Fall 2006 Nurs 253 Neuro/endocrine Exam

Front 1

What is the normal intracranial pressure and what are the normal values?

Lewis page: 1491-1492

Back 1

Intracranial pressure is the pressure that three different components (brain tissue, CSF, and cerebral blood volume) exert inside the rigid, unyielding skull.

Normal Values: 0-15mmHg
Normal Values: 60-150mm/H2O

Front 2

What is the significance of (IICP) increased intracranial pressure?

Lewis page: 1493

Back 2

IICP is a life threatening situation that results from an increase in any or all of the three components (brain tissue, CSF, cerebral blood volume)of the skull. Cerebral edema is an important factor contributing to IICP.

Front 3

What are three types of cerebral edema?

Lewis page: 1493-1494

Back 3

Vasogenic Cerebral Edema
Cytotoxic Cerebral Edema
Interstitial Cerebral Edema

Front 4

Briefly describe Vasogenic Cerebral Edema.

Lewis page: 1493

Back 4

Vasogenic Cerebral Edema is the most common type of edema, it occurs mainly in the white matter and is attributed to changes in the endothelial lining of the cerebral capillaries. These changes allow leakage of macromolecules from the capillaries into the surrounding extracellular space, resulting in an osmotic gradient that favors the flow if water from the intravascular to the extravascular space.

Front 5

Describe briefly Cytotoxic Cerebral Edema.

Lewis Page: 1494

Back 5

Results from local disruption of the functional or morphologic integrity of cell membranes and occurs most often in the gray matter. Cytotoxic Cerebral Edema develops from destructive lesions or trauma to brain tissue resulting in cerebral hypoxia or anoxia, sodium depletion, and syndrome of inappropriate antidiuretic hormone (SIADH). Cerebral edema results as fluid and protein shift from the extracellular space directly into the cells, with subsequent swelling and loss of cellular function.

Front 6

Briefly describe Interstitial Cerebral Edema.

Lewis page: 1494

Back 6

Is the result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus. It can also be caused by enlargement of the extracellular space as a result of systemic water excess (hyponatremia). Fluid moves into the cells to equilibrate with the hypoosmotic interstitial fluid. Regardless of the cause of the cerebral edema, manifestations of IICP result unless compensation is adequate.

Front 7

What is CPP and how do changes effect the patient?

Lewis page:1492

Back 7

CPP or cerebral perfusion pressure is the pressure needed to ensure blood flow to the brain or simply the pressure at which the blood perfuses the brain cells.

Front 8

What is the formula to calculate CPP?

Lewis page: 1492

Back 8

CPP=MAP-ICP

MAP=SBP + 2(DBP)/3

Front 9

Describe the effects of CO2 factors have on cerebral blood flow.

Lewis page: 1493

Back 9

The partial pressure if arterial carbon dioxide (PaCO2) is a potent vasoactive agent. An increase in PaCO2 relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance and increases CBF. Alternately, a decrease in PaCO2 reverses this process and decreases CBF.

Front 10

Describe the effects of oxygen factors have on cerebral blood flow.

Lewis page: 1493

Back 10

Cerebral oxygen tension below 50mmHg results in cerebral vascular dilation. This dilation decreases cerebral vascular resistane, increases CBF, and raises oxygen tension. However, if oxygen tension is not raised, anaerobic metabolism begins, resulting in an accumulation of lactic acid. As lactic acid increases and hydrogen ions accumulate, the environment becomes more acidic.

Front 11

Describe the effects hydrogen ion concentration factors have on cerebral blood flow.

Lewis page: 1493

Back 11

As lactic acid increases and hydrogen ions accumulate, the environment becomes more acidic. Within the acidic environment, further vasodilation occurs in a continued attempt to increase blood flow. The combination of a severely low PaCO2 and an elevated hydrogen ion concentration (acidosis), which are both potent cerebral vasodilators, may produce a state where in auto regulation is lost and compensatory mechanisms fail to meet tissue metabolic demands.

Front 12

Describe how vomiting assessments are related to and increase in ICP.

Lewis page: 1496

Back 12

* Usually not preceeded by nausea
* Nonspecific sign of IICP

This is called unexpected vomiting and is related to pressure changes in the cranium. Projectile vomiting may also be seen and is related to increased ICP.

Front 13

Describe how headache assessments are related to and increase in ICP.

Lewis page: 1496

Back 13

* Compression of the intracranial structures such as the walls of the arteries and veins and the cranial nerves can cause a headache.
* Usually worse in the morning.

Front 14

Describe how a decrease in motor function assessments are related to and increase in ICP.

Lewis page 1495

Back 14

As the ICP continues to rise, the patient manifests changes in motor ability. A contralateral hemiparesis or hemiplegia may be seen, depending on the location of the source of the increased ICP. If painful stimuli are used to elicit a motor response, the patient may enhibit localization to the stimulior a withdrawl from the stimuli. Decorticate (flexor) and decerebrate (extensor) posturing may also be elicited by noxious stimuli.

Front 15

Describe how ocular signs assessments are related to and increase in ICP.

Lewis page: 1495

Back 15

* Changes in pupil size, equality, and reaction to light, and extraocular movements are indicative of compression of the 3rd, 4th and 6th cranial nerves.