Hello, everyone! Here are the answers to your inquiries about our diagram.
1) Regarding the medications the patient is taking, is there a connection between his regular usage of carvedilol to the observed manifestations? Why does it not have a line connected to the other mechanisms?
To provide a brief background, Carvedilol is a nonselective beta-blocker, which reduces the SNS activity and blocks the effects of epinephrine (and alpha receptors) by relaxing smooth muscle vasculature, leading to a reduced peripheral vascular resistance and blood pressure; hence, it is used to treat HPN, and target HR, BP, and heart strain.
However, despite these effects of Carvedilol, there is no connection between the client’s intake of it with his observed manifestations, particularly his bradycardia, and lowered BP and RR. First and foremost, Carvedilol exerts a lesser effect in HR as compared to other beta-blockers (Singh & Preuss, 2024). Most importantly, the clinical manifestations, which are collectively called the Cushing’s Triad, were due to the pathophysiological compensations for the client’s low cerebral perfusion, as brought about by his increased ICP. The compensatory mechanisms are as follows:
- Stage 1: HPN compensates for the decreased cerebral blood flow and oxygenation.
- Stage 2: Once the baroreceptors in the aortic arch detect a high MAP (which, in this case is 110), the vagus nerve is stimulated by the PNS to produce a reflex bradycardia to compensate for the HPN
- Stage 3: As long as there is an increased ICP, and since the nervous system components are confined in one space, the brainstem is distorted and compressed, resulting in apnea (aeb by the lowered RR post-initial examination).
The group believes that Carvedilol at 6.25 mg twice a day paves its major role as a risk factor that predisposes the patient to the stroke; literature says that a 6.25 mg dosage for this medication is a starting dose that can be increased in increments, according to its effectiveness. Unfortunately, the client’s usual BP prior to the stroke attack was unremarkable, but IF it was sustainedly increased, the client’s maintenance medication might be ineffective and is subject to augmentation as he has other innumerable factors: Has a family history of T2DM, a male, 65 y/o, a smoker - among the others and not taking into consideration his health belief and management and activity and exercise patterns.
2) How did you hypothesize that the patient underwent hemorrhagic stroke and not ischemic stroke?
First, let's differentiate ischemic stroke from hemorrhagic stroke. Ischemic stroke is characterized by the presence of a blood clot or thrombus present in the vessels of the brain; this prevents oxygenation of the brain, hence leading to stroke. On the other hand, hemorrhagic stroke refers to the hemorrhage or bleeding present in the brain due to cerebral vessel rupture.
The CT Scan showed intracranial bleeding, specifically intraparenchymal hemorrhage. It is usually caused by hypertension, aneurysm rupture, tumors, and even trauma. Consequently, hemorrhagic stroke is due to bleeding into the brain by the rupture of a blood vessel, which may be attributed to hypertension and aneurysm ruptures similar to the case of the client. In addition, the CT Scan did not reflect any information on the presence of a blood clot, but we do not completely rule out Hemorrhagic Stroke as a complication of Ischemic Stroke since it may actually be possible. For example, a thrombus may be present in a cerebral artery, and may dislodge. The dislodging of the thrombus may lead to a rupture of the vessel, thus leading to Hemorrhagic Stroke. But since there are incomplete details in the case, the condition leans towards Hemorrhagic Stroke.
As reported by Sechzter (2012), Vaghdati et al. (2017), and Lekoubou (2019), certain manifestations such as seizures are more significantly common in hemorrhagic stroke than in ischemic stroke. Out of 503 respondents, 17.4% of hemorrhagic stroke patients manifested seizure while ischemic stroke patients had 0%. Moreover, as per Unnithan et al. (2023), cranial nerve dysfunction with contralateral (opposite side, aeb Intraparenchymal hemorrhage in the RIGHT parietal but left) weakness, seizures (shaking ng legs and arms), and aphasia (slurring of speech, sa broca’s area affected) indicates hematoma in various locations in the brain.
3) The CT scan only showed damage to the parietal area. With this, how did the condition affect the patient’s brain stem and areas of the frontal lobe?
Monro-kellie Hypothesis Principle - The combined volume of neuronal tissue, blood, and CSF is constant. To maintain homeostatic intracranial pressure, any increase or decrease in one of these elements leads to a reciprocal and opposite change in the others or an increase in one should cause a decrease in one or both of the remaining two.
Although CT scan only showed intraparenchymal hemorrhage only in the right parietal area, the accumulated blood in the area can expand. This expansion has the potential to elevate intracranial pressure by triggering an inflammatory response in the body, which leads to cerebral edema and the compression of surrounding brain structures.
In relation to the Monro-kellie Hypothesis, the total volume inside the skull, the total volume of the parenchyma, cerebrospinal fluid, and blood, must remain constant. This means that an increase in the volume of one component (blood due to hemorrhage) must be compensated by a decrease in the volume of another component (csf/brain tissue/ both), forcing a displacement of components → increasing intracranial pressure, which impacts/ can compress other parts of the brain, such as the brainstem and areas of frontal lobe.
