of the brain and initiates the ischemic cascade. Brain tissue ceases to function when deprived of oxygen for more than 60 to 90 seconds. After approximately three hours, tissue death and infarction may occur, causing permanent functional injury. This is why thrombolytic medications such as alteplase must be administered within the early treatment window after symptom onset. Atherosclerosis may compromise blood supply by narrowing the vascular lumen, reducing blood flow, and promoting intravascular thrombus formation.
An embolic infarction occurs when an embolus forms elsewhere in the circulation—commonly in the heart as a result of atrial fibrillation or in the carotid arteries—and then enters the cerebral circulation, obstructing a blood vessel in the brain. The resulting reduction in cellular energy forces the ischemic area to rely on anaerobic metabolism. Oxygen deprivation disrupts normal neuronal processes responsible for producing adenosine triphosphate (ATP), which is required for energy production. Lactic acid accumulates and may damage cells, disrupt cerebral acid-base balance, cause cellular depolarization, and permit ions, including calcium (Ca++), to enter the cell. Calcium influx may trigger further glutamate release. Phospholipases then break down the cell membrane, increasing its permeability and allowing additional ions and harmful chemicals to enter the cell.
Cerebral edema (brain swelling) occurs when large molecules, such as albumin, leak from blood vessels through a damaged blood-brain barrier. These molecules draw water into brain tissue by osmosis. This vasogenic edema compresses and damages brain tissue. Ischemia also stimulates the production of oxygen free radicals and other reactive oxygen species, which interact with and damage multiple intracellular and extracellular components.
Brain tissue is particularly vulnerable to ischemia because it has minimal respiratory reserve and depends almost entirely on aerobic metabolism, unlike most other organs.
Bleeding within the cranial cavity may occur for several reasons. Subdural and epidural hemorrhages are most often caused by trauma, whereas hemorrhagic strokes occur within the brain parenchyma or the ventricular spaces.