1. Nursing Management of Patients with Respiratory Disorders
Winter Quarter 2012
Teresa M. Champion, RN MSN

2. ASSESSMENT OF PATIENTS WITH RESPIRATORY DISORDERS

3. Anatomy Physiology of Pulmonary System
Ventilation – movement of air in and out of lungs
Respiration – consists of diffusion of oxygen across alveolar-capillary membrane into pulmonary circulation and release of carbon dioxide molecules across the alveolar- capillary membrane through the airways out into the environment

4. Exchange of Gases during Respiration
Respiration Perfusion – the exchange of O2 and CO2 across the alveolar membrane
Alveoli – place in lungs where exchange occurs and must be adequately expanded by air to have adequate contact with hemoglobin
If alveoli are expanded adequately but unable to exchange due to edema or secretions – a ventilation(V)/perfusion(Q) mismatch occurs
If alveoli are not expanded adequately despite blood flow – Ventilation (V) and Perfusion (Q) mismatch will also occur
Anemic patients have fewer binding sites for O2. Other compromising conditions – shock, heart failure can also affect gas exchange because blood flow Is diverted from the alveoli and decreases gas exchange

5. Mechanisms of Respiration
Ventilation – dependent on neuromuscular and musculoskeletal integrity
CNS – medulla and Pons respond to changes to carbon dioxide and oxygen levels in the blood by increasing or decreasing rate and depth of respiration
Musculoskeletal – assist and influence respiration - intercostal muscles, diaphragm, abdominal muscles, thoracic muscles (scalene, sternomastoid and trapezius)

6. Inspiration and Expiration
Influenced by intrapleural pressures
When the pressure of air in the lungs reaches capacity during inspiration, expiration begins
Inspiration is active
Expiration is passive
Movement of air in one breath is the tidal volume
Movement of air over one minute is minute ventilation
Normal tidal volume at rest is ~500ml, but can increase if more is demanded by the body (i.e. exercise and stress)

7. Collection of Patient Data
History
Biographic and demographic data
Chief complaint - dyspnea
Past medical history, allergies
Family history
Risk factors
Social history, Cultures
Medications
Nutrition
Travel and Areas of Residence
Biographic and Demographic – age, race, gender and cultures that affect perceptions of health conditions like pulmonary disorders.
Chief complaint – s/s of respiratory malfunctions (dyspnea, fatigue)
Systems that affect the patients ability to carry out or perform normal daily activities
Past medical history – cancers like breast and testicular – mets to lungs OR other prior illnesses. Cardiovascular complications and medication related pulmonary fibrosis that occurs with amiodarone. Thyroid disorders (myxedema or thyroitoxosis) Childhood diseases – cystic fibrosis, asthma, lack of immunizations, premature infants that were intubated and mechanically ventilated at birth. Childhood or past trauma. Past pulmonary dysfunctions, history of DVT.
Allergies – allergies can trigger respiratory problems – Pts that are allergic to soy or nuts should not use atrovent and combivent
Family history – genetic related conditions or family members that smoke or family history of lung disease, cardiovascular disease and lung cancers.
Risk factors – smoking, substance abuse, lack of physical activity and obesity
Social – lifestyles and habits – occupational exposures via work (asbestos, pesticides) – exposures in the home (mold, pet dander, cock roach infestations, meth labs)
Cultures – affect how and when people seek and accept diagnostics and treatments. Cultural Practices like use of amulets, cupping, coining, and herbal remedies
Medication like ACE inhibitors cause cough, amiodarone cause pulmonary fibrosis, address OTC like cough suppressants, expectorants, antihistamines Herbals
Proper use of inhaled treatment – bronchodilators first then steroids, Advair a combo of the two should not be given with a spacer.
Traveling to other countries like the (SARS) outbreak was traced to a specific location in the world. High altitudes (HAPE), living near livestock or factories that emit possible environmental exposures

8. PHYSICAL EXAMINATION Inspection General Appearance Mentation
Rate, Depth and Rhythm of Respirations
Tachypenea, Bradypnea, Orthopnea, Apnea, Hyperpnea
Thoracic Size and Shape
Thoracic Expansion and Symmetry
Use of Accessory Muscles
Color and Appearance of Skin and Extremities
Pallor
Cyanosis
Neck Inspection – Tracheal Deviation
General Appearance – does patient appear capable to take care of themselves, comfortable. Facial appearance non-distressed. No evidence of tripod posture – leans forward resting on both arms to allow chest expansion. Nasal flaring, pursed lip breathing?
Mentation – the brain needs oxygen…any confusion or agitation, lethargy? Decreased level of consciousness
Regular rate of breathing is between 12 and 20 per minute.
FOR EACH INCREASE IN ONE DEGREE OF TEMPERATURE – HEART RATE WILL INCREASE 4 BEATS PER MIN AND RESPIRATORY RATE INCREASES ONE BREATH PER MINUTE.
Orthopnea – difficulty breathing while lying down
Hyperpnea – increased rate and depth of respirations
Thoracic size and shape – clues for pulmonary disease are structural abnormalities like sternal depression, pigeon chest, barrel chest and scoliosis or kyphoscoliosis. These abnormalities will limit chest expansion needed for breathing
Chest expansion and symmetry – inspiration diaphragm flattens and rises with expiration
Accessory muscles – trapezius, sternomastoid, scalenous, abdominal muscles
Color and appearance – clubbing of fingers, pallor – pale, cyanosis - blue

10. ABNORMAL BREATHING PATTERNS
Cheyenne Stokes
Breaths are deep than become shallow followed by periods of apnea
Causes: severe brain pathology - brain stem herniation, Increased ICP, compression on Brain Stem
Kussmal’s
Breaths are deep, rapid and labored
Rates are >20 bpm
Causes: metabolic acidosis, renal failure, diabetic ketoacidosis

