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By Laurie Dickson. Respiration Exchange of O2 and CO2 gas exchange Respiratory Failure the inability of the cardiac and pulmonary systems to maintain.

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Presentation on theme: "By Laurie Dickson. Respiration Exchange of O2 and CO2 gas exchange Respiratory Failure the inability of the cardiac and pulmonary systems to maintain."— Presentation transcript:

1 By Laurie Dickson

2 Respiration Exchange of O2 and CO2 gas exchange Respiratory Failure the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

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5 Hypoxemic Respiratory Failure- (Affects the pO2) Causes- 4 Physiologic Mechanisms 1. V/Q Mismatch 2. Shunt 3. Diffusion Limitation 4. Alveolar Hypoventilation- CO2 andPO2

6 VentilationPerfusion Mismatch (V/Q) Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs Perfusion or Q=perfusion

7 Pulmonary Embolus Pulmonary Embolus- (VQ scan)

8 Shunt Anatomic Intrapulmonary blood passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect 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

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

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

11 Hypercapnic Respiratory Failure Failure of Ventilation PaCO2>45 mmHg in combination with acidemia (arterial pH< 7.35) Caused by conditions that keep the air in

12 Hypercapnic Respiratory Failure Abnormalities of the: Airways and Alveoli-air flow obstruction and air trapping Asthma, COPD, and cystic fibrosis CNS-suppresses drive to breathe drug OD, narcotics, head injury, spinal cord injury Chest wall-Restrict chest movement Flail chest, morbid obesity, kyphoscoliosis Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis

13 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

14 Signs and Symptoms of Respiratory Failure hypoxemia pO2<50-60 May be hypercapnia pCO2>45-50 only one cause- hypoventilation *In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02

15 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

16 Hypoxemia Tachycardia and Hypertension to comp. Dyspnea and tachypnea to comp. Cyanosis Restlessness and apprehension Confusion and impaired judgment Later dysrhythmias and metabolic acidosis, decreased B/P and CO.

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

18 Diagnosis Physical Assessment Pulse oximetry ABG CXR CBC Electrolytes EKG Sputum and blood cultures, UA V/Q scan if ?pulmonary embolus Pulmonary function tests

19 Treatment Goal- to correct Hypoxia O2 therapy Mobilization of secretions Positive pressure ventilation(PPV) Noninvasively( NIPPV) through mask Invasively through oro or nasotracheal intubation

20 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

21 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

22 Positive Pressure Ventilation Noninvasive ( 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. NPPV

23 Endotracheal Tube Fig Endotracheal intubation

24 Tracheostomy Surgical procedure Used when need for artificial airway is expected to be long term Research shows benefit to early trach

25 Exhaled C02 (ETC02) normal Used when trying to wean patient from a ventilator

26 Drug Therapy Relief of bronchospasm- Bronchodilators metaproterenol (Alupent) and albuterol-(Ventolin, Proventil, Proventil-HFA, AccuNeb, Vospire, ProAir ) 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

27 Drug Therapy Treatment of pulmonary infections- IV antibiotics- vancomycin and ceftriaxone (Rocephin) Reduction of anxiety, pain and agitation propofol (Diprivan), lorazepam (Ativan), midazolam (Versed), opioids May need sedation or neuromuscular blocking agent if on ventilator vecuronium (Norcuron), cisatracurium besylate (Nimbex ) assess with peripheral nerve stim.

28 Medical Supportive Treatment Treat underlying cause Maintain adequate cardiac output- monitor B/P and MAP. **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs Maintain adequate Hemoglobin concentration- need 9g/dl or greater Nutrition- During acute phase- enteral or parenteral nurtition In a hypermetabolic state- need more calories If retain CO2- avoid high carb diet

29 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

30 a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias

31 Memory Jogger A ssault to the pulmonary system R espiratory distress D ecreased lung compliance S evere respiratory failure

32 150,000 adults develop ARDS About 50% survive Patients with gram negative septic shock and ARDS have mortality rate of 70-90%

33 Direct Causes Inflammatory process is involved Pneumonia* Aspiration of gastric contents* Pulmonary contusion Near drowning Inhalation injury

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

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36 *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

37 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

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39 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

40 The essential disturbances of ARDS Interstitial and alveolar edema and atelectasis Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS

