Clinical Decision-Making, Technology, and Treatment


The rationale behind the tortuous aorta stems from the calcification or accumulation of fat on the epithelial tissues of the aortic lumen. It is evidenced by high cholesterol, low-density lipoproteins, and triglycerides in the patient’s laboratory blood test findings. Mrs. Larsen’s chest x-ray results show that she has cardiomegaly, which evidence in the literature shows is one of the cardinal signs of atrial fibrillation. The patient’s fever might indicate an infection, but tests are required to determine the type of infection. One of the most common symptoms of atrial fibrillation is palpitations characterized by a fast and irregular pulse (Feske, 2021). Additional physical examination should focus on the cardiovascular system, such as checking for heart murmurs through auscultation or irregularities in arterial pulse, which might indicate the presence of aortic or mitral stenosis and hypertrophic cardiomyopathy.

It should be noted that apical-radial pulse insufficiency might be expected in patients with atrial fibrillation. Following the assessment of the left ventricular apex and the radial pulse simultaneously, the radial heart rate might be lower than the apical heart rate (Phipps & Cronin, 2020). Additionally, it is essential to examine the lungs for the presence of stridor, fluid overload, bronchospasm, or breath sounds. The head should be examined for any signs of trauma.

Etiology and Risk Factors

The etiology and risk factors of cerebrovascular accident (stroke) for Mr. Larsen include atherosclerosis which the high blood low-density lipoproteins and cholesterol might cause. Additionally, hyperglycemia due to high blood glucose levels and hypertension, as evidenced by blood pressure levels of 144/88, places the patient at risk of a cerebrovascular accident. Embolism is one of the leading causes of cerebrovascular accidents, which can also be caused by atrial fibrillation and paroxysmal atrial fibrillation shown in the patient’s electrocardiogram (Herpich & Rincon, 2020).

Technology and Treatment

Diagnostic Testing and Assessments

The noncontract brain computed tomography (CT) angiography of the head should be carried out since the patient might be eligible for a thrombectomy. Additionally, these neuroimaging tests will be instrumental in excluding hemorrhage as the cause of the deficit, the degree of brain injury, and the identification of the vascular lesion responsible for the stroke. The advanced CT and MRI technologies will help discern between brain tissue that can be irreversibly infarcted and repaired, leading to determining whether Mrs. Larsen will benefit from therapy. Magnetic resonance imaging (MRI) with diffusion-weighted imaging will be essential if the patient qualifies for thrombectomy. The MRI with DWI will be instrumental in identifying patients having a wake-up stroke with lesions that respond positively to DWI but negatively impact the fluid-attenuated inversion recovery. Cardiac monitoring through the use of ECG are essential in detecting the types of arrhythmias such as atrial fibrillation, which might predispose Mrs. Larsen to thrombotic incidents, coupled with finding direct evidence of atrial enlargement, which might predispose her to the development of a thrombus. The most recent guidelines recommend monitoring of the heart functions following the cerebrovascular accident. Transthoracic and transesophageal echocardiography should be carried out to determine cardiogenic and aortic sources of cerebral ischemia besides atrial fibrillation.


Pathophysiological Basis

It is worth noting that in the normal physiologic state, the cerebral blood flow rate is mainly determined by the resistance rate in the cerebral blood vessels. The dilatation of the arteries leads to increased blood volume in the brain and increased blood supply in the cerebral tissue of the brain. Cerebral blood flow is also subject to blood perfusion pressure in the brain. The brain is susceptible to shortchanges of ischemia. Brain ischemia leads to the depletion of adenosine triphosphate and changes in the sodium, potassium, and calcium concentration, acidosis, high lactate level, and acidosis. Electrical failure ensures the following ischemia leading to glutamate release and activation of glutamate receptors. Therefore, the ion channels open and facilitates the opening of ion channels which helps potassium ions to move out of the cells and sodium ions enter. This explains the rationale behind Mrs. Larsen’s hyponatremia and hyperkalemia, which have worsened atrial fibrillation. Blood pressure might increase to enhance the supply of oxygen and nutrients to the ischemic brain tissues. Cell death after cerebral ischemia can occur through necrosis or apoptosis. Because of the low levels of ATP at the epicenter of the infarct, cell death through apoptosis is not possible, leading to cell death through necrosis.

Clinical Manifestations

          The cardiac findings in Mrs. Larsen, such s atrial fibrillation and cardiac enlargement, clearly indicate that their ischemic stroke has a cardiac origin. The presence of fever evidenced by temperatures of 38 degrees Celsius points towards suspicion of endocarditis and the following embolic stroke. It should be noted that infections are responsible for activating the acute phase blood reactants leading to an increased risk of thrombosis.


Mrs. Larsen should be evaluated to determine if she qualifies for reperfusion therapy using iv thrombolytics. Aspirin and other thrombotic should not be administered alone or in combination following intravenous thrombolytic therapy. Following the diagnosis of transient ischemic attack, the patient should be started on antiplatelets. Since Mrs. Larsen has been diagnosed with atrial fibrillation, she must be put on oral anticoagulation with warfarin to prevent the recurrence of secondary strokes. It should be noted that even though it is widely practiced for patients with atrial fibrillation, early treatment with heparin causes significant damage to the patients. Blood pressure should not necessarily be reduced during an acute ischemic attack because elevated blood pressure is essential in maintaining perfusion among the borderline ischemia areas (Sandset et al., 2021). Lowering the systematic blood pressure among patients within 24 hours of acute ischemic stroke is linked to clinical deterioration in most observational studies (Vitt et al., 2019).