11. PHYSICAL EXAMINATION Palpatation of Skin and Extremities
Edema – Caused by Pulmonary HTN
8mm – 4+, 6mm – 3+, 4mm – 2+, 2 mm – 1+
Skin Temperature & Moisture
warm moist skin r/t increased effort of breathing, possible fever from pulmonary infection
Dry skin-moisture lost from increased respirations
Clinical Reference Points – landmarks
Trachea, nipple line, sternum, intercostals, axillary line, midaxillary line, midclavicular line
Chest Excursion – should be equal and up to 5-10 cm
Tactile Fremitus – palpations of vibration in thorax
Tenderness
Crepitus – also called “subcutaneous emphysema – air trapped under the subcutaneous tissue
EDEMA – press finger down over 5 seconds – depth related to the rating of pitting – caused by Right sided Heart Failure or Right and Left Heart Failure
Right sided heart failure is caused by Pulmonary Hypertension and the increased resistance of forward flow causes the right ventricle to hypertrophy in an attempt to increase the flow through the pulmonary tree.
SKIN TEMP and MOISTURE – COPD and Asthma Exacerbations may have dry skin due to moisture lost through the respiratory tract from increased breathing rates. Causes dehydration as they may not be able to replace fluids.
Clinical Reference points during the pulmonary assessments and lesions, adventitious lung sounds heard along these reference points/lines.
Tactile Fremitis – palpated over the thorax by having the patient vocalize “99” . Palpate with ulnar side of hand from scapula (back) Clavicles on front of chest – move down bilaterally. Vibrations should be the strongest over large airways on upper thorax, and decrease as you move down. Unequal fremitis could indicate unilateral airway obstruction, pneumothorax, or pleural effusion. Decreased fremitis could also be palpated with pneumonia or consolidations
Tenderness – from coughing, intercostals are strained and thoracic muscles. Pneumonia and consolidation can also cause tenderness, people may not breath as deep
Crepitus – caused by ruptured pulmonary bullae, pneumothorax or around chest tube sites.

13. PHYSICAL EXAMINATION
Auscultation of the lungs – 4 types of breath sounds
Tracheal Breath Sounds –
loud and high pitched – over the largest airway and are the loudest – length of time heard is equal during expiration and inspiration
Bronchial Breath Sounds –
loud and high pitch, harsh and less turbulent and lower in frequency than tracheal – Expiration is heard longer than inspiration
Bronchovesicular –
Midway in pitch between Bronchial and Vesicular and are heard during inspiration and expiration
Vesicular
Soft and low pitched – heard longer during expiration, heard over most of thorax
Tracheal – best heard over the trachea and neck – Largest airway
Bronchial - from 2nd to 4th intercostals on anterior chest and between 3rd and 6th on posterior chest -
Bronchovesicular best heard over 1st and 2nd intercostals on anterior chest and between scapulae of the posterior chest – air movement in the moderate airways between the bronchi and the smaller airways.
Vesicular – air moving through the smaller airways
Expiration last longer than inspiration so most breath sounds are heard longer during expiration than inspiration.

14. Bronchial – 2nd to 4th intercostals
Bronchovesicular – 1st and 2nd intercostals
Vesicular – heard all over thorax

15. Bronchial – 3rd and 6th intercostals
Bronchovesicular – between scapulas

16. ADVENTITIOUS BREATH SOUNDS
Crackles (Rales)
Indicate fluid, inflammation in airways – snapping sound when airways open – can be heard when airways close too but softer sounding than on inspiration
Intermittent or discontinuous.
Fine or Course
Wheezes
High-pitched musical sounds caused by inflammation in narrowing airways or bronchospasms
Rhonchi – indicate mucus secretions in the airways
Caused by air passing through mucus strands
Can be heard on inspiration and expiration
Continuous/ discontinuous (intermittent),
Mild/moderate/severe
Crackles are described as snapping, popping sounds
Rales and Rhonchi terms not used according to this book.
Rhonchi is classified as Wheezes, according to this book. Low pitched wheezes – sounds like rattling, snoring, gurgling and usually clear with coughing and or suctioning.

17. ADVENTITIOUS BREATH SOUNDS
Stridor
Heard only during inspiration as air attempts to flow though an obstruction, high pitched crowing sound – needs immediate intervention
Pleural Friction Rub
Indicate inflamed pleural surfaces – easily heard on inspiration – hold breath to determine it is not pericardial

18. Page 878 in book

19. USING THE STEHASCOPE
Diaphragm - best for higher pitched sounds, like breath sounds and normal heart sounds.
Bell - is best for detecting lower pitch sounds, like some heart murmurs, and some bowel sounds. It is used for the detection of bruits, and for heart sounds (for a cardiac exam, listen with the diaphragm, and repeat with the bell).

20. PHYSICAL EXAMINATION Percussion Dull - Abnormal Finding
Heard over solid tissue, occurs when air is absent, can be heard over consolidation areas with pneumonia, pleural effusion, hemothorax, solid tumors
Dull thumping sound without vibration
Resonant – Normal Finding
heard over lung fields during inspiration while lungs are full of air
low pitched clear sounds – Normal Finding
Hyperresonant – Abnormal Finding
Very loud, lower pitched longer sound than resonance
Drum like sound with vibration
indicates hyperinflamation – emphysema, pneumothorax
Tympanic – like hyperresonance like tapping on air filled cheeks

21. PAIN
Pain in association with breathing may be related to Pulmonary Embolism, Pneumothorax, Pleural Disease, Pericarditis, Musculoskeletal Disease or Pneumonia
Sudden onset shortness of breath may be related to Pulmonary Embolism or pneumothorax
Pain during respiration may decrease tidal volumes
Pain management enables participation in rehabilitative activities and promotes deep breathing to prevent pneumonia and atelectasis
Use cough suppressants with caution

22. GERONTOLOGICAL CONSIDERATIONS
Aging decreases respiratory function
Osteoporosis – stooped posture, decreased rib expansion
Anterior to posterior diameter increases
Alveolar surface decreases
Decreased elasticity
Increased atelectisis
Lower arterial oxygen values – decreased exchange of O2/CO2
Increase risk of pneumonia – Decreased tidal volumes, ineffective cough
Risk of aspiration may increase with aging
Aging may affect patient comfort needs during the examination

