Term
|
Definition
| Prerenal- is kidney dysfunction caused by inadequate renal blood flow, resulting in renal hypoperfusion and renal ischemia. Structural damage has not yet occurred and the condition is reversible. The kidneys are able to tolerate a wide variation in blood flow without causing tissue damage, however, as blood flow falls so does glomerular filtration rate (GFR). As CO, BP, and blood flow all decrease, the kidneys intrinsic compensatory mechanisms fail and ischemic changes occur. |
|
|
Term
| prerenal Maintain MAP and hourly urinary output |
|
Definition
| . Maintain MAP of at least 70mmHg and an hourly urinary output of 25-30mL/hr as indicators of adequate GFR. |
|
|
Term
| common causes of acute prerenal renal injury |
|
Definition
Excessive Fluid loss (vascular: Hemorrhage, skin: Severe burns, gastrointestinal: Vomiting and diarrhea, Renal: Polyuria, Endocrine: diabetes insipid us).
Decreased renal perfusion (Decreased CO, Heart failure, Myocardial Infarction, third spacing of fluids).
Increased vascular capacity (Shock states).
Vascular obstruction (Embolus, Dissecting aortic aneurysm, tumor).
Drugs that alter renal hemodynamics (Angiotensin converting enzyme inhibitors, Amphotericin B, Angiotensin receptor blockers, Cocaine, Cyclosporine, NSAIDS) |
|
|
Term
|
Definition
| is caused by problems involving the renal parenchyma (renal tissue) and is categorized further by the primary injury site. |
|
|
Term
|
Definition
| syndrome characterized by excessive muscle breakdown that causes release of muscle cell contents in large quantities. The most common cause is severe crush injuries seen in multiple traumatic injuries. |
|
|
Term
| common causes of acute intrarenal injury |
|
Definition
Ischemia (secondary to prerenal failure),
Nephrotoxicity (drugs, aminoglycosides, contrast dyes, ethylene glycol, NSAIDS),
Rhabdomyolysis (crush injuries, severe burns, compartment syndrome, severe exertion, seizure activity, certain drug side effects [HMG Co-A reductase inhibitors for hypercholesterolemia]),
Intratubular obstruction (cellular debris, myoglobin casts, uric acid crystals). |
|
|
Term
|
Definition
| causes of renal injury include any obstruction to the outflow or urine from the kidneys. Bilateral obstruction will precipitate renal injury resulting from backup pressure caused by increasing volume of urine proximal to the obstruction. |
|
|
Term
| common causes of acute postrenal injury- |
|
Definition
Mechanical causes (Blood clots, calculi, tumors, prostatic hypertrophy, prostate cancer, urethral strictures),
Functional causes (Diabetic neuropathy, neurogenic bladder, certain drugs [parasympatholytics]). |
|
|
Term
|
Definition
Risk
Injury
Failure
Loss
ESRD |
|
|
Term
|
Definition
| Risk: GFR criteria- Increased serum Cr by 1.5 times or more GFR decreased by more than 25%. Urinary Criteria- Urine output less than 0.5mL/kg for 6 hours. |
|
|
Term
|
Definition
| Increase serum Cr by 2 times or GFR decreased by more than 50%. Urine criteria- Urine output less than 0.5mL/kg for 12 hours. |
|
|
Term
|
Definition
| Increased serum Cr by 3 times or GFR decreased by 75% or serum Cr at or above 4mg/dl. Urine criteria: - Urine output less than 0.3mL/kg or anuria for 12 hours. |
|
|
Term
|
Definition
| GFR Criteria- Complete loss of renal function for at least four weeks. End-stage kidney disease: Need renal replacement therapy for more than three months. |
|
|
Term
|
Definition
| End-stage kidney disease: Need renal replacement therapy for more than three months. |
|
|
Term
| two most important ongoing measurements of renal status |
|
Definition
|
|
Term
|
Definition
Glomerular filtration and urine-concentrating capacity is reflected by the concentration of urea in the blood.
Urea is the major end product of protein metabolism and is filtered in the glomerulus and eliminated in the urine.
The BUN levels increase as glomerular filtration decreases.
BUN is NOT considered a reliable measure of GFR. |
|
|
Term
|
Definition
Creatinine is the end product of muscle metabolism and is released into the blood at a constant rate.
It is eliminated at a rate related to the level of renal function and is a more reliable measure of the state of renal health.
The Cr level is not elevated until approximately 25% of the nephrons are nonfunctioning.
Osmolality of urine or of serum is dependent on the number of molecules in the solution. |
|
|
Term
| The relationship of urine and blood osmolality |
|
Definition
monitored as an indicator of adequate renal function.
renal function is normal=the urine & blood (plasma) osmolality maintains a direct relationship- one rises so does the other.
If renal perfusion becomes diminished, the urine osmolality becomes more elevated than the blood osmolality and urine specific gravity increases. |
|
|
Term
| Ways to restore renal perfusion: |
|
Definition
Prerenal injury is kidney dysfunction caused by inadequate blood flow, resulting in renal hypoperfusion and renal ischemia. As filtration pressures decline in the face of reduced renal blood flow, the glomerular filtration pressures also fall.
No structure damage, still reversible.
Some causes of prerenal injury include low CO, renal vasoconstriction or vascular obstruction, and drug induced alterations in glomerular hemodynamics.
Prevent sudden superimposes stress of cardiac or vascular nature.
If prolonged, renal tissue ischemia results. The ischemia can result in necrosis of the kidney.
Prevent vascular obstruction.
Prevent decreased CO.
as blood flow falls, so does GFR. |
|
|
Term
| For the nurse, it is important to use BP/MAP and urinary output as clinical measures of renal blood flow. |
|
Definition
| Important to maintain MAP >70 and an hourly urinary output of 25-30mL/hr as indicators of adequate GFR. Drugs that are nephrotoxic cause prerenal injury. |
|
|
Term
|
Definition
Use of NSAID’s should be restricted in those patients with evidence of reduced renal function.
Contrast dyes can be nephrotoxic. Steps must be taken to minimize nephrotoxicity:
The patient should be adequately hydrated with sodium chloride.
N-acetylcystine (mucomyst) may be given orally or IV before contrast administration |
|
|
Term
| Explain measures the nurse may use to prevent renal injury and/or care for the client with acute kidney injury (AKI). |
|
Definition
| Nursing interventions focus on monitoring the patient for fluid volume excess and signs of worsening heart failure and pulmonary edema. A key role of the nurse lies in monitoring the patient’s status and reporting changes to the healthcare provider. |
|
|
Term
collaborative management of the electrolyte imbalances commonly seen in acute renal failure
potassium |
|
Definition
| Treatment may include drug therapy or dialysis. Cation exchange resins (kayexalate) may be used rectally or orally to bind the potassium and result in its excretion through the GI tract. Sodium bicarbonate, calcium gluconate, insulin or hypotonic glucose may be ordered to attempt to drive potassium back to the intracellular space and out of the serum. Dialysis may be ordered to control potassium, when hyperkalemia is accompanied by excess fluid volume. |
|
|
Term
collaborative management of the electrolyte imbalances commonly seen in acute renal failure
sodium |
|
Definition
| a close relationship between sodium and water make it important to control. Sodium restricted in the diet and IV fluids to control fluid excess and prevent dilutional hyponatremia. Maintaining a balance of intake and output helps prevent or control hypernatremia. If renal function is sufficient, diuretic therapy may be ordered to lower sodium. |
|
|
Term
| Describe fluid volume management in acute renal failure |
|
Definition
Fluid restriction requires very careful assessment of the patient’s volume output status.
All output must be carefully documented.
How to divide available free water over 24 hours is imperative.
Meals and medication timing and treatments must be considered.
Diuretic therapy is useful to remove volume from patients with AKI.
The type of diuretic is an important consideration given the patient’s needs, symptoms of overload, electrolyte and acid-base status. |
|
|
Term
| Explain why peritoneal dialysis is of limited use in patients with acute renal failure |
|
Definition
It is used when hemodialysis is not available and when less rapid treatment is available.
It is slower than hemodialysis. Hemodialysis and CRRT are used for acute renal failure. (Hemodialysis is also used for chronic renal failure. (Wagner pg. 646).
In peritoneal dialysis, the catheter is inserted through the anterior abdominal wall by surgery. The tip of the catheter in the peritoneal cavity and has many perforations spaced along the distal end of the tubing to allow fluid to flow in and out of the catheter. In the nonsurgical bedside approach, an area of approximately 2 cm below thumbilicus is numbed with a local anesthetic, and a small stab wound is made.
A stylet is inserted and the abdomen is distended with dialysis solution. The catheter is placed into the peritoneal cavity. Before the start of PD, it is preferable to allow a waiting period of 7-14 days for proper sealing of the catheter and for tissue to grow into the cuffs.
However, some centers will start dialysis 5-7 days after the catheter insertion. About 2-4 weeks after catheter implantation, the exit site should be clean, dry, and free of redness and tenderness. Once the catheter incision site is healed, the patient may shower and then pat the catheter and exit site dry.
Daily catheter care includes the application of an antiseptic solution and a clean dressing, as well as examination of the catheter site for signs of infection (Lewis pg. 1218). This would be too lengthy of a solution for acute renal failure. |
|
|
Term
| Hemodialysis- disadvantages: |
|
Definition
HD
Disadvantages: requires vascular access and heparin, restricts activity level; complications such as infection, decreased CO, Cardiac arrhythmias, disequilibrium syndrome, air embolism and disconnected hemorrhage.
Disadvantages: Vascular access problems, Dietary and fluid restrictions, heparinization may be necessary, Extensive equipment necessary, Hypotension during dialysis, Added blood loss that contributes to anemia, Specially trained personnel necessary, Surgery for permanent access placement, Self-image problems with permanent access. |
|
|
Term
| Hemodialysis- advantages: |
|
Definition
Advantages: Rapid fluid removal, Rapid removal of urea and creatinine, Effective potassium removal, Less protein loss, Lowering of serum triglycerides, Home dialysis possible, Temporary access can be placed at bedside. (Lewis pg. 1217)
Advantages: provides more efficient clearance of excess fluid and solutes |
|
|
Term
| CRRT (continuous renal replacement therapy) - disadvantages/complications |
|
Definition
| equires vascular access, slow process, restricts activity level, risk of contamination. Complications include infection, bleeding, infiltration, air embolism. |
|
|
Term
|
Definition
| smaller volume of blood in the extracorporeal circuit therefore has less hemodynamic side effects. |
|
|
Term
| Describe nursing management of the patient requiring hemodialysis or continuous renal replacement therapy. |
|
Definition
| Monitor the patient for fluid and volume excess and for evidence of heart failure and electrolyte imbalance associated with therapies. Focus on adequate nutritional support- the diet should be restricted in protein, sodium, potassium, and fluids and high in carbohydrates, fats and essential amino acids. Consistently monitor the patient for clinical manifestations of electrolyte imbalances especially sodium, potassium, calcium, phosphate and magnesium. Arterial blood gases monitored. Monitor for s/s of infection. |
|
|
Term
| Describe the nurse’s role in the care of the client with Cushing’s triad. |
|
Definition
Cushing’s triad is a classic syndrome of increased ICP characterized by a specific change in vital signs evidenced by 1) an increase in systolic blood pressure, 2) a decrease in diastolic blood pressure, 3) bradycardia.
