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RESPIRATORY FAILURE and ARDS

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1 RESPIRATORY FAILURE and ARDS
BY NANCY JENKINS

2 Exchange of O2 and CO2 gas exchange

3 For normal functioning

4

5 Respiratory Failure the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

6 Acute Respiratory Failure
Hypoxemia- inadequate O2 transfer PaO2 of 60mmHg or less when pt. Receiving 60% or greater O2 Hypercapnia- insufficient CO2 removal Increases PaCO2

7 Inhaling Affects PaO2 Exhaling Affects PCO2

8 Hypoxemic Respiratory Failure- (Affects the pO2)
V/Q Mismatch Shunt Diffusion Limitation Alveolar Hypoventilation- inc. CO2 and dec. PO2

9 Range of V/Q Relationships
Fig. 68-4

10 VentilationPerfusion Mismatch (V/Q)
Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs Perfusion or Q=perfusion Pulmonary Embolus- (VQ scan) pulmonary embolism

11 Pulmonary Embolus

12 Shunt 2 Types 1. Anatomic- passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect 2. Intrapulmonary shunt- blood flows through pulmonary capillaries without participating in gas exchange ex: alveoli filled with fluid * Patients with shunts are more hypoxemic than those with VQ mismatch and they may require mechanical ventilators

13 Diffusion Limitations
Gas exchange is compromised by a process that thickens or destroys the membrane 1. Pulmonary fibrosis 2. ARDS * A classic sign of diffusion limitation is hypoxemia during exercise but not at rest

14 Diffusion Limitation Fig. 68-5

15 Alveolar Hypoventilation
Mainly due to hypercapnic respiratory failure but can cause hypoxemia Increased pCO2 with decreased PO2 Restrictive lung disease CNS diseases Neuromuscular diseases

16 Hypercapnic Respiratory Failure Ventilatory Failure- affects CO2
1. Abnormalities of the airways and alveoli- air flow obstruction and air trapping Asthma, COPD, and cystic fibrosis 2. Abnormalities of the CNS- suppresses drive to breathe drug OD, narcotics, head injury, spinal cord injury

17 Hypercapnic Respiratory Failure
3. Abnormalities of the chest wall Flail chest, morbid obesity, kyphoscoliosis 4. Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis

18 Tissue Oxygen needs Tissue O2 delivery is determined by:
Amount of O2 in hemoglobin Cardiac output *Respiratory failure places patient at more risk if cardiac problems or anemia

19 Signs and Symptoms of Respiratory Failure- ABG’s
hypoxemia pO2<50-60 May be hypercapnia pCO2>50 only one cause- hypoventilation *In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02 and KNOW BASELINE!!!

20 Hypoxemia Compensatory Mechanisms- early Restlessness and apprehension
Tachycardia- more O2 to tissues Hypertension- fight or flight Tachypnea –take in more O2 Restlessness and apprehension Dyspnea Cyanosis Confusion and impaired judgment **Later dysrhythmias and metabolic acidosis, dec. B/P and Dec. CO.

21 Hypercapnia Dyspnea to respiratory depression- if too high CO2 narcosis Headache-vasodilation- Increases ICP Papilledema Tachycardia and inc. B/P Drowsiness and coma Respiratory acidosis **Administering O2 may eliminate drive to breathe especially with COPD patients- WHY??

22 Specific Clinical Manifestations
Respirations- depth and rate Patient position- tripod position Pursed lip breathing Orthopnea Inspiratory to expiratory ratio (normal 1:2) Retractions and use of accessory muscles Breath sounds

23 Diagnosis Physical Assessment Pulse oximetry (90% is PaO2 of 60) ABG
CXR CBC Electrolytes EKG Sputum and blood cultures, UA V/Q scan if ?pulmonary embolus Pulmonary function tests (PFT’s)

24 Exhaled C02 (ETC02) normal 35-45
Used when trying to wean patient from a ventilator

25 Treatment Goals O2 therapy Mobilization of secretions
Positive pressure ventilation(PPV)

26 O2 Therapy If secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by mask
If secondary to intrapulmonary shunt- positive pressure ventilation-PPV May be via ET tube Tight fitting mask **Goal is PaO2 of with SaO2 at 90% or more at lowest O2 concentration possible **O2 at high concentrations for longer than 48 hours causes O2 toxicity