23. HEALTH PROMOTION Smoking cessation
Decrease exposure to second-hand smoke
Hand Hygiene
Flu and Pneumonia Vaccines
Instruction and use of Personal Protective Equipment (PPE) especially in the workplace for workers exposed to allergens, mold, bird, bat and rat feces and other toxins like asbestos

24. STANDARD OF CARE
For patients with cardiac and respiratory illness, standard is:
Continuous or intermittent observation of the patient’s oxygen saturation (most cost effective)
End-tidal carbon dioxide levels (being used more, but is more costly but most accurate).
Monitoring Peak Flow results is utilized to trend treatment effectiveness in patients with asthma

25. RESPIRATORY MONITORING
Pulse Oximetry
Measures saturation of hemoglobin
May NOT be accurate with patients with low Hgb, hypovolemia and shock states
Nail polish, ambient light may interfere with reading
Wave forms should match pulse rate and should not be dampened
Pulse Ox Probes should not be placed on extremities with blood pressure cuffs, fistulas or arterial lines due to lack of blood flow
Pulse Ox Saturations do not necessarily match calculated Oxygen Saturation in ABG – SPO2%

26. RESPIRATORY MONITORING
Peak Flow Meters
Evaluate air movement to determine severity of asthma exacerbation
Measure Peak Expiratory Flow Rate
Measurements are based on age and body size
Red Zone (Dangerous) – less than 50% of the normal value
Yellow Zone (caution) – Between 50% to 80% below normal value
Green Zone (Good) – meets 80% to 100% of normal value

27. RESPIRATORY MONITORING
Arterial Blood Gases
Determine Respiratory Acidosis and Alkalosis
PaO2 levels below 80mmHg and/or SaO2 <95% indicate hypoxemia
Cost $800 to $ per draw
Invasive procedure

28. RESPIRATORY MONITORING
Capnography
Measures exhaled carbon dioxide or End Tidal CO2 (ETCO2)
Small disposable capnographers are used to check ET Tube placement after intubation and/or continuous monitoring of tube placement
Capnography monitoring has been added to the – 2015 ACLS Guidelines for Compression Effectiveness.
Normal ETCO2 values are 35mmHg to 45mmHg.
ETCO2 values between 10-20mmHg indicate high quality compressions
ETCO2 less than 10mmHg – quality of chest compressions need improvement

29. MONITOR SHOWING ETCO2 WAVEFORM

30. RESPIRATORY PATHWAY DISORDERS
SLEEP APNEA
AIRWAY OBSTRUCTION
TRACHEOSTOMY

31. ANATOMY OF RESPIRATORY TRACT
Nose to pharynx-behind the mouth to esophagus (approx. 5 inches)
Epiglottis – above Larynx covers when swallowing
Larynx - voice box: air passes between pharynx and trachea
Trachea - windpipe
Bronchi - main branch that air passes through divides into left and right branch
Bronchioles - subdivides and connects with alveoli for gas exchange

32. SLEEP APNEA
Defined – a person stops breathing for more than 10 seconds, more that times in an hour
3 types –
Central
Brain fails to send signal to the breathing muscles to initiate respirations (less common)
Obstructive
Physical obstruction from tissues in upper airway
Combination of both or Mixed Sleep Apnea

33. RISK FOR SLEEP APNEA Overweight/Obesity High Blood Pressure
Decreased Airway Size – congestion, inflammation (allergies), anatomical abnormalities
Family History

34. MEDICAL MANAGEMENT FOR SLEEP APNEA
Weight loss
Avoid alcohol, tobacco and sleeping pills (sedatives)
Use side-lying positions when sleeping
Dental devises that move tongue or mandible forward
Continuous Positive Airway Pressure (CPAP) Machines
Surgical Interventions – UVPPP – resection of the uvula and soft palate, Tracheotomy
Focus is on airway patency

35. AIRWAY OBSTRUCTION
Potentially life threatening – requires immediate intervention
Types: foreign object, allergy, lesions, stenosis, swelling
Causes:
Viral and Bacterial Infections, fire or inhalation burns, allergic reactions (foods/medications/bee stings)
Infections after dental extractions
Laryngeal trauma-MVA, Strangulation or surgical procedures
Large tumors
Aspiration of foreign objects

36. Clinical Manifestations of Airway Obstruction
STRIDOR
Inability to speak (partial or complete)
Labored breathing and use of accessory muscles
Air Hunger (mild)
Cyanosis (severe)

37. Medical Management of Airway Obstruction
Diagnosis and treat the cause
Provide Oxygenation Support!!
Sit in upright position
Keep patient’s airway patent (if partial or mild obstructions get worse – need immediate intervention)
Secure and protect airway – Endotracheal Intubation, Cricothyroidotomy or tracheotomy – bag/mask ventilation will not work with obstruction!
Treat cause – if infection provide anti-infectives, .steroids, bronchodilators, epinephrine if anaphylaxis allergy with airway swelling

38. Tracheotomy Insertion of artificial airway in the trachea
Recommended for oral/nasal endotracheal intubations lasting longer than 1 – 2 weeks. (book says 7 – 10 days)
Usually is temporary to protect airway until underlying cause can be fixed or corrected
Decreases risk of permanent injury to the airway, and vocal cords

39. Tracheotomy
Incision is below the prominent thyroid cartilage (Adam’s Apple) and below the cricoid cartilage – between 2 – 3 OR 3 – 4 tracheal cartilages
A tube is placed and secured (Sutured) to keep the tracheal stoma open
The tube is also secured with ties
The tube remains in place until the tracheal stoma is well established and won’t close back up
A post tracheotomy kit is kept at bedside or on the nursing unit if accidental decannulation occurs
An Obturator is kept at bedside to prevent stoma closure if decannulation occurs until new tracheotomy tube can be put in immediately

40. Tracheostomy tubes can be fitted with an inflatable cuff that blocks off the top of the windpipe, preventing aspiration.
Most people do better with uncuffed tubes, since they can push secretions up and out, and prevent accumulation of unswallowed food above the cuff. Also, cuff inflation interferes with passage of air up to vocal cords needed for speech.