This response is activated when ICP rises to a point where it equals or exceeds MAP.
Signs of a widening pulse pressure should alert the nurse of this complication (impending brain herniation) in the setting of severe intracranial hypertension.
Nurse role: monitor for signs and symptoms. |
|
|
Term
| Describe the assessment with the client with traumatic brain injury. |
|
Definition
Assessment: past health history: motor vehicle collision, sports injury, industrial incident, assault, falls. Medications: anticoagulant medication use.
Health management: Use of alcohol or recreational drugs, at risk behavior.
Cognitive: Headache, mood, behavioral change, mentation changes, aphasia, dysphasia, impaired judgment. Coping: Fear, denial, anger, aggression.
General: altered mental status.
Integumentary: Laceration, contusions, abrasions, hematoma, Battle’s sign, periorbital edema and ecchymosis, exposed brain matter.
Respiratory: Rhinorrhea, impaired gag reflex, inability to maintain a patent airway. Impending herniation: altered/irregular respiratory rate and pattern. Cushing’s response.
Gastrointestinal: Vomiting, projectile vomiting, bowel incontinence.
Neurological: Altered LOC, seizure activity, pupil dysfunction.
Musculoskeletal: Motor deficit/impairment, weakness, palmar drift, paralysis, spasticity, decorticate or decerebrate posturing, muscle rigidity, flaccidity, ataxia. (Lewis Table 57-10) |
|
|
Term
| Describe the diagnostic procedures with the client with traumatic brain injury. |
|
Definition
Dx procedures: CT scan is considered the best diagnostic test because it allows rapid diagnosis and interventions in the acute setting.
MRI, PET and evoked potential studies may also be used in the diagnosis and differentiation of head injuries.
Transcranial Doppler studies allow for the measurement of CBF velocity.
A cervical spine x-ray series or CT scan of the spine may also be indicated since cervical spine trauma often occurs concomitantly with head injury.
GCS (coma scale) can be used to classify head injury as mild (13-15), moderate (9-12), or severe (3-8). (Lewis pg.1484) |
|
|
Term
| Describe the collaborative care with the client with traumatic brain injury. |
|
Definition
Collaborative Care: A craniotomy is generally performed to visualize and allow control of the bleeding vessels.
Burr-hole openings may be used in an extreme emergency for a more rapid decompression, followed by a craniotomy. (Lewis pg. 1485). |
|
|
Term
| Describe the evaluation of cerebral tissue perfusion |
|
Definition
Evaluation of cerebral tissue perfusion:
Attain maximal cognitive, motor, and sensory function.
Maintain adequate cerebral oxygenation and perfusion. Remain normothermic. |
|
|
Term
| Subarachnoid hemorrhages: |
|
Definition
the accumulation of blood/hematoma between arachnoid layer of the menings and the brain.
Additional accumulation of blood results in blood leaking into the cerebrospinal fluid. The bleeding associated with SAH can be focal with little consequence or it can be massive and diffuse with subsequent intracranial hypotension.
Patients with this type of hematoma may manifest nuchal rigidity (neck stiffness).
A severe headache is also a common finding, often described as the worse headache the person has ever experienced. (Wagner pg. 558).
Leakage of blood from aneurysms, usually found at the arterial bifurcations where blood velocity is higher, can be lethal with rupture and is usually located in the circle of Willis.
Develops suddenly and without warning. (Wagner pg. 532). |
|
|
Term
|
Definition
is the accumulation of blood between the dura and the arachnoid layers of the menings.
Subdural hematoma usually develops secondary to venous injury. This results in a slower onset of symptoms.
It is categorized by the time between the injury took place and the development of neurological changes.
There are 3 categories:
acute- less than 48 hours after injury,
subacute- 48 hours to two weeks,
chronic-more than two weeks after the injury.
Manifestations of acute subdural hematoma include: drowsiness,
headache,
confusion,
slowed thinking
or agitation.
Because of the expansion of the hematoma is over a longer period of time with subacute subdural hematoma, neurological deterioration may not occur for days or weeks.
Clinical manifestations of chronic subdural hematoma are vague and are often attributed to other conditions.
The patient may complain of headache, lethargy, absent-mindedness, and vomiting.
Other more serious symptoms may be present including seizures, stiff neck, pupil changes or hemiparesis.
Medical management involves surgical evacuation of the hematoma and possible placement of a subdural drain which may remain in place for a few days postoperatively.
Nursing includes monitoring LOC and performing regular and frequent Neurological assessments. |
|
|
Term
|
Definition
occurs in the space between the dura mater and the skull.
High impact to the temporal areas of the brain can induce an epidural hematoma.
When the force of the impact is transferred to the brain, small arteries are sheared. This results in an accumulation of blood between the skull and the dura.
May have a brief loss of consciousness immediately following the injury, followed by an episode of being alert and oriented and then a loss of consciousness again.
A fixed and dilated pupil on the same side as the impact area may be present. Because an artery is most often the source of the hematoma, the rapid accumulation of blood makes it essential to identify and treat these injuries quickly before intracranial pressure reaches a critical point causing brain herniation.
Medical management of the epidural hematoma involves surgical evacuation of the hematoma with possible placement of the ICP monitor.
Nursing: diligent neurological assessment, look for sudden changes in LOC and for presence of a fixed and dilated pupil on the side of the injury. These findings suggest bleeding has recurred and represents an emergent medical situation. |
|
|
Term
|
Definition
the spine is composed of 33 individual and fused vertebrae. There are 7 cervical (C),
12 thoracic (T), and
5 lumbar (L) vertebrae.
The sacral and coccygeal vertebrae are fused in the adult. Each vertebra consists of a body (anterior) and an arch (posterior).
The arch section is composed of two pedicles that attach the arch to the body and two laminae that form the roof of the arch.
The spinous process is located at the rear of the vertebrae. Vertebral bodies increase in size as they descend in order to bear additional weight.
The spine is conceptualized as having three columns: an anterior column that includes the anterior part of the vertebral body, a middle column that houses the posterior wall of the vertebral body and a posterior column that includes the vertebral arch.
If two or more of these columns are damaged, the injury is considered to be unstable.
Unstable spinal injury exists when the vertebral and ligamentous structures are unable to support and protect the injured area. (Wagner pg. 569) |
|
|
Term
| Complete Spinal Cord Injury: |
|
Definition
results in one of two conditions- paraplegia or tetraplegia.
Paraplegia is the result of injury to the thoracolumbar region (T1-L1) causing loss of motor and sensory function of the lower extremities, upper remains intact.
Tetraplegia (Quadriplegia) is the result of injury to the cervical or thoracic regions (C1-T1). Muscle function depends on specific segments involved but impaired function of arms, trunk, legs and pelvic organs may occur |
|
|
Term
| . Incomplete Spinal Cord Injury: |
|
Definition
has evidence of partially interrupted motor and sensory pathways.
Alterations in function that occur vary greatly, depending on amount and location of injury and level of injury. |
|
|
Term
Table 23-1 Incomplete Spinal Cord Injury-
Anterior Cord: |
|
Definition
| Anterior Cord: motor, pain, temp. Touch, paralysis below the injury level. Proprioception, vibration, and pressure sense. |
|
|
Term
Table 23-1 Incomplete Spinal Cord Injury-
Brown-Sequard: |
|
Definition
| Brown-Sequard: loss of voluntary motor movement on same side of injury, loss of pain, temp, sensation on opposite side (below level of injury). Side of the body with the best motor control has little or no sensation. |
|
|
Term
Table 23-1 Incomplete Spinal Cord Injury-
Central Cord: |
|
Definition
| Central Cord: motor, sensory deficit in upper extremities, often spastic; variable paralysis of lower extremities. Motor, sensory pathways in lower extremities; some Bowel/bladder function. |
|
|
Term
Table 23-1 Incomplete Spinal Cord Injury-
Posterior Cord: |
|
Definition
| Posterior Cord: Proprioception, vibration sensation below the level of injury. Motor function, sense of pain and light touch. |
|
|
Term
Primary SCI
Hyperextension Injury- |
|
Definition
caused by a forward and backward motion of the head (rear end collision).
