Nursing reflection in icu cardiac arrest

University of Virginia Residency: Hospital of the University of Pennsylvania Fellowship:

Nursing reflection in icu cardiac arrest

Paralysis of the palate, pharynx, and vocal cord Loss of taste in posterior third of the tongue Contralateral loss of pain and temperature sensation in the trunk and limbs Tachycardia and dyspnea Palatal myoclonus involuntary jerking of the soft palate, pharyngeal muscles, and diaphragm Kaye, ; Tidy, Basilar Artery Stroke Syndrome Cutting off the blood supply to the entire field of the basilar artery will result in: Bilateral neurological problems, such as bilateral sensory and motor deficits Combined cerebellar and cranial nerve problems Hemiparesis with contralateral cranial nerve dysfunction or with ipsilateral ataxia Behavioral abnormalities Occlusion of the basilar artery is commonly catastrophic, resulting in: Growth of the lesion begins immediately after the onset, and the largest volume of tissue infarction occurs within 10 minutes of stroke Nursing reflection in icu cardiac arrest.

Over half of the total infarct volume occurs within 30 minutes of stroke onset Zhang et al. The acute stage begins six hours after the onset of the stroke. During this stage, release of inflammatory mediators from ischemic brain tissue leads to vasogenic edema with extravasation of water molecules from blood vessels to expand the interstitial spaces.

This is a major deleterious type of brain edema, which persists for several days. Imaging during this period shows the involved area is soft and edematous, with a blurring of anatomic detail. During the subacute stage there is obvious tissue destruction and liquefactive necrosis of the involved brain.

Liquefactive necrosis results in a transformation of tissue into a liquid mass. In the chronic stage of stroke, the damaged tissue has been phagocytized and there is cavitation with surrounding gliosis, a process leading to scarring ISC, Cell and Tissue Injuries Caused by Strokes Stroke pathophysiology includes ischemic and mechanical damage.

For decisions about acute treatment, the particular stroke syndrome is usually less important than the type of vascular injury that has occurred. Both ischemic and hemorrhagic strokes cause ischemic damage. Hemorrhagic strokes cause additional ischemic damage due to the pressure that builds from the excess blood that has been released into the brain or the cerebrospinal fluid.

This increase in intracranial pressure presents additional problems for the hemorrhagic stroke patient, particularly in the acute phase and within the early recovery period.

When cerebral blood flow is reduced, the affected regions of the brain begin to stop functioning and the patient begins to lose the ability to perform the tasks that are localized in those regions. Complete Global Ischemia If the blood supply to a brain region is cut off entirely, as occurs most commonly during cardiac arrest, cell damage is widespread and neurons begin to die quickly.

The brain uses energy at a high rate, but it can only store a small back-up supply of energy. Complete ischemia immediately decreases the available oxygen and glucose in the affected region of the brain, and without continual nourishment, local neurons will run low on their internal back-up stores of adenosine triphosphate ATP within seconds.

The depolarization also sets off the release of unusually large amounts of extracellular excitatory neurotransmitters. These events cause the influx of calcium ions, which set off an unregulated intracellular cascade of calcium-triggered processes, including the activation of catabolic enzymes, such as proteases, phospholipases, and endonucleases.

In a short time, the neuron self-destructs and dies. Incomplete Ischemia Most strokes do not produce complete ischemia. Many ischemic strokes leave arteries only partially blocked. Even when an artery is entirely occluded, the cerebral circulation has some collateral coverage with overlap and interconnections, and some blood usually gets to the affected brain regions via other routes.

The perfusion that remains will vary throughout the ischemic region. A common pattern is severely reduced perfusion in the core of an ischemic region, with gradually increasing perfusion toward the edges.

Abstract | European Association of Hospital Pharmacists

Neurons become functionally silent when their arterial perfusion drops by a small amount. In a stroke, as soon as cerebral blood flow is reduced, electrical activity stops in the affected region of the brain and neurological deficits appear.

For a time, the silent neurons remain alive, but they no longer have the energy to generate membrane potentials that are sufficient to respond to stimuli or to transmit signals.

However, to remain alive, the silent neurons still need some arterial perfusion.

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In most strokes, patients lose neurologic functions early, before all the neurons in the affected area are irreversibly damaged. Typically, strokes leave enough arterial perfusion that many neurons can maintain a low level of energy production sufficient to slow the onset of their deaths Joseph, In those parts of the affected region that have no blood flow, neurons begin to die in less than 10 minutes, and for every hour untreated, the brain ages 3.

Nursing reflection in icu cardiac arrest

In every infarct there is a central core of total ischemia and cell death that is irreversible. This central core is surrounded by a zone of borderline ischemic tissue called the ischemic penumbra.– The role of Cardiac Rehabilitation in Secondary Prevention: looking back and moving forward Meshal AlModhy.

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