41. TYPES OF TRACHEAL TUBES
Made of silicone, plastic, stainless steel or silver
With or without an inner cannula
With or with out a cuff
Mechanical ventilation requires cuffed tubes to seal the airway to maintain pressures for ventilation
Cuffed tracheal tubes decrease aspiration risk
Inner cannulas prevent tube obstructions from thick crusted secretions
Average adult size are 7 to 8
Shiley or Bivona are most common

44. Assessment of New Tracheal Artificial Airway
Auscultation of the lungs
Monitoring Oxygenation saturations
Assessment of increased amount of blood in the sputum and around site
Subcutaneous emphysema (crepitis) around the neck
Respiratory distress
Patency of tracheal tube
Postoperative pulmonary edema (POPE)
Post operative edema (POPE) is a potentially life-threatening complication of acute airway obstruction. The predominant mechanism is forced inspiration against a closed or occluded airway. Forceful attempts to inhale against an obstruction create highly negative intrathoracic pressure, which causes increased venous return, decreased cardiac output and fluid transudation into the alveolar space.

45. Interventions following Tracheostomy
Encourage cough and deep breathing
Suction as necessary, but keep to a minimum
Provide supplemental oxygen
Pre-oxygenate with 100% Oxygen when suctioning
Hyperventilate (bag – suction) when necessary
Suction limited to 5-10 seconds with each pass
Insert catheter till patient starts to cough or meet slight resistance – do not use force

46. Tracheostomy Cares
Tracheotomy cares should be done every 8 to 12 hours with cleaning the inner cannula or changing the disposable cannula
Most medical institutions no longer use Hydrogen peroxide to clean around tracheostomy site (book says use half- strength)
Aseptic technique is used when cleaning the inner cannula (sterile gloves)

47. Laryngectomy Trachea is sutured to the stoma
Oral airway is permanently bypassed
Patients lose the ability to speak because the vocal cords are bypassed permanently
Patient only breath out of their stoma
The esophagus still follows the normal pathway and patients can still eat normally

48. LOWER AIRWAY DISORDERS

49. Restrictive lung diseases (interstitial lung diseases)
Result in reduced lung volumes
Alteration in lung parenchyma (alveolar tissue w/ terminal bronchioles, respiratory bronchioles, alveolar ducts)
Disease of pleura, chest wall or neuromuscular apparatus
Characterized by reduced total lung capacity, vital capacity, or resting lung volume

50. Obstructive lung diseases
Common characteristic – chronic and recurring blockage of airways
Limit airflow through the airways and out of the lungs

51. LOWER AIRWAY DISORDERS
Infections and Inflammatory Disorders of the Lungs
Acute or Chronic Bronchitis
Influenza – complication - pneumonia
Pneumonia – 6th leading cause of death
Tuberculosis – Mycrobacterium tuberculosis
Lung Abcesses/Empyema
Globally, pneumonia causes more deaths than any other infectious disease.
Empyema is a collection of pus in the space between the lung and the inner surface of the chest wall (pleural space).

52. Pneumonia
Inflammatory process that results in edema of the parenchymal lung tissue (aveoli and bronchioles) caused by inhalation of bacteria, viruses, fungi, protozoa or parasites or enter lungs via the blood stream
Aspiration of water, food, vomitus, toxic gases, chemicals and smoke
Radiation therapy
Effects terminal gas exchange

53. Classifications of pneumonia
Type of agent causing infection
Distribution of the infection (lobar - consolidation of a lobe, or bronchial – patchy consolidation)
Setting (community or healthcare (hospital) aquired

54. Community Acquired Pneumonia (CAP)
CAP: begins outside hospital or is diagnosed w/in 48 hours after admission
Patient did not reside in a long-term facility prior to admission
Incidence of CAP is highest in winter months
Smoking an important risk factor

55. Healthcare (Hospital) Acquired Pneumonia (HAP)
HAP: occurs > 48 hours after hospital admission
HAP has a mortality rate of 20% to 50%
90% of HAP infections are bacterial
Compromised immune systems, chronic lung disease, intubation and mechanical ventilation increase risk

56. Severe Acute Respiratory Syndrome
Severe acute respiratory syndrome (SARS) is a serious form of pneumonia. It is caused by a virus that was first identified in Infection with the SARS virus causes acute respiratory distress (severe breathing difficulty) and sometimes death.
SARS is a dramatic example of how quickly world travel can spread a disease. It is also an example of how quickly a connected health system can respond to a new health threat
World Health Organization (WHO) physician Dr. Carlo Urbani identified SARS as a new disease in

57. Clinical Manifestations of Pneumonia
Fever, chills
Increased respiratory rates
Rusty bloody sputum
Crackles
X-ray abnormalities
Chest discomfort
Cough
Fatigue, muscle aches, headache, nausea

58. Nursing Management of Pneumonia
Administer antibiotics (prime treatment)
Antibiotic Type depend on organism
Primary nursing intervention: Maintain airway and O2 saturation above 93%
Promote nutrition and hydration
Provide small, frequent, high-carb, high- protein meals

59. Discharge Priorities/Prevention
Teach patient about
Continue deep breathing and coughing exercises 4x/day, 6-8 weeks
Signs and symptoms to report to health care provider
Continue and complete antibiotic therapy as directed
Rest, fluids and nutrition important

60. Pulmonary Tuberculosis
Mycobacterium tuberculosis (bacteria)
Transmitted via aerosolization (i.e., an airborne route)
Affects people with repeated close contact with an infected but undiagnosed person
TB an opportunistic infections common with HIV/AIDS
The newest form of TB is multidrug-resistant tuberculosis (MDRTB)
Resistant TB is difficult and costly to treat and can be fatal

61. Clinical Manifestations
Dyspnea
Weight loss
Cough
Sputum production, streaked with blood
Sleep disturbances
Lethargy, exhaustive fatigue, activity intolerance, nausea, irregular menses
Low-grade fever may have occurred for weeks or months
Fever also may be accompanied by night sweats

