Respiratory system_1_

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Respiratory system_1_ Powered By Docstoc
					By: Diana Blum MSN
              MCC
        NURS 2140
2
 Nose to pharynx}behind the mouth to
  esophagus (approx. 5 inches)
 Larynx} voice box: air passes between
  pharynx and trachea
 Trachea} windpipe
 Bronchi}this is the main branch that air passes
  through divides into left and right branch
 Bronchioles} subdivides and connects with
  alveoli for gas exchange
                                                3
 Epiglottis} behind the thyroid cartilage
   Has a hinged door action to larynx
 Glottis} space between the folds of vocal cords
   Air from the lungs promote it to open and close
 Lungs} 3 lobes on the right and 2 lobes on the
  left
 Pleura}membrane that covers the lungs
   Has a lubricant between the layers to allow inhalation
    and exhalation to occur
 Cilia} hair like projections that trap debris

                                                             4
• Inspiration : air enters lungs
   – Active process where Chest muscles and
     diaphragm contract causing chest cavity to enlarge
• Expiration: air leaves lungs
   – Passive process where muscles relax and the chest
     returns to normal.
• Normal quiet breathing = 500ml of air
  exchanged with each breath
• Pg

                                                      5
• Temporary interruption in the normal breathing
  pattern in which NO air movement occurs
  – May occur during sleep and at end of life
• http://www.blinkx.com/video/understanding-
  obstructive-sleep-apnea-osa-
  1/WDHzxnb1t77AkBsdYIYwdg
• http://www.blinkx.com/video/answered-patient-
  sleep-disorders-living-with-sleep-
  apnea/FjusOmVoqIX3V0lKzcwlKQ


                                                   7
• Dyspnea} difficulty breathing or shortness of
  breath
• Orthopnea} difficulty with breathing while in a
  lying position
• Tachypnea} respiratory rate >20
• Bradypnea} respiratory rate <12



                                                    8
   Normal Breath Sounds
            To be able to distinguish between types of abnormal breath sounds and their location, it is important to
    understand normal respiration and its effect on airway noises that make up breath sounds. Normal breath sounds are
    bronchovesicular in nature. They are loud pipe-like sounds in the large airways, and softer blowing-like sounds in the
    small airways. Normal breath sounds are loudest during inspiration and softest during expiration. The inspiratory
    phase is shorter with faster airflow. Although abnormal sounds may be louder during inspiration, they may be difficult
    to distinguish due to their short duration.
   Normal Air Flow through the Lungs
            Flow is greatest in the trachea and diminishes in the distal lung fields, until it reaches the alveoli, where there is
    no flow. Breath sounds are loudest over areas with greater flow, and distal pathology may be communicated to these
    areas. Therefore, auscultation over the trachea may reveal pathology there or communicated from distal regions of
    the lung.
   **If breath sounds are really diminished, listen over the trachea**
   Adventitious sounds
   Wheezing: musical, whistling sound
   Usually more pronounced during expiration
   From narrowed airways
      Bronchoconstriction
      Secretions
   Interventions:
      Bronchodilation
      Hydration
      Coughing
   http://www.ed4nurses.com/breathsnds.htm



                                                                                                                           9
•   Rales: crackling sound
•   Heard at the end of inspiration
•   From collapsed or waterlogged alveoli
•   Fine: beginning of fluid buildup / or atelectasis
•   Coarse: greater volume of fluid buildup
•   Interventions:
•   Manage fluids
      – Budget volume resuscitation
      – Diuretics
•   Expectorate
      – Turn & position
      – Deep breathing
      – Forced expiration
      – Vibration & percussion
•   Rhonchi: bubbling
•   The sound will be heard throughout inspiration and expiration.
•   Louder than rales due to larger secretions
•   Results from air bubbling past secretions in the airways
•   Interventions:
      – Deep breathing
      – Coughing
      – Hydration (encourage fluids, if no restriction)
      – Humidify air
      – Mobilize
•   Friction rub: creaking, leathery sound
•   End of inspiration and beginning of expiration
•   Caused by rubbing of inflamed pleural surfaces against lung tissue.
•   Interventions:
      – Chest x-ray
      – Anti-inflammatory medications
Cheyenne Stokes                Kussmal’s