27 Mobilization of secretions
Effective coughing- quad cough, huff cough, staged cough Positioning- HOB 45 degrees or recliner chair or bed “Good lung down” Hydration - fluid intake 2-3 L/day Humidification- aerosol treatments- mucolytic agents Chest PT- postural drainage, percussion and vibration Airway suctioning

28 Positive Pressure Ventilation
Invasively through oro or nasotracheal intubation Noninvasively( NIPPV) through mask Used for acute and chronic resp failure BiPAP- different levels of pressure for inspiration and expiration- (IPAP) higher for inspiration,(EPAP) lower for expiration CPAP- for sleep apnea **Used best in chronic resp failure in patients with chest wall and neuromuscular disease, also with HF and COPD.

29 NPPV NPPV

30 Should hear equal breath sounds if in correct place
Should hear equal breath sounds if in correct place. Always get a CXR to check placement also

31 Endotracheal Tube Fig

32 Surgical Intervention-Tracheostomy
If tube in greater than 4-5 days, perform a trach Tracheotomy Surgical procedure performed when need for an artificial airway is expected to be long term

33 Drug Therapy Relief of bronchospasm- bronchodilators
alupent and albuterol-(Watch for what side effect?) Reduction of airway inflammation-Corticosteroids by inhalation or IV or po Reduction of pulmonary congestion-diuretics and nitroglycerine with heart failure- why HF with pulmonary problems? Treatment of pulmonary infections- IV antibiotics, vancomycin and rocephin Reduction of anxiety, pain and agitation- diprivan, ativan, versed, propofol, opioids May need sedation or neuromuscular blocking agent if on ventilator.(Norcuron, nimbex) assess with peripheral nerve stim.

34 Medical Supportive Treatment
Treat underlying cause Maintain adequate cardiac output- monitor B/P and MAP. Maintain adequate Hemoglobin concentration- need 9g/dl or greater **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs

35 Nutrition During acute phase- enteral or parenteral nutrition
In a hypermetabolic state- need more calories If retain CO2- avoid high carb diet

36 Acute Respiratory Failure Gerontologic Considerations
Physiologic aging results in ↓ Ventilatory capacity Alveolar dilation Larger air spaces Loss of surface area Diminished elastic recoil Decreased respiratory muscle strength ↓ Chest wall compliance **Dec. PO2 and inc. CO2

37 ARDS Also known as DAD (diffuse alveolar disease) or ALI (acute lung injury)
a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias

38 Memory Jogger Assault to the pulmonary system Respiratory distress
Decreased lung compliance Severe respiratory failure

39

40 150,000 adults dev. ARDS About 50% survive
**Patients with gram negative septic shock and ARDS have mortality rate of 70-90%

41 Direct Causes (Inflammatory process is involved in all)
Pneumonia* Aspiration of gastric contents* Pulmonary contusion Near drowning Inhalation injury

42 Indirect Causes (Inflammatory process is involved)
Sepsis* (most common) gm - Severe trauma with shock state that requires multiple blood transfusions* Drug overdose Acute pancreatitis

43

44 ↓CO ↑CO *Causes (see notes) DIFFUSE lung injury (SIRS or MODS)
Damage to alveolar capillary membrane Pulmonary capillary leak Interstitial & alveolar edema Inactivation of surfactant Alveolar atalectasis ↓CO Metabolic acidosis ↑CO Severe & refractory hypoxemia Hypoventilation Hypercapnea Respiratory Acidosis Hyperventilation Hypocapnea Respiratory Alkalosis SHUNTING Stiff lungs

45

46 Pathophysiology of ARDS
Damage to alveolar-capillary membrane Increased capillary hydrostatic pressure Decreased colloidal osmotic pressure Interstitial edema Alveolar edema or pulmonary edema Loss of surfactant