62. Laboratory and Diagnostic Procedures
Tuberculin skin test
Chest x-ray
Acid-fast bacillus smear
Sputum culture

63. Nursing Management
Administer drug therapy as ordered by health care provider
Report the diagnosis to the local health department
Keep patient in negative pressure room with respiratory airborne isolation
Maintain isolation until three consecutive sputum cultures have tested negative
Focus on preventing the spread of the infection
Discuss pain management, handling fatigue, importance of good nutrition

64. Health Promotion and Prevention of TB
The main focus of TB management is preventing spread of the infection
Patient typically must take drugs for 9 months
Test and treat all persons in close contact with the infected individual

65. Lung Abcess
Most often abscess is secondary to anaerobic and aerobic organisms that colonize the upper respiratory tract.
Formation of multiple abscesses and cavities occurs commonly in patients with TB or fungal infections of the lung.
Pulmonary Empyema - is a collection of pus in the space between the lung and the inner surface of the chest wall (pleural space).

66. Clinical Manifestations of Lung Abcess
Spiking temperature with rigors and night sweats
Cough with foul sputum
Pleural chest pain
Tachycardia
Dullness on percussion over the abcessed area.
Oxygen saturation may decrease with larger abcesses

67. Laboratory and Diagnostic Procedures for Lung Abcess
CT scan
Pleural fluid and blood cultures may be obtained (thoracentesis)
Bronchoscopy
Transtracheal aspiration via suction sputum collection for cultures

68. Nursing Management of Lung Abcess
Penicillin G or clindamycin is the pharmacologic therapy of choice
Administer antipyretic, antibiotic, and pain medications
Assess for recent history of influenza, pneumonia, febrile illness, cough, and sputum production
Space physical care to allow for periods of rest between activities

69. Chronic Obstructive Pulmonary Disease (COPD)
Characterized by chronic, recurrent obstruction in pulmonary airways
Encompasses chronic bronchitis and emphysema
Obstruction is generally permanent and progressive
Unifying symptoms
Dyspnea
Wheezing
Use of accessory muscles
Ventilation/perfusion (V/Q) mismatching
Decreased forced expiratory volume

70. Chronic Obstructive Pulomary Disease (COPD)
Emphysema: abnormal, permanent enlargement of the aveoli (air sacs) accompanied by destruction of their walls
Chronic bronchitis: characterized by hypersecretion of mucus and chronic productive cough that continues at least 3 months of the year for at least two consecutive years

71. Etiology of COPD
The primary cause of COPD is exposure to tobacco smoke. Clinically significant COPD develops in 15% of cigarette smokers.
Age of initiation, total pack-years, and current smoking status predict COPD mortality

72. Pathophysiology of COPD
Obstructed airways close on expiration and traps air in the distal portions of the lung, causing:
Hypoventilation (increased PaCO2)
Ventilation/perfusion mismatching
Hypoxemia
Edema and accumulation of inflammatory cells lead to bronchial wall inflammation and thickening
Airway enlargement, loss of elastic recoil in the alveoli trap air, limit outflow
Enzymes called proteases break down elastin, cause alveolar destruction

73. Nursing Management
Assess for dyspnea, muscle fatigue,↑ work of breathing, worsening symptoms
Monitor ABG results
Manage the anxiety
A major role of the nurse is patient and family education
Breathing retraining
Use of postural drainage techniques
Energy conservation
Single most important factor in preventing COPD – smoking cessation

74. Cystic Fibrosis (CF)
A person is born with CF, and it affects boys more than girls
Affects Caucasians 5 times more often than African American people
Typical features: mucous plugging, chronic inflammation, infection
Peripheral bullae or blebs may develop due to obstruction, airway wall weakening
Affects mucous glands of the lungs, liver, pancreas, and intestines
Causes progressive disability due to multiple- system failure
Bullae or blebs – cyst like air pockets

75. Clinical Manifestations of CF
Acute exacerbation characterized by:
Increasing breathlessness
Change in sputum volume, color, and viscosity
Tiredness
Loss of appetite
Weight loss
Include barrel chest and digital clubbing
GI: malabsorptive symptoms e.g. frequent loose and oily stools, cramping, rectal prolapse
Signs and symptoms of diabetes including abnormal glucose tolerance, polydipsia, polyuria, and polyphagia
Subtle manifestations: chronic sinusitis, nasal polyps

76. Nursing Management of CF
Assist patient to maintain adequate airway clearance, reduce risk factors, perform ADLs
Involve patient/family in planning and implementing the therapeutic regimen
Encourage use of corticosteroids, bronchodilators, and antibiotics
Postural drainage techniques – percussion and vibration

77. Diagnostic Tests for CF
Possibly abnormal ABGs and PFTs
Abnormal sweat chloride test >60 mEq/L
Chest x-ray – densities w/o consolidation
Fecal fat analysis – fat concentration is elevated
Pacreatic Enzymes decreased
Serum Glucose Increased
Sperm count low
Genetic Analysis – positive for CF
Liver enzymes - elevated

78. Pulmonary Embolism (PE)
Thrombus breaks loose and blocks a pulmonary artery
Produces widespread pulmonary vasoconstriction and impairs ventilation and perfusion (V/Q) resulting in life- threatening hypoxemia, pulmonary ischemia and pulmonary infarction

79. Epidemiology of PE
Occurs mostly in older individuals, males more than females
Highest incidence in hospitalized patients
In patients younger than 55 yrs of age occurs more in females
Patients who have survived PE have higher incidence of recurring PE and the development of pulmonary hypertension and cor pulmonale

80. Etiology of PE
Complication of a Deep Vein Thrombosis (DVT) common after surgery, trauma, childbirth, stroke, heart failure, Myocardial Infarction (MI), Atrial Fibrillation, Cancer and prolonged immobilization
Arise from thrombi in proximal deep veins
Can also arise from pelvis from childbirth or pelvic fractures

81. Risk Factors of PE Most common – prior history of DVT or PE
Venous stasis with hypercoagulation states or a clotting tendency of the blood
Long trips in airplanes, trains and cars
Oral contraception
Pelvic, Hip or femur fractures
Central venous catheters
Genetic conditions causing increased clotting disorders
Genetic factors – Mutations in Factor V, antithrombin II deficiency, protein C or protein S deficiency, fibrinolysis defects

82. Pathophysiology of PE
Pulmonary occlusion occurs when a bloodborne substance occludes a branch of the pulmonary artery and obstructs blood flow
Embolism – thrombus, air (accidental air injection), fat from bone marrow after a fracture, amniotic fluid that enters the mother’s blood stream after rupture of membranes at birth, piece of an IV catheter that sheared off
Atelectasis (lung collaspe) may occur from loss of surfactant, pulmonary infiltrates can occur
Systemic hypotension, decreased cardiac output, pulmonary hypertension and right ventricular failure and death.