• Breaths are deep than        • Regular breathing but
  become shallow followed by     breaths are deep
  periods of apnea             • Rates are >20 bpm
• Cause: severe brain          • Causes: metabolic acidosis,
  pathology                      renal failure, diabetic
                                 ketoacidosis




                                                               11
• http://rnbob.tripod.com/breath.htm
• Lung sounds
  http://www.med.ucla.edu/wilkes/lungintro.htm
• http://www.rnceus.com/resp/respabn.html
• case studies
  http://www.meddean.luc.edu/lumen/MedEd/me
  dicine/pulmonar/pd/step29e.htm


                                             12
 Muscle atrophy in pharynx and larynx and change in vocal
  cords
 Loss of lung elasticity
 Decreased number of alveoli
 Weaker chest muscles
 Diminished chest movement
 Less effective cough
 Work harder to breath
 Enlargement of bronchioles
 More suseptible to lung infections r/t decreased defense
  mechanisms
 Rib cage becomes more rigid and diaphragm flattens

                                                             13
Nasal Cannula: 1-6 liter flow
Simple mask: 6-8 liters/ 40-60% o2
prercentage
Partial rebreather: has reservoir bag so
patient can rebreath part of inhaled gas: 8-
11 liters/ 50-75%
Non rebreather mask: non of exhaled gas
rebreathed. 12 liters ; 80-100%


See figure 35-3




                                               14
• - a thrombus (most originate from lower
  extremities) that travels thru venous circulation
  to pulmonary circ. & partially OR
  completely occludes a pulm. artery

- - a massive PE: occlusion of >50% of
   pulmonary artery bed
 150,000 deaths annually in US

Pg 973
19
• Obstruction in pulmonary blood vessel causing a
  ventilation-perfusion mismatch resulting in hypoxemia,
  followed by < CO, bronchial constriction, collapsed alveoli
  and may result in sudden death
• Cause: blood clot, fat , air, amniotic fluid, clumps of bacteria
• Diagnosis: H&P, ABGs,VQ scan, EKG
• S/S: sudden severe chest pain increases on inspiration,
  tachypnea, dyspnea, diaphoresis, hemoptysis, abnormal lung
  sounds, fever, tachycardia
• Tx: Anticoagulation: PTT 2-21/2 normal
   – Heparin then oral Coumadin using PT and INR to
      regulate doses
       • Therapeutic coumadin range varies per doctor but most use
         goal of 2.0-3.0
   – O2, IV ms, support CV system
   – Surgically may do embolectomy and insert a vena cava
     filter
                                                                     22
• How does PE occur??
•     Deep venous thrombus breaks loose (MOST
  COMMON CAUSE)
•                  ↓
•      flows through venous circulation
•                   ↓
•       enters right ventricle
•                    ↓
•        lodges in small pulmonary arteries
•                    ↓
•        embolus may dissolve, grow or fragment
• Embolus will most often lodge in Rt LL
• - - increases pulmonary artery pressure
• - - increases vascular resistance
• - - increased dead space ( disruption of
  blood flow to alveoli = nonfunctioning units)
• Virchow’s triad:
•      1. damaged vascular endothelium
•      2. venous stasis
•      3. hypercoagulability
• What would cause release of a thrombus?
•     - direct trauma
•     - muscle contraction
•     - changes in perfusion
• - may have no predisposing factors
• - immobilization, obesity, pregnancy,
•     estrogen use, aging, major trauma
•     or surgery within 4 weeks, malignancy
•     DVT, indwelling catheter, electrodes in
•     right heart (pacer), CHF, acquired
•     disorder (heparin-induced
  thrombocytopenia, postspleenectomy)
•   Hx of DVT
•   > 40 yrs of age
•   Extensive abdominal or pelvic surgery
•      (many PE originate in femoral – iliac-
•        pelvic veins)
•   Long-bone or pelvic fractures
• - - occurs suddenly
• - - associated with acute Rt hrt failure
•        (  ‘d pulmonary artery systolic
•          pressure & pulm. vasc resistance)
• - - ↓’d CO
• - - may have crushing substernal CP
• - - Shock: hypotension, dypnea, cyanosis,
  apprehension, coma
• - - resp rapid, shallow, gasping
• “impending doom” if pt conscious