The anterior ligaments are torn and the spinal cord is stretched (whiplash). |
|
|
Term
Primary SCI
Rotation injury |
|
Definition
| causes a tearing of the posterior ligaments and rotation of the spinal column (non-belted person in a car hit broadside). |
|
|
Term
Primary SCI
Axial Loading Injury- |
|
Definition
| (compression fracture) caused by a vertical force along the spinal cord. Bony fragments sent into the spinal cord. Occur with diving into shallow water, jumping from tall heights and landing on feet or butt. |
|
|
Term
| Secondary Spinal Cord Injury: |
|
Definition
| the 24 hour period immediately following SCI involves a series of pathophysiologic processes. |
|
|
Term
| Secondary SCI ______ & ______ |
|
Definition
Ischemia &
Elevated Intracellular Calcium |
|
|
Term
|
Definition
| Ischemia- blood flow to the spinal cord decreases on injury as a result of hypotension and vasospasm induced thrombosis. Thrombi impede blood flow. Edema further impairs perfusion to the cord. The zone of ischemia can spread if perfusion to the cord is not restored. |
|
|
Term
| Elevated Intracellular Calcium- |
|
Definition
| Elevated Intracellular Calcium-calcium ions accumulate in injured cells, causing a breakdown of intracellular protein and phospholipids. Demyelination and destruction of the cell membrane occur when these substances are broken down. Fatty acids produce arachidonic acid which produces leukotrienes and prostaglandins (inflammatory process). Once cell membrane is damaged, neuronal death occurs. Inflammatory Processes- Leukocytes infiltrate the injured area immediately post-injury, causing edema which further decreases blood supply to the injured area. |
|
|
Term
| A PATIENT WITH A C4 INJURY MAY HAVE EDEMA UP TO THE C2 LEVEL. |
|
Definition
|
|
Term
| BECAUSE EDEMA CAN EXTEND THE LEVEL OF INJURY FOR SEVERAL CORD SEGMENTS ABOVE AND BELOW THE AFFECTED LEVEL, |
|
Definition
| THE EXTENT OF INJURY MAY NOT BE DETERMINED FOR SEVERAL DAYS, UNTIL AFTER THE CORD EDEMA HAS RESOLVED. |
|
|
Term
| ) Describe physical assessment techniques and diagnostic test frequently used to identify the type and severity of spinal cord injury. |
|
Definition
| The diagnosis of spinal cord injury (SCI) begins with a detailed history of events surrounding the incident, radiographic studies of the spine and as assessment of sensory and motor function. Assume an unconscious patient has an SCI until it is ruled out. Also suspect a patient with maxillofacial injuries and clavicle or upper rib fractures has SCI. |
|
|
Term
|
Definition
Radiographs
Computed Tomography Scan
MRI
Angiography
Somatosensory-Evoked Potentials |
|
|
Term
|
Definition
| Radiographs-documents the level of injury and provides information regarding the stability of the cord injury. |
|
|
Term
|
Definition
| Computed Tomography Scan- ordered if the spine is not well visualized in x-ray or there are suspicious findings. Provides superior visualization of bony structures of the spine and identifies spinal fractures, more accurate for detecting posterior and central column injuries as well as cord impingement. |
|
|
Term
|
Definition
| MRI- identifies injuries to the spinal cord, ligaments and disk. Also used to detect tumors, inflammation, infection, degenerative disorders and vascular disruptions in the spinal cord and brain. Has greater sensitivity than CT for contusions, hematomas and edema. |
|
|
Term
|
Definition
| Angiography- because of the proximity of the cervical spine and vertebral arteries, routine screening should be used in patients with complex cervical spine fractures involving subluxation, extension into the foramen transversarium or upper C1-C3 fractures. Remains the standard test. |
|
|
Term
| Somatosensory-Evoked Potentials |
|
Definition
| are used to establish a functional prognosis after resolution of spinal cord edema. A peripheral nerve is stimulated below the level of the injury. Response is recorded using scalp electrodes. |
|
|
Term
|
Definition
serial neurologic exams are performed hourly for at least the first 24 hours after SCI.
Motor Assessment-
Sensory
Reflex activity |
|
|
Term
|
Definition
| Motor Assessment- voluntary movement requires both upper and lower motor neuron activity. Motor activity is assessed for strength. The examiner begins at the head and moves toward the toes. |
|
|
Term
|
Definition
| Sensory Assessment- the most important data to collect in the sensory examination is the exact point on the patient where normal sensation is present. The assessment begins by moving from the lower to the upper body regions because it is easier for the patient to recognize the onset of a sensory stimulus rather than cessation of a stimulus. |
|
|
Term
|
Definition
| Reflex activity- the presence of deep tendon reflexes below the level of injury indicates an incomplete lesion. The presence of perineal reflexes indicates that bowel and bladder training may be feasible. Priapism (persistent penile erection) may be present in males. The anal wink reflex is initiated by a pin prick in the perianal area. The presence of the anal wink and bulbocavernosus reflexes indicate that the injury is an upper motor neuron injury. |
|
|
Term
| Assessing for Shock States- |
|
Definition
Assessing for Shock States-
The degree of dysfunction varies by level and severity of injury. Autonomic dysfunction is more extensive when the level of injury is higher. |
|
|
Term
| Following severe cord trauma, two types of shock commonly develop |
|
Definition
| spinal shock and neurogenic shock |
|
|
Term
|
Definition
Spinal Shock-
occurs within 30-60 minutes after injury.
Manifested by
absence of all reflex activity,
flaccidity and
loss of sensation below the level of injury.
Subsides within 24 hours, but may last 7-20 days post-injury. Treatment is symptomatic. End is seen with the return of deep tendon reflexes, spasticity and increased muscle tone |
|
|
Term
|
Definition
Neurogenic Shock- occurs in patients with injury above T6.
The loss of sympathetic control from the brainstem and higher centers allows the parasympathetic output to go unchecked.
The patient experiences:
hypotension, bradycardia, decreased CO, hypothermia with loss of ability to sweat below the level of the lesion.
Treatment will involve both fluid resuscitation and vasopressor medications. Bradycardia with hypotension differentiates neurogenic shock from hypovolemic shock. |
|
|
Term
| Discuss stabilization techniques used for spinal cord injuries-- then 2 techniques: |
|
Definition
Stabilization in the high- acuity unit includes bedrest with log rolling maneuvers and a hard cervical collar until the spine has been stabilized with surgery or traction.
Surgical stabilization and
Manual stabilization |
|
|
Term
|
Definition
| Surgical stabilization-spinal segments are fused during surgery abd spinal canal decompression is accomplished. Rods are inserted to stabilized thoracic spinal injuries. External traction may be required postoperatively. Special braces, such as the Jewett orthosis may be used postoperatively to maintain hyperextension when the patient is supine. Surgery is reserved for patients not sufficiently aligned with manual stabilization |
|
|
Term
|
Definition
| Manual stabilization-Tong devices (Gardner-Wells, Vinke), may be used to reduce a fracture. Screws are implanted into the patient’s skull a few cm above the ears, patient feels pressure but not pain. Weights are added (10lbs no fracture, 5lbs per interspace beginning with C1 to level of lesion is applied). Muscle relaxants promote the efficacy of the traction. Halo device- prevents flexion, extension, rotational movement of the head and neck, and allows for early mobilization. Attached to a rigid plastic vest. Braces- a hard cervical collar and a molded plastic body jacket (clam shell) brace for stabilization of some injuries. Jewett orthosis most frequently used with thoracic and lumbar injuries. |
|
|
Term
| Describe the assessment, diagnostic procedures, collaborative care and evaluation of cerebral tissue perfusion with the client with spinal cord injury. |
|
Definition
Assessment: begins using ABC’s, monitor for signs of pulmonary dysfunction, breath sounds, respiration pattern and rate, temperature, sputum color and consistency, pulmonary function tests, pulse oximetry.
Interventions: Quad assist cough, suction, deep breathe, incentive spirometer, reposition every two hours, elevate head of bed 30 degrees, intake and output. Administer drug therapy: Administer O2.
Assessment: monitor for signs of decreased CO, Heart rate and rhythm, mentation, BP, extremities for warmth, capillary refill, pulses
. Interventions: continuous cardiac monitoring. Administer Drug therapy: IV fluids and vasopressors |
|
|
Term
|
Definition
| are caused by an interruption of cerebral blood flow by a thrombus or embolus. |
|
|
Term
| Interruption of cerebral blood flow can result in |
|
Definition
TIA
transient ischemic attacks. |
|
|
Term
|
Definition
| episodes of focal neurologic deficits that usually resolve in a few minutes or hours but are always completely resolved within 24 hours. |
|
|
Term
|
Definition
sudden unilateral dimness or partial loss of vision in one eye,
weakness,
numbness,
tingling,
severe headache,
speechlessness or
unexplained dizziness. |
|
|
Term
| TIAs are warnings of ____ and requires _____ |
|
Definition
| TIAs are warnings of an impending stroke and require immediate referral for treatment. The highest incidence for stroke occurs within the first few weeks after the TIA. |
|
|
Term
| most common cause of ischemic stroke. |
|
Definition
| Atherosclerosis of cerebral arteries |
|
|
Term
|
Definition
| Thrombotic strokes are more common in older persons and are frequently accompanied by evidence of atherosclerotic plaque deposits in the coronary (heart) or peripheral vasculature. May occur at rest and are not associated with activity. |
|
|
Term
|
Definition
An embolic stroke is caused by a blood clot that travels from its original site and eventually becomes lodged in a vessel.
Most embolic originate from a thrombus in the heart that develops with certain cardiac conditions (Atrial fibrillation, rheumatic heart disease, recent myocardial infarction or endocarditis).
Occurs commonly in younger individuals, and occurs suddenly when the person is awake and active. |
|
|
Term
| Recombinant tissue plasminogen activator (tPA) |
|
Definition
| administered IV is used to reestablish blood flow through a blocked artery to prevent cell death in patients with the acute onset of ischemic stroke symptoms. |
|
|
Term
| tPA must be administered within |
|
Definition
tPA must be administered within 3 hours of the onset of clinical signs of ischemic stroke.
The single most important factor is timing. |
|
|
Term
|
Definition
noncontrast CT or MRI scan to rule out hemorrhagic stroke,
blood tests for coagulation disorders,
and screening for recent history of gastrointestinal bleeding,
stroke,
or head trauma within the past 3 months,
or major surgery within the past 14 days. |
|
|
Term
| During/After infusion RN ____ and ____ |
|
Definition
performs frequent neurological assessments
evaluates the patient’s blood pressure. |
|
|
Term
| Assessment schedule x2 hrs, x6 hrs, 24hrs.... |
|
Definition
The schedule for both of these assessments is every 15 minutes for the first 2 hours,
every 30 minutes for the next 6 hours
then every hour for 24 hours after treatment. |
|
|
Term
| During the infusion, if the patient develops discontinue the IV and and call the DR |
|
Definition
nausea, vomiting,
severe headache,
or acute hypertension, |
|
|
Term
| The patient with acute ischemic stroke presenting to the emergency department within 48 hours of the onset of symptoms are given |
|
Definition
| aspirin (50-325mg/day) to reduce stroke mortality and decrease morbidity, provided contraindications are absent and the patient has not or will not be treated with tissue plasminogen activator. |
|
|
Term
| Surgical Management of strokes: |
|
Definition
For ischemic cerebrovascular disease, surgery may be performed to prevent recurring cerebral infarcts and TIAs.
This procedure is done to remove the source of the occlusion and to increase cerebral blood flow to the ischemic area.
A carotid endartectomy is a surgical procedure performed to remove atherosclerotic plaque. |
|
|
Term
|
Definition
| Intracerebral hemorrhage and Subarachnoid hemorrhage |
|
|
Term
|
Definition
Intracerebral hemorrhage is a type of hemorrhagic stroke that occurs when a cerebral blood vessel ruptures and blood accumulates in brain tissue.
Hypertension is a common cause of intracerebral hemorrhage; however, a variety of factors can also cause intracerebral hemorrhage including arteriovenous malformation, anticoagulant therapy, aneurysms, trauma, and erosions of blood vessels by tumors.
They appear suddenly and without warning. A spontaneous intracerebral hemorrhage is the most common cause of a fatal stroke. Chronic hypertension a major cause. |
|
|
Term
|
Definition
leakage of blood from aneurysms, usually found at arterial bifurcations where blood velocity is high can be lethal with rupture and is usually located in the circle of Willis.