47 What does surfactant do?

48

49 Pathophysiologic Stages in ARDS
Injury or Exudative- 1-7 days Interstitial and alveolar edema and atelectasis Refractory hypoxemia and stiff lungs Reparative or Proliferative-1-2 weeks after Dense fibrous tissue, increased PVR and pulmonary hypertension occurs Fibrotic-2-3 week after Diffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension

50 The essential disturbances of ARDS
**interstitial and alveolar edema and atelectasis

51 **Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS

52 Clinical Manifestations: Early
Dyspnea-(almost always present), tachypnea, cough, restlessness Chest auscultation may be normal or reveal fine, scattered crackles ABGs **Mild hypoxemia and respiratory alkalosis caused by hyperventilation

53 Clinical Manifestations: Early
Chest x-ray may be normal or show minimal scattered interstitial infiltrates Edema may not show until 30% increase in lung fluid content

54 Clinical Manifestations: Late
Symptoms worsen with progression of fluid accumulation and decreased lung compliance Pulmonary function tests reveal decreased compliance and lung volume Evident discomfort and increased WOB

55 Clinical Manifestations: Late
Suprasternal retractions Tachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 ( ex: 80/.8=100)

56 Clinical Manifestations
As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs

57

58 Chest X-Ray of ARDS Fig

59 Clinical Manifestations
If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue

60 Nursing Diagnoses Ineffective airway clearance
Ineffective breathing pattern Risk for fluid volume imbalance Anxiety Impaired gas exchange Imbalanced nutrition: Less than body requirements

61 Planning Following recovery PaO2 within normal limits or at baseline
SaO2 > 90% Patent airway Clear lungs or auscultation

62 Dyspnea and Tachypnea The Auscultation Assistant - Breath Sounds

63 Cyanosis

64 Nursing Assessment Lung sounds ABG’s CXR Capillary refill
Neuro assessment Vital signs O2 sats Hemodynamic monitoring values

65

66 Diagnostic Tests ABG-review CXR
Pulmonary Function Tests- dec. compliance and dec vital capacity - (max exhaled after max inhale) Hemodynamic Monitoring- (Pulmonary artery pressures) to rule out pulmonary edema

67 ABG Review and Practice
RealNurseEd (Education for Real Nurses by a Real Nurse)

68 ARDS X-Ray

69 Severe ARDS

70 X-RAY on Autopsy

71 *Goal of Treatment for ARDS
Maintain adequate ventilation and respirations. Prevent injury Manage anxiety

72 Treatment Mechanical Ventilation-goal PO2>60 and 02 sat 90% with FIO2 < 50 PEEP- can cause dec. CO, B/P and barotrauma Positioning- prone, continuous lateral rotation therapy and kinetic therapy Hemodynamic Monitoring- fluid replacement or diuretics Enteral or Parenteral Feeding- high calorie, high fat. Research shows that formulas enriched with omega -3 fatty acids may improve the outcomes of those with ARDS

73 Cont. Crystalloids versus colloids
Mild fluid restriction and diuretics

74 pt. can not expire completely. Causes alveoli to remain inflated
PEEP pt. can not expire completely. Causes alveoli to remain inflated (Complications can include decreased cardiac output, pneumothorax, and increased intracranial pressure). YouTube - Peep

75

76 FRC- air in after normal exhalation

77 PEEP ( Positive end-expiratory pressure)

78

79

80 Proning Proning typically reserved for refractory hypoxemia not responding to other therapies Plan for immediate repositioning for cardiopulmonary resuscitation

81 Proning-Principles Positioning strategies
Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone Predisposes to atelectasis Turn from supine to prone position May be sufficient to reduce inspired O2 or PEEP Fluid pools in dependent regions of lung

82 Prone Device No benefit in mortality Prone positioning
With position change to prone, previously nondependent air-filled alveoli become dependent, perfusion becomes greater to air-filled alveoli opposed to previously fluid-filled dependent alveoli, thereby improving ventilation-perfusion matching. No benefit in mortality

83 Benefits to Proning Before proning ABG on 100%O2 7.28/70/70
After proning ABG on 100% 7.37/56/227

84 Positioning Other positioning strategies Kinetic therapy
Continuous lateral rotation therapy

85 Continuous Lateral Rotation
Fig

86 Oxygen Therapy Oxygen High flow systems used to maximize O2 delivery
SaO2 continuously monitored, Usually have arterial line for frequent ABG’s Give lowest concentration that results in PaO2 60 mm Hg or greater