41 Clinical Manifestations: Early Dyspnea-(almost always present), tachypnea, cough, restlessness Lung sounds-may be normal or reveal fine, scattered crackles ABGs -Mild hypoxemia and respiratory alkalosis caused by hyperventilation Chest x-ray -may be normal or show minimal scattered interstitial infiltrates Edema -may not show until 30% increase in lung fluid content

42 Clinical Manifestations: Late Symptoms worsen with progression of fluid accumulation and decreased lung compliance PFTs show decreased compliance and lung volume Evident discomfort and increased WOB Suprasternal retractions Tachycardia, Diaphoresis Changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO 2 /FIO 2 ratio <200 despite increased FIO 2 ( ex: 80/.8=100)

43 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

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

45 Nursing Diagnoses Ineffective airway clearance Ineffective breathing pattern Risk for fluid volume imbalance Anxiety Impaired gas exchange Imbalanced nutrition

46 Planning Following recovery PaO 2 within normal limits or at baseline SaO 2 > 90% Patent airway Clear lungs or auscultation

47 ARDS Diagnosis Progressive hypoxemia due to shunting Decreased lung compliance Bilateral diffuse lung infiltrate

48 Nursing Assessment Lung sounds ABG’s CXR Capillary refill Neuro assessment Vital signs O2 sats Hemodynamic monitoring values The Auscultation Assistant - Breath Sounds

49 Diagnostic Tests ABG CXR Pulmonary Function Tests Hemodynamic Monitoring ABG review RealNurseEd (Education for Real Nurses by a Real Nurse)

50 ARDSSevere ARDS

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

52 Treatment Mechanical Ventilation- goal PO2>60 and O2 sat 90% with FIO2 < 50 PEEP- can cause CO + B/P and barotrauma Positioning- prone, continuous lateral rotation therapy and kinetic therapy Hemodynamic Monitoring- fluid replacement or diuretics Crystalloids vs Colloids Enteral or Parenteral Feeding- high calorie, high fat.

53 PEEP Cannot expire completely. Causes alveoli to remain inflated Peep Peep Complications can include decreased cardiac output, pneumothorax, and increased intracranial pressure

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

56 Proning Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone Fluid pools in dependent regions of lung Predisposes to atelectasis With prone position nondependent air-filled alveoli become dependent perfusion becomes greater to air-filled alveoli thereby improving ventilation-perfusion matching. May be sufficient to reduce inspired O 2 or PEEP

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

58 Other positioning strategies Kinetic therapy Continuous lateral rotation therapy

59 Oxygen Therapy High flow systems used to maximize O 2 delivery SaO 2 continuously monitored Give lowest concentration that results in PaO 2 60 mm Hg or greater Risk for O 2 toxicity increases when FIO 2 exceeds 60% for more than 48 hours Patients will commonly need intubation with mechanical ventilation because PaO 2 cannot be maintained at acceptable levels

60 Mechanical ventilation PEEP at 5 cm H 2 O compensates for loss of glottic function Opens collapsed alveoli Higher levels of PEEP are often needed to maintain PaO 2 at 60 mm Hg or greater High levels of PEEP can compromise venous return ↓ Preload, CO, and BP

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

62 Medical Supportive Therapy Use of inotropic drugs may be necessary Hemoglobin usually kept at levels greater than 9 or 10 with SaO 2 ≥90% Packed RBCs Maintenance of fluid balance May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEP Monitor PAWP, daily weights, and I and Os to assess fluid status

63 Medical Supportive Therapy Pulmonary Artery Wedge Pressure Pressure in pulmonary artery Indirect estimate of L Arterial pressure Keep as low as possible without imparing cardiac output (normal 6-12) Prevent pulmonary edema PAWP increases with Heart Failure PAWP does not increase with ARDS

64 Other Treatments Inhaled Nitric Oxide Surfactant therapy NSAIDS and Corticosteroids

65 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 100% O2 and call the Dr.

66 #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.

