CVA Pathophysiology

OT Dude Academy’s Free NBCOT® Exam Prep Course Stroke (CVA) CVA Pathophysiology
  • Stroke is a neurological impairment of perfusion of blood vessels to the brain.
  • The Circle of Willis – blood flow inside the brain involves two internal carotids anteriorly and two vertebral arteries posteriorly.
  • Ischemic stroke involves deficient blood and oxygen supply the brain.
    • 85% of strokes are ischemic, which are thrombotic or embolic in nature.1 
    • The most common type of stroke.
    • Results in tissue anoxia from the interruption of cerebral flood flow.
    • Embolic stroke is the most common subtype of ischemic stroke.
    • In an embolic stroke, a blood clot forms elsewhere breaks loose and travels to the brain.2 
      • Characterized by an abrupt onset.
      • 40% of cases are unknown.
      • Known causes have a cardiac origin.3 
      • Atherothrombotic lesions result in artery-to-artery embolism with lesions in the aorta, carotid, and vertebrobasil systems.
    • Thrombosis involves blow flow being affected by the narrowing of vessels due to atherosclerosis.
      • Plaque build-up eventually constricts the vascular chamber and forms clots.
  • Hemorrhagic stroke is caused by bleeding or leaky blood vessels.4 
    • 10-15% are hemorrhagic and often with a high mortality rate.
    • Stress on brain tissue and internal injuries cause the blood vessels to rupture.
    • The excess of blood has a toxic on the vascular system and results in infarction.5 
    • Classified as intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH).
    • ICH involves blood vessel rupture and the abnormal accumulation of blood in the brain caused by hypertension, disrupted vasculature, excessive anticoagulants and thrombolytic agents.
    • SAH involves blood accumulation in the subarachnoid space due to a head injury or cerebral aneurysm.6 7 
    • Hemorrhagic conversion occurs when an ischemic infarct converts into a hemorrhagic lesion.
      • Due to damaged blood vessels no longer maintaining their integrity from an ischemic stroke and hemorrhaging.
      • Common in large infarcts.
      • Anticoagulation therapy is not used with infarcts that have a possibility of hemorrhage because of the risk of hemorrhagic conversion.
  • A transient ischemic attack (TIA) are reversible neurological defects as no cerebral infarction occurs.
    • Typically resolves in less than 24 hours.
    • 35% chance of having a stroke within 5 years.8 

Signs/Symptoms of Acute Stroke

  • Aphasia
  • Hemiparesis
  • Hemisensory loss
  • Hemineglect
  • Visual Field Deficit
  • Gaze deviation and eye movement abnormalities
  • Dysarthria
  • Gait instability and incoordination9 
  1. Musuka, T.D.; Wilton, S.B.; Traboulsi, M.; Hill, M.D. Diagnosis and management of acute ischemic stroke: Speed is critical. CMAJ 2015, 187, 887–893.[↩]
  2. Ibrahim F, Murr N. Embolic Stroke. [Updated 2021 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564351/[↩]
  3. Cerebral Embolism Study Group: Immediate anticoagulation of embolic stroke, Brain Hemorrhage and Cerebral Embolism Task Force: cardiogenic brain embolism—the second report of the Cerebral Embolism Task Force. Arch Neurol 46(7):727, 1989.[↩]
  4. Kuriakose, D., & Xiao, Z. (2020). Pathophysiology and treatment of stroke: present status and future perspectives. International journal of molecular sciences, 21(20), 7609.[↩]
  5. Flaherty, M.L.; Woo, D.; Haverbusch, M.; Sekar, P.; Khoury, J.; Sauerbeck, L.; Moomaw, C.J.; Schneider, A.; Kissela, B.; Kleindorfer, D.; et al. Racial variations in location and risk of intracerebral hemorrhage. Stroke 2005, 36, 934–937.[↩]
  6. Testai, F.D.; Aiyagari, V. Acute hemorrhagic stroke pathophysiology and medical interventions: Blood pressure control, management of anticoagulant-associated brain hemorrhage and general management principles. Neurol. Clin. 2008, 26, 963–985.[↩]
  7. Aronowski, J.; Zhao, X. Molecular pathophysiology of cerebral hemorrhage: secondary brain injury. Stroke
    2011, 42, 1781–1786[↩]
  8. Whisnant JP, Matsumotoa N, Elveback LR: The effect of anticoagulant therapy on the prognosis of patients with transient cerebral ischemic attacks in a community: Rochester, Minnesota, 1955–1969. Mayo Clinic Proc 48(12):844–848, 1973.[↩]
  9. Furie, K. L., & Jayaraman, M. V. (2018). 2018 guidelines for the early management of patients with acute ischemic stroke.[↩]
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