Pathophysiology of Cerebral Vascular Accidents

Abstract 

Cerebral vascular accident (CVA), or commonly known as a stroke, is a serious neurological disease and a major cause of death across the globe. According to the CDC (2016), 133,000 individuals died due to CVA in 2015 in the U.S making CVA the fifth cause of mortality with a mortality rate of 41.7 deaths per 100,000. The Pathophysiology of CVA is complicated; it involves excitotoxicity mechanisms, oxidative damage, apoptosis and neuroprotection (Guo et al., 2013). The ultimate consequence of CVA is neuronal death with permanent loss of neuronal function. Extensive research has been done on pathophysiology of CVA to come up with therapeutic strategies. Nonetheless, an effective neuroprotectant is yet to be discovered. This research paper evaluates the pathophysiology of CVA with emphasis on risk factors, diagnosis, symptoms, and management strategies.

Introduction to Population

According to Barker-Collo et al. (2015), various epidemiological studies show that CVA is more frequent in men than women. However, by the age of 55 the difference is significantly reduced. Age and gender plays an important role, such that as one gets older the risk for CVA increases, thus the aging population is the primary population affected by CVA. The risk of getting CVA doubles every decade after the age of 55. While women under the age of 55 have slightly lower chances in comparison to men, there are factors within women that make them experience severe CVA (Barker-Collo et al., 2015). Use of birth control pills, pregnancies and history of gestational diabetes in women are risk factors that apply to women only (Arboix, 2015).

Though CVA is common among the aging population, there are other demographic related factors that make one susceptible to CVA. Feigin et al. (2016), note that CVA occurs more often among African Americans, Hispanics, Asian Americans and Native Americans. According to Mozaffarian et al. (2016), African Americans and Hispanics have unique biomarkers that differentiate them from the white populations, making them high-risk populations in relations to CVA. African Americans and the minority races are known to have high cases of blood pressure, diabetes and obesity incidents; all being key risk factors for CVA. 

Lastly, individuals (populations) with family histories of CVA have greater chances of getting CVA as they grow old, regardless of their gender or race. On certain occasions, CVA is seen as a sign of genetic disorder like CADASIL, caused by a gene mutation that leads to damage of blood vessel walls (Guo et al., 2013). For example, in the case of CADASIL, a child has a 50% chance of inheriting the disease from the parent, hence such populations have extremely high risks of getting CVA. 

Risk Factors for Primary Diagnosis 

CVA is life threatening, it represents a disturbance to the flow of blood to the brain due to a blockage or a rupture of a blood vessel (Jean et al., 2012). The severity of CVA depends on the location of the blockage or the rupture blood vessel. Loss of blood supply to a part of the brain leads to ischemic cascade, which changes the metabolism in the cells to anaerobic. The final consequence is widespread cell death (Jauch et al., 2013). 

There are risk factors that are evaluated by medical professionals when diagnosing CVA. Awareness of risk factors is also necessary to guide the treatment process. CVA risk factors are classified as traditional and novel, modifiable and non-modifiable (George & Steinberg, 2015). The risk of CVA will vary depending on the individual differences in the identified risk factors. Non-modifiable risk includes age, gender, ethnicity and family history. A detailed analysis of the non-modifiable factors is necessary to ascertain the impact of CVA. 

Traditional risk factors such as history of diabetes, hypertension, obesity, smoking and carotid artery disease are considered modifiable. Fortunately, their effects can be changed, unlike the effects of non-modifiable factors. Lastly, novel risk factors such as hyperhomocysteinemia, hypercoagulable states, and select biomarkers must be identified (George & Steinberg, 2015). 

The identification of different risk factors can be challenging to health care professionals when the patient and immediate family members are unaware of the risk factors. The awareness of traditional modifiable risk factors such as hypertension and diabetes is necessary for diagnosis and proper treatment once the patient presents common symptoms of CVA such as dizziness, loss of balance and coordination, headaches, nausea and blurred vision. 