83. Four types of PE Occurances
Massive occlusion of pulmonary circulation
Infarction of a portion of the lung
Embolus without infarction
Multiple pulmonary emboli that may be chronic or recurrent

84. Clinical Manefestations
Triad of symptoms – hemoptysis, dyspnea (sudden onset), and chest pain
Many signs and symptoms are atypical – pleural chest pain, chest wall tenderness, friction rub
Small repeating emboli – decreases pulmonary bed
Massive PE – tachypnea, S3 and S4 gallop, tachycardia, sudden crushing chest pain and are usually fatal

85. Diagnostic Testing for PE
AGB’s – abnormal in some cases
Pulse Oximetry – sometimes abnormal
WBC – may be elevated
ECG – tachycardia, peaked T-waves in lead II, right axis deviation, right bundle branch block
D-dimer – positive >500 mg/L
V/Q scan – somes shows abnormal perfusion patern
Pulmonary Angiogram – positive
Lower extremity dopplers (U/S) – positive for DVT
Echocardiography – right sided heart failure
Spiral CT - positive
If d-dimer is positive and is combined with tachycardia, crackes, dyspnea, pleuritic chest pain and cough PE is diagnosed

86. Nursing Management of PE
Evaluation of risk factors on admission and during hospital stay
Encourage maximal mobility, range of motion and ambulation when appropriate or leg compression devices if on bed rest
Administer anticoagulant medication - heparin continuous IV drip until coumadin started and PT/INR is theraputic
Monitor liver function when patients receive anticoagulants
Monitor Lab for anticoagulant effectiveness (Heparin - PTT q 6 hrs till in range then q day)
Assess for symptoms of bleeding and heparin-induced thrombocytopenia (HIT)
IVC Filter – vena cava filter

87. Discharge Teaching
Discharge priorities include educating the patient and family about risk factors and following treatment regimes (anticoagulant therapy)
Coumadin – routine INR
Diet – low in vitamin K

89. Saddle
Pulmonary
Embolism

90. Cor Pulmonale
Alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system
Chronic lung disease
Pulmonary embolism
Interstitial lung disease
Primary pulmonary hypertension
Right sided heart failure caused by the left side of the heart or congenital heart disease is NOT considered cor pulmonale

91. Pathophysiological causes of Cor Pulmonale
Pathophysiological respiratory mechanisms lead to Primary Pulmonary Hypertension (PPH) then to cor pulmonale these include:
Pulmonary vasoconstriction due to alveolar hypoxia
Anatomic compromise of the pulmonary vascular bed
Increased blood viscosity secondary to blood disorders
Idiopathic primary pulmonary hypertension

92. Two types of Cor Pulmonale
Acute: usually results from massive PE or injury d/t mechanical ventilation for ARDS
Chronic cor pulmonale usually caused by COPD

93. Diagnostic Testing for Cor Pulmonale
Echocardiography gives information about the size of the heart
Chest x-rays and CAT scan
PFT evaluate ventilation/perfusion mismatch
ABG tests identify gas exchange, presence of acidosis and alkalosis

94. Clinical Manifestations of Cor Pulmonale
Asymptomatic initially
Later, as right ventricular (RV) pressures increase, physical signs commonly include:
Left parasternal systolic lift (visible pulsations to left midsternal)
Loud pulmonic component of the second heart sound (S2)
Murmurs of functional tricuspid and pulmonic insufficiency
Then even later, an RV gallop rhythm (third [S3] and fourth [S4] heart sounds)
Distended jugular veins, hepatomegaly
Lower extremity edema, fatigue, dyspnea, chest pain on exertion, cough
In advanced stages, hepatic congestion leads to anorexia, RUQ abdominal discomfort

95. Physical Assessment Findings and Nursing Management
Increased chest diameter
Labored respirations with retractions of the chest wall and use of accessory muscles
Hyperresonance to percussion
Diminished breath sounds
Cyanosis
Manage dyspnea by administration of oxygen
Administer medications to treat right ventricular hypertrophy and pulmonary hypertension
Provide patient education re: managing equipment and medications
Refer to home health and pulmonary rehabilitation

96. Nursing Management of Cor Pulmonale
Manage dyspnea by administration of oxygen
Administer medications to treat right ventricular hypertrophy and pulmonary hypertension (vasodilators, calcium channel blockers)
Provide patient education re: managing equipment and medications
Refer to home health and pulmonary rehabilitation
Regularly assess oxygen needs and medications
Single most preventive measure – encourage smoking cessation
Avoid exposure to secondhand smoke and respiratory pollutants

97. Complex Respiratory Disorders

98. The Alveolar-Capillary (A-C) Membrane

99. Ventilation/Perfusion
Ventilation (V) – movement of air
Perfusion (Q) – the movement of blood carrying oxygen
Near equal relationship of ventilation is 4L/min and perfusion 5L/min
Acute Respiratory Failure commonly caused by mismatch of ventilation and perfusion

100. Ventilation is 4L/Min and Perfusion is 5L/min
Normal ventilation to perfusion is 4/5 or 0.8
V/Q is equal to 0.8 – no miss match
V/Q is >0.8 – there is ventilation but no perfusion
V/Q is <0.8 – there is perfusion but little or no ventilation
V/Q no perfusion and no ventilation

