Increasing carbon dioxide (PaCO2) causes vasodilatation of cerebral arterioles, thus increasing cerebral blood flow.
The decrease vasocontriccion produces carbon dioxide. thus reducing central blood flow.
Two mechanisms of ECT.
1.The impact that receives the skull and its contents to be beaten by a strong element while at rest. This produces a lesion on the scalp, bone, dura and brain parenchyma.
2. Injuries resulting from rotational acceleration and deceleration during which forces occur conclusion.
Pathophysiologic
Basal condition or preinjuria: Conditions of the patient that can influence evolution. Age, background morbid, accident severity.
Primary Injury: A direct consequence of trauma, child may be avoided. Ex erosions scalp, scalp wounds.
The diffuse axonal injury is characterized by tearing and micorscopicamente axonal disruption with formation of small hemorrhages in the brain stem. What that translates into impairment of consciousness.


The secondary injury is the result of worsening primary or local or systemic conditions.
Intracranial lesions: They generate varying degrees of ischemia, altering the metabolic environment, they increase susceptibility to brain injury:
Intracranial hematomas.
Extradural hematomas,
Acute subdural hematomas
Seizures
Cerebral Edema
Cerebral ischemia

Systemic lesions: lead to a reduction in transport of O2

Hypotension, pain
Hypoxemia
Hypercarbia
Anemia
Hyperthermia
Acidosis
Alterations of glucose.

Intracranial Pathophysiology:
Intracranial contents: brain parenchyma, blood volume, cerebrospinal fluid. Usually these three are in balance.
The intracranial pressure volume equals the volume of CSF + blood + brain size.
The increase in any of these causes increased ICP.
In a TEC this balance is lost:
Increases in ICP that produces a decrease in cerebral perfusion by decreasing the hypercarbia which is the increase in CO2 causes vasodilatation Concentrates thus increasing blood volume and thus the edema.
Intracranial Hipertencion stages.
First Stage: changes in intracranial volume at the expense of displacement of CSF and / or blood. No change yet in ICP.
Second Stage: gradual elevation of ICP, bradycardia and hypertension.
Stage Three: Lack of regulatory mechanisms to compensate for changes in ICP and formation of herniations.
Fourth Stage: Irreversible
Headaches occur expansive process difficult manejopor
Projectile vomiting
Autonomic signs (Cushing triad)
Homolateral mydriasis
Signs of herniation
If the increase in ICP and hypercarbia, arterial hypotension plus hypoxia and ischemia appears.
The increased arterial systolic pressure reflects the increase in ICP and is part of the Cushing reflex.
Diagnostic tests: skull radiographs
CT skull
MRI
Examanes hematological: hemoglobin, hematocrit, clotting time ELP, Glucose, Urea, Creatinine, arterial blood gases.
The TEC is classified by severity according to the Glasgow.
Mild: 14 to 15 G
Moderate: G 9 a13
Grave: G 3 to 8

Handling:
A) handling of the airway and cervical spine (oxygen and ventilation)
Lifting head 30 °
B) oxygen and ventilation to maintain PCO 2 at 25 to 30 mmHg. Saturation above 95%
Hyperventilation to reduce CO2.
C) Fluid: isotonic solutions at a given speed to reduce the risk of cerebral edema. Use of sedatives, analgesics (minimize secondary injury)
Use of Diuretics: Mannitol: ICP decreases plasma expansion by reducing the hematocrit and blood viscosity. The osmotic effect increases the serum tonicity extracting liquid brain parenchyma edema, improving microcirculation by increasing cerebral blood flow and O2 transport. This is done after intubation if required EIT.

Nursing Diagnosis:
Altered cerebral tissue perfusion related to increased intracranial pressure and inflammatory process manifested by edema, hemorrhage, hypoxia, hypoxia and Glasgow.
Objectives: To improve cerebral perfumer restore ICP to normal levels
Posts: Administer O2 as Saturations requirement to maintain 95% or more.
Position 30 ° -45 °
Administer Medication EV
Monitorizacion vital signs
Rating Glasgow.
Rating: patient improves blood perfusion without evidence of Cushing, oximetry improved.
Head injury-related pain VAS expressed verbally and fascia.
Objective reduce pain.
Posts: administer analgesia as directed.
Position semisitting
Comfortable
Oxygenation
Comfortable and quiet.
Evaluate EVA.
Evaluation: Patient reducing pain.
You will be equipped with required knowledge from proper CNA training.

• Hypertension associated with:
  • Acute left ventricular failure
  • Acute coronary insufficiency
  • Dissecting aortic aneurysm
  • Severe hypertension more acute
    nephritic syndrome
  • Scleroderma renal crisis
  • Microangiopathic hemolytic anemia

  
  

  • Intracranial hemorrhage
    • Subarachnoid hemorrhage
    • Cerebral hemorrhage
  • Arterial surgery sutures
• Hypertensive encephalopathy
• Eclampsia
• Pheochromocytoma in hypertensive crisis and further increases in catecholamines
• Hypertensive crisis post:
  • Abrupt withdrawal of clonidine
  • Food and Drug Interactions with MAO inhibitors
  • Cocaine
• Severe hypertension after emergency surgery or in the immediate postoperative

• Hypertension with DBP> 130 mm Hg uncomplicated
• Hypertension associated with:
• Heart failure without EPA
• Stable angina
• Stroke

Hypertensive Urgency

• Adequate ventilation (arterial PCO2 approximately 35 mmHg).
• Maintain adequate oxygen saturation (arterial Po2 from 80 to 100 mmHg): Use the lowest pressure positive end-expiratory possible.





• Arterial pH = 7.3 to 7.5.
• Immobilization (neuromuscular paralysis), if necessary.
• Sedation (eg. Morphine or diazepam), if necessary.
• Anticonvulsants (eg. Diazepam, phenytoin or barbiturates), if necessary.




• Standardized blood values (hematocrit, electrolytes, osmolality and glucose). Administer a bolus of glucose if hypoglycemia, administer insulin if glucose> 200 mg%.
  Administer thiamine (100 mg) in case of malnutrition or alcoholism.
• Osmotherapy (mannitol or glycerol), if required for elevated ICP monitored or secondary neurological deterioration.
• Avoid hypotonic fluids, keep the serum sodium concentration and prevent fluid overload.
• If the temperature is> 37.5 ° C, start treatment.
• Initiate nutritional support within 48 hours.