Health Promotion and Risk Reduction Recommendations

CVA is a serious condition, it is necessary to promote prevention strategies and risk reduction measures because the effects of CVA are life threatening. Different health organizations and research studies recommend various strategies and frameworks for health promotion and risk reduction. The CDC in particular recommends six steps for health promotion with regards to CVA (Jauch et al., 2013). The first step involves recognizing the cost of CVA; CVA often leads to death and serious disability. CVA is one of the most costly health conditions, thus when patients recognize how CVA will affect their lives they are more likely to lead healthy lifestyles. The second step is recognizing the risk factors; individuals and employers must make themselves aware of the risk factors that put them at risk for CVA (Feigin et al., 2016). The next step involves learning from others what they know about CVA. Patients can inquire from their primary caregivers about CVA and how to avoid it. The fourth step is the implementation of cardiovascular health strategies, such as wellness programs that involve regular check ups and healthy lifestyles (Jauch et al., 2013). The fifth step is about working within the health plan, by taking advantage of the cardiovascular services provided. Lastly, it is imperative to establish useful partnerships with care givers and organizations dedicated to cardiovascular conditions. 

Alternatively, American Heart Association (AHA) has created a framework for risk reduction in case of a CVA incident. The FAST (face, arms, speech and time) framework promoted a decade ago has helped in reducing the effects of CVA. When a patient presents a weakened/ drooped one side of the face, weak arms or numbness and slurred speech, these are primary symptoms of CVA (Powers et al., 2015). AHA is running a public education program to educate the public on FAST framework. This message is crucial as it will help the members of the public to recognize serious cases of CVA from other conditions and to seek immediate help. 

Powers et al. (2015), explores the Framingham Stroke Risk Profile (FSRP) developed over four decades ago. FSRP model provides sex specific information on the probability of CVA based on available clinical information. The model sums individual risk factors based on at least 10-year clinical information. It identifies the traditional, novel, modifiable and non-modifiable factors. Powers et al. (2015), notes that the tool has been useful in educating patients with a history of cardiovascular conditions on their risk of getting CVA. Health care providers must educate patients, immediate families and the general public on tools such as FAST and FSRP. They must also furnish them with adequate information to enable them to use the tools effectively to minimize risks in case of an occurrence of CVA. 

Pathophysiology of Primary Diagnosis

According to Larsson et al. (2015) the pathophysiology of CVA is quite complex. Before analyzing the pathophysiology, it is necessary to understand the two mechanisms that cause CVA, ischemia and hemorrhage (Larsson et al., 2015). Ischemic stroke is the most common type of stroke, representing 80% of all strokes. An ischemic stroke is caused by the lack of or decreased circulation of blood in the brain, which deprives the cells of the necessary substrates. Ischemic CVA is severe and the effects are felt immediately since the brain does not store glucose, which is a major substrate driving the operation of brain cells. 

On the other hand, CVA that originates from intracerebral hemorrhage causes injury to the brain tissue. It represents 10-15 percent of CVA cases (Larsson et al., 2015). Regardless of the cause of CVA, the condition is lethal as it disrupts the biochemical processes in the brain. Health professionals differentiate ischemic from hemorrhagic CVA using a CT scan. 

Ciccone et al. (2013) note ischemic CVA manifests itself in three forms: thrombotic CVA, embolic CVA and systemic hypoperfusion. The different forms are characterized by different effects on the organs affected, for instance, thrombotic CVA affects large and small vessel types. Regardless of the form, they are all characterized by compromised vascular supply of blood in the brain, hence the occurrence of acute stroke. The severity of CVA will depend on the section of the brain affected. The lower respiratory reserve and reliance of aerobic metabolism makes CVA dangerous. Some commonly affected parts of the brain will not recover, while others might recover when the situation is addressed immediately. For example, the brain parenchyma will undergo immediate death due to lack of blood supply, while areas such as penumbra have the potential to be recovered (Ciccone et al., 2013). 

Ischemic CVA activates ischemic cascade, a progressive depletion of oxygen and glucose compounds in the brain. The process is accompanied by the release of high energy phosphate compounds, particularly adenine triphosphate (ATP). ATP will adversely affect energy dependent processes in the brain while setting a series of cellular injury and death (Mandalenakis et al., 2016). 