• Core pulomonale pg 980
• Pulmonary hypertension from pulmonary
  arterial obstruction
• Sudden obstruction & total: sudden
  death
• Pulmonary infarction
• Stroke, MI, dysrhythmias, liver failure,
  acute respiratory distress syndrome,
  shock, death
• Ultrasound
• D-dimer test: not specific, fibrin product – if
  positive will do further testing
• Pulmonary Venography: gold standard, inject
  dye noninvasive tests first
• MRI with contrast
• CT contrast spiral
• V/Q scanning (dye give IV AND inhaled )
• Heparin: Load 80 Units/kg
•           Drip 18 Units/kg/hr
• Measure PTT every 6 hours
•          Goal: PTT 1.5 to 2.0 X control
• Vena Cava Filter: for contraind. anticoag OR
  clot develops while adeq anticoagulated
• Embolectomy: if not anticoag candidate &
•      acutely unstable
• Thrombolytics: tPA
•
• Platelet count monitored about every 3 days
  for heparin-induced thrombocytopenia
• Oral Coumadin by day 3 of heparin
• Titrate dose heparin so PTT is 1.5-2.5 times
  normal control.
• ADVERSE EFFECTS:
•    hemorrhage, hypersensitivity,
  thrombocytopenia
•    measured PTT          Heparin adjust
•     <35 sec (1.2 X )     80U/kg then 
•                           rate by 4U/kg/hr
• 35-45 sec (1.2-1.5X)   40U/kg bolus
•                          then  rate by 2U/
•                          kg/hr
• 46-70 sec (1.5-2.3X)   NO CHANGE
• 71-90 sec (2.3-3X)     ↓rate by 2U/kg/hr
  >90 sec (3X control)    Stop infusionX1hr
                          then ↓ rate by 3U/kg/hr
• Leg elevation
• Sequential compression devices
• EARLY POSTOPERATIVE AMBULATION ( THE
•   MOST IMPORTANT)
•   High-fowler’s
•   Oxygen (prepare for intubation)
•   Auscultate breath sounds
•   Admin thrombolytics/anticoag (monitor
•     bleeding)
•   ***HEPARIN/THROMBOLYTICS IV
    – INCOMPATIBLE IN SAME IV LINE
• Analgesics to ↓pain, ↓ anxiety
• Maintain calm environment
•   Impaired gas exchange
•   Ineffective breathing pattern
•   Anxiety
•   Decreased CO
•   Risk for inability to sustain spontaneous
•     ventilation
• Adequate oxygenation
• Reversal of thrombus
• Reduction in risk for additional
  thrombus formation
• Prevention of pulmonary infarction
• Improved V/Q ratio
• V = ventilation
• Q = perfusion
• The amt of air reaching lung must be equal to
  blood reaching lung for the ideal exchange of O2
  and CO2, ratio is 0.8
• If airway is blocked, then ventilation zero
• If blood flow blocked, (PE) VQ is infinite “dead
  space”
• Pg 974
• V/Q ratio > 0.8 dead space producing
•   - PE, pneumothorax
•   - increased vent with decrease perfusion
• V/Q ratio < 0.8 Shunt producing
•    - hypoventilation, obstructive
•    - decreased vent with increase perfusion

• Pg 1005
• Situation: 55 yr old woman returned to her room at
  2 pm yesterday following abdominal hysterectomy.
  Her vitals have been stable & dressing dry, intact. She
  was up to the side of the bed & ambulated a few feet
  before returning to bed. A few minutes later, she
  turns on her call light stating she is having difficulty
  breathing. The nurse hurries to her room & finds the
  pt tachycardic, diaphoretic, gasping for air, & C/O
  Chest pain.
• 1. How can the nurse determine if the pt is
  experiencing a PE or a MI?
• 2. Why is it essential to establish the cause of
  the pt’s symptoms as rapidly as possible?
• 3. What risk factors does the woman have for
  development of PE?
• 4. What can nurses do to help identify those
  pts at  ‘d risk for PE?
• - the result of abnormalities in
  ventilation, perfusion, or compliance
  which leads to hypercapnia &/or
  hypoxemia
• - respiratory acidosis
• - must identify underlying condition
  before treatment

