Stroke: Cerebrovascular Accident - NURS 210B Spring 2024-2025 PDF

Stroke: Cerebrovascular Accident Marina Gharibian Adra PhD RN NURS 210B Spring 2024-2025  Cerebral Circulation  Anatomy and Physiology  The blood flow to the brain is supplied by the two internal carotid arteries anteriorly and the vertebral arteries posteriorl...

Stroke: Cerebrovascular Accident Marina Gharibian Adra PhD RN NURS 210B Spring 2024-2025  Cerebral Circulation  Anatomy and Physiology  The blood flow to the brain is supplied by the two internal carotid arteries anteriorly and the vertebral arteries posteriorly.  The internal carotid artery, branches into several arteries: ophthalmic, posterior communicating, choroidal, anterior cerebral, and middle cerebral. The brain is supplied by two systems of arteries: (a) vertebral system, consisting of a pair of vertebral arteries, and (b) carotid system, consisting of pair of internal carotid arteries Vertebral arteries  The approximate locations of the V1 and V2 segments of the vertebral artery are shown. Branches of the Aorta. This illustration includes the right common carotid artery, right vertebral artery, right subclavian artery, brachiocephalic artery, ascending aorta, left coronary artery, right coronary artery, left common carotid artery, left vertebral artery, left subclavian artery, left axillary artery, left brachial artery, arch of aorta, and descending aorta. The common carotid artery  There is one common carotid artery on either side of the body and these arteries differ in their origin. The left common carotid artery arises from the aortic arch within the superior mediastinum, whilst the right common carotid artery arises from the brachiocephalic trunk posterior to the right sternoclavicular joint. Blood supply to the brain  The vertebral and internal carotid arteries begin in the neck and travel up to the cranium.  Once in the cranial vault, the terminal branches form an anastomotic circle, commonly known as the Circle of Willis.  Branches arise from the circle to supply most of the cerebrum. Circle of Willis (circulus arteriosus) The major arteries supplying the cerebrum (i.e., branches of basilar and internal carotid arteries) get interconnected to one another at the base of the brain to form a six- sided polygon of arteries called circulus arteriosus or circle of Willis. It contributes most of the arterial blood supply to the brain.  Stroke Stroke (or Brain Attack) is an acute neurologic deficit from a vascular disorder that injures brain tissue. Stroke remains one of the leading causes of mortality and morbidity in the United States. Ischemic/Hemorrhagic Stroke Lacunar stroke  Lacunar Stroke Strokes can damage brain tissue in the outer part of the brain (the cortex) or deeper structures in the brain underneath the cortex. A stroke in a deep area of the brain (for example, a stroke in the thalamus, the basal ganglia or pons) is called a lacunar stroke. Ischemic strokes are caused by an interruption of blood flow in a cerebral vessel and are the most common type of stroke, accounting for 70% to 80% of all strokes. The less common hemorrhage strokes are caused by bleeding into brain tissue. This type of stroke usually is from a blood vessel rupture caused by hypertension, aneurysms, head injury, and has a much higher fatality rate than ischemic strokes.  Ischemic stroke (thrombotic, embolic) The common pathway of ischemic stroke is lack of sufficient blood flow to perfuse cerebral tissue, due to narrowed or blocked arteries leading to or within the brain. Ischemic strokes can be broadly subdivided into thrombotic and embolic strokes. Narrowing is commonly the result of atherosclerosis – the occurrence of fatty plaques lining the blood vessels. As the plaques grow, the blood vessel becomes narrowed and the blood flow to the area beyond is reduced. Damaged areas of an atherosclerotic plaque can cause a blood clot to form, which blocks the blood vessel – a thrombotic stroke. In an embolic stroke, blood clots from elsewhere in the body, typically the heart valves, travel through the circulatory system and block narrower blood vessels.  Ischemic Stroke Ischemic stroke Thromboti Embolic c Thrombotic Stroke vs Embolic Stroke Subclassification of ischemic stroke Based on the etiology of ischemic stroke, a more accurate sub-classification is generally used:  Large artery disease – atherosclerosis of large vessels, including the internal carotid artery, vertebral artery, basilar artery, and other major branches of the Circle of Willis.  Small vessel disease – changes due to chronic disease, such as diabetes, hypertension, hyperlipidemia, and smoking, that lead decreased compliance of the arterial walls and/or narrowing and occlusion of the lumen of smaller vessels.  Embolic stroke – the most common cause of an embolic stroke is atrial fibrillation.  Stroke of determined etiology – such as inherited diseases (Antiphospholipid Antibody Syndrome, APS) metabolic disorders, and coagulopathies.  Stroke of undetermined etiology – after exclusion of all the above. Pathophysiology of ischemic stroke (Cont’d) In the core area of a stroke, blood flow is so drastically reduced that cells usually cannot recover and subsequently undergo cellular death. The tissue in the region bordering the infarct core, known as the ischemic penumbra, is less severely affected. This region is rendered functionally silent by reduced blood flow but remains metabolically active. Cells in this area are endangered but not yet irreversibly damaged. They may undergo apoptosis after several hours or days but if blood flow and oxygen delivery is restored shortly after the onset of stroke, they are potentially recoverable. Ischemic penumbra – Potential to reverse neurologic impairment with post-stroke therapy Oligemia: hypo perfused parenchyma with a cerebral blood flow (CBF) value of approximately 22–60 mL/100 g/min, which is above the ischemic threshold (22 mL/100 g/ min).  