101. Acute Respiratory Failure
Respiratory system unable to provide O2 and remove CO2
Lungs can not meet the physiological needs of the body due to failure of heart, lungs or both.
Hallmark of Acute Respiratory Failure is respiratory difficulty with abnormal ABG’s

102. Three main categories of Acute Respiratory Failure
Hypoxemia (deprived of oxygen)
Caused by failure of oxygenation
Hypercapnea (high CO2 in blood)
Caused by failure of respiratory system to ventilate
Failure of respiratory centers in the brain

103. ABG Findings for ARF Hypoxemia: Hypercapnea:
PaO2 below normal (<60 mmHg)
SaO2 <90% on room air
Hypercapnea:
PaCO2 above normal (>50 mmHg)
pH <7.3

104. Pathophysiology of Acute Respiratory Failure
Alteration in oxygenation is most common form of Acute Respiratory Failure
Perfusion (Q)exceeds ventilation (V)
A low V/Q ratio causes decreased oxygenation of venous blood & a mixing of less oxygenated blood with arterial blood
Reduced arterial oxygen value (hypoxemia)
Hypoventilation

105. Pulmonary Edema Types Acute Pulmonary Edema
Cardiogenic Pulmonary Edema (CPE)
Noncardiogenic Pulmonary Edema (NCPE)
Neruogenic Pulonary Edema
Negative Pressure Pulmonary Edema
Pulmonary Edema in Specific Populations

106. Acute Pulmonary Edema Abnormal accumulation of fluid in the lungs
Occurs rapidly – over minutes or hours
Etiologies – all relate to failure of heart and/or lungs

107. Cardiogenic Pulmonary Edema (CPE)
Initial insult is caused by heart failure
↑ Pulmonary venous pressure leads to
↑ Hydrostatic pressure in pulmonary capillaries
Result: pulmonary edema
Cardiac dysfunction is most common factor
Fluid overload, and chronic hypoxemia may also be present

108. Noncardiogenic Pulmonary Edema (NCPE)
Insult to the A-C membrane
Changes the permeability of the A-C membrane
Major causes: sepsis, inflammation, inhaled toxins, drugs

109. Clinical Manifestations of Cardiogenic PE/Non-Cardiogenic PE
Respiratory clues are identical
Agitation, confusion common to both CPE and NCPE
Distinguishing factors are subtle
Most evident in cardiac assessment, skin appearance

110. Differentiating CPE/Non-CPE
Mostly evident in cardiac assessment, skin appearance
Example 1: tachycardia with hypotension and cool diaphoretic skin suggests CPE
Example 2: tachycardia with hypertension, bounding pulses and dry skin suggests NCPE

111. Differentiating CPE/Non-CPE
Other Distinguishing Factors
Jugular Vein Distension more common in CPE
If coronary artery catheter is used, Pulmonary Artery Occlusion Pressures (PAOP) or Pulmonary Capillary Wedge Pressure (PCWP) above 18mmHg confirms CPE

112. Neurogenic Pulmonary Edema
Direct insult to central nervous system
Examples: seizures, cerebral hemorrhage, head injury
Dyspnea (shortness of breath) is primary presenting symptom
Other symptoms may be present
Crackles, pink frothy sputum

113. Negative Pressure Pulmonary Edema
Caused by ventilation with airway obstruction
High pressures required
When obstruction is relieved
Hydrostatic pressure pushes fluid into lungs

114. Pulmonary Edema and Specific Populations
Mountain climbers – HAPE (high altitude pulmonary edema) – causes vasoconstriction and hypoxemia and confusion – vasoconstriction causes increased pulonary pressures and forses fluid in the aveoli and interstical spaces
Heroin users
Scuba divers/hyperbaric chamber users
Excessive intravenous fluid administration

115. Acute Respiratory Distress Syndrome (ARDS)
Most severe type of respiratory failure
Caused by injury to A-C membrane
Mortality rate = 40%
Acute lung injury (ALI) less severe than ARDS

116. Acute Respiratory Distress Syndrome (ARDS)
ARDS leads to a buildup of fluid in the air sacs. This fluid prevents enough oxygen from passing into the bloodstream.
The fluid buildup also makes the lungs heavy and stiff, and decreases the lungs' ability to expand.
The level of oxygen in the blood can stay dangerously low, even if the person receives oxygen from a breathing machine (mechanical ventilator) through a breathing tube (endotracheal tube).
ARDS often occurs along with the failure of other organ systems, such as the liver or kidneys. Cigarette smoking and heavy alcohol use may be risk factors.

117. Treatment for ARDS
Typically people with ARDS need to be in an intensive care unit (ICU).
The goal of treatment is to provide breathing support and treat the cause of ARDS. This may involve medications to treat infections, reduce inflammation, and remove fluid from the lungs.
A breathing machine is used to deliver high doses of oxygen and continued pressure called PEEP (positive end- expiratory pressure) to the damaged lungs. Patients often need to be deeply sedated with medications when using this equipment. Some research suggests that giving medications to temporarily paralyze a person with ARDS will increase the chance of recovery.
Treatment continues until you are well enough to breathe on your own.

118. Causes of ARDS
ARDS can be caused by any major injury to the lung. Some common causes include:
Breathing vomit into the lungs (aspiration)
Inhaling chemicals
Lung transplant
Pneumonia
Septic shock (infection throughout the body)
Trauma

119. How the Ventilator Works
Monitors respiratory rate, pressure, volume
Delivers specified volume, pressure, or both
Controls concentration of oxygen
Mixes compressed air with oxygen to reach desired FiO2

120. Nursing Issues Complexity of equipment is increasing
Variety of equipment is increasing
No standard terminology among manufacturers

121. Terminology Spontaneous breaths Mandatory breaths Assisted breaths
Types of ventilation
Modes

122. Types of Breath Spontaneous breaths Assisted breaths
Patient initiates breath
Patient controls switch from inspiration to expiration
Assisted breaths
Ventilator controls switch to expiration
Ventilator controls volume and pressure