• Pg 1006
• - an alteration in oxygenation is most
  common form of resp. failure
• - perfusion (Q)exceeds ventilation (V)
• which is a low V/Q ratio causes
  decreased oxygenation of venous blood
  & a mixing of less oxygenated blood
  with arterial blood
• - so have reduced arterial oxygen value
PE
Pneumonia
CVA
COPD
Pneumothorax
Lung trauma
atlectasis
Pulm. Edema
• Tachycardia, atrial dysrhythmias tachypnea,
  dyspnea on exertion or rest, labored
  breathing, use of accessory muscles, rales
• - correct hypoxia & acidosis with CPAP
  or may need intubation, ventilator, PEEP
• - if medication induced: discontinue med
• - if due to trauma or ICP must focus on
  relieving the ICP
• - if due to high V/Q ratio (dead-space)
  must reestablish perfusion (if from PE,
  thromolytic therapy)
• Ability to sustain spontaneous ventilation
• Adeq. Ventilation: pH 7.35-7.45
•    PCO2 35-45
• SaO2: >92%
•   Correction of hypoxia & acidosis:
•          - CPAP, ET, mechanical vent, PEEP
•   Resp. muscle rest
•   Control of shock
•   nutrition
•   Severe resp & met acidosis
•   Infection
•   Failure to wean from ventilator
•   Lack of adeq. Nutitional support
51
• Progressive pulmonary disorder after chest trauma 1-
  96 hrs after
• Also seen with aspiration, prolonged mechanical
  ventilation, severe infection and open heart surgery
• Involves: pulmonary capillary damage with loss
  of fluid and interstitial fluid, Impaired alveolar
  gas exchange and tissue hypoxia due to
  pulmonary edema, Altered surfactant
  production, Collapse of alveoli, Atelectasis
  resulting in labored breathing and ineffective
  respirations

• Pg 1014


                                                         52
• The damaged tissue of the lungs has increased capillary
  permeability and fluid accumulates in the tissues of the
  lungs. The production of pulmonary surfactant < and
  atelectasis occurs. Lung compliance < meaning the lungs
  are losing the ability to carry out the process of
  breathing.
• As a result, hypoxia develops. Some clients recover but
  the scar tissue becomes fibrous and lung fibrosis may
  progress.
• Systemic effects: cardiac dysrhythmia, renal failure, stress
  ulcers

                                                             53
• H&P
• S/S: > respirations, rapid and shallow, adventitious lung sounds-crackles,
  agitation, tachycardia, mental confusion, cyanosis, etc.
• CXR-non cardiac pulmonary edema
• ABGs (hypoxia-respiratory acidosis)> PC02 and < PO2
• Rapid identification of the problem
• Intubate and place on ventilator with PEEP (keeps airways open and
  decreases hypoxia)
• Maintain patent airway, suction as needed
• Diuretics to reduce pulmonary edema
• Steroids



                                                                          54
• AIMED TO; preserve O2 consumption &
•    tissue perfusion
•         - reduce fever
•         - use sedatives to reduce muscle
•              activity & prevent further
•              excessive O2 use
•      May also need corticosteroid therapy
• DEATH USUALLY OCCUS AS RESULT OF THE
  PRECIPITATING EVENT OF ARDS (NOT JUST ARDS
  ALONE)
• Mechanical ventilation
• - alveoli to remain open (or further
  damage results)
• - PEEP used to stabilize alveoli & keep
•       open. (PEEP of 10-15 cmH2O)
•   - tidal volume of 4 – 6 mL/kg needed
•       to avoid overdistention of alveoli
• - supports ventilating function to improve
  oxygenation thru supplemental O2 & positive
  pressure
• PRIMARY OBJECTIVE:
•    - decrease work of breathing,
•    - reverse hypoxia
•     - reverse hypercapnea

