Ischemic Stroke
Pathophysiology
The brain has a high metabolic demand and requires a constant blood supply that provides
metabolic substrates such as glucose and oxygen. The brain contains no energy reserves and
very little oxygen reserves that can be used in the event of inadequate tissue perfusion
(Peschillo, 2016). Ischemic strokes occur as a result of hypoperfusion of the brain due to some
form of arterial obstruction, hypovolemia (low blood volume), hypotension, or cardiogenic shock.
Inadequate perfusion initially leads to ischemia (insufficient oxygen supply) and impairment,
which progresses to infarction (tissue death) if perfusion is not restored within minutes (Huether
& McCance, 2017).
Obstruction of cerebral arterial blood flow generally results from a thrombus or an embolism. A
thrombus is a blood clot that forms in the lumen of a blood vessel. Thrombi that cause ischemic
strokes form on the inside of an artery that serves part of the brain. Thrombus formation is much
more likely if atherosclerosis is present and has progressed for many years. If part of a
thrombus in another part of the body detaches and travels to the brain, it is termed an embolus.
A piece of a thrombus that detaches within the brain and becomes lodged in a smaller vessel in
the brain is still considered a thrombus, not an embolus. Due to years of atherosclerosis
progression, thrombi can form in the larger arteries in the brain. An embolism will usually
(though not always) become lodged in and occlude smaller vessels in the brain, since they are
generally small enough to pass through the larger vessels. The smaller the vessel that is
occluded, the more focal the area of affected tissue. Clots in embolic strokes usually form in the
valves or chambers of the heart (cardioembolic) prior to travelling to the brain, due to a heart
defect such as atrial fibrillation (Huether & McCance, 2017).
Ischemic strokes can also be the result of lesions to small deep arteries or systemic
hypoperfusion. The former etiology, classified as a lacunar stroke, is usually caused by chronic
hypertension or diabetes mellitus without atherosclerosis (Martin-Schild, Hallevi, & Barreto,
2018). During a lacunar stroke, only small cortical structures are affected, so usually only
isolated sensory impairment or isolated motor impairment will result. Systemic hypoperfusion
can also cause an ischemic stroke. Causes of systemic hypoperfusion are cardiac failure,
pulmonary embolism, and hypovolemia. Systemic hypoperfusion causes whole brain ischemia,
which leads to death if perfusion to the brain is not restored within minutes (Huether &
McCance, 2017).
Ischemia lasting longer than a couple minutes deprives brain cells of ATP production, and ion
pumps cease to function. This results in a loss of the ion gradient used in neuronal signaling.
Extracellular potassium concentrations and intracellular sodium concentrations rise. Increased
intracellular sodium concentration leads to increased osmotic pressure that eventually causes
lysis of the cell (Peschillo, 2016). In brain tissue that becomes infarcted due to prolonged
ischemia, the affected region has a central core of necrotic tissue surrounded by a region called
the ischemic penumbra. The central core is unsalvageable tissue, but tissue in the ischemic
penumbra can be salvaged if reperfusion is achieved within three hours (Huether & McCance,
2017).
References:
Huether, S.E., & McCance, K.L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
Missouri: Elsevier
Martin-Schild, S., Hallevi, H., & Barreto, A. (2018). Ischemic stroke : diagnosis and treatment.
Rutgers University Press.
Peschillo, S. (2016). Brain ischemic stroke : from diagnosis to treatment. Bentham Science
Publishers Ltd.