87 Respiratory Therapy Risk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hours Patients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels

88 Mechanical ventilation
PEEP Higher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater **High levels of PEEP can compromise venous return ↓ Preload, CO, and BP

89 Medical Supportive Therapy
Maintenance of cardiac output and tissue perfusion Continuous hemodynamic monitoring Continuous BP measurement via arterial catheter

90 Medical Supportive Therapy
Pulmonary artery catheter to monitor pulmonary artery pressure, pulmonary artery wedge pressures, and CO Administration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls

91 Medical Supportive Therapy
Use of inotropic drugs may be necessary Hemoglobin usually kept at levels greater than 9 or 10 with SaO2 ≥90% Packed RBCs Maintenance of fluid balance

92 Medical Supportive Therapy
May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEP Monitor PAWP, daily weights, and I and O’s to assess fluid status

93 Medications Inhaled Nitric Oxide Surfactant therapy NSAIDS and
corticosteroids

94 Nitric Oxide Dilates pulmonary blood vessels and helps reduce shunting

95 Case Study Case Study: Case Study Assignments

96 Assessment Data and Priority
Respiratory rate of 10 Absent breath sounds on the left O2 sat 82% High pressure alarm on vent going off Bilateral wheezing Respiratory rate of 30 ABG respiratory acidosis

97 ARDS Prioritization and Critical Thinking Questions #28
When assessing a 22 Y/o client admitted 3 days ago with pulmonary contusions after an MVA, the nurse finds shallow respirations at a rate of 38. The client states he feels dizzy and scared. O2 sat is 80% on 6 Ln/c. which action is most appropriate? A.Inc. flow rate of O2 to 10 L/min and reassess in 10 min. B.Assist client to use IS and splint chest using a pillow as he coughs. C.Adminster ordered MSO4 to client to dec. anxiety and reduce hyperventilation. D.Place client on non-rebreather mask at % FiO2 and call the Dr.

98 #25.The nursing assistant is taking VS for an intubated client after being suctioned by RT. Which VS should be immediately reported to the RN? A. HR 98 B.RR 24 C.B/P 168/90 D.Temp 101.4

99 #15. After change of shift report, you are assigned to care of the following clients.
Which should be assessed first? 68 y/o on ventilator who needs a sterile sputum specimen sent to the lab. 59y/o with COPD and has a pulse ox on previous shift of 90%. 72y/o with pneumonia who needs to be started on IV antibiotics. 51y/o with asthma c/o shortness of breath after using his bronchodilator inhaler.

100 Ventilators song Ventilate me

101 a machine that moves air in and out of the lungs
Ventilator VentWorld - What is a Ventilator? a machine that moves air in and out of the lungs

102 Mechanical Ventilation
Indications Apnea or impending inability to breathe Acute respiratory failure Severe hypoxia Respiratory muscle fatigue

103 Mechanical Vent Objective
support circulation and maintain pt. respirations until can breathe on own

104 Goal of Mechanical Ventilation
adequate controlled ventilation relief of hypoxia without hypercapnia relief of work of breathing access to airways

105 Criteria to put on vent Apnea or impending inability to breathe
Acute respiratory failure pH<7.25 pCO2>50 Severe hypoxia - pO2<50 Respiratory muscle fatigue

106 Mechanical Ventilation
Types of mechanical ventilation Negative pressure ventilation Uses chambers that encase chest or body and surround it with intermittent subatmospheric or negative pressure Noninvasive ventilation that does not require an artificial airway Not used extensively for acutely ill patients Mostly used for neuromuscular diseases, CNS and injuries of the spinal cord

107 Mechanical Ventilation
Types of mechanical ventilation (cont’d) Positive pressure ventilation (PPV) Used primarily in acutely ill patients Pushes air into lungs under positive pressure during inspiration Expiration occurs passively

108 Patient Receiving PPV Fig

109 Mechanical Ventilator

110 Settings to Monitor FIO2 -% of O2 TV-<5ml/kg for ARDS (normal 8-10)
Rate 12-15 Control (CMV) Continuous Mandatory Ventilation assist control SIMV inspiratory pressure and flow Pressure support- only in spontaneous breathes (gets the balloon started) Pt. controls all but pressure limit

111

112 Ventilator Modes- depends on WOB
Mode refers to how the machine will ventilate the patient in relation to the patient’s own respiratory efforts. There is a mode for nearly every patient situation, plus many can be used in conjunction with each other.