• Pg 1021
• 1. inability to adeq ventilate
       - chest trauma, excessive sedation,
  neuromuscular disease, fatigued respiratory
  muscles
• 2. Inability to adequately oxygenate
   - pneumonia, PE, pulm edema, ARDS
• 3. Excessive work of breathing
     - severe bronchospasm, airway obstruction
• 4. Airway protection
   - unconscious, massive resuscitation, facial or
  head trauma
• 1. Resp impairment
•     - tachypnea >30 breaths/minute
•     - dyspnea
• 2. Neurological impairment
•     - loss of gag reflex
•     - altered mental status
• 3. Gas exchange impaired
•     PaCO2 >60, PaO2 <70, SaO2 <90
• Endotracheal Tubes
•     - may insert nasal or oral
•     - must be trained to insert
•     - Post-intubation MUST have CXR for
•         confirmation of placement
•     - complications: laryngeal trauma
•             - intubation into right mainstem
•               bronchus
•              - infection
• Nasal intubation:
• - not used with ICP, head trauma
• - disadvantages: tissue necrosis,
  nosebleed, rupture of nasal polyps,
  submucosal dissection
• - increases susceptibility to infection due
  to increased mucus production from the
  irritant properties of the tube itself
• Oral intubation:
•   - direct visualizaition, rapid intubatoin
•    - must reposition to opposite side of
•       mouth every 24 hr
•   Disadvantages:
•        - increased dryness of oral mucosa
•        -produx of mucus
•        - susceptibility to infection
• Tracheostomy
•        - May need to be performed for
•          long-term ventilatory support
•        - this can bypass upper airway
•            obstrux
•        -maxillofacial injuries
•         - may help prevent aspiration
•         - may decrease necrosis or
•             tracheoesophageal fistula
•   Improves pt comfort
•   Oral hygiene
•   Ease of secretion removal
•   More secure airway
• - to maintain airway patency
• - closed system, multiple use catheter
• - hyperoxygenation prior to suctioning reduces hypoxemia
  from suctioning
    – - instillation of saline should not be done as increases risk of
      ventilator associated pneumonia (thin secretions by
      adequate fluid intake)]
• - stimulation of cough, very effective to remove
  secretions
• - inflatable cuff provides seal & reduces aspiration of fluids
  into lungs
• - must use soft- low pressure cuffs to minimize tracheal
  necrosis/fistulas
• - must have pressure of 25 cmH20 or less
•       ( if more pressure is needed then may
•         need an larger tube inserted)
• - CUFF IS NOT DEFLATED WHILE ON VENTILATOR
• - always suction pt orally before deflating cuff to
•        remove secretions on top of cuff so will not
•       aspirate these secretions
• - risk for airway plugging (tube is foreign
  body)
• - tube can become misplaced
• -Tension pneumothorax
• -tracheal dilation, ischemia, necrosis
• - infection
• MUST GIVE FREQUEST ORAL HYGIENE FOR
  COMFORT AS WELL AS DECREASE
  INFECTION
• Goal} improve to improve oxygen and CO2 exchange by removing
  excess mucus with a suction catheter…Follow facility guidelines!
• Procedure:
    – Use sterile technique for tracheal and clean technique for oral.
    – Administer O2 before inserting catheter WHY?
    – Moisten cath in sterile water and insert through nose or mouth before applying suction
    – Apply suction as the catheter is withdrawn from the airway
    – Maintain pressure gauge b/w 80-100 mmHg
    – Limit EACH pass to 10 seconds
    – Allow the patient to rest briefly, encourage deep breathing and rinse catheter with
      sterile water before each pass.
    – Monitor for patient’s response
        • If tachycardia or increased respiratory distress develops, stop the procedure
            immediately and give the patient oxygen as ordered
    – Document the amount, color, odor, and consistency of the secretions as well as pt status
      before and after procedure.