This type of stroke usually a subarachnoid hemorrhage (SAH) develops suddenly without warning.
The patient often complains of a sudden severe unilateral headache- “the worst headache of my life”-neck pain or stiffness (nuchal rigidity) and vomiting. |
|
|
Term
| Cerebellar lesions are critical because of |
|
Definition
| hemorrhage or infarction can rapidly become life threatening by compromising the brainstem. |
|
|
Term
| Emergency surgery is indicated for cerebellar infarction or hemorrhage with... |
|
Definition
clinical evidence of
brainstem compression and increased ICP, such as decreasing level of consciousness, restlessness or cranial nerve palsies.
Bleeding into the subarachnoid space, such as ruptured aneurysm, requires immediate medical attention. |
|
|
Term
|
Definition
| the severity of neurological symptoms. |
|
|
Term
| Persons with no neurological deficits may require______ within_______ to ________ |
|
Definition
cerebral arteriography and early surgery.
The surgery performed within 72 hours is known as an “aneurysm clipping”
to prevent re-bleeding. |
|
|
Term
| Postoperative complications |
|
Definition
|
|
Term
|
Definition
| decreases perfusion to brain tissue. |
|
|
Term
| Vasospasm is prevented and treated with |
|
Definition
|
|
Term
|
Definition
| hypervolemia, hypertension and hemodilution. |
|
|
Term
| This combination of therapies augment cerebral perfusion pressure (CPP) by |
|
Definition
raising:
systolic blood pressure, cardiac output and intravascular volume to increase cerebral blood flow and minimize cerebral ischemia. |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Thrombotic Risk factors include: |
|
Definition
| Hypertension, smoking, high cholesterol, DM, atherosclerosis. |
|
|
Term
| Thrombotic Characteristics |
|
Definition
May have TIAs,
Develop during sleep or when awake, may have mild headache,
predictable locations and symptoms,
intermittent attacks and progression. |
|
|
Term
|
Definition
|
|
Term
|
Definition
Cardiac abnormalities:
Atrial fibrillation,
valvular heart disease,
carotid plaque or thrombosis. |
|
|
Term
|
Definition
no warning,
sudden attack,
symptoms vary with attack,
usually occur during daytime. |
|
|
Term
|
Definition
| young, middle aged adults. |
|
|
Term
|
Definition
: Ruptured aneurysms,
Arteriovenous malformation,
Trauma. |
|
|
Term
|
Definition
usually no warning,
sudden attack,
very severe headache,
nausea/vomiting,
photophobia,
hypertension,
decreasing level of consciousness,
bloody CSF,
nuchal rigidity. |
|
|
Term
| Intracerebral hemorrhage age |
|
Definition
|
|
Term
| Intracerebral hemorrhage Risks |
|
Definition
Chronic hypertension,
Aneurysms,
Anticoagulant Therapy,
Trauma,
Brain tumors,
Arteriovenous malformations |
|
|
Term
| Intracerebral hemorrhage Characteristics |
|
Definition
Usually no warning,
gradual development,
headache,
nausea/vomiting,
photophobia,
hypertension,
decreased level of consciousness,
motor-sensory deficit of face, arm, leg. |
|
|
Term
|
Definition
Hypertension and hypotension,
cardiac disease,
dysrhythmias (A fib),
Coagulopathies,
Diabetes mellitus,
Drug abuse (cigarette smoking, excessive alcohol consumption, cocaine),
physical inactivity,
hypercholesterolemia. |
|
|
Term
| Non-modifiable risk factors: |
|
Definition
Age,
Gender,
Race/ethnicity,
Genetic factors,
Prior stroke of heart attack. |
|
|
Term
| In the evolution of a stroke there are usually two zones of affected neurons |
|
Definition
|
|
Term
| In the central zone are neurons that are |
|
Definition
infarcted.
They do not function and do not regain function. |
|
|
Term
|
Definition
| Surrounding the infarcted zone is a zone of neurons that are minimally perfused but not totally ischemic. This zone of neurons is called the penumbra. These neurons are impaired, but are viable and capable of responding to therapy. |
|
|
Term
|
Definition
| Agnosia- is a cortical impairment that results in the inability to recognize or interpret familiar sensory information although there is no important of sensory input or dementia. Can be tactile, visual or auditory. Tactile: inability to recognize objects by touch. Visual: inability to recognize or name familiar objects or faces. Auditory: inability to recognize familiar sounds. |
|
|
Term
|
Definition
| Apraxia-is the inability to carry out a purposeful movement although movement, coordination and sensation are intact. Motor: memory deficit for motor sequences affecting only upper limbs, although muscle and sensory function are intact. Ideomotor: Inability to perform a motor act on command even though the patient understands the act and has muscle and sensory function; can perform spontaneous, simple, isolated acts but not complex acts such as writing or dressing. Ideational: inability to perform activities automatically or on command. Constructional: inability to copy, draw, or construct designs to two or three dimensions on command or spontaneously. Dressing: Inability to dress self because of a disorder in body schema, unilateral neglect, and or spatial relations. |
|
|
Term
|
Definition
| Aphasia- means a total inability to understand of formulate language. Language comprehension, speech expression or writing ability may be lost. |
|
|
Term
|
Definition
| Dysphasia-refers to difficulty with comprehending, speaking or writing. |
|
|
Term
|
Definition
| Wernicke’s aphasia- the patient receives auditory impulses but is unable to comprehend them. It is a receptive aphasia characterized by fluent, well- articulated speech with intact tone but inappropriate speech content that is unintelligible because of poor word choices. The patient makes up words. Reading and speech comprehension, repetition of speech and naming of objects is impaired. The patient is unable to write coherently. Motor deficits are seldom seen in these patients because the lesion is in the left temporal lobe. The goal of therapy for patients is to develop an awareness of the language problem and to increase comprehension. |
|
|
Term
|
Definition
| Broca’s aphasia-is an expressive aphasia characterized by non-fluent, telegraphic speech with outbursts of profanity, uninhibited speech and word finding difficulty, which reflects impaired memory for language. The patient uses nouns or phrases with pauses between words and lacks grammar. An awareness of speech errors is present and speech production is labored and frustrating. A poor capacity for repetition and difficulty naming objects exists although recognition of objects is present. Comprehension is usually intact and responses are appropriate. The goal is to establish reliable language output to express needs. This may be in the form of yes or no questions. |
|
|
Term
|
Definition
| Global aphasia- is a combination of Broca’s and Wernicke’s aphasia with an almost complete loss of comprehension and expression of speech. The lesion involves the frontal and temporal lobes. The patient has non fluent speech and an inability to express his or her ideas in speech or writing. The goal is to improve the ability to communicate. |
|
|
Term
|
Definition
| Dysarthria- is an impairment of the muscle that control speech. Hemispheric or brainstem stroks produce dysarthria, which is characterized by slurred, muffled or indistinct speech. Uncoordinated, slow, monotone speech results if the basal ganglia or cerebellum are involved. |
|
|
Term
| Traumatic brain Injury (TBI) is often referred to as a closed head injury (CHI) and is a brain insult that results from a |
|
Definition
| mechanical disruption of brain tissue from an external impact or injury to the head. |
|
|
Term
|
Definition
| simplest form of closed head injury |
|
|
Term
| severe traumatic brain injury occurs with |
|
Definition
| epidural hematoma and diffuse axonal injury |
|
|
Term
| epidural hematoma and diffuse axonal injury |
|
Definition
| are both associated with high mortality. |
|
|
Term
| Acceleration/deceleration injury |
|
Definition
| The most common mechanism of TBI is the result of acceleration and deceleration forces. |
|
|
Term
|
Definition
occurs when the stationary brain is suddenly and rapidly moved in one direction along a linear path.
This type of injury is seen in victims of assault who have been hit in the head with a fist or bat.
The sudden acceleration causes brain injury at the site of impact. |
|
|
Term
|
Definition
occurs when the brain stops rapidly in the cranial vault.
As the skull ceases movement, the brain continues to move until it hits the skull.
The force of deceleration causes injury at the site of impact with the skull. Victim of a fall.
As the rapid deceleration of the persons head hitting the ground results in a deceleration injury of the brain as it it’s the boney wall of the cranium. |
|
|
Term
| Acceleration and deceleration injuries can _______ together |
|
Definition
| occur. E.g., coup and countercoup |
|
|
Term
| injury affects the cerebral tissue directly under the point of impact. |
|
Definition
|
|
Term
| injury occurs in a line directly opposite the point of impact. |
|
Definition
| Countrecoup (deceleration) |
|
|
Term
|
Definition
Occurs when the force impacting the head transfers energy to the brain in a nonlinear fashion, resulting in shearing forces being exerted throughout the brain.
An example of this type is in boxing. When a boxer is punched in the side of the head, the force causes rapid rotational movement of the head and its contents which causes tearing of the axons in the brain. |
|
|
Term
|
Definition
Occurs when a foreign object invades the brain.
The penetrating object may be a bullet, knife, or a falling object.
The penetrating object may pass completely through the brain and exit on the opposite side or it may bounce around causing multiple injuries.
A bullet may cause additional injury from shock waves transmitted throughout the brain. |
|
|
Term
|
Definition
simple fracture involving the entire boney thickness without bone movement;
considered the most benign type of skull fracture; associated with low velocity blunt trauma; usually requires no interventions. |
|
|
Term
|
Definition
| liner skull fractures are not life threatening and are allowed to heal over time without surgical interventions. |
|
|
Term
|
Definition
fracture in which a high energy force depresses the skull inward;
usually causes bone fragmentation (comminuted) with fragments potentially tearing though the dura and into brain tissue;
called an open depressed fracture if the scalp is lacerated to the bone or called a closed depressed fracture if the scalp is intact. |
|
|
Term
| RN and Depressed skull fx |
|
Definition
Medical interventions include
surgical repair of the fracture and meninges
evacuation of any hematomas beneath the fracture.
Nursing interventions focus on
frequent neurological assessment
pain management.