The pathophysiology of ischemic CVA follows a complex path, which begins with the depletion of cellular energy store. Consequently, there will be a loss of ion pump function characterized by an inflow of water and swelling of neurons (Mandalenakis et al., 2016). Excitatory neurotransmitters such as glutamate and Synaptosomal-associated protein 25 (SNAP-25) are released, but when released in high quantity they can be damaging to the neurons. Glutamate is necessary for neuronal plasticity, but it can enhance the excitotoxic synaptic transmission via activation of N-methyl-d-aspartate (NMDA), amino-3-hydroxy-5-methyl-4-propionate (AMPA) or kainite receptors, which allows the Na+and Ca2+ influx. These components and their metabolic products such as oxygen free radicals are damaging to the neuronal membrane, gene material and structure of proteins in the neurons, consequently leading to cell death. Mandalenakis et al. (2016) add that the oxygen free radicals do not just damage the structure of cells, but they can initiate the apoptotic pathway. Apoptosis represents one of the most destructive and last stages of ischemic CVA, it refers to programmed cell death that occurs in the peripheral neurons. It is an early response in gene expression of Bcl-2 and p53, proceeded by the release of proapoptotic molecules and apoptosis-inducing factor from the mitochondria. Eventually, the caspase cascade will be activated by either extrinsic or intrinsic factors, and when combined with the availability of damaging oxygen free radicals, the ultimate result is cell death (Guo et al., 2013). 

From the description above, the brain is the most affected organ. However, other organs such as the mouth and bones are also affected. Depending on the sector of the brain affected, the patient will have difficulty with speech and mobility. 

It is worth noting that ischemic CVA also activities cell neuroprotection to protect the brain from the damaging effects of apoptosis and necrotic cell death (Guo et al., 2013). Various neuroprotective components are released during the various stages of CVA. Heat shock protein 70 (HSP70) is one of the earliest components released during the first 1-2 hours of ischemia; it limits infarct volume and increases the Bcl-2 expression. Bcl-2 gene family is antiapoptotic in nature and they can modulate calcium fluxes hindering caspase activation. 

Pathophysiology of Primary Symptoms of Primary Illness

The primary symptoms can be used to determine the exact cause of the CVA (Feigin et al., 2016). The primary symptoms are intrinsically associated with the disease, and they are of greatest significance to the health providers if they want to properly manage CVA. Feigin et al., (2016), note that the primary symptoms of CVA are identified in the prehospital setting and throughout the care provision process in the hospital. A common tool used to identify symptoms of CVA is the FAST tool. When a patient shows the signs described in the FAST tool, emergency medical care must be sought as the pathophysiology of CVA has began (Feigin et al., 2016). 

The neurological assessment of the patient will be based on subjective and objective data. Subjective information is derived from the symptoms possessed by the patients as well as visible risk factors. Park & Park (2015) describe a process for evaluating all the symptoms in an effort to judge the severity of CVA and the extent of damage. The process is conclusive; it focuses on various factors regarding the level of consciousness of the patient. If the patient is still alert, it shows that the damage to brain cells is in its initial phase, and the healthcare professionals have a better chance of helping the patient recover brain function. However, when the patient is experiencing visual loss, severe aphasia, sensory loss and damage to motor function, it shows that CVA has progressed and it has damaged a lot of brain cells. 

The objective data shows the health history and genetic history of the patient. Ischemic CVA is common among patients with other primary conditions such as obesity, hypertension, coronary artery disease, cigarette smoking and substance abuse in general and sleep apnea (Guo et al., 2013). Stress in women is also known to increases chances for ischemic CVA. 

According to Guo et al. (2013) ischemic CVA remains the most studied forms of CVA because it is responsible for 85-87% of CVA cases. The average cerebral blood flow (CBF) for an adult is 50-55ml/100g/min. The number is drastically reduced during ischemia, triggering the pathophysiology of CVA. Ultimately, when CBF is reduced up to 6ml/100g/min, the brain damage becomes fatal, and brain cells experience increased infarction. In such situations, medical professionals work hard to salvage the penumbra. 