113 Mechanical Ventilation
Modes of volume ventilation Based on how much work of breathing (WOB) patient should or can perform Determined by patient’s ventilatory status, respiratory drive, and ABGs

114 Control Mode or CMV TV and RR are fixed.
Used for patients who are unable to initiate a breath (anesthetized or paralyzed). CMV delivers the preset volume or pressure at pre-set rate regardless of the patient’s own inspiratory effort Spontaneously breathing patients must be sedated and/or pharmacologically paralyzed so they don’t breathe out of synchrony with the ventilator. *Ventilator does all the work

115 Assist Contol A/C delivers the preset volume or pressure in response to the patient’s own inspiratory effort, but will initiate the breath if the patient does not do so within the set amount of time. Patient Assists or triggers the vent –can breathe faster but not slower Vent has back-up rate May need to be sedated to limit the number of spontaneous breaths since hyperventilation can occur. This mode is used for patients who can initiate a breath but who have weakened respiratory muscles.

116 Synchronous Intermittent Mandatory Ventilation-SIMV
SIMV delivers the preset volume or pressure and rate while allowing the patient to breathe spontaneously in between ventilator breaths. Each ventilator breath is delivered in synchrony with the patient’s breaths, yet the patient is allowed to completely control the spontaneous breaths at own TV. SIMV is used as a primary mode of ventilation, as well as a weaning mode. During weaning, the preset rate is gradually reduced, allowing the patient to slowly regain breathing on their own. The disadvantage of this mode is that it may increase the work of breathing and respiratory muscle fatigue

117

118

119 Pressure Support Ventilation
PSV is preset pressure that augments the patient’s spontaneous inspiratory effort and decreases the work of breathing. The patient completely controls the respiratory rate and tidal volume. PSV is used for patients with a stable respiratory status and is often used with SIMV to overcome the resistance of breathing through ventilator circuits and tubing.

120 Pressure support

121 High Frequency Ventilation
HFV delivers a small amount of gas at a rapid rate (as much as breaths per minute.) This is used when conventional mechanical ventilation would compromise hemodynamic stability, during short-term procedures, or for patients who are at high risk for pneumothorax. Sedation and pharmacological paralysis are required.

122 Inverse Ratio Ventilation
The normal inspiratory:expiratory ratio is 1:2 but this is reversed during IRV to 2:1 or greater (the maximum is 4:1). This mode is used for patients who are still hypoxic even with the use of PEEP. The longer inspiratory time increases the amount of air in the lungs at the end of expiration (the functional residual capacity) and improves oxygenation by re-expanding collapsed alveoli- acts like PEEP. The shorter expiratory time prevents the alveoli from collapsing again. Sedation and pharmacological paralysis are required since it’s very uncomfortable for the patient. For patients with ARDS continuing refractory hypoxemia despite high levels of PEEP

123 Case Study Mr. Hill has been on the ventilator for 24 hours. You volunteered to care for him today, since you know him from the intubation yesterday. The settings ordered by the pulmonologist after intubation were as follows: A/C, rate 14, VT 700, FIO2 60%. Since 0700, Mr. Hill has been assisting the ventilator with a respiratory rate of 24 (It’s now 1100). 1.        1. Describe the ventilator settings.

124 Answer The ventilator delivers 14 breaths per minute, each with a tidal volume of 700 ml. The A/C mode delivers the breaths in response to Mr. Hill’s own respiratory effort, but will initiate the breath if he doesn’t within the set amount of time. (He’s currently breathing above the vent setting.) The oxygen concentration is 60%.