Cerebral edema → Increased intracranial pressure → Brainstem (Medulla Oblongata) compression → Dysfunction in the pacemaker cells of the brain stem → Pneumotaxic center in the upper pons is affected → Disruption of respiratory signals from the brainstem to the spinal cord → Impaired signaling to the phrenic nerve → Ineffective/uneven diaphragm movement → Cheyne-stokes respirations (irregular respirations) → Increased risk for herniation → Drop in SPO2
4) How are you able to determine that MAP was needed in the progression of the case?
Cerebral perfusion pressure is the pressure required to maintain blood flow to the brain, determined by the equilibrium between mean arterial pressure (MAP) and intracranial pressure (ICP). The need to monitor MAP was determined by maintaining CPP amidst increasing ICP. The increase in ICP compromised cerebral perfusion, prompting the need to ensure CPP remained adequate to prevent further ischemic damage.
5) Is there a mechanism involved in why the patient suddenly experienced worse manifestations compared to the initial examination?
Increased ICP: Hematoma expansion leads to increased ICP due to the sudden increase of volume in the brain, to which cannot be compensated right away. The longer the patient experiences increased ICP, the lower the GCS score due to the shifting of the compensation stages: from the end of stage 1 to stage 2. The pressure begins to compromise neuronal oxygenation. Stage 2 of intracranial hypertension shows signs of: confusion and lethargy– manifestations the patient experienced (Huether & McCance, 2019).
Brainstem Compression: In patients with hemorrhagic stroke, lowering target SBP to <130 mmHg can significantly reduce the risk of ICH (Hemphill et al., 2015). However, given the patient’s blood pressures, the target SBP wasn’t met which possibly resulted in an increase in ICH. Here, due to overcrowding, the blood can make its way to the foramen magnum. When the brainstem is pressed, there will be a decrease in GCS that can lead to other complications such as cardiac arrest and decrease in respiratory function. (Note: brainstem functions: breathing, consciousness, blood pressure, heart rate)
Prolonged Postictal Phase: The postictal phase is considered as the recovery period after a seizure where the patient may experience cognitive deficits, behavior changes, and psychiatric symptoms (Pottkamper et al., 2020). The risk of having these negative outcomes increases with the time it takes for someone to fully recover from a seizure (Vickrey et al., 2000). In the patient’s case, his GCS decreased as time passed by — from during to after initial examination. (Note: The mechanisms of the postictal state are poorly understood, although electrophysiological changes in the brain and cerebral blood flow alterations are thought to be involved in the mechanisms (Ohira et al., 2019).)
Vital Signs: Increased ICP results in a lack of oxygen in brain tissue and a restriction of cerebral blood flow in the brain. This activates the cushing reflex that then leads to cushing’s triad. To compensate for the lack of oxygen, the sympathetic nervous system is activated, causing an increase in systemic blood pressure and an initial increase in heart rate. The increased blood pressure then signals the carotid and aortic baroreceptors to activate the parasympathetic nervous system, causing the heart rate to decrease. As the pressure in the brain continues to rise, the brain stem may start to dysfunction, resulting in irregular respirations followed by periods where breathing ceases completely. This progression is indicative of a worsening prognosis.
6) In relation to the post-initial exam, what directly contributed to the overall lower MAP?
The lowered mean arterial pressure is an effect of the inflammatory response (release of cytokines and vasodilation) leading to decreased vascular resistance and if combined with decreased myocardial contractility, there is a decrease in cardiac output. Cardiac output has a direct relationship with the MAP; hence, it is more likely to be lowered.
7) If, for instance, there was already a lipid analysis result stated, how would the diagram change depending on the result?
Cholesterol is a waxy, fat-like substance that's found in all the cells in your body. There are two types of cholesterol or lipoproteins: (1) LDL stands for low-density lipoproteins. It is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries, and (2) HDL stands for high-density lipoproteins. It is sometimes called the "good" cholesterol because it carries cholesterol from other parts of your body back to your liver. Your liver then removes the cholesterol from your body.
Circulating lipid and lipoprotein biomarkers have consistently been associated with cardiovascular diseases such as myocardial infarction and stroke Denti et al. (2003) reported that low density Lipoprotein cholesterol concentrations over 100 mg/dl along with low high density lipoprotein cholesterol levels were associated with higher stroke risk. This is due to the fact that population studies have demonstrated that elevated levels of LDL cholesterol and apolipoprotein B (apoB) 100, the main structural protein of LDL, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE).
If the cholesterol levels were already released and stated, there could be multiple changes. If there is high LDL and low HDL, it would be safe to consider atherosclerosis in the diagram indicating it with a SOLID line.
If there is low LDL and high HDL in a person with hypertension, it could rule out atherosclerosis and attribute the condition to other risk factors such as family history or working habits
According to Ma, et al. (2019), a significant association between lower LDL-C and higher risk of ICH when LDL-C was <70 mg/dL.
8) Is hemorrhagic stroke curable or reversible?
According to Garg et al. (2021), intracranial hemorrhage (ICH) is the most common neurologic complication of reversible cerebral vasoconstriction syndrome (RCVS). So, yes, it is curable or reversible as long as medical attention is promptly given. According to O'Carroll (2024), different therapies and management interventions such as iv fluids and rest can be employed to counteract the manifestations; mainly, it focuses on stopping the hemorrhage and increasing the blood clotting mechanisms of the body. Management of blood pressure is also given priority; surgical repair of the ruptured vessel may also be considered relative to the case.
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