According to Parker & Parker (2015) the symptoms of ischemic CVA occur according to the areas of the brain affected as the condition progresses. Different sectors of the brain are responsible for various functions; the dominant hemisphere is responsible for language function. The handedness is used to determine the dominant brain hemisphere, such that right-handed people have left hemisphere as the dominant side of their brain, though 60% of left-handed people have the left side as the dominant too. When the blood flow to the dominant hemisphere is compromised in case of a CVA, a patient will present symptoms such as aphasia, agraphia, acalculia, apraxias, left gaze preference and a right visual field (Clarke, 2014). 

Alternatively, when the blood supply to the nondominant hemisphere is compromised, a patient will present right gaze preference and left visual field deficit. Other symptoms include dysarthia, flat affect and left-sided hemisensory loss (Clarke, 2014). When the patient is presenting symptoms like aphasia and left gaze preference, it becomes evident that the CVA has affected the dominant hemisphere. Medical professionals have to be aware of the differences between the symptoms of transient ischemic attack (TIA) and ischemic CVA. Diagnostic tests will be used to rule out TIA, and better yet the symptoms of TIA are temporary. 

Typical Lab and Diagnostic Test Data

Though the symptoms of CVA are unique, lab and diagnostic tests are necessary to ascertain the extent of the damage and to sub classify CVA (Jauch et al., 2013). Once the medical professionals have accessed common symptoms such as difficulty with speech and paralysis in half of the body, extensive study of the patient’s history and tests are needed to rule out CVA mimics. A physical exam is the first exam used to determine the exact time in which the symptoms started showing, personal and medical history and blood pressure. During a physical exam, the doctor will use a stethoscope to listen to the heart rhythm, and an opthalmoscope to check for signs of cholesterol clots.

Jauch et al. (2013) state that neuroimaging is the only way to distinguish between intracerebral hemorrhage and ischemic CVA. Both of the two forms of CVA are characterized by acute onset of similar symptoms which will be differentiated through neuroimaging. Patients with intracerebral hemorrhage show gradual worsening of symptoms due to increasing size of hematoma (Bushnell & Goldstein, 2000). A CT scan will be used to differentiate CVA from tumors and other brain masses. However, MRI scans are better than CT scans in differentiating CVAs from other masses, and it can successfully show the changes and the time course. 

Nurse-sensitive Outcomes or Care Management

CVA stands out as one of the leading causes of mortality across the globe. If caregivers want to make a difference in the lives of patients with CVA, they must equip themselves with key information on how to address the situation as soon as possible. CVA does not leave much room for error and care; hence nurses dealing with CVA patients must educate themselves on the various facets of CVA (Jauch et al., 2013).

The treatment plan for CVA patients mainly focuses on reversing the damage, though in severe cases the damage cannot be reversed. The state of the patient after treatment will determine a care management plan for nurses. Nurses have to be aware of the motor and functional rehabilitation skills in order to assist patients with their recovery process (Bushnell et al., 2014). Studies show that early onset of motor and functional rehabilitation will help the patient regain their functionality. 

Another crucial aspect of care management is drug administration. CVA patients are in critical shape, and drugs must be administered properly and on time for the patients to improve. Nurses must be aware of the effects of different CVA drugs such as thrombolytic drug recombinant tissue plasminogen activator (r-TPA). r-TPA is administered after one hour after the patient’s admission. Nurses are responsible for administering the drug, monitoring the effects for any complications and informing the doctor in case changes in the vital signs (Liu et al., 2015). 

The American Heart Association recommends various nurse-sensitive care management strategies for CVA patients. Nurses must check on the patient after every 15 minutes during r-TPA infusion (Liu et al., 2015), every 30 minutes during the next six hours and every hour during the next 16 hours. The temperature must be checked after every four hours, and oxygen must be administered using nasal cannular if it decreases below 92% (Liu et al, 2015). Nurses must closely monitor the patient for 72 hours until the patient is out of the danger. 

The complex pathophysiology of CVA entails various excitotoxity mechanisms, inflammatory pathways, ionic imbalances and apoptosis. The complex nature of CVA has made it hard to come up with suitable therapeutic advances to reduce the burden of CVA. Further research on the pathophysiology of CVA is necessary to identify all the patterns and outcomes. This will also open avenues of CVA management beyond the realms of r-TPA. Well designed and executed clinical trials on pathophysiology of CVA must be encouraged. 

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