By Laurie Dickson Slide 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 Slide 3 Slide 4 Slide 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 Slide 6 VentilationPerfusion Mismatch
(V/Q) Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs
Perfusion or Q=perfusion Slide 7 Pulmonary Embolus Pulmonary
Embolus- (VQ scan) Slide 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 Slide 9 Diffusion Limitation Gas exchange is
compromised by a process that thickens or destroys the membrane 1.
Pulmonary fibrosis 2. 2. ARDS * A classic sign of diffusion
limitation is hypoxemia during exercise but not at rest Slide 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 Slide 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 Slide 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 Slide 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 Slide 14 Signs and Symptoms of Respiratory
Failure hypoxemia pO245-50 only one cause- hypoventilation *In
patients with COPD watch for acute drop in pO2 and O2 sats along
with inc. C02 Slide 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
Slide 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. Slide 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 Slide 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 Slide 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 Slide 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 55-60 with SaO2 at 90% or more at lowest O2 concentration
possible O2 at high concentrations for longer than 48 hours causes
O2 toxicity Slide 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
Slide 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 Slide 23
Endotracheal Tube Fig. 66-17 Endotracheal intubation Slide 24
Tracheostomy Surgical procedure Used when need for artificial
airway is expected to be long term Research shows benefit to early
trach Slide 25 Exhaled C02 (ETC02) normal 35-45 Used when trying to
wean patient from a ventilator Slide 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 Slide 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. Slide 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 Slide 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 Slide 30 a variety of acute and
diffuse infiltrative lesions which cause severe refractory arterial
hypoxemia and life-threatening arrhythmias Slide 31 Memory Jogger A
ssault to the pulmonary system R espiratory distress D ecreased
lung compliance S evere respiratory failure Slide 32 150,000 adults
develop ARDS About 50% survive Patients with gram negative septic
shock and ARDS have mortality rate of 70-90% Slide 33 Direct Causes
Inflammatory process is involved Pneumonia* Aspiration of gastric
contents* Pulmonary contusion Near drowning Inhalation injury Slide
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 Slide 35 Slide
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 Slide 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 Slide 38 Slide 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 Slide 40 The essential disturbances of ARDS
Interstitial and alveolar edema and atelectasis Progressive
arterial hypoxemia in spite of inc. O2 is hallmark of ARDS Slide 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 Slide 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 ratioSlide 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 Slide 44 Clinical Manifestations If
prompt therapy not initiated, severe hypoxemia, hypercapnia, and
metabolic acidosis may ensue Slide 45 Nursing Diagnoses Ineffective
airway clearance Ineffective breathing pattern Risk for fluid
volume imbalance Anxiety Impaired gas exchange Imbalanced nutrition
Slide 46 Planning Following recovery PaO 2 within normal limits or
at baseline SaO 2 > 90% Patent airway Clear lungs or
auscultation Slide 47 ARDS Diagnosis Progressive hypoxemia due to
shunting Decreased lung compliance Bilateral diffuse lung
infiltrate Slide 48 Nursing Assessment Lung sounds ABGs CXR
Capillary refill Neuro assessment Vital signs O2 sats Hemodynamic
monitoring values The Auscultation Assistant - Breath Sounds Slide
49 Diagnostic Tests ABG CXR Pulmonary Function Tests Hemodynamic
Monitoring ABG review RealNurseEd (Education for Real Nurses by a
Real Nurse) Slide 50 ARDSSevere ARDS Slide 51 Goal of Treatment for
ARDS Maintain adequate ventilation and respirations. Prevent injury
Manage anxiety Slide 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. Slide 53 PEEP Cannot
expire completely. Causes alveoli to remain inflated Peep Peep
Complications can include decreased cardiac output, pneumothorax,
and increased intracranial pressure Slide 54 Slide 55 Proning
typically reserved for refractory hypoxemia not responding to other
therapies Plan for immediate repositioning for cardiopulmonary
resuscitation *** Slide 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 Slide 57 Benefits to Proning Before
proning ABG on 100%O2 7.28/70/70 After proning ABG on 100%
7.37/56/227 Slide 58 Other positioning strategies Kinetic therapy
Continuous lateral rotation therapy Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide
64 Other Treatments Inhaled Nitric Oxide Surfactant therapy NSAIDS
and Corticosteroids Slide 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. Slide 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. Slide 67 a machine
that moves air in and out of the lungs Slide 68 Mechanical
Ventilation Indications Apnea or impending inability to breathe
Acute respiratory failure pH50 Severe hypoxia pO25 cm H 2 O Slide
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 Slide 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
Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 Slide 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 clients need for suctioning q 2 hours.
