A Synthesis of The Relationship Between Reproduction and Intracranial Regulation Kaitlyn Walters Nurs 4000 Dr

A Synthesis of The Relationship Between Reproduction and Intracranial Regulation
Kaitlyn Walters
Nurs 4000
Dr. Souter
University of Mary Hardin-Baylor Scott and White College of Nursing
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Abstract
This paper explores the correlation between reproduction and intracranial regulation. Information retrieved from Porth’s pathophysiology and Concepts of nursing Practice were used to define and describe signs and symptoms of exemplars of reproduction and intracranial regulation. Additionally, research conducted by Swearingen and Donnelly, Ball, Dains, Flynn, Solomon, ; Stewart further explores seizures, increased intracranial pressure, pre-eclampsia, and gestational diabetes. The conclusion of this paper relates complications of reproduction to the effect it has on intracranial regulation and incidence of seizures. Further explanation of how research will be applied in the clinical setting will be noted along with the knowledge gained while constructing this paper.

A Synthesis of The Relationship Between Reproduction and Intracranial Regulation
Introduction
With each passing year, medical and nursing care becomes more advanced. There are new evidence-based techniques, procedures, and interventions introduced to the healthcare team. Often, it is easy to get caught up in the glamour of all the new that the foundation of practice is overlooked.
Within this synthesis, I will compare the concepts of reproduction and intracranial regulation. With each concept, a review of the pathophysiology, exemplars, medications, adverse effects of medications, expected outcomes, medical interventions, and nursing interventions will be researched along with the relationship of the two concepts and how the knowledge gained will be implemented into practice.
Reproduction
Reproduction is a common concept that has multiple different alterations and subparts that are often overlooked. While the overall idea of reproduction is the union of the sperm and an egg, the actual pathophysiology is quite complex. For reproduction of the human to be possible, both the male and the female reproductive systems must be working. This means that the female must be both menstruating and ovulating and the male must be producing sperm.
After the sperm reaches the egg and achieves fertilization, the egg travels to the uvula to implant. Here is where the concept gets perplex. Amidst the joining of the sperm and the egg to form the gamete, there are multiple divisions of cells and exchanges of chromosomes to form the individual. A multitude of alterations could occur such as that known as down syndrome, the condition of having an extra chromosome. This division is a crucial time for the gamete which is referred to as just a “clump of cells” by many but with research, you understand that this is the very making of the innermost individual. It Is now that hair color is determined, features are picked based on dominant or recessive genes, and even personality traits are inscribed in the cells of the gamete all in 8 weeks of conception.
The remarkable characteristic of reproduction that sets it apart from all other concepts is that it does not affect just one person, the entire physiology of the woman carrying the child is altered at the same time. The blood supply of the mother now must facilitate another life’s blood supply, hormones from the mother help form the fetus and even the diet of the mother can alter the fetus’ metabolic state and effect the birth of the baby.
Two exemplars of reproduction that will be discussed in this synthesis is pre-eclampsia/eclampsia and gestational diabetes. Both exemplars have variable risk factors, life threatening effects, and can alter the reproductive state of the carrying mother and viability of the fetus all together.
Pre-eclampsia
Pre-eclampsia is defined by Swearingen as, “blood pressure is elevated (more than 140 mm Hg systolic, more than 90 mmHg diastolic) and accompanied by significant proteinuria” (Swearingen, 2016). Pre-eclampsia may seem as though it is only hypertension while pregnant, but it is its potential complications that make the diagnosis so deadly. If pre-eclampsia continues to progress, the mother may develop HELLP syndrome (hemolysis of red blood cells, elevated liver enzymes, and low platelets), a deadly diagnosis for both mom and baby. Additionally, pre-eclampsia can progress to eclampsia. This is when the mother begins having seizures because of the elevated blood pressure. Porth suggests that the etiology of preeclampsia is widely unknown however, it occurs primarily during the first pregnancies, and during subsequent pregnancies in women with multiple fetuses, diabetes mellitus, collagen vascular disease, or underlying kidney disease (Porth, 2015). Also, preeclampsia is associated with a condition called a hydatidiform mole, an abnormal mass of cysts that develops due to an abnormal pregnancy caused by a pathologic ovum (Porth, 2015). Porth further poses the suggestion that preeclampsia could be attributed to the placenta as considerable evidence suggests that the definitive cure of the manifestations is delivery. Pregnancy induced hypertension is thought to involve an overall decrease in blood flow to the placenta which leads to the release of toxic mediators that cause endothelial cells of blood vessels throughout the body to constrict and alters their function entirely which results in the manifestations of preeclampsia (Porth, 2015).