                                                                                             71
• Hypotension (positive pressure decreases
•    venous return to heart which decreases
•    CO which decreases BP)
• So, may see decreased UO, cardiac
  arrythmias
• INFECTION: most common WHY??
• Atelectasis
• Pneumothorax (esp with PEEP)
• 1. FiO2 (avoid >60%)
•        - start low, maintain O2 sat >90%
•        - PEEP helpful to decrease FiO2
•     requirements while maintain O2 sats
•    O2 TOXICITY: damage to lungs with FiO2
  >60%
• 2. Minute Ventilation:
• MV= Tidal volume x breaths/min
• (tidal vol: the vol inspired or expired with
  each normal breath)
• 3. Pressure support: 5-10 cm H20
• 4. PEEP (positive end expiratory pressure)
• - increases alveolar vent by preventing small
  airway collapse
• - FiO2 can be decreased ( decrease O2
  toxicity)
• - too hi PEEP, compromises venous return
• - affects ICP (caution)
• 5. Inspiratory to expiratory (I/E) ratio
•       Normal ½ or 1/3
Controlled Mechanical Ventilation:
     - pt receives ONLY ventilator breaths
Assist-control ventilation:
    -resp rate can be determined by pt but
 the ventilator delivers full tidal volume with each breath
   (watch for respiratory alkalosis with tachypneic pts)
Synchronous Intermittent Mandatory Ventilation (SIMV):
   ventilator delivers set
  tidal volume with a minimum set rate (pt assumes more
   work of breathing) USE THIS MODE For FULL SUPPORT OR
   CAN USE FOR WEANING
  - decrease rate over time to wean
• CPAP: Continuous Positive Airway Pressure
•   - pt breathes at own effort
•   - pressure set for up to 20 cm H20
•   - used to assess extub potential
•   Mode: intermittent mandatory vent
•   TV: 6-8 mL/kg
•   Vent rate: 10 breaths/min
•   Fi02: 100% but wean down
•   PEEP: 5 cm H20
•          -change according to ABG
•   Airway or ET tube obstruction
•   Bronchospasm
•   ARDS
•   Mucous plug
•   CHF (pulm edema)
• 1. increase FiO2
• 2. increase PEEP
• HOW CAN YOU DECREASE PCO2 IN THE
  VENTILATED PT?
•      1. increase resp rate
•      2. increase tidal vol
• 1. may need sedation
•     - IV benzodiazepine & opiates
• 2. decubitus ulcers
•            - repositioning
•            - air mattress
• 3. venous thrombosis
•            - SQ Heparin, LMWH
•            - pneumatic compression boots
• 4. GI mucosal injury
•     - H2 receptor antagonists
•     - antacids
• 5. Nutrition needs
•     - delayed gastric emptying with sedatives
•     - metoclopramide (promotility agent)
•       - if GI works, use It
•       - enteral feedings
•        - parenteral nutrition for severe GI
    pathology
•   Barotrauma (high pressure=overdistends lung tissue)
•          - pneumomediastinum
•          -SQ emphysema
•          - pneumothorax
•   Nosocomial pneumonia
•   Vent assoc. pneumonia =leakage around cuff
•   O2 toxicity
•   Tracheal stenosis
•    deconditioning of respiratory muscles
•   Hypotension (from elevated intrathoracic pressures
    will decrease venous return)
• GI: stress ulceration
• Gallbladder: Cholestasis from increased
  intrathoracic pressure on portal veins