123. Terminology Mandatory breaths – controlled entirely by ventilator
Inspiration
Expiration
Volume/pressure of gas delivery

124. Types of Ventilation
Volume – clinician controls tidal volume; pressure can vary – can set rate, set volume
Pressure – clinician controls pressure; tidal volume can vary - set rate, set pressure, need to monitor minute volumes – pressure is determined by lung compliance – used for ARDS
No clinical consensus on preferred type

125. Common Ventilator Modes
Mode: describes the pattern of breath delivery
Common modes
Assist control mode (ACM) (A/C)
Synchronized mandatory intermittent ventilation (SIMV)
Pressure support (PS or PSV) – assists spontaneous breathing
Pressure controlled ventilation (PCV)

126. Assist Control Mode
ACM delivers a preset volume or a preset pressure for each breath
Patient can trigger a breath or the breath can be time triggered (CMV, A/C)
Commonly used in care of in the postoperative patient

127. Assist Control Mode Nursing Implications of ACM
As patient awakens, she or he may begin initiating breaths
Machine may not have time to deliver set volume
Patient can become hypoxic by attempt to breathe faster, stacking breaths
Pressure builds; lungs may be injured

128. Assist Control Mode Nursing Implications of ACM
Nurse must monitor to assure that patient and machine are working together
At high respiratory rates – air trapping may occur and cause high pressures and the high pressure to alarm on the ventilator

129. Synchronized Intermittent Mandatory Ventilation
Very common mode in US
SIMV sets the mandatory respiratory rate (VE )
Ventilator will deliver a set volume or pressure
Patient can also initiate a breath
Ventilator waits for the patient, to breathe
Synchronizes delivery of breath in concert with the patient

130. Synchronized Intermittent Mandatory Ventilation
Nursing Implications of SIMV
Desirable for patient to “overbreathe” the machine; i.e. breathe faster than the VE
In SIMV, patient may initiate breaths, some are assisted and some are not
Team should evaluate VE, level of sedation or analgesia

131. Pressure Support PS is a form of assisted ventilation
Requires stable respiratory effort from patient
IF ventilator senses negative pressure on inspiration
THEN ventilator supports the patient- initiated breath

132. Pressure Support Does not control the rate or tidal volume
Therefore, usually used with SIMV, CPAP mode
PS not triggered unless patient breathes above the VE (mandatory rate)

133. Pressure Support Nursing Implications of PS with SIMV
If patient does not “overbreathe” the machine, no benefit from PS
The nurse should assess the patient and talk to the team to determine a course of action

134. Pressure Control Ventilation
Clinician sets rate and pressure
Tidal volume is allowed to vary
Usually reserved for patients with noncompliant lungs, difficult to ventilate and oxygenate
Gas delivery distinguishes PCV from PS
Breath triggers rapid delivery of gas to reach set pressure, then the flow is decelerated

135. Pressure Control Ventilation
Nursing Implications of PCV
The nurse should trend the VE and the expiratory volume over time
Volume decrease may indicate lungs are becoming less compliant
Adjust Pressure to Achieve the Same Volume

136. Positive End-Expiratory Pressure
PEEP is a ventilator setting, not a mode
Provides resistance at end of exhalation
Prevents alveoli from collapsing
CPAP – continuous positive airway pressure – related to PEEP

137. Three Types of PEEP Physiological PEEP – 5 cm of H2O
Treatment PEEP – >5 cm of H2O
Auto-PEEP - gas trapped in alveoli at end expiration, due to inadequate time for expiration, bronchoconstriction or mucus plugging. It increased the work of breathing.
For most ventilated patients, PEEP of at least 5 cm of H2O required to prevent alveolar collapse

138. Nursing Implications of PEEP
PEEP of greater than 5 cm of H2O can cause decreased cardiac output – and CAUSE HYPOTENSION
Pneumothorax at higher levels of PEEP
The nurse should be aware of the level of PEEP, especially if patient is hypotensive

139. Auto-PEEP Potential problems Result: pressure builds in the lungs
Ventilator set rate is too high
Overaggressive use of an Ambu bag
Result: pressure builds in the lungs
Disconnect the ventilator or Ambu briefly
Allows the excess pressure to dissipate

140. CPAP Commonly used prior to extubation
Patient is breathing spontaneously
Ventilator support at end of expiration only

141. Nursing Assessment in ARF
Priorities are airway and oxygenation status
Frequent, ongoing assessment is vital

142. Assessment Data Ask if the patient feels s/he is getting enough air
Evaluate for anxiety
Respiratory rate, work of breathing, SO2, vital signs
Assess skin and nail beds for cyanosis and pallor

143. Nursing Diagnosis Impaired gas exchange
Ineffective tissue perfusion: cardiopulmonary and peripheral
Deficient knowledge related to the disease process
Self-care deficit
Ineffective airway clearance
Ineffective breathing pattern

144. Nursing Interventions in ARF
Encourage deep breathing and coughing
Encourage incentive spirometer use, if ordered
Frequent turning and repositioning

145. Indications for Endotracheal Intubation
Inability to maintain oxygenation/ ventilation
Airway protection
Elective surgery

146. Nurse’s Role Know the proper equipment and its use
Anticipate the health provider’s needs
Position the patient
Preoxygenate the patient
Provide suction as necessary
Monitor the patient
Provide information and reassurance

147. Figure 36.6 Endotracheal tube.
How Intubation Works
Figure Endotracheal tube.

148. Documentation Size of ET tube Location of ET tube in airway
Medications administered
Patient’s tolerance of procedure

149. Suctioning Performed based on assessment only Never routinely ordered
DO: Hyperoxegenate before/after suctioning
DON’T: Routinely instill normal saline before suctioning
10 seconds for each pass, up to three times only

150. Complications Hypoxemia Bronchospasm Cardiac arrhythmias Tissue injury
Increased risk of infection

151. Closed Suctioning System
Patient with high PEEP, high FiO2
Closed system keeps pressure up
Patient cannot tolerate use of open system
Patient with airborne infectious disease
Avoids exposing others to aerosolized infectious secretions