Manifestations. Swearingen notes that in assessment, patients with pre-eclampsia present with elevated blood pressure with proteinuria, decreased fetal movement, spontaneous bruising, prolonged bleeding, and epistaxis. The definitive range of blood pressure to diagnose the patient with preeclampsia is a systolic blood pressure greater than 140 mmHg or a diastolic blood pressure greater than 90 mmHg with the greater than 300 mg of protein present in the urine in a 24-hour period after the 20th week of gestation (Porth, 2015). The client can present with more than 1.5 kg/ month or more in the third trimester and risk of oligohydramnios. Additionally, hyperreflexia is evident in severe pre-eclampsia along with, a continuous headache, nausea and vomiting, blurred vision, epigastric pain, oliguria, edema, pulmonary edema, elevated liver studies, elevated creatinine, late decelerations, and placental ischemic necrosis with the baby small for gestational age (Swearingen, 2016). These signs and symptoms occur after the 20th week of pregnancy with proteinuria without the presence of hypertension before conception.
Nursing management. Nursing management includes monitoring the lab studies and frequently assessing the client every four hours. Diagnostic tests that should be ordered include, Complete Blood Count (CBC), renal function studies that detect proteinuria, rising serum creatinine, uric acid, and blood urea nitrogen, Liver function tests such as ALT, AST, and LDH that rise with severe preeclampsia and HELLP syndrome, platelet count, obstetric ultrasound, and daily fetal activity monitoring, such as nonstress testing and biophysical profile (Swearingen, 2016). Assessment should be of urine output, presence of mental changes and/or headache, blood pressure, heart rate, rhythm and quality along with respiratory rate and lung sounds. Fluid intake should be monitored along with fundal height, ultrasound for fetal movement, asse4ssment of fetal heart rate and patterns, assess for signs of placental abruption and vaginal bleeding and frequent assessment of fetal response to any medication or treatment. The nurse should maintain a therapeutic environment for the client by keeping the room quiet and dark and limiting visitors to decrease stress on the client. The client should be positioned in the left lateral position and seizure precautions should be implemented. The nurse should teach the client to eat a healthy and balanced diet full of nutrients and explain that salt should not be added as the blood pressure does not need to be increased. Baseline parameters of fetal heart rate (FHR), maternal vital signs, and uterine activity should be obtained before administering any drug related therapy. Invasive procedures should be kept to a minimum. The nurse should develop an educational plan tailored to the patients and family’s cognitive ability. The client should be informed of the effects of preeclampsia on pregnancy, delivery, and both fetal and maternal wellbeing (Swearingen, 2016).
Medical Management. Porth suggests that early prenatal care is key to diagnose and detect preeclampsia. If preeclampsia is detected, close monitoring and bed rest is the traditional therapy. Antihypertensive medications may be required and chosen carefully because of their potential adverse effects on uteroplacental blood flow (Porth, 2015).
Medication Management. Magnesium sulfate, though dangerous and potentially toxic, along with Labetalol is the gold standard for preeclampsia treatment. Calcium Gluconate may have to be administered if the client begins to reach toxic levels of magnesium or present signs of magnesium toxicity. Agents such as Misoprostol and oxytocin may be used to induce labor. Oxygen via facemask and maternal corticosteroid therapy with betamethasone is recommended (Swearingen, 2016).
