POWERED BY: Silverspeed Site Builder

SILVERSPEED SELECTIONS:

Share


I made this widget at MyFlashFetish.com.

.

September 17, 2010

N-Trivia

N-Trivia

Arteriovenous Malformation (AVM)

Posted: 16 Sep 2010 10:43 PM PDT


Arteriovenous are malformation of the cerebrovascular system in which tortuous, tangled, and malformed arterial channels drain directly into the venous system without an intervening capillary bed. The arteries supplying the AVM tend to dilate with time as a result of increased flow through the lesion. The veins enlarge as the flow increases; creating a vicious cycle that can make this lesion increase in size. This large flow or shunting of the blood through the AVM can render adjacent areas (and sometimes distal areas) of the brain ischemic. The high flow state can lead to increased pressure and eventually hemorrhage, typically into the subarachnoid space and parenchymal tissue.

Signs and Symptoms

  • Headache
  • Seizures
  • Syncope
  • Progressive neurologic deficits
  • Hemorrhage

Physical Examination

Vital signs:

  • BP: Normotensive or hypertensive
  • HR: Mild tachycardia may be present
  • RR: Eupnea

Neurologic: depending on the area of the brain in which the AVM is located, there may be speech, motor, or sensory deficits. There also may be problems with vision, memory, and coordination.

Acute Care Patient Management

Nursing Diagnosis: Ineffective tissue perfusion: Cerebral related to shunting of blood from cerebral tissue and/ or intracerebral hemorrhage (ICH).

Outcome Criteria

  • Alert and oriented
  • Pupils equal and normoreactive
  • BP 90 to 140 mmHg
  • HR 60 to 100 beats/minute
  • RR 12 to 20 breaths/minute, eupnea
  • Motor function equal bilaterally
  • Absence of headache, nystagmus, and nausea
  • Intracranial pressure (ICP) <20 mm Hg
  • Cerebral perfusion pressure (CPP) 60 to 100 mm Hg

Nursing Interventions

Patient Monitoring

  1. Monitor ECG continuously because hypoxemia and cerebral bleeding are risk factors for pronounced ST segment and T-wave changes and life-threatening dysrhythmias.
  2. Monitor ICP, analyze the ICP waveform, and calculate CPP every hour.
  3. Monitor BP and pulse every 15 to 30 minutes initially, then hourly.
  4. Obtain CVP and/ or PA pressures if available, every hour or more frequently if indicated.

Patient Assessment

  1. Assess pain using the patient's self-repot whenever possible.
  2. Note headache onset and severity; presence of stiff neck; and insidious onset of confusion, disoreintatio, decline in consciousness, and/or focal deficits (weakness of extremity).
  3. Assess neurologic status using Glascow Coma scale and assess for changes suggesting increased ICP and herniation.
  4. Be alert for subtle changes and new focal deficits.
  5. Assess for factors that can cause increased ICP, evaluate the patient for restlessness, distended bladder, constipation, hypovolemia, headache, fear, or anxiety.

Diagnostic Assessment

  • Review serial ABGs for decreasing Pao2 (<60 mm Hg) or increasing Paco2 (.40 mm Hg) to identify causes for increased ICP.

Nursing Interventions

  1. Maintain patent airway and administer oxygen as ordered to prevent hypoxemia.
  2. Institute measures to minimize external stimuli and maintain BP level.
  3. Administer antihypertensive drugs as ordered. To control blood pressure.
  4. Sedatives and stool softeners may be prescribed to reduce agitation and straining.
  5. Anticipate interventions such as embolization, resection, clipping, ligation of feeding vessels, proton-beam therapy, or gamma radiation.

Related posts:

  1. Hypovolemic Shock
  2. Encephalitis
  3. Nursing Care Plan (TB Meningitis)

Pulmonary Embolus

Posted: 16 Sep 2010 10:28 PM PDT


pulmonary embolus A pulmonary embolus is pulmonary vasculature that occurs from a fibrin or blood clot. Most commonly emboli are detached thrombi from the deep veins of the legs. Predisposing factors include:

Virchow's triad:

  • Acute injury to blood vessels wall
  • Venous stasis
  • Hypercoagulable states.

Air emboli usually result from air entering the sirculatory system through intravascular catheters. Fat emboli occur with long-bone fractures.

Signs and Symptoms

  • The signs and symptoms are non-specific. The hemodynamic effects depend on the size of embolus, presence of cardiopulmonary disease, and the neurohormonal response to the embolus.
  • The patient may be apprehensive and exhibit dyspnea, pleuritic pain, hemoptysis, tachycardia, tachypnea, crackles, cough, diaphoresis, and syncope.

Physical Examination

Appearance:

  • Restless
  • Anxious

Vital signs:

  • BP: Normal or increased BP as a result of anxiety
  • HR: Normal or increased HR > 100 beats/minute
  • RR: Increase rate

Acute Care Patient Management

Nursing Diagnosis: Impaired gas exchange related to ventilation perfusion mismatch and/ or hypoventilation secondary to pain.

Outcome Criteria

  • Alert and oriented
  • RR 12 to 20 breaths/minute, eupnea.
  • Absence of adventitious breath sounds
  • Pao2 80 to 100 mm Hg
  • O2 saturation ? 95%
  • P (a/A)O2 ratio > 0.60

Nursing Interventions

Patient Monitoring

  1. Continuously monitor oxygen saturation with pulse oximetry (Spo2).
  2. Carefully monitor patient activities and interventions that may adversely affect oxygen saturation.
  3. Continuously monitor ECG for dysrhythmias or ischemic changes.
  4. Calculate P (a/A) o2 ratio to evaluate intrapulmonary shunt.