• Pg 1031
• First assess:
•         - vital capacity: the amount expired
  after maximum inspiration
•         - tidal volume: The vol. of inspired
  gas during a normal breath (6-8 mL/kg)
•         - spontaneous resp rate
•         - lung compliance
• 1. reduce Fi02 to 40% while monitoring
•     SpO2
• 2. reduce IMV rate to 4-8 breaths/min
• 3. reduce PEEP in increments of 2 to 3 cm
  water while maintaining Sp02 >90% until a
  level of 5 cm of water is reached
• 4. reduce PS by increments of 2-3 cm water
  monitor resp rate, work of breathing, minute
  ventilation
• Change of LOC
• Change in Vitals
•    - diastolic BP >100
•    -fall in systolic BP
•    - heart rate >110/min OR >10 breaths
•       per minute increase over baseline
• Falling Pulse Ox
• Tidal vol <250 ml
• increase CO2
• ECG: PVC’s >5 minute, ST segment elevation,
•        ventricular conduction changes
• 1. Explain procedure to pt
• 2. Elevate HOB 45 to 90 degrees
• 3. Disconnect ET tube from vent tubing
• 4. suction ET tube & oropharynx
• 5. have pt take deep breath
• 6. as pt expires forcefully, deflate cuff, remove tube
• 7. suction any secretions & admin 02 through nasal cannula at
  2-4 L/min
• 8. check postextubation ABGs
• 9. Be prepared to reintubate if necessary
• - coronaviruses
• -affects cells from resp tract with triggers
  inflam process
• -spread easily by droplet, also on surfaces of
  objects (but not long periods)
• -high fever
• Headache, aches
• Xray: pneumonia like pattern
•   Not test specific
•   No agents to kill virus at this time
•   Oxygen
•   Full isolation
•   Pt’s door closed
• Mycobacterium tuberculosis
• Inhaled into lungs
• Infection: host susceptibility, virulence, number
  inhaled
• Requires prolonged exposure
• Those at Risk: malnurished, crowded living,
  compromised immune systems, HC workers
  providing care to hi risk pop
                                                  93
94
•   Develop gradually
•   Low grade fever-specific pattern
•   Persistent cough
•   Hemoptysis
•   Hoarseness
•   Dyspnea on exertion
•   Night sweats, fatigue, wgt loss
•   TB IS COMMON CAUSE OF FEVER OF
    UNKNOWN ORIGIN
                                       95
• Mantoux skin test-0.1cc purified protein
  derivative (ppd),
• ID
• Read test @ 48 – 72 hrs
• Palpable swelling 5mm = induration = +
• + indicates only exposure and development of
  antibodies


                                             96
97
• + finding = INH 6-12 months prophylactic.
• CXR & Sputum for AFB to confirm active TB
• Active = Isonaizid, Rifampin, Pyrazinamide & after 3 weeks
  no longer contagious but requires long term TX
• Well balanced nutrition
• Hydration to liquefy pulmonary secretion
• Activity as tolerates
• Hospitalized client:
   – Airborne & Standard Precautions
   – Isolation room with neg air pressure
   – Doors and windows closed
   – Staff to wear particulate respirator that fits securely


                                                           98
• - all cases reported to state/local health
• -resp isolation
• -DRUGS: “RIPE”
•    Rifampin (body fluids turn orange)
•    INH (Vit B6 to prevent periph neuritis)
•    Pyrazinamide
•    Ethambutol
• Well balanced meals with adequate hydration
• Instruct: TB is spread by airborne droplets—protect others by
  covering mouth when coughing and wash hands often
• Keep all clinic appts, continue meds for
• the prescribed length of time and take all meds as directed
• If on isoniazid, avoid foods containing tyramine (aged cheese,
  smoked fish) and histamine (tuna and sauerkraut). Meds +
  these foods will make client ill.
• Rifampin causes body fluids to become red-orange and may
  stain contact lenses



                                                              100
• Instruct: takes 3 weeks of med before no
  longer considered contagious, so if home
  needs to: Cover mouth and nose when
  cough/sneeze and wash hands freq, dispose of
  tissue in a closed bag, avoid close contact with
  others, sleep alone in bedroom, clean all eating
  utensils thoroughly and separate



                                                101
• Wedge resection- small triangular resection of
  tissue
• Lobectomy- remove lobe
• Pneumonectomy-remove entire lung
• Segmental resection-remove section of lung
• Bronchoscopic laser



                                               102
•   s/s: fever, sepsis, fatigue
•   Diagnostic: CXR
•        CT scan
•        bronchoscopy
•   Treat: antib
•   Surgery: lobectomy of lobe with abscess
• -most common severe genetic disease in US
• -DIAGNOSIS
•         -sweat chloride test
• S/S:
•    - recurrent infections, cyanosis, digital clubbing,
  cough, dyspnea, hemoptysis
• - fatty stools, pancreatitis
• Fat soluble vitamin deficiency due to
  malabsorption
•   - aims to improve quality of life
•   -decrease # exacerbations & hospitalizations
•   -decrease mortality
•   THERAPY FOCUS; CLEAR PULMONARY
    SECRETIONS & CONTROL INFECTIONS
• Treatment:
• - inhaled bronchodilators
• - airway clearance: postural drainage with
  chest percussion & vibration (vest)
• Dnase (decrease viscosity of sputum)
• Hypertonic saline (4 ml of 7% saline) inhaled
  BID to reduce exacerbations (admin.
  Bronchodilator first to avoid bronchospasm)
•   - antibiotics (sputum cultures)
•   -short term glucocorticoid
•   Pulm rehab
•   Oxygen
•   May need lung transplant
•   Yearly flu vaccine
• -defined at mean pulmonary arterial pressure of
  >25 mmHg (most often with young or mid-age
  women)
• CAUSES:
• - left side hrt failure
•    - COPD (hypoxic vasoconstriction)
•    - thromboembolic disease