Outcomes of medication. Magnesium Sulfate is used to depress the central nervous system (CNS). By depressing the CNS, the medication helps to decrease the blood pressure of the mother and therefore, decreases the risk of seizure activity. However, Magnesium can depress the respiratory system causing respiratory arrest if at toxic levels. Furthermore, magnesium toxicity can depress deep tendon reflexes (DTR) and cause kidney compromise (Karch, 2015). These same effects can present in the fetus as the medication crosses the placenta. Labetalol is a betablocker used to lower the maternal blood pressure. Calcium gluconate is to counteract the depressing effects of magnesium. Misoprostol and Oxytocin are uterine ripening agents that stimulate the uterus to induce birth however, with overstimulation, the uterus could potentially rupture. Oxytocin can also cause fetal hypoxia, and CNS injury in the preterm new born. Betamethasone is a corticosteroid administered to the mother that helps stimulate the lung growth in the fetus in case of premature delivery (Swearingen, 2016).
Relationship Between Medications. Karch states that magnesium sulfate acts as a sedative on the uterus but has a systemic effect. This will decrease the contractions of the uterus and stop the premature labor. Calcium Gluconate should be kept at the bedside in case of magnesium toxicity as evidenced by decreased respiratory status and/or decreased deep tendon reflexes. Labetalol is a beta blocker medication used for hypertension and safe to use in pregnancy. By using this medication, the vessels will become relaxed and decrease blood pressure.
In the event of eclampsia, induction of birth is the only cure. To induce labor, Misoprostol and Oxytocin are used to ripen the uterus and stimulate contractions. Finally, betamethasone is a steroid used in the event of a premature birth to help mature the infant’s lungs. Betamethasone is used as soon as birth is imminent to aide in the production of the most mature lungs possible (Karch, 2015).
Gestational Diabetes
The culprit that alters the endocrine system and metabolism of glucose during pregnancy is the increase of estrogen and progesterone in the pregnant body (Trakolo, 2015). In the second half of pregnancy, the increased levels of prolactin, placental secretions of Human Placental Lactogen (hPL), cortisol, and glycogen causes a peripheral resistance to insulin. This happens as a type of protective mechanism, ensuring that glucose is readily available for the fetus (Trakolo, 2015). Gestational Diabetes (GDM) is a combination of insulin resistance and impaired insulin secretion. Insulin resistance is defined by Porth as “the failure of target tissues to respond to insulin (Porth, 2015).”
Manifestations. Typically, gestational diabetes is discovered when a standard glucose test is performed at 24 weeks. The diagnosis of gestational diabetes is reached if two or more of the following values are equaled or exceeded when taking the glucose test. A fasting glucose of 92 mg/dL, 1-hour glucose of 180 mg/dL or 2-hour glucose of 153 mg/dL. Typically, infants born from a mother with gestational diabetes are large for gestational age and are predisposed to macrosomia. An infant with macrosomia are predisposed to birth trauma like shoulder dystocia and clavicle fractures. Within 2-4 hours, the newborn’s body becomes hypoglycemic because of the increased insulin levels and depleted glycemic supply from the mother. Additionally, mothers with hyperglycemia have intrauterine growth restriction (IUGR). IUGR is caused by vascular changes in the mother that decrease the efficacy of placental perfusion. Respiratory distress syndrome is seen in the neonate with high levels of fetal insulin because of insulins ability to inhibit surfactant producing enzymes. The neonate is also susceptible to hyperbilirubinemia, this is a result of immature liver enzymes to metabolize the increased bilirubin because of the diminished ability of glycosylated hemoglobin in the mother’s blood to release oxygen.
Nursing management. Trakolo gives detailed management of gestational diabetes. Trakolo states gestational diabetes is managed by dietary measures, nonstress test, ultrasounds, birth timing, management of labor, and assessment of the neonate after birth.