Patient Assessment

  1. Assess respiratory status: note rate and depth of respirations.
  2. Observe for dyspnea and restlessness. Hypoxia may be manifested as increased restlessness or change in level of consciousness and respiratory rate > 30 breaths/min.
  3. Auscultate breath sounds such as crackles and pleuritic rub may be present.
  4. Perform systematic initial and ongoing pain assessment such as intensity, location, quality, aggravating and relieving factors.
  5. Use a self-report pain rating scale, such as 0-to-10 numerical pain rating scale, to assess pain intensity in patients who are awake and oriented.
  6. Assess for behaviors such as grimacing, groaning, grunting, sobbing, crying, irritability, withdrawing, or hostility because they may be signs of pain. However, the absence of these behaviors does not necessarily mean the absence of pain.
  7. Assess for physiologic indicators, such as increased RR, HR, and B; dilated or constricted pupils and pallor, which may be signs of pain.

Diagnostic Assessment

  • Review ABGs for changes inSao2 and Pao2 to evaluate improvement or deterioration in the patient's pulmonary status.

Patient Management

  1. Place the patient on bed rest initially and assist the patient to assume a comfortable position.
  2. Administer supplemental oxygen as ordered.
  3. Intubation and mechanical ventilation may be required.
  4. Pace activities to decrease the patient's oxygen demand, allowing adequate time for patient recovery.
  5. Administer analgesics as ordered to prevent splinting and improve chest excursion.

Related posts:

  1. Cardiogenic Pulmonary Edema
  2. Arteriovenous Malformation (AVM)
  3. Hypovolemic Shock

Cardiogenic Pulmonary Edema

Posted: 16 Sep 2010 09:05 PM PDT


Pulmonary edema is an abnormal accumulation of extravascular fluid as the lung parenchyma that interferes with adequate gas exchange. This is a life threatening situation that needs immediate treatment. The most common cause of cardiogenic pulmonary edema is left ventricular failure exhibited by increased left atrial ventricular pressures. Risk factors include ischemic heart disease, cardiomyopathy, valvular disease, myocardial infarction, and acute septal defects.

Signs And Symptoms

  • Shortness of breath
  • Orthopnea
  • Moist cough with pink frothy sputum
  • Chest discomfort
  • Palpitations
  • Fatigue
  • Syncope
  • Cyanosis
  • Respiratory distress

Physical Examination

Appearance:

  • Anxious
  • Diaphoretic
  • Clammy skin

Vital signs:

  • HR: sustained tachycardia
  • BP: < 90 mm Hg
  • RR: > 30 breaths/minute
  • Falling O2 saturations

Cardiovascular:

  • Tachydysrhythmias with possible ectopy
  • Laterally displaced point of maximal impulse (PMI)
  • Murmur – mitral valve regurgitation
  • S3 with possible S4

Pulmonary:

  • Respiratory distress
  • Respiratory failure
  • Orthopnea
  • Coarse bilateral crackles
  • Wheezing
  • Rhonchi
  • Cough with frothy sputum

Acute Care Patient Management

Nursing Diagnosis: Impaired gas exchange related to increased pulmonary congestion secondary to increased left ventricular end diastolic pressure (LVEDP).

Outcome Criteria

  • RR 12 to 20 breaths/min
  • Eupnea
  • Lungs clear to auscultation
  • pH 7.35 to 7.45
  • Pao2 80 to 100 mm Hg
  • Paco2 35 to 45 mm Hg
  • O2 sat ? 95%
  • Svo2 60% to 80%
  • P (a/A) O2 ratio 0.75 to 0.95

Nursing Interventions

Patient Monitoring

  1. Continuously monitor oxygenation status with pulse oximetry monitoring.
  2. Monitor ECG for dysrhythmia development that may be related to hypoxemia, acid-base imbalance, or ventricular irritability.
  3. Calculate arterial-alveolar oxygen tension ratio as an index of gas exchange efficiency.
  4. Document hourly the input and output to monitor fluid status. Obtain daily weights.

Patient Assessment

  1. Measure HR, RR, and BP every 15 minutes to evaluate the patient's response to therapy and to detect cardiopulmonary deterioration.
  2. Assess the patient for changes that may indicate respiratory compromise, necessitating intubation and mechanical ventilation.

Diagnostic Assessment

  1. Review ABGs for hypoxemia (Pao2 < 60 mm Hg) and acidosis (pH < 7.35), which may further compromise tissue perfusion and to indicate need for mechanical ventilation.
  2. Review serial chest radiographs for worsening or resolving pulmonary congestion.
  3. Review lactate levels as an indicator of anaerobic metabolism.

Patient Management

  1. Provide supplemental oxygen via mask as indicated.
  2. Administer diuretic agents or nesiritide to reduce circulating volume, which will improve gas exchange.
  3. Monitor urine output and electrolytes.
  4. Administer vasodilating agents to redistribute fluid volumes, which will facilitate gas exchange.
  5. Morphine sulfate maybe ordered to promote preload and afterload reduction and to decrease anxiety.

Related posts:

  1. Pulmonary Embolus
  2. Hypovolemic Shock
  3. Nursing Care Plan Chronic Obstructive Pulmonary Disease (COPD)
POWERED BY: Silverspeed Site Builder