The nurse must be cautious when administering pain medications to patients with head injuries. The presence of narcotics may obscure the neurological exam and make it difficult during an assessment to differentiate changes in mental status as a result of actual injury for changes caused by the narcotic |
|
|
Term
|
Definition
a fracture that develops at the base of the skull;
usually located in the temporal or occipital regions;
associated with a high energy force;
if dura is torn, can result in rhinorrhea (CSF draining from the nose) or otorrhea (CSF draining from the ear). |
|
|
Term
| RN assessment findings and Basilar skull fx |
|
Definition
the presence of periorbital ecchymosis (raccoon eyes),
or mastoid ecchymosis (Battle’s sign),
otorrhea,
rhinorrhea
or facial nerve paralysis. |
|
|
Term
| drainage from the nares and ear canals |
|
Definition
|
|
Term
| indicates the meninges are torn |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Any drainage from the ear or nose should be tested for |
|
Definition
| the presence of glucose with a glucose reagent strip. |
|
|
Term
| What is a positive CSF test? |
|
Definition
| Clear drainage that tests positive for glucose indicates the fluid is CSF. |
|
|
Term
|
Definition
neurological assessment,
pain management
monitoring the patient for s/s infection associated with the disrupted meningeal layer.
All dressing should be changed with aseptic technique in an effort to reduce the possibility of an infection.
Sterile cotton gauzes are placed in the ear or under nose.
Dressings are changed when wet because moisture facilitates the movement of microorganisms and predisposes the patient to infection. |
|
|
Term
|
Definition
includes allowing the CSF to drain & the dura to close on its own.
If not healed on own within 2 weeks, surgical repair may be necessary. |
|
|
Term
|
Definition
Cerebral hematomas represent a group of focal cerebral injuries associated with the accumulation of blood in the cranial vault.
Occur as the result of injury to a cerebral vein or artery. |
|
|
Term
| 1) Subdural hematoma (SDH)- |
|
Definition
| the accumulation of blood between the dura and the arachnoid layers of the meninges. |
|
|
Term
| SDH usually Develops secondary to |
|
Definition
|
|
Term
SDH is categorized by the time between the injury took place and the development of neurological changes.
3 categories & durations |
|
Definition
acute (less than 48 hours),
subacute (48 hours to 2 weeks),
and chronic (more than 2 weeks). |
|
|
Term
| SDH acute duration and manifestation |
|
Definition
(less than 48 hours),
Manifestations of acute include drowsiness, headache, confusion, slow thinking or agitation. |
|
|
Term
| SDH subacute duration and manifestation |
|
Definition
subacute (48 hours to 2 weeks),
Subacute neurological deterioration may not occur for days or weeks. |
|
|
Term
| SDH chronic duration and manifestations |
|
Definition
(more than 2 weeks).
Chronic are vague and are attributed to other conditions. The patient may complain of headache, lethargy, absent mindedness and vomiting. |
|
|
Term
|
Definition
may be present including:
seizures,
stiff neck,
pupil changes
or hemiparesis. |
|
|
Term
|
Definition
| involves surgical evacuation of the hematoma and possible placement of a subdural drain which may remain in place for a few days. |
|
|
Term
|
Definition
| Nursing priorities include monitoring level consciousness and performing regular and frequent focused neurological assessments. |
|
|
Term
|
Definition
occurs in the space between the dura mater and the skull.
High impact to the temporal areas of the brain can induce an epidural hematoma.
When the force of the impact is transferred to the brain, small arteries are sheared.
This results in an accumulation of blood between the skull and the dura mater. |
|
|
Term
|
Definition
may have a brief loss of consciousness immediately following the injury, followed by an episode of being alert and oriented and then a loss of consciousness again.
Clients present with a fixed and dilated pupil on the same side as the impact area. |
|
|
Term
|
Definition
| involves surgical evacuation of the hematoma with possible placement of an intracranial pressure monitor (ICP). |
|
|
Term
|
Definition
Nursing care focuses on diligent neurological assessment.
The nurse must look for sudden changes in level of consciousness and for the presence of a fixed dilated pupil on the side of the injury.
These finding suggest bleeding has recurred and represents an emergency medical situation. |
|
|
Term
| 3) Intracerebral hematoma |
|
Definition
| is the accumulation of blood in the parenchyma of brain tissue rather than between the meninges. Result from uncontrolled hypertension, ruptured aneurysm, trauma with high impact blow to the head. |
|
|
Term
|
Definition
Manifestations vary according to the location of the hematoma and may include
headache along with decreasing level of consciousness, dilation of one pupil and hemiplegia. |
|
|
Term
|
Definition
| Surgical evacuation is usually not possible. Medical management includes management of intracranial pressure and cerebral perfusion pressure. |
|
|
Term
|
Definition
refers to a bruising of soft tissue and is considered a moderate-to-severe injury.
It is commonly seen in traumatic brain injury that may begin local but become more diffuse over time. |
|
|
Term
|
Definition
| macroscopic tissue and vessel damage that is detectable through CT or MRI scanning; |
|
|
Term
| contusions are associated with |
|
Definition
| longer periods of unconsciousness and a more guarded prognosis, depending on the severity of injury. |
|
|
Term
|
Definition
| Glasgow coma scale (GCS) is useful in determining the severity of the injury. |
|
|
Term
|
Definition
| contusion only causes mild alterations in level of consciousness (GCS of 13-15) |
|
|
Term
|
Definition
| , a contusion is associated with more significant alterations, moderate injury |
|
|
Term
|
Definition
|
|
Term
|
Definition
| are those that involve the brain more globally |
|
|
Term
|
Definition
classified as mild traumatic brain injury (MTBI) is caused by blunt trauma to the head.
Patient will require a CT scan of the head.
Symptoms may last up to 3 months or more. |
|
|
Term
| Cerebral damage is at the |
|
Definition
| microscopic level and not detectable through radiographic or other testing. |
|
|
Term
|
Definition
Signs include a transient period of unconsciousness (lasting up to 20 minutes) and a Glasgow coma scale score of 13-15;
however signs of neurological deficits (unilateral weakness, pupillary abnormalities) are usually absent. |
|
|
Term
| the injury can have devastating effects including the |
|
Definition
| inability to function at pre-injury levels. |
|
|
Term
| On presentation to the emergency department |
|
Definition
the patient may report having amnesia about the event that caused the injury.
may ℅
headache,
dizziness,
vertigo,
nausea,
vomiting,
slurred speech or confusion. |
|
|
Term
| 2) Diffuse Axonal injury (DAI) |
|
Definition
| occurs when shearing forces disrupt the structure of neurons and their nearby blood vessels. |
|
|
Term
|
Definition
| without bleeding, making it difficult to visualize on CT or MRI. |
|
|
Term
|
Definition
| high speed acceleration/deceleration injury that occurs with motor vehicle crashes. |
|
|
Term
|
Definition
| involves a rotational (twisting motion) movement of the brain within the skull that causes widespread shearing of axons in the white matter. |
|
|
Term
| The outcome of the patient with DAI |
|
Definition
unpredictable.
Mild DAI can result in a comatose state lasting hours to days followed by recovery with minimal residual neurological damage.
In more severe DAI, the prognosis is poor and may include: prolonged coma, death or a persistent vegetative state. |
|
|
Term
| 3) Subarachnoid hemorrhage- SAH |
|
Definition
| is the accumulation of blood/hematoma between the arachnoid layer of the meninges and the brain |
|
|
Term
| The bleeding can be focal with little consequence or |
|
Definition
| it can be massive and diffuse with subsequent intracranial hypotension. |
|
|
Term
| Patients may present with |
|
Definition
| nuchal rigidity (stiff neck). A severe headache is also common and often described as the worse headache the person has ever had |
|
|
Term
| Management of diffuse head injury: |
|
Definition
In the acute care phase includes diligent and frequent neurological assessments and pain management.
When moderate-to-severe, management may include interventions to lower ICP, increase cerebral perfusion, and stabilize vital signs, all of which contribute to an improved outcome. |
|
|
Term
| Management of Traumatic Brain Injury, 2 injuries |
|
Definition
|
|
Term
|
Definition
| occurs when neurons sustain direct injury from the offending event. Primary injury is immediate and often irreversible damage. |
|
|
Term
|
Definition
| occurs in response to the primary injury. |
|
|
Term
| Four causes of secondary injury: |
|
Definition
ischemia,
neuronal death,
cerebral swelling
and inflammation. |
|
|
Term
| Collaborative interventions are directed at |
|
Definition
preventing these causes of secondary injury.
Many methods target the reduction of intracranial pressure (ICP) and improvement of cerebral perfusion pressure (CPP), thus minimizing ischemic injury to the brain. |
|
|
Term
| Maintain CPP greater than |
|
Definition
| 60 mm Hg to reduce secondary injury. |
|
|
Term
|
Definition
| osmotic diuretics, hypertonic saline, hypothermia, and hyperventilation may be used to help CPP. |
|
|
Term
| The first goal in treating TBI |
|
Definition
| The first goal in treating TBI is to limit the primary ischemic tissue injury by aggressive prevention and treatment of hypoxia and hypotension. |
|
|
Term
| This is accomplished with |
|
Definition
| upplemental oxygen and mechanical ventilation |
|
|
Term
TBI & Resp.
RN Maintain PaO2 |
|
Definition
|
|
Term
TBI & Resp
RN Maintain PaCO2 |
|
Definition
| PaCO2 between 35-45 mm Hg. |
|
|
Term
| Systolic BP should be maintained at |
|
Definition
| > 90 mm Hg with fluids and vasopressors. |
|
|
Term
| CPP should be maintained at |
|
Definition
|
|
Term
|
Definition
| pain and sedation medications, maintain normothermia, patient positioning with head of bed elevation and midline neck alignment. |
|
|
Term
|
Definition
| consideration of external ventricular drainage, hyperosmolar therapy, mechanical ventilation maintaining PaO2 greater than 60 mm Hg and PaCO2 35-45. |
|
|
Term
|
Definition
| Neuromuscular blockade, mild hyperventilation, mild hypothermia |
|
|
Term
|
Definition
| Barbiturate coma, decompression craniotomy |
|
|
Term
traumatic brain injury and normalizing intracranial pressure (ICP)
Nursing Interventions: |
|
Definition
, nursing activities are spaced out to allow recovery time for the patient.
The patient’s neck is kept in proper neutral alignment (no flexion or rotation)
hip flexion is kept at less than 90 degrees to allow for proper venous return and prevention of elevated ICP.
Elevating the head of bed to 30 degrees reduces ICP without compromising CPP and may decrease the risk of pneumonia. |
|
|
Term
|
Definition
hyperthermia increases cerebral metabolic rate and increases cerebral oxygen requirements,
antipyretics and cooling measures are used to reduce body temperature. |
|
|
Term
|
Definition
| the nurse pre-oxygenates the patient and limits passage time of the suction catheter to 10 seconds or less x2 |
|
|
Term
Complications associated with traumatic brain injury:
Diabetes Insipidus |
|
Definition
is a condition associated with improper water balance.