Diet therapy and exercise are the gold standard management of gestational diabetes. The pregnant woman is taught that fruits and vegetables with lean meat should be most of her diet with cardiovascular exercise such as walking at least five times a week.
Nonstress testing is typically started around 28 weeks gestation and are increased to twice a week at 32 weeks gestation. Ultrasounds at 18 weeks confirm gestational age, multiple pregnancies, congenital anomalies, and monitor for IUGR or macrosomia.
While most diabetic pregnancy’s go to term, a cesarean birth may be indicated if the fetal status is no reassuring. Birth before term may also be indicated if women with vascular changes and worsening hypertension or evidence of IUGR exists.
During labor, the maternal insulin needs decrease however, it is imperative to control maternal glucose level to prevent neonatal hypoglycemia. Often, an intravenous (IV) line infusing 5% dextrose is utilized to help control maternal glucose levels (Trakolo, 2015).
Medical Management. Porth includes in the treatment of GDM, close observation of both the mother and fetus. Additionally, maternal fasting and postprandial blood glucose levels should be tested regularly along with a healthy diet, ensuring that both the mother and fetus are receiving necessary nutrients (Porth, 2015). Appropriate measures should be taken to make sure that normoglycemia and proper weight is gained along with the prevention of ketosis.
Medication management. The best medication for gestational diabetes is a change in eating habits. The pregnant mother should focus on eating fruits and vegetables rather than pastries and sweets. A diet change may be enough to combat the increased blood glucose and insulin resistance. Medications used in GDM include insulin and oral agents such as glyburide (Porth, 2015). Karch provides insight into the recommended medication management for gestational diabetes including use of Insulin, Metformin, Glyburide and 5% dextrose. Insulin is used to transport glucose into the cells and out of the vascular space. Metformin has been proven to cross the placenta, therefore, is not recommended for use in pregnancy. Glyburide facilitates management of gestational diabetes by stimulating increased insulin production. Finally, during birth, a bag of 5% dextrose is infused with a fixed dose of insulin to ensure that the mother has adequate glucose to be utilized during the stressful and exhausting event (Karch, 2015).
Outcomes of medication. These medications act to lower the blood glucose level by either pushing glucose into the cell or stimulating the pancreas to produce insulin. Overall, these medications ultimately get glucose out of the vascular space and into the cells so that it can be utilized and will not pose the mother and/or fetus to complications because of high blood glucose. With every medication, they can work “too” good. By this I mean that while they are used to lower blood glucose, they can lower the blood glucose to dangerously low levels resulting in alterations of overall health status, lower level of consciousness, or even injury from fainting (Karch, 2015).
Relationship between medications. Both Glyburide and Insulin ultimately produce the effect of decreasing blood glucose. Glyburide stimulates increased insulin production while insulin directly pushes glucose into cells. 5% dextrose is used for energy purposes and to ensure that hypoglycemia does not occur during labor. While it sounds counterintuitive to infuse a type of glucose into the already glucose dense patient, it is vital to make sure that the mother can make it through the birthing process without putting stress on the fetus (Karch, 2015).
Intracranial Regulation
Intracranial regulation is a concept that has the potential to affect all aspects and processes of the body. The brain is the control center for the body and from it stems all potentials. The pathophysiology as stated by the Critical Care Journal by Donnelly et. Al, the brain requires adequate supply of oxygen and nutrients. To do so, a circulatory system must be able to maintain optimal cerebral blood flow to allow the brain to achieve its diverse needs. Important regulators for cerebral blood flow include cardiovascular and cerebrovascular health and intracranial pressure as cerebral blood flow equals arterial blood pressure minus intracranial pressure divided by cerebral vascular resistance. Two exemplars that will be discussed that directly impact intracranial regulation are seizures and increased intracranial pressure. Both exemplars will alter cerebral blood flow/perfusion and the body’s ability to carry out otherwise natural processes (Donnelly, Budohoski, Smielewski, ; Czosnyka, 2016).