125 Case Study You notice that Mr. Hill’s pulse oximetry has been consistently documented as 100% since intubation. You also notice that his respiratory rate is quite high and that he’s fidgety, doesn’t follow commands, and doesn’t maintain eye contact when you talk to him. He hasn’t had any sedation since he was intubated. 2.        2. Which lab test should you check to find out what his true ventilatory status is?

126 Answer Arterial blood gas (ABG) - which he should have had done with his morning labs. If not, check with the pulmonologist about getting one.

127 Case Study 3. Which two parameters on the ABG will give you a quick overview of Mr. Hill’s status?

128 Answer PaCO2 (which affects the pH) and PaO2. With his high respiratory rate, Mr. Hill is at risk for hypocapnia from “blowing off CO2.” If the PaO2 is adequate, the FIO2 could be decreased, since his oxygen saturation has been consistently 100%.

129 Case Study 4. What are some possible causes of Mr. Hill’s increased respiratory rate? (Give the corresponding nursing interventions as well.)

130 Answer 1. Secretions - suction through the ETT, as well as his mouth.
2. Anxiety or pain - Mr. Hill hasn’t received any sedation since he was intubated. At this point, he should at least have a prn order for sedation, if not a continuous IV infusion. 3. The vent settings may not be appropriate – check the ABG’s and notify the pulmonologist

131 Case Study Mr. Hill didn’t have an ABG done this morning, so you get an order from the pulmonologist to get one now (1130). When it comes back, the PaCO2 is 28, the pH is 7.48, and the PaO2 is 120 (normals: PaCO mm Hg, pH mm Hg, PaO mm Hg). 5.         Based on the ABG, the pulmonologist changes the vent settings to SIMV, rate 10, PS 10, FIO2 40%. The VT remains 700. How will these new settings help Mr. Hill?

132 Answer SIMV will deliver 10 breaths with the full tidal volume each minute, but in synchrony with Mr. Hill’s spontaneous breaths. This mode is not triggered to deliver a breath each time Mr. Hill inhales, and the tidal volume of his spontaneous breaths is under his control. Pressure support decreases the work of breathing that results from breathing through the ventilator circuits and tubing. The PaO2 was higher than desired, indicating that the FIO2 could be decreased. We need to be careful to prevent oxygen toxicity. The pulmonologist also orders midazolam (Versed) 1-2 mg every hour prn for sedation.

133

134

135

136 Alarms high pressure low pressure

137 Low Pressure Alarms Circuit leaks  Airway leaks  Chest tube leaks  Patient disconnection  High Pressure Alarms Patient coughing  Secretions or mucus in the airway  Patient biting tube  Airway problems  Reduced lung compliance (eg. pneumothorax)  Patient fighting the ventilator  Accumulation of water in the circuit  Kinking in the circuit 

138

139 NEVER TURN ALARMS OFF!

140 Assess your patient not the alarms

141 Mechanical Ventilation
Complications of PPV (cont’d) Cardiovascular system (cont’d) ↑ Intrathoracic pressure compresses thoracic vessels ↓ Venous return to heart, ↓ left ventricular end- diastolic volume (preload), ↓ cardiac output Hypotension Mean airway pressure is further ↑ if PEEP >5 cm H2O

142 Mechanical Ventilation
Complications of PPV (cont’d) Pulmonary system Barotrauma Air can escape into pleural space from alveoli or interstitium, accumulate, and become trapped pneumothorax , subcutaneous emphysema Patients with compliant lungs are at ↑ risk Chest tubes may be placed prophylactically

143 Subcutaneous Emphysema

144 Mechanical Ventilation
Complications of PPV (cont’d) Ventilator-associated pneumonia (VAP) Pneumonia that occurs 48 hours or more after ET intubation Clinical evidence Fever and/or elevated white blood cell count Purulent or odorous sputum Crackles or rhonchi on auscultation Pulmonary infiltrates on chest x-ray

145 Mechanical Ventilation
Complications of PPV (cont’d) Guidelines to prevent VAP HOB elevation at least 30 to 45 degrees unless medically contraindicated No routine changes of ventilator circuit tubing

146 Mechanical Ventilation
Complications of PPV (cont’d) Guidelines to prevent VAP (cont’d) Use of an ET that allows continuous suctioning of secretions in subglottic area Drain condensation that collects in ventilator tubing