• Pg 976
• -dypnea with exertion, fatigue, lethargy
• Snycope with exertion,
• Diagnosis:
•    - CXR: enlargement of central pulm
  arteries
• - echocardiogram: rt vent overload
• Treatment:
•    - oxygen
•    - anticoagulation
•    - vasodilators
•    -diuretics
• Inflammation of both layers of the pleura
   – It may develop with pneumonia, TB, upper respiratory
     infection, after trauma, PE, Cancer
   – Viseral layer has nerves
   – Parietal layer does not
• S/S: SOB, severe pain with inspiration. As fluid
  accumulates pain diminishes
   – Described like stabbing knife
• Dx: friction rub with auscultation, chest x-ray, sputum
  analysis, thoracentesis, biopsy
• Tx: pain management, NSAID (indocin), splint with
  cough and movement
• Accumulation of thick purulent fluid in the pleural
  space. May or may not encapsulate.
• Most occur from bacterial pneumonia, lung
  abscess, chest trauma, post surgery
• S/S: similar to pneumonia (fever, nite sweats,
  pleural pain, cough, dyspnea, anorexia, wt loss),
  decreased or absent sounds over affected area
• Dx: CT, thoracentesis
• Tx: Thoracentesis, Chest tube, education on tube
  and infection
• Removal of pleural fluid for examination or to
  allow for lung re-expansion
  – Obtain consent
  – Post :
     • Assess respiratory status
     • Document amount, color of fluid
     • Monitor dressing for bleeding
     • Label specimen bottle and send to lab
     http://www.youtube.com/watch?v=noDxydboLrA&featur
       e=related

                                                     116
 • Chest tubes are inserted to drain blood, fluid, or air and allow full
   expansion of the lungs. The tube is placed in the pleural space. The area
   where the tube will be inserted is numbed (local anesthesia). The
   patient may also be sedated. The chest tube is inserted between the
   ribs into the chest and is connected to a bottle or canister that
   contains sterile water. Suction is attached to the system to encourage
   drainage. A stitch (suture) and adhesive tape is used to keep the tube in
   place.
 • The chest tube usually remains in place until the X-rays show that all
   the blood, fluid, or air has drained from the chest and the lung has fully
   re-expanded. When the chest tube is no longer needed, it can be easily
   removed, usually without the need for medications to sedate or numb
   the patient. Medications may be used to prevent or treat infection
   (antibiotics).
http://www.atriummed.com/PDF/ManagingChestDrainage.ppt#438,37,Remove fluid & air
                                                                              117
• Tidaling: the middle water seal chamber is observed for expected rise
  in fluid level with expiration.
• Air leak: noted when continuous bubbling is observed in the main
  water seal chamber
• Suction may be wet or dry
   – A gentle bubbling sound is normal to hear with a wet system
   – Dry systems have a orange accordion looking object visible when
       suction is applied
• Change the recepticle only when chambers are full using sterile
  technique
• Heimlich Flutter Valve: air and fluid are expelled and not rebreathed in
• READ THORACIC SURGERY page 530-531



                                                                         118
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122
• Stomach content/ food in the lung
• May cause pneumonia
• S/S: tachycardia, dyspnea, cyanosis, hyper or
  hypo tension, death
• May be silent
• Death/ complications a result of volume and
  type of aspirate
• If fecal matter is the aspirate=fatal
•   Seizures
•   Decreases LOC
•   N/V
•   Stroke
•   Swallow disorders
•   Cardiac arrest
•   Silent aspiration
•   This is the goal!!!
•   HOB at least 30-45 degrees
•   Chin tuck
•   Monitor tube placements
•   Speech therapy
•   May need antibiotics
•   Remember ABCs
127

				
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