67 a machine that moves air in and out of the lungs

68 Mechanical Ventilation Indications Apnea or impending inability to breathe Acute respiratory failure pH<7.25 pCO2>50 Severe hypoxia pO2<50 Respiratory muscle fatigue RR<12

69 Mechanical Ventilation Purpose Support circulation and Maintain pt. respirations until can breathe on own Goal Adequate controlled ventilation Relief of hypoxia without hypercapnia Relief of work of breathing Access to airways

70 Types of Mechanical Ventilation Negative Pressure Ventilation Chambers encase chest or body Surround with intermittent subatmospheric or negative pressure Noninvasive ventilation Does not require an artificial airway Not used extensively for acutely ill patients Used for neuromuscular diseases, CNS and injuries of the spinal cord

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

72 Mechanical Ventilator

73 Settings to Monitor FIO2 -% of O2 Vt-<5ml/kg for ARDS (normal 10-12) rate Control (CMV) Continuous Mandatory Ventilation assist control IMV SIMV inspiratory pressure Pressure support- only in spontaneous breaths (gets the balloon started) Pt. controls all but pressure limit

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75 Ventilator Modes Mode 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 Can be used in conjunction with each other Two types Volume Pressure

76 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 Types CMV- Control Mode AC- Assist Control SIMV- Synchronous Intermittent Mandatory Ventilation

77 Control Mode- CMV Volume 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 a preset rate regardless of 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

78 Assist Control Preset Volume or pressure in response to the patient’s own inspiratory effort Will initiate the breath if the patient does not do so with in the set amount of time Patient Assists of triggers the vent Can breathe faster but not slower Vent has back up rate May need sedation to limit the number of spontaneous breaths- can hyperventilate For patients who can initiate a breath but have weakened respiratory muscles

79 Synchronous Intermittent Mandatory Ventilation- SIMV Preset volume or pressure and rate while allowing the patient to breathe spontaneously in between breaths. Each ventilator breath is delivered in synchrony with the patients breaths The patient is allowed to completely control the spontaneous breaths at own tidal volume (Vt) Used as primary mode and for weaning Weaning- preset rate gradually reduced Risk- may increase work of breathing and cause respiratory muscle fatigue

80 Pressure Support Ventilation Preset pressure that augments patients own inspiratory effort Decreases WOB Patient completely controls rate and volume Used for stable patients often with SIMV to overcome resistance of breathing through ventilator tubing

81 High Frequency Ventilation Small amounts of gas delivered at a rapid rate As much as breaths /minute Used when conventional mechanical ventilation would compromise hemodynamic stability For short term procedures For patients at high risk for pneumothorax Sedation and pharmacological paralysis required

82 Inverse Ration Ventilation Inspiratory/expiratory ratio set at 2:1 or greater max 4:1 Normal inspiratory/expiratory ratio is 1:2 Longer inspiratory time Increases the amount of air in the lungs at the end of expiration (FRC) Improves oxygenation by re-expanding collapsed alveolI Acts like PEEP Shorter expiratory time prevents alveoli from collapsing again Very uncomfortable, sedation required For patients with continuing refractory hypoxemia despite high levels of PEEP- (ARDS)

83 Ventilator Alarms Low Pressure High Pressure Circuit Leaks Airway leaks Chest tube leaks Patient disconnection NEVER TURN OFF ALARMS!! Assess the patient NOT the Alarm!! Coughing Patient biting tube Fighting Ventilator Secretions or mucus in the airway Airway problems Reduced lung compliance Water in the circuit Kink

84 Complications of PPV Cardiovascular system ↑ 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 H 2 O

85 Complications of PPV 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

86 Complications of PPV 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

87 Complications of PPV Guidelines to prevent VAP HOB at least 45 degrees No routine changing of ventilator circuit tubing Use ET that allows continuous suctioning of secretions Drain condensation that collects in ventilator tubing

88 Complicationof PPV 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

89 Complications of PPV Fluid retention Pressure changes within thorax ↓ release of atrial natriuretic peptide (ANP) Causing sodium retention Stress response Antidiuretic hormone and cortisol may be ↑ Contributes to sodium and water retention

90 Complications of PPV 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

91 Complications of PPV 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 (H 2 )-receptor blockers Proton pump inhibitors Tube feedings ↓ Gastric acidity ↓ risk of stress ulcer/hemorrhage

92 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

93 Psychosocial needs Involve patients in decision making Encourage hope and build trusting relationships with patient and family Provide sedation and/or analgesia to facilitate optimal ventilation 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

94 Alternative modes If hypoxemia persists Pressure support ventilation Pressure release ventilation Pressure control ventilation Inverse ratio ventilation High-frequency ventilation Permissive hypercapnia Independent Lung Ventilation

95 Mechanical Ventilation Extracorporeal membrane oxygenation Alternative form of pulmonary support for patient with severe respiratory failure Modification of cardiopulmonary bypass Involves partially removing blood through use of large- bore catheters, infusing oxygen, removing CO 2, and returning blood back to patient

96 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.


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