147 Mechanical Ventilation
Complications of PPV (cont’d) Fluid retention Occurs after 48 to 72 hours of PPV, especially PPV with PEEP May be due to ↓ cardiac output Results Diminished renal perfusion Release of renin-angiotensin-aldosterone Leads to sodium and water retention

148 Mechanical Ventilation
Complications of PPV (cont’d) Fluid retention (cont’d) Pressure changes within thorax are associated with ↓ release of atrial natriuretic peptide, also causing sodium retention As part of the stress response, antidiuretic hormone and cortisol may be ↑ Contributes to sodium and water retention

149 Mechanical Ventilation
Complications of PPV (cont’d) Gastrointestinal system Risk for stress ulcers and GI bleeding ↑ Risk of translocation of GI bacteria ↓ Cardiac output may contribute to gut ischemia Peptic ulcer prophylaxis Histamine (H2)-receptor blockers, proton pump inhibitors, tube feedings ↓ Gastric acidity, ↓ risk of stress ulcer/hemorrhage

150 Mechanical Ventilation
Complications of PPV (cont’d) Musculoskeletal system Maintain muscle strength and prevent problems associated with immobility Progressive ambulation of patients receiving long-term PPV can be attained without interruption of mechanical ventilation

151 Mechanical Ventilation
Psychosocial needs Physical and emotional stress due to inability to speak, eat, move, or breathe normally Pain, fear, and anxiety related to tubes/ machines Ordinary ADLs are complicated or impossible

152 Mechanical Ventilation
Psychosocial needs (cont’d) Involve patients in decision making Encourage hope and build trusting relationships with patient and family Provide sedation and/or analgesia to facilitate optimal ventilation

153 Mechanical Ventilation
Psychosocial needs (cont’d) If necessary, provide paralysis to achieve more effective synchrony with ventilator and increase oxygenation Paralyzed patient can hear, see, think, feel Sedation and analgesia must always be administered concurrently

154 Respiratory Therapy Alternative modes of mechanical ventilation if hypoxemia persists Pressure support ventilation Pressure release ventilation Pressure control ventilation Inverse ratio ventilation High-frequency ventilation Permissive hypercapnia Independent Lung Ventilation

155 Independent Lung Ventilation

156 Research LiquiVent is an oxygen-carrying liquid drug (perflubron) used for respiratory distress syndrome. The goal of "liquid ventilation" therapy is to open up collapsed alveoli (air sacs) and facilitate the exchange of respiratory gases while protecting the lungs from the harmful effects of conventional mechanical ventilation.

157 Liquid Ventilation Partial liquid ventilation with perflubron
Perflubron is an inert, biocompatible, clear, odorless liquid that has affinity for O2 and CO2 and surfactant-like qualities Trickled down ET tube into lungs

158 Blood drains by gravity from the patient through a tube (catheter) placed in a large neck vein. This blood passes through a plastic pouch, or bladder, and then in pumped through the membrane oxygenator that serves as an artificial lung, putting oxygen into the blood and removing carbon dioxide. The blood then passes through a heat exchanger that maintains the blood at normal body temperature. Finally, the blood reenters the body through a large catheter placed in an artery in the neck.

159 Research and New video YouTube - Superman breather - USA

160 Prioritization and Delegation Questions on Vent
The nurse is assigned to provide nursing care for a client receiving mechanical ventilation. Which action should be delegated to the experienced nursing assistant? A. Assess respiratory status q 4 hours. B. Take VS and pulse ox reading q4 hours. C. Check ventilator settings to make sure they are as prescribed. D.Observe client’s need for suctioning q 2 hours.

161 #27 The high pressure alarm on the vent goes off and when you enter the room to assess a client with ARDS, her O2 sat is 87% and she is struggling to sit up. What action should be taken next? A. Reassure client that the vent will do the work of breathing for her. B. Manually ventilate the client while assessing possible reasons for the alarm. C. Inc. the FiO2 to 100% in preparation for endotracheal suction. D. Insert an oral airway to prevent client from biting the endotracheal tube.


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