Seizure
Porth states that seizures represent “an abrupt and transient occurrence of signs and/or symptoms resulting from an abnormal, excessive discharge from an aggregate of neurons in the brain (Porth, 2015). Porth further breaks down the etiology of seizures to be provoked or unprovoked (epileptic) seizures. Provoked seizures are just as they sound, provoked. They are brought on by a cause such as a high fever, systemic metabolic disturbance, electrolyte imbalance, hypoglycemia, hypoxia, hypocalcemia, uremia, alkalosis, rapid withdrawal of sedative drugs and even specific central nervous system (CNS) injuries including, toxemia of pregnancy, water intoxication, meningitis, trauma, cerebral hemorrhage, stroke, and brain tumors (Porth, 2015).
Manifestations. Overall, seizures are merely manifestations of abnormal spontaneous electrical discharges from neural networks in the brain. They result from electrical changes of excitability of a single neuron or an entire network of neurons. Porth describes seizure activity as, “Seizure activity has the potential to impair the consciousness, involuntary motor movements, somatosensory disturbances, special sensory sensations, flushing, tachycardia, diaphoresis, hypotension or hypertension, or pupillary changes due to changes of the autonomic nervous system” (Porth, p. 947-948. 2015).
Manifestations of seizures can be further subdivided into phases. These phases are named the tonic phase, clonic phase, and postictal period. During the tonic phase, Trakolo describes it as an unconscious state with continuous muscular contraction (Trakolo, 2015). During this phase, the basal metabolic rate (BMR), rises and increases the body’s demand for glucose and oxygen. Following the tonic phase is the clonic phase. The clonic phase is characterized by continuous alternating muscular contraction and relaxation. Finally, the postictal period occurs following the seizure activity and is a state of decreased level of consciousness (LOC) when the client is sleepy but arousable (Trakolo, 2015).
Nursing management. Nursing management during seizures is focused on safety of the patient. The nurse should focus on maintaining the airway and be aware to never place anything in the mouth of a patient that is having a seizure. Along with maintaining the airway, the nurse should think of positioning. The client should be positioned on their side so that secretions can drain. Continuous monitoring of oxygenation by checking the color of mucous membranes, monitoring heart rate and pulse ox readings are vital along with administering oxygen if the oxygen saturation reading falls below 95%. The nurse should also be aware that patients with seizures can harm themselves even while in bed so special precautions of padding the bed rails should be taken. When administering medications, the nurse should be sure to push the medications slowly to minimize the risk of respiratory or circulatory collapse (Trakolo, 2015). In emergency situations, a jaw thrust maneuver may have to be performed to open an obstructed airway, suction equipment should be readily available at the bedside in case of copious secretions, vital signs and circulation should be monitored along with a complete neurological assessment. An IV line should be infusing in case of a need to administer necessary fluids or glucose, a nasogastric (NG) tube should be inserted and thermoregulation should be managed.
Medication management. Medication management for seizures focuses on benzodiazepines and antiepileptic drugs. Benzodiazepines include diazepam, lorazepam, or midazolam. If seizure activity continues, the next step is often antiepileptic drugs. Drugs in this category include, Phenytoin, phenobarbital, primidone, carbamazepine, valproic acid, ethosuximide, clonazepam, gabapentin, lamotrigine, and tiagabine hydrochloride. The main mechanism of action of these drugs as stated by Trakolo is that they act in the motor cortex of the brain to reduce the spread of electrical discharges from the rapidly firing epileptic foci in this area. These agents control seizures without impairing the normal functions of the CNS (Trakolo, 2015).
Outcomes of medication. These medications alter activity in the CNS system and essentially slow it down so adverse reactions such as decrease in blood pressure, pulse, and respirations should be monitored. Other CNS activity that could be dangerous to the patient is blurred vision, dimmed vision, slurred speech, nystagmus, confusion or even gingival hyperplasia in the client taking phenytoin (Trakolo, 2015).