Regulatory T lymphocytes (Treg) Liesz et al found that Treg cells antagonize enhanced TNF-α and IFN-γ production, which induce delayed inflammatory brain damage, and that Treg cell-derived secretion of IL-10 is the key mediator of the Cerebro protective effect via suppression of proinflammatory cytokine production. IL-10 potently reduced infarct size in normal mice and prevented delayed lesion growth after Treg cells depletion.   Excitotoxicity,  oxidative stress,  microvascular injury, What is the  blood-brain barrier dysfunction ischemic cascade  postischemic inflammation of a stroke? leading to cell death of neurons, glia and endothelial cells.  The degree and duration of ischemia determines the extent of cerebral damage. Ischemic cascade leading to cerebral damage. Ischemic stroke leads to hypoperfusion of a brain area that initiates a complex series of events. Excitotoxicity, oxidative stress, microvascular injury, blood-brain barrier dysfunction and postischemic inflammation lead ultimately to cell death of neurons, glia and endothelial cells. The degree and duration of ischemia determines the extent of cerebral damage.  Important steps of the ischemic cascade  Without adequate blood supply and thus lack of oxygen, brain cells lose their ability to produce energy - particularly adenosine triphosphate (ATP).  Cells in the affected area switch to anaerobic metabolism, which leads to a lesser production of ATP but releases a by-product called lactic acid.  Lactic acid is an irritant, which has the potential to destroy cells by disruption of the normal acid-base balance in the brain.  ATP-reliant ion transport pumps fail, causing the cell membrane to become depolarized; leading to a large influx of ions, including calcium (Ca), and an efflux of potassium.  Intracellular calcium levels become too high and trigger the release of the excitatory amino acid neurotransmitter glutamate.  Glutamate stimulates AMPA receptors and Ca-permeable NMDA receptors, which leads to even more calcium influx into cells.  Important steps of the ischemic cascade Excess calcium entry overexcites cells and activates proteases (enzymes which digest cell proteins), lipases (enzymes which digest cell membranes) and free radicals formed permeable, the ischemic cascade in a process called excitotoxicity. As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more ions and harmful chemicals enter the cell. Mitochondria break down, releasing toxins and apoptotic factors into the cell. Cells experience apoptosis. If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier and contributes to cerebral edema, which can cause secondary progression of the brain injury.   A door-to-treatment time of 60 minutes or less is the goal. This 60-minute period is often referred to as the “golden hour” Golden period of of acute ischemic stroke treatment during which a focused ischemic stroke diagnostic workup must be completed to rule out conditions that may mimic stroke as well as contraindications to rt-PA administration.  Hemorrhagic strokes are due to the rupture of a blood vessels leading to compression of brain tissue from an expanding hematoma. Pathophysiology This can distort and injure tissue. In addition, the of hemorrhagic pressure may lead to a loss of blood supply to stroke affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature. Pathophysiology of hemorrhagic stroke Intracerebral hemorrhage – caused by rupture of a blood vessel and accumulation of blood within the brain. This is commonly the result of blood vessel damage from chronic hypertension, vascular malformations, or the use of medications associated with increased bleeding rates, such as anticoagulants, thrombolytics, and antiplatelet agents. Subarachnoid hemorrhage is the gradual collection of blood in the subarachnoid space of the brain dura, typically caused by trauma to the head or rupture of a cerebral aneurysm. The Key Differences Between Ischemic vs. Hemorrhagic Stroke Symptoms: Pathophysiology of hemorrhagic stroke Hemorrhagic Stroke The most frequently fatal stroke is a spontaneous hemorrhage into the brain substance. With rupture of a blood vessel, hemorrhage into the brain tissue occurs, resulting in edema, compression of the brain contents, or spasm of the adjacent blood vessels. The most common predisposing factors are advancing age and hypertension. Other causes of hemorrhage are aneurysm, trauma, drugs. Hemorrhagic Stroke A cerebral hemorrhage occurs suddenly, usually when the person is active. Vomiting commonly occurs at the onset, and headache sometimes occurs. In the most common situation, hemorrhage into the basal ganglia results in contralateral hemiplegia. The hemorrhage and resultant edema exert great pressure on the brain substance, and the clinical course progresses rapidly to coma and frequently to death. If you think someone may be having a stroke, act F.A.S.T. and do the following test: F—Face: Ask the person to smile. Does one side of the face droop? A—Arms: Ask the person to raise both arms. Does one arm drift downward? S—Speech: Ask the person to repeat a simple phrase. Is the speech slurred or strange? T—Time: If you see any of these signs, call 9-1-1 right away. Transient ischemic attack-TIA  Transient ischemic attacks are characterized by ischemic cerebral neurologic deficits that last for less than 24 hours.  TIA or ministroke is equivalent to brain angina and reflects a temporary disturbance in cerebral blood flow, which reverses before infarction occurs, analogous to angina in relation to heart attack.  TIAs are important because they may provide warning or impending stroke.  In fact, the risk of stroke after a TIA is maximal immediately after the event.