Loss of ADH secretion results in polyuria. Any patient with TBI and ICP is at risk for developing diabetes insipidus. |
|
|
Term
|
Definition
| polyuria and polydipsia resulting from either inadequate ADH secretion or from a decrease renal response to ADH. |
|
|
Term
| Traumatic brain injury may result in |
|
Definition
| pressure on or damage to the pituitary gland and loss of ADH secretion. |
|
|
Term
| Loss of ADH secretion results in |
|
Definition
| Loss of ADH secretion results in polyuria. |
|
|
Term
| Any patient with TBI and ICP |
|
Definition
| is at risk for developing diabetes insipidus. |
|
|
Term
|
Definition
| The time of onset is 5-10 days following initial injury. |
|
|
Term
|
Definition
| large amounts of pale, clear, “water like” urine and hypotension. |
|
|
Term
| The classic diagnostic profile of DI includes |
|
Definition
| output, urine concentration, Na |
|
|
Term
|
Definition
| production of large output (>200mL/hr) |
|
|
Term
|
Definition
| dilute urine (specific gravity <1.005) |
|
|
Term
|
Definition
| associated increase in serum sodium (> 145 mEq/L). |
|
|
Term
|
Definition
| aggressive replacement of intravascular volume with IV fluids and administration of synthetic antidiuretic hormone (ADH) . |
|
|
Term
| Administration of ADH may be either in the form of |
|
Definition
a vasopressin infusion or desmopressin
either IV, subQ or intranasal. |
|
|
Term
| Indications of DI improvement |
|
Definition
| are decreased urine output and increased specific gravity. |
|
|
Term
| Syndrome of Inappropriate Antidiuresis Hormone |
|
Definition
| -increases total body water because excess antidiuretic hormone (ADH) secretion results in retention of water. |
|
|
Term
| The classic profile of SIADH |
|
Definition
|
|
Term
|
Definition
| includes the production of small amounts (less than 400mL/DAY) |
|
|
Term
| Urine Concentration & SIADH |
|
Definition
| concentrated (specific gravity >1.020) |
|
|
Term
|
Definition
| urine with an associated decrease in serum sodium (dilutional hyponatremia). |
|
|
Term
| The presence of the hypoosmolar state results in |
|
Definition
| cellular swelling, systemically and intracerebrally. |
|
|
Term
| Cerebral swelling increases_____ and leads to________ |
|
Definition
| intracranial pressure & secondary injury. |
|
|
Term
|
Definition
| restricting fluid intake to prevent further dilution of the serum. |
|
|
Term
| Nursing interventions for the patient with SIADH |
|
Definition
| include monitoring intake and output, neurologic status, and enforcement of fluid restrictions. |
|
|
Term
|
Definition
is similar to SIADH because patients with low serum sodium and low serum and urine osmolality.
CSW is a state of hypovolemia.
The end result is the loss of sodium into the urine causing water to follow.
It is important to differentiate CSW from SIADH because restricting fluid in the CSW patient, who is already volume depleted, can lead to disastrous results.
The patient with CSW is treated with salt replacement via IV saline and oral salt tablets.
Cerebral salt wasting tends to correct itself over the course of 3-4 weeks.
In more severe cases, hypertonic saline and fludrocortisones (Florinef) may be used. |
|
|
Term
| Seizure Activity are classified as ___ or -___ |
|
Definition
early (occurring within seven days of the injury)
late (occurring more than seven days after the injury). |
|
|
Term
| Early onset of seizure activity |
|
Definition
| may cause increased intracranial pressure, hypoxia, and increased metabolic demands increasing severity of secondary injury. |
|
|
Term
|
Definition
| IV lorazepam (Ativan) 0.1mg/kg up to 10mg |
|
|
Term
| lorazepam Ativan can be followed by ____ or ____ |
|
Definition
phenytoin (Dilantin)
fosphenytoin (Cerebyx) |
|
|
Term
| Phenytoin loading dose is |
|
Definition
| 15-20mg/kg IV at 50mg/min followed by a |
|
|
Term
|
Definition
|
|
Term
| The loading dose of fosphenytoin |
|
Definition
| The loading dose of fosphenytoin is 15-20mg/kg IV at 150mg/min |
|
|
Term
| The maint dose of fosphenytoin |
|
Definition
| maintenance dose of 4-6mg/kg/day. |
|
|
Term
|
Definition
a catastrophic complication of traumatic brain injury caused by increased intracranial pressure. '
The direction in which the brain herniates depends on the type and location of injury.
Cingulate herniation occurs when one hemisphere of the brain is forced across the falx cerebri into the space occupied by the contralateral hemisphere. Central herniation occurs when cerebral swelling forces both hemispheres to be displaced downward across the tentorium.
Herniation of either type is devastating as increased pressure is placed on the medulla where basic functions needed to sustain life are located.
When occurring, the nurse will see drastic deterioration patterns in the patient’s neurologic status and vital signs.
The classic vital sign changes are called “Cushing’s Triad” which consists of bradycardia, severe systolic hypertension with a widened pulse pressure and irregular breathing.
Another sign of herniation is the classic pupillary pattern of development of unequal pupils with fixed or sluggish or no reaction to light followed by bilateral fixed and fully dilated pupils.
Management requires emergent interventions to relieve the intracranial pressure which may require emergency surgery. |
|
|
Term
|
Definition
is an irreversible cessation of all brain function, including brainstem function.
Brain death is suspected when there is no evidence of brainstem function for up to 24 hours in a patient with a normal temperature who is not under any influence of depressant drugs, paralytics or alcohol.
Signs of impending death include loss of the body’s ability to maintain adequate blood pressure, profound bradycardia, loss of basic neurological functioning.
The diagnosis- the physician must be able to document coma, absence of brainstem reflexes and apnea. Spontaneous respiratory effort is absent (apnea is present), pupils are fixed and dilated, ocular responses to head turning and cold caloric stimulation are absent. |
|
|
Term
|
Definition
33 individual and fused vertebrae.
There are
7 cervical (C),
12 thoracic (T), and
5 lumbar (L).
The sacral and coccygeal are fused in the adult. |
|
|
Term
| Unstable spinal injury exists when |
|
Definition
| the vertebral and ligamentous structures are unable to support and protect the injured area. |
|
|
Term
| The most frequent neurological level of injury is |
|
Definition
| incomplete tetraplegia, followed by complete paraplegia. |
|
|
Term
|
Definition
1-Motor vehicle crashes account for most SCI cases, next to 2-falls, then
3-acts of violence (gunshot wounds), and then
4-sport injuries. |
|
|
Term
| most frequent causes of death in SCI |
|
Definition
| Pneumonia, pulmonary emboli, and septicemia are the |
|
|
Term
| Non-traumatic Etiologies SCI |
|
Definition
| Degenerative changes r/t osteoarthritis in the spine predispose a person to hyperextension injuries. |
|
|
Term
| SCI precipitating factors ____ and _____ |
|
Definition
Ankylosing spondylitis-calcification of ligaments and soft tissue
and rheumatoid arthritis-inflammation causing osteoporosis and decreased mobility |
|
|
Term
| The first sign of spinal cord compression from tumor growth |
|
Definition
constant dull back pain aggravated by coughing or sneezing.
Leg weakness, urinary retention and sexual dysfunction may also develop. |
|
|
Term
| Acute spinal cord infarction |
|
Definition
is an uncommon but clinically important disease
Onset is sudden, evolving over minutes.
Sudden severe back pain which may radiate with bilateral weakness, tingling and numbness occur. Vascular disease of the aorta is the most common cause of infarction. |
|
|
Term
| Hard cervical collar (short term) |
|
Definition
Philadelphia collar and stiff neck collar
- pre-hospital immobilization, un-cleared C-spine; pre-evaluation, presumptive.
Used for less than 48 hours.
Ensure good collar fit, skin care, decubitus ulcers. |
|
|
Term
| Hard cervical collar (long term) |
|
Definition
Hard cervical collar (long term)
- Miami J collar and Aspen collar- stable C-spine fracture,
Ligamentous injury; hasten healing, diminished pain.
Used for 8-12 weeks.
Ensure good collar fit, warn continuously- provide second collar for washing, meticulous skin care. |
|
|
Term
|
Definition
| cervical strain, whiplash; symptom management; uses varies depending on symptom severity, limit use to avoid dependence (nighttime, riding in car only). |
|
|
Term
| Cervical traction- Gardner-Wells tongs- |
|
Definition
unstable malaligned c-spine fracture,
dislocation, or ligamentous injury; cervical reduction, bridge to operative therapy,
used for varies times,
pin site care and assessment, reposition patients every two hours. |
|
|
Term
|
Definition
unstable c-spine fracture, dislocation, or ligamentous injury; definitive cervical immobilization,
used for 8-12 weeks,
pin site assessment and care, decubitus ulcers beneath vest. |
|
|
Term
| Four poster or Yale brace- |
|
Definition
stable C-spine injuries or adjunct to surgery for unstable c-spine injuries; hasten healing, diminish pain.
Used for 8-12 weeks. |
|
|
Term
|
Definition
Stable thoracic or lumbar spine column fractures, anterior compression fracture with <40% loss of height, burst fractures with no neurologic deficit, <50% vertebral body involvement, <30% canal compromise, angulation <20% degree; hastens healing, diminish pain, after spinal decompressive and stabilization surgery for support and comfort.
Used for 8-12 weeks, requires custom fit, meticulous skin care. Elastic thoraco-lumbar supports- minor compression fractures or transverse process fractures, lumbar strain; symptom management, used for varies time, depending on symptom severity. |
|
|
Term
| Steroid Therapy- methylprednisolone |
|
Definition
| administered post-SCI, may decrease free fatty acid production, inhibit phospholipid breakdown and reduce infiltration of leukocytes. |
|
|
Term
| Steroid Therapy- methylprednisolone |
|
Definition
| By these actions, secondary injury to the spinal cord is prevented because blood flow to the cord is improved and mediators of the inflammatory process are not released. Secondary injury may be diminished if initiated within 8 hours of injury with an |
|
|
Term
| Steroid Therapy- methylprednisolone |
|
Definition
initial bolus of 30mg/kg,
followed by a continuous infusion of 5.4mg/kg/hr over 24-48 hours.