Relationship between medications. The medications work cohesively to create an environment in the brain to decrease the risk of seizures. These measures include, closing or disabling sodium channel gates, increasing GABA at receptor sites, or sedating the patient all together (Karch, 2015).
Increased intracranial pressure
Intracranial pressure is the pressure inside of the brain. The pressure is composed of brain tissue, cerebral spinal fluid (CSF) and blood. According to the Monroe Kellie hypothesis, the volumes of the three intracranial components compensate for one or both other components without a marked change in ICP (Porth, 2015). Intracranial Pressure increases most commonly when a traumatic event occurs. Ischemia and elevated partial pressures of carbon dioxide in the blood which causes systemic vasodilation increases intracranial pressure.
Pathophysiology. The cranial cavity contains about 10% blood, 80% brain tissue, and 10% CSF (Porth, 2015). These components are kept in a rigid, nonexpendable skull. Each of these components contribute to the ICP which is normally within a range of zero to fifteen mmHG (Poth, 2015). An increase in intracranial pressure can lead to ischemic injury and damaged neurons.
Porth explains, “ICP is the pressure within the intracranial cavity. It is determined by the pressure volume relationships among the brain tissue, cerebrospinal fluid, and blood in the intracranial cavity; the monro-kellie hypothesis, which relates to reciprocal changes among the intracranial volumes; and the compliance of the brain and its ability to buffer changes in intracranial volume (Porth, p. 930, 2015)”.
Of the three components, blood and cerebrospinal fluid are most easily manipulated. CSF can be translocated to the subarachnoid space and re-absorbed and blood is contained in a low-pressure system than can be changed by vasoconstriction or vasodilation. Brain tissue however, is restricted to much change or compensation. ICP is managed by the body’s natural recognition of pressure changes and displacement of fluid. When there’s too much CO2, the body vasodilates and increases the ICP. When there is increased fluid volume in the intracranial space, the body displaces CSF to the subarachnoid space to lower ICP (Porth, 2015).
Manifestations. Headache, vomiting, papilledema or deviation in eye movements due to pressure on the cranial nerves and abnormal posturing (Porth, 2015). Because the brain controls all bodily functions, any alteration of intracranial regulation causes normal control of body functions to be lost. Increased pressure in the brain can place pressure on the nerves causing involuntary movements. Ball, Dains, Flynn, Solomon, & Stewart explains that the high-pressure environment facilitates vessel constriction and the formation of headaches, vomiting and abnormal decerebrate or decorticate posturing. Decorticate posturing is caused by damaged nerve pathways between the brain and spinal cord. Decorticate posturing indicates that a hemisphere, the thalamus, or the midbrain is damaged. Decorticate posturing presents as all extremities being tightly brought to the center of the patient. (Ball, J., Dains, J. E., Flynn, J. A., Solomon, B. S., & Stewart. 2014). Decerebrate posturing is the hyper extension of all extremities. Decerebrate posturing is often thought to be worse than decorticate posturing as decerebrate posturing indicates brainstem damage or even herniation (Ball, et al. 2014).
According to Swearingen, early indicator of changes in increased ICP include, declining Glasgow coma scale score (GCS), alterations and changes in LOC ranging from irritability, restlessness, confusion and lethargy. Other signs indicating an increased intracranial pressure is onset or worsening of headache, pupils that are not equal, round, reactive to light, or do not accommodate. Visual disturbances such as diplopia or blurred vision can begin to occur along with sluggish or weakening sensorimotor activity of muscles.
Late indicators include a continuing decline and GCS, continued deterioration in LOC leading to stupor and coma, projectile vomiting, hemiplegia, abnormal posturing, widening pulse pressure, decreased heart rate, increased systolic blood pressure, Cheyne-Stokes breathing or other respiratory irregularity, papilledema, and impaired brain stem reflexes (Swearingen, 2016).
