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Nursing Management of Patients with Respiratory Disorders NURS 2140 Winter Quarter 2012 Teresa M. Champion, RN MSN.

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1 Nursing Management of Patients with Respiratory Disorders NURS 2140 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

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

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

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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

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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

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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

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

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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

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

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 $1500.00 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 2010 – 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

32 SLEEP APNEA Defined – a person stops breathing for more than 10 seconds, more that 20-30 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!

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

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

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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

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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)

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 – 6 th leading cause of death ◦ Tuberculosis – Mycrobacterium tuberculosis ◦ Lung Abcesses/Empyema

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 2003. 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 2003.

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 O 2 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 PaCO 2 ) ◦ 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

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

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

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

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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 (S 2 ) ◦ Murmurs of functional tricuspid and pulmonic insufficiency ◦ Then even later, an RV gallop rhythm (third [S 3 ] and fourth [S 4 ] 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 (a) V/Q is equal to 0.8 – no miss match (b) V/Q is >0.8 – there is ventilation but no perfusion (c) V/Q is <0.8 – there is perfusion but little or no ventilation (d) V/Q no perfusion and no ventilation Ventilation is 4L/Min and Perfusion is 5L/min Normal ventilation to perfusion is 4/5 or 0.8

101 Acute Respiratory Failure Respiratory system unable to provide O 2 and remove CO 2 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: ◦ PaO 2 below normal (<60 mmHg) ◦ SaO 2 <90% on room air Hypercapnea: ◦ PaCO 2 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 FiO 2

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 ◦ Patient initiates breath ◦ Patient controls switch from inspiration to expiration Assisted breaths ◦ Patient initiates breath ◦ 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 (V E ) 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 V E ◦ In SIMV, patient may initiate breaths, some are assisted and some are not ◦ Team should evaluate V E, 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 V E (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 V E 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 H 2 O Treatment PEEP – >5 cm of H 2 O 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 H 2 O required to prevent alveolar collapse

138 Nursing Implications of PEEP PEEP of greater than 5 cm of H 2 O 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 ◦ 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, SO 2, 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 How Intubation Works Figure 36.6 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 FiO 2 ◦ Closed system keeps pressure up Patient cannot tolerate use of open system Patient with airborne infectious disease ◦ Avoids exposing others to aerosolized infectious secretions


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