Potential adverse reactions include gastric ulceration, electrolyte imbalances and delayed wound healing. |
|
|
Term
|
Definition
| a potentially life threatening complication, occurs when a stimulus triggers excessive sympathetic nervous system activation below the level of the SCI. Systemic vasoconstriction results, producing sweating, anxiety, headache, blurred vision, and hypertension. The most serious danger is severe hypertension (Systolic BP >200) which can trigger cerebral hemorrhage and stroke, myocardial infarction or seizures. The parasympathetic nervous system compensates for this reaction by producing massive Vasodilation above the level of the lesion and bradycardia. This phenomenon occurs after spinal shock has resolved, usually within the first 6 months. Remains a potential problem throughout the patient’s life. Factors that produce Autonomic dysreflexia: Bladder distention/spasm, bowel impaction, stimulation of anal reflex, labor, temperature change, ingrown toenails, tight irritating clothes, urinary tract infection, decubitus ulcer, pain. While the search for the trigger is conducted, antihypertensive agents are administered. Medications to manage hypertension associated with this include: nifedipine (Procardia), nitroglycerine (nitrostat sublingual or nitrol topical ointment). It is more prevalent in lesion at or above T6. |
|
|
Term
|
Definition
| chronic peripheral vasodilation causes orthostatic hypotension, particularly for patients with injuries at T6 or above. Medications to reduce include ephedrine and medorine. |
|
|
Term
|
Definition
| bladder function is dependent on level of injury. Because of the effects of spinal shock and usual need for aggressive fluid replacement immediately after SCI, patients with acute SCI are best managed with an indwelling urinary catheter, it is best to facilitate a catheter free status as soon as reflex activity returns, the patient is medically stable, urine output average 2L in 24 hours. Most injuries above the T12 level will result in an upper motor neuron (hyper-reflexic or spastic) bladder dysfunction. Intermittent catheterization is the management technique of choice in this type of bladder. Bladder spasticity may lead to problems of leaking; anticholinergic (antispasticity) agents may be required to prevent leaking. |
|
|
Term
|
Definition
| the bowel is innervated by the sacral segments of the spinal cord. Normal bowel function is preserved in incomplete SCI above the sacral level. In complete SCI or during spinal shock, the bowel is flaccid or areflexic. With resolution of spinal shock, the bowel in a SCI above the sacrum will become reflexic. The presence of this reflex activity facilitates bowel evacuation. Bowel training with ducolax suppository or digital stimulation. If SCI is lower (below the sacral level), then the bowel will remain areflexic and retention of stool becomes a problem. The use of stool softeners and suppositories are indicated. Manual removal may be necessary. Anticholinergic agents, vitamins, iron supplements and opioids increase the risk of constipation, ileus and fecal impaction in the patient with SCI. |
|
|
Term
|
Definition
| referred to as phantom or central pain is frequently experienced. This pain is described as burning, stabbing, shooting, aching, numbness and or tingling or electric shock like pain that occurs at or just above the level of the injury or may be experienced at or below the level of injury. Gabapentin (Neurontin) is a first line treatment for neuropathic pain. Antiepileptics and antidepressants are the most common treatment prescribed. Gabapentin, pregabalin and amitriptyline can reduce the pain following SCI. Serotonin noradrenalin reuptake inhibitors as well as steroids may also be used to treat patients with SCI neuropathic pain. |
|
|
Term
| 1) Describe the mechanism of impaired oxygenation for each the four functional classifications of shock states. |
|
Definition
|
|
Term
Hypovolemic Shock State:
results from two conditions- |
|
Definition
either the fluid volume in the circulation has decreased
or the size of the intravascular compartment has increased on proportion to fluid volume. |
|
|
Term
Hypovolemic Shock State:
Venous return |
|
Definition
to the right atrium decreases.
This reduces:
ventricular filling pressure,
stroke volume,
cardiac output,
and blood pressure. |
|
|
Term
Hypovolemic Shock State:
Loss of intravascular volume can be caused by |
|
Definition
loss of blood volume (hemorrhage),
loss of intravascular fluid from the skin (dehydration or burns),
loss of fluid from persistent vomiting or diarrhea,
loss of fluid from intravascular compartment to interstitial spaces (third spacing). |
|
|
Term
Hypovolemic Shock State:
A diminished fluid volume leads to |
|
Definition
| a decreased cardiac output, resulting in impaired oxygen delivery. |
|
|
Term
Transport Shock States:
Hg & O2 |
|
Definition
the common pathologic mechanism in transport shock states is a diminished supply of Hg to carry O2 to tissue.
Anemia and hemorrhage are characterized by a decrease in red blood cells and Hb for O2 to bind to. |
|
|
Term
Transport Shock States:
Carbon Monoxide |
|
Definition
| Carbon monoxide toxicity represents another form of transport shock state. Carbon monoxide binds rapidly to Hb and leaves no room for O2 to bind therefore oxygen cannot be transported to tissue. Carbon monoxide interferes with the release of O2 from Hb and also interferes with the cells ability to use O2. |
|
|
Term
|
Definition
| occurs as a result of a mechanical barrier to blood flow that blocks O2 delivery. |
|
|
Term
Obstructive Shock State:
causes |
|
Definition
| pulmonary embolism, tension pneumothorax or cardiac tamponade. |
|
|
Term
Obstructive Shock State:
PULMONARY ARTERIES BECOME |
|
Definition
partially obstructed which results in an increase in alveolar dead space and a lentiltion-perfusion mismatch which impairs gas exchange.
Obstruction of the pulmonary arteries by emboli also results in increased pulmonary vascular resistance. Shock states in response to a pulmonary embolism can result from inadequate systemic O2 delivery because of impaired gas exchange and cardiac dysfunction.
A tension pneumothorax occurs when air enters the pleural space during inspiration but cannot leave during expiration. The progressive accumulation of air within the thoracic cavity leads to a shift of the mediastinal structures and compression of the opposite lung. The increased pleural pressure impedes venous return and serves as a barrier to O2 delivery.
Cardiac tamponade is caused by bleeding into a nonflexible pericardial sac. The accumulating pressure around the heart impairs ventricular filling and decreased CO. |
|
|
Term
|
Definition
| occurs as a result of impaired O2 delivery due to cardiac dysfunction. |
|
|
Term
Cardiogenic Shock State:
The most common cause |
|
Definition
| is an extensive myocardial infarction (MI), particularly in the anterior portion of the left ventricle. |
|
|
Term
Cardiogenic Shock State:
Causes of cardiogenic shock include |
|
Definition
extensive acute myocardial infarction,
mechanical complications (papillary muscle rupture, acute mitral regurgitation, ventricular septal rupture or cardiomyopathy). |
|
|
Term
Cardiogenic Shock State:
Failure can occur when the |
|
Definition
| right ventricle fails to pump the volume of blood it receives or when the left ventricle fails to pump oxygenated blood into the systemic circulation. |
|
|
Term
Cardiogenic Shock State:
An infarction in the left ventricle produces a |
|
Definition
| necrotic area that impairs contractility and CO. |
|
|
Term
Cardiogenic Shock State:
As stroke volume decreases, |
|
Definition
| so do CO and blood pressure. |
|
|
Term
Cardiogenic Shock State:
Because the damaged left ventricle cannot propel all of its contents forward, blood begins to “back up” into the pulmonary system, causing pulmonary congestion. |
|
Definition
| Increased pulmonary congestion leads to increased afterload for the right ventricle. In right ventricle dysfunction, the right ventricle ejects too little blood and therefore less blood enters the left ventricle. As left ventricle stroke volume decreases, CO and blood pressure decreases as well. Because right ventricle cannot effectively pump all the blood it receives, blood begins to “back up” into systemic circulation. |
|
|
Term
| 2) Describe the compensatory mechanism that occurs in response to shock states. |
|
Definition
Low pressure stretch receptors in the right atrium sense a decrease in circulating blood volume when there is a decrease in venous return to the right atrium.
Baroreceptors in the aorta and carotid arteries sense a decrease in blood volume and CO. Carotid body chemoreceptors sense alterations in pH and partial pressure of arterial Carbon dioxide (PaCO2).
The baroreceptors and chemoreceptors alert the hypothalamus to activate the sympathetic nervous system’s flight or fight response. This releases a massive amount of norepinephrine, epinephrine and cortisol, which causes an increase in venous return, an increase in CO and an increase in O2 delivery. The endocrine system is activated to increase oxygen delivery by increasing blood volume.
The hypothalamus releases adrenocorticotropic hormone (ACTH) which activates the adrenals to secrete aldosterone. Aldosterone causes sodium and water retention, attempting to increase the blood volume and blood pressure. Sodium and water retention stimulates the release of antidiuretic hormone (ADH), which increases reabsorption of water in the kidney tubules and increase blood volume. CO must be augmented in shock for adequate tissue perfusion. CO is proportional to venous return. To increase venous return, sodium and water are retained by aldosterone and ADH.
As a result of decreased blood flow to the kidneys, the juxtaglomerular cells in the kidneys excrete renin. Renin catalyzes angiotensinogen in the liver which then converts to angiotensin 1. In the lungs angiotensin 1 turns to angiotensin 2, which is a potent vasoconstrictor, which increases blood pressure by increasing afterload. The effects of these hormonal mechanisms are increased blood pressure through vasoconstriction and increased venous rerturn through retention of sodium and water and decreased urine output. |
|
|
Term
3) Discuss the clinical manifestations of each of the four functional shock states.
Hypovolemic Shock State |
|
Definition
With fluid loss, the signs and symptoms are related to the degree of volume depletion.
The skin is cool and capillary refill is poor.
The blood pressure may be low and orthostatic blood pressure changes may be noted.
Tachycardia is evident and urine output is low.
Hemodynamically, as less volume is returned to the right atrium, the right atrial pressure (RAP) is low.
As less fluid is delivered to the pulmonary vasculature and left ventricle, pressures are low, as evidenced by a low pulmonary artery wedge pressure (PAWP) and low CO.
They systemic vascular resistance (SVR) is elevated as vasoconstriction occurs in efforts to increase venous return and CO. |
|
|
Term
3) Discuss the clinical manifestations of each of the four functional shock states.
Hypovolemic Shock State |
|
Definition
increased: HR, SVR
Decreased: RAP, UO, BP, PAWP, CO,
Skin cool & sluggish cap refill |
|
|
Term
| In Neurogenic shock, S/S are related |
|
Definition
to the loss of sympathetic innervation.
Persistent vasodilation produces a decreased SVR.
Pooling of blood in dilated vessels results in diminished venous return, producing a lower RAP, PAP, PAWP, and CO.
Heart rate is decreased as a result of parasympathetic innervation.
Peripheral vasodilation produces warm skin. Hypothermia and absence of sweating below the level of spinal cord injury may be present. |
|
|
Term
| Severe anaphylactic shock frequently involves multiple |
|
Definition
multiple organ systems,
but the most life threatening are those involving the cardiovascular and pulmonary systems. |
|
|
Term
|
Definition
Typical pattern of generalized itching followed by cutaneous flushing, urticarial, and loss of consciousness.