Nursing management. Nursing management of increased ICP is continuous monitoring and assessment of worsening condition and/or impending herniation. Preventative measures should be taken for patients with increased ICP such as ensuring a patent airway, delivering O2 as prescribed, and collection and assessment of arterial blood gasses (ABG) and pulse ox values may be required as well. The nurse should place the patients head in a neutral position and the head of the bed slightly elevated at 30 degrees as hyperextension or flexion of the neck, hips, supine and Trendelenburg positions increase the ICP. The nurse should also perform passive range of motion exercises on the patient so that muscle integrity is maintained during their stuporous condition. Analgesics and epileptic drugs might be prescribed to be administered. A quiet and calming environment should be maintained by decreasing noise and stimuli. This means the nurse should cluster cares and encourage family members to talk in a quiet voice. Stress should be reduced for the patient so painful procedures should be limited, unnecessary touch should be avoided and continuous tension such as a blood pressure cuff left on the patient should be avoided at all costs. The nurse and family should also be careful to not say anything in front of the patient that would not be said if they were awake. The nurse should take the time to individualize care so that rest periods and activities are spaced adequately for the patient (Swearingen, 2016).
Medical management. Being that the brain is the control center for the body, the medical team must be proactive and consider all preventative interventions in case the brain is unable to regulate systems of the body anymore. Doctors will order labs and levels to be checked daily. Labs are vital to monitoring brain function, perfusion, nutrition status, glucose level, kidney function, and alkalosis or acidosis in the body, all which effect healing and ICP. The doctor will also order medications as needed to control symptoms of ICP and to decrease stress on the body such as antihypertensives, sedatives, osmotic and loop diuretics, muscle relaxants, stool softeners and sedatives. Orders for drains and tubes to be placed are the doctor’s responsibility and should only be placed if necessary as catheters, rectal tubes, and nasogastric tubes can twist and kink causing an increase in ICP. To directly lower the ICP, the doctor can place a shunt to drain excess fluid and monitor ICP. An electroencephalography (EEG) should be ordered to monitor brain function and perfusion. The patient may have to be intubated and placed on a ventilator if the respiratory center begins to fail although, the positive end expiratory pressure (PEEP) should be kept as low as possible so not to increase ICP.
Medication management. Karch lists many methods of managing increased intracranial pressure via medications. Labetalol acts on the beta cells to relax the vessels to decrease blood pressure, a component of ICP. The patient should be kept in a sedated state to allow for healing of the brain. However, should the patient become agitated or restless, noninvasive measures such as relieving kinks in lines, decreasing painful stimuli, or removing restraints should be taken first before medication. Diphenhydramine, Haloperidol, lorazepam, midazolam sedates the patient by enhancing the effect of the neurotransmitter gamma-aminobutyric acid (GABA). Muscle relaxants can be used for the same reason as sedatives and promotes comfort for the patient. Propofol, Atracurium, Pancuronium are neuromuscular blocking agents that compete for acetycholestine receptor sites. Antiepileptic drugs such as Phenobarbital, Methylphenobarbital, Barbexaclone, and Phenytoin, Gabapentin, decrease risk of seizures by increasing the amount of GABA at receptor sites, or by causing voltage-dependent block of voltage gated sodium channels. Loop or osmotic diuretics such as Furosemide and Mannitol, decrease ICP by removing excess fluid from the intracranial space (Karch, 2015).
Outcomes of medications. The purpose of every medication ordered is to reduce stress on the body and lower ICP. Antihypertensive medications decrease cerebral perfusion which lowers ICP, sedatives relax the patient and decrease stress on the body as does antianxiety agent and muscle relaxants, antiepileptic drugs help prevent seizures that could be caused from increased ICP, and diuretics decrease volume in the intracranial space (Karch, 2015).
Relationships between medication. All the medications work different actions to create the same effect, a decreased ICP. Antihypertensives decrease perfusion pressure along with diuretics by taking fluid out of the intravascular space and surrounding area. Anticonvulsants work to prevent seizures so that ICP does not increase even more and cause additional deficits while sedatives create a calm and stress-free environment for the patient to promote healing (Karch, 2015).
Relationships between the concepts
At first thought, the correlation between reproduction and intracranial regulation is difficult to see however, they are very closely related. Ultimately, it is the complications of reproduction that link the concepts together and increase the ICP.
When the pregnant female begins to enter pre-eclamptic state, the blood pressure is at an alarmingly high level that increases the cerebral perfusion pressure and intracranial pressure to a point to even eclampsia, the presence of seizures.
Gestational diabetes increases the metabolic demand on the body. If blood sugar reaches dangerously high levels, the vessels could become damaged as the intravascular volume expands, increasing ICP. Gestational diabetes also makes the mothers diagnosed with the ailment more prone to having seizures and altered LOC.
Summary and conclusions
In conclusion, factors that cause increased ICP are all prevalent in alterations during pregnancy. It is the high blood sugar that could predispose pre-eclampsia, that could cause seizures, that increase intracranial pressure. The body has a design to help compensate for slight alterations, but it is the nurses job to be one step ahead and prevent adverse events from potentially occurring.
I learned that reproduction and intracranial regulation are tightly connected, and it is the nurse who should be the first to catch signs of increasing ICP in the pregnant woman. The signs are often subtle, but a watchful eye could notice the slight changes. Pregnancy can cause a decreased amount of blood return to the brain if the pressure of the baby sits on major vessels, especially when the pregnant mother is sleeping on her back. It is essential to reinforce education of proper sleeping habits during pregnancy to reduce this risk that can cause an avoidable problem. Other factors influencing intracranial regulation during pregnancy include habits that can cause complications. These habits include, consuming too much sugar and/or salt, decrease in amount of exercise, and increased stress because of changes in daily life. It is imperative to closely monitor pregnant women for any changes in baseline as that could be the signs of gestational diabetes or pre-eclampsia forming.
Gestational diabetes and Pre-eclampsia are can cause such changes in the brain that a seizure can be induced, increasing ICP, and depriving both mom and baby of oxygen. This is a particularly fatal effect of pregnancy complications as they can result in death of one of or both fetus and mother.
I will relate all of this to practice by being diligent in performing basic nursing duties. Although assessment is the foundation for nursing care, it is often brushed off as a routine chore rather than a vital component of quality nursing care. I will be sure to know my patients baselines and do a thorough objective and subjective assessment of my patients. If a change in level of consciousness or increase of blood pressure and/or blood glucose is found, I will reassess and then utilize my healthcare team to determine what interventions to take and call the doctor to update him on patient changes. A nurse should always step onto the unit expecting a change so that she can be one step ahead to give patients the care they need immediately. Ultimately, I will remember that there is a reason that fundamentals are the foundation of nursing care. While cutting edge interventions and skills are fun, it is the assessment of the patients that will save their lives and make a great nurse.

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References
Ball, J., Dains, J. E., Flynn, J. A., Solomon, B. S., & Stewart, R. W. (2014). Seidel’s guide to physical examination.
Donnelly, J., Budohoski, K. P., Smielewski, P., & Czosnyka, M. (2016). Regulation of the cerebral circulation: bedside assessment and clinical implications. Critical Care, 20, 129. http://dewey.umhb.edu:2363/10.1186/s13054-016-1293-6
Karch, A. M. (2015). 2015 Lippincott pocket drug guide for nurses. Philadelphia: Wolters Kluwer.
Swearingen, P. L. (2016). All-in-one care planning resource: medical-surgical, pediatric, maternity & psychiatric nursing care plans (4th ed.). Philadelphia, PA: Elsevier/Mosby.
Porth, C. (2015). Essentials of pathophysiology: Concepts of altered health states (4th ed.). Philadelphia: Wolters Kluwer.
Trakolo, K. (Ed.). (2015). Nursing: A concept-based approach to learning (2nd ed., Vol. 1 & 2). Upper Saddle River: Pearson.