Severe upper airway obstruction by edema can lead to asphyxia, whereas lower airway obstruction with wheezing and chest tightness is caused by bronchospasm. |
|
|
Term
|
Definition
Diminished oxygen carrying capacity of the blood produces the clinical manifestations seen in transport shock states.
In shock caused by anemia or hemorrhage, a low hematocrit and hemoglobin will be present.
RAP and PAWP may be normal depending on the patient’s volume status. |
|
|
Term
| carbon monoxide poisoning |
|
Definition
| Symptoms caused by carbon monoxide poising can result from exposure to low levels of carbon monoxide for prolonged periods or can arise from exposure to higher levels for a shorter duration. Common symptoms of carbon monoxide poising include headache, malaise, nausea, difficulties with memory and personality changes as well as gross neurologic dysfunction. |
|
|
Term
| Obstructive Shock states: |
|
Definition
Pulsus paradoxus is one of classic signs of cardiac tamponade.
Pulsus paradoxus is an exaggerated decrease (>10 mm Hg) of the systolic blood pressure during inspiration.
Increased pericardial fluid may produce distant heart sounds.
In tamponade, RAP usually is elevated and equaled by the PAWP.
Beck’s triad- elevated RAP, decreased BP, muffled heart sounds- may be present.
Some patients demonstrate S/S of dysphoria. Patients with cardiac tamponade reported feelings of restlessness and impending death.
They exhibited restless body movements and facial expressions. Increased pleural pressure as a result of tension pneumothorax puts direct pressure on the heart, vena cava and contralateral lungs, which decrease venous return and CO.
Decreased breath sounds and tracheal deviation may be present. Pulmonary embolism the most frequent symptom is dyspnea, the most frequent sign is tachypnea.
The presence of pleuritic pain, cough, or hemoptysis suggests a small embolism near the pleura and the presence of dyspnea, syncope or cyanosis indicates a massive pulmonary embolism.
ECG abnormalities are T wave inversion in the anterior leads (V1, V2) and a right bundle branch block. Acute pulmonary embolism may also have a unique pattern on ECG and includes an S wave in lead 1 and a Q wave with T wave inversion in lead 2. ABGs may be normal or indicate hypoxemia or hypercapnia. |
|
|
Term
|
Definition
left ventricular failure produces clinical manifestations associated with hypoperfusion and pulmonary congestion including
dyspnea, bilateral crackles and distant heart sounds and 3rd and 4th heart sounds are usually present.
Hemodynamic profile includes and elevated PAWP (>15 mmHg), low cardiac index (<1.8 L/min/m2 without inotropic support, or < 2.2 L/min/m2 with inotropic support), sustained hypotension (systolic BP less than 90 mm Hg and mean BP 30 mmHg lower than baseline).
Right Ventricular failure is associated with systemic venous congestion. Peripheral edema may be present.
Lung sounds will be clear unless there is also left ventricular dysfunction.
A split-second heart sound may be heard. Hemodynamic profile includes elevated RAP in the presence of normal or low PAWP. |
|
|
Term
4) State the medical and nursing interventions used in the treatment of shock states that optimize oxygen delivery and decrease oxygen consumption.
Interventions to optimize O2 delivery |
|
Definition
Supplemental O2 may be administered; intubation and mechanical ventilation may be required.
IV fluids combination of crystalloid solution (lactated ringer) and colloids may assist in restoring optimal tissue perfusion. Positive inotropic drugs increase contractility.
Inotropic drugs that increase cardiac output and enhance tissue perfusion include dopamine, dobutamine and milrinone.
Vasoactive drugs act on smooth muscle layer of blood vessels and affect preload and afterload.
Vasopressors include epinephrine, norepinephrine, dopamine and vasopressin.
These drugs increase SVR and BP and should only be given to patients with adequate volume status.
Afterload reducing (vasodilating) drugs improve cardiac output and oxygen delivery. Peripheral arterial vasodilators (nitroprusside, nitroglycerine) decrease SVR. |
|
|
Term
| Interventions to decrease O2 consumption |
|
Definition
should be directed toward decreasing total body work, decreasing pain and anxiety, and decreasing temperature.
Hyperventilation occurs in an effort to increase O2 delivery to meet demands, ventilation is ensured with intubation and mechanical ventilation.
Neuromuscular blocking agents such as pavulon and norcuron. These drugs eliminate unnecessary muscle activity and allow O2 to be redirected for use in involuntary muscles such as the heart.
Hyperthermia increases metabolic demands and O2 requirements. This is controlled with antipyretic drugs (acetaminophen) or physical cooling measures such as fan or cooling blanket. |
|
|
Term
|
Definition
treatment goal is to restore fluid volume.
The source of the fluid loss is identified and controlled. |
|
|
Term
| Neurogenic shock treatment goals are to |
|
Definition
| maintain stability of the spine and optimize O2 delivery with IV fluids or vasopressors. |
|
|
Term
| Anaphylactic shock treatments |
|
Definition
| are to maintain airway and support blood pressure. |
|
|
Term
| Sepsis and septic shock are treated with antibiotics within |
|
Definition
| one hour after HCP initiates order. |
|
|
Term
| Initial fluid resuscitation (colloid or crystalloids) is given until RAP |
|
Definition
| Initial fluid resuscitation (colloid or crystalloids) is given until RAP is 8-12 mm Hg, |
|
|
Term
| Initial fluid resuscitation (colloid or crystalloids) is given until MAP |
|
Definition
| MAP greater than 65 mm Hg, |
|
|
Term
| Initial fluid resuscitation (colloid or crystalloids) is given until UO |
|
Definition
| urine output greater than 0.5mL/kg/hr |
|
|
Term
| Initial fluid resuscitation (colloid or crystalloids) is given until central venous O2 sat |
|
Definition
|
|
Term
|
Definition
The treatment goal is to restore the oxygen-carrying capacity of red blood cells.
For the treatment of anemia or hemorrhage, packed red blood cells may be administered in an effort to provide an adequate Hb concentration.
Treatment for carbon monoxide poisoning consists of the administration of high fractional concentrations of supplemental oxygen. Hyperbaric oxygen therapy may decrease the negative sequelae of carbon monoxide poisoning. |
|
|
Term
|
Definition
treatment is to remove the mechanical barrier to blood flow.
For tension pneumothorax, trapped air is decompressed by a physician with the insertion of a 14 gauge needle or a chest tube. Needle pericardiocentesis may decompress the pericardium for cardiac tamponade or thoracotomy may be required to surgically control and decompress the tamponade.
Pulmonary embolism management is with heparin.
Inferior vena cava filters may be used in the presence of active hemorrhage, contraindications to anticoagulation or recurrent pulmonary embolism. Thrombolytic therapy or surgical embolectomy may be necessary in the face of hemodynamic instability and shock. |
|
|
Term
|
Definition
treatment is based on the cardiac abnormality and whether the shock is caused by left sided or right sided heart failure.
Treatment is directed toward decreasing myocardial oxygen demand and improving myocardial oxygen supply.
Initial management may include fluid resuscitation (unless pulmonary edema is present), placement of central venous and arterial catheters, urinary catheterization, pulse oximetry, airway protection, correction of electrolyte abnormalities and relief of pain and anxiety.
Dobutamine can be used to improve myocardial contractility and increase cardiac output in patients with normovolemia but inadequate tissue perfusion.
Diuretics may be used to treat pulmonary congestion.
Vasodilators may be used (after blood pressure is stabilized) to decrease both preload and afterload.
Further treatment may include thrombolytic therapy, an intra-aortic balloon pump, and revascularization (angioplasty or coronary artery bypass surgery). |
|
|
Term
5) Describe the nursing care plan for clients with shock.
Risk for shock: |
|
Definition
risk factors may include- relative or actual hypovolemia; Reduction of arterial/venous blood flow: selective vasoconstriction, vascular occlusion-intimal damage, microemboli.
Desired outcomes-
Circulation status: display adequate perfusion as evidenced by stable vital signs, palpable peripheral pulses, skin warm and dry, usual level of mentation, individual appropriate urinary output and active bowel sounds.
Actions/interventions: maintain bedrest and assist with care activities. Monitor trends in BP, especially noting progressive hypotension and widening pulse pressure. Monitor HR and rhythm. Note dysrhythmias. Note quality and strength of peripheral pulses. Assess respiratory rate, depth and quality. Note onset of severe dyspnea. Investigate changes in sensorium- mental cloudiness, agitation, restlessness, personality changes, delirium, stupor and coma. Assess skin for changes in color, temperature and moisture. Record hourly output and specific gravity. Auscultate bowel sounds. Hematest gastric secretions and stools for occult blood. Evaluate lower extremities for local tissue swelling, erythema, and positive Homan’s sign. Maintain sequential compression devices (SCD’s) as indicated. Monitor for signs of bleeding: oozing from puncture sites or suture sites, petechiae, ecchymoses, hematuria, epistaxis, hemoptysis and hematemesis, note drug effects and monitor for signs of toxicity. Collaborative: administer parenteral fluids, administer drugs, as indicated, inotropic agents and vasopressors, corticosteroids , low molecular weight heparin, histamine 2 receptor blockers, monitor laboratory studies (ABG’s and Lactate), provide supplemental O2, maintain stable body temperature, prepare for and transfer to critical care setting as indicated. |
|
|
Term
| Nursing care: cardiogenic Shock: Expected Patient Outcomes- |
|
Definition
Assess and compare to established norms, patient baseline and trends. Assess for clinical manifestations of left ventricular failure including dyspnea, bilateral crackles, distant heart sounds, 3rd and 4th sounds, elevated PAWP, low Cl, sustained systolic hypotension. Assess for clinical manifestations of right ventricular failure including peripheral edema, split S2 heart sounds, elevated RAP in the presence of normal or low PAWP.
Implement interventions to increase O2 delivery: administer supplemental O2 as ordered. Administer IV fluids as ordered. Administer inotropic agents as ordered (Dobutamine). Administer afterload reducing (Vasodilating) drugs as ordered. Implement IABP as ordered. Implement interventions to decrease O2 consumption: Mechanical ventilation as ordered. Administer sedative, analgesics, anxiolytics as ordered. Implement nonpharmacologic interventions to decrease pain and anxiety. Position patient to maximize comfort. Provide calm, quiet environment. Offer support to decrease anxiety. Administer related drug therapy and monitor for therapeutic and non-therapeutic effects: Diuretics (Lasix). Vasodilators (Nipride). Inotropic agents (Primacor). Thrombolytic therapy.
Related Nursing Diagnosis: Ineffective Cardiopulmonary tissue perfusion related to acute myocardial ischemia.
Decreased cardiac output related to altered contractility. Decreased cardiac output related to altered heart rate. |
|
|
