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شبكة منتديات تمريض مستشفى غزة الأوروبيegh-nsg.forumpalestine.com
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Hala Ayyash
EGH-NSG.ForumPalestine.com
Respiratory Failure (RF)
&
ARDS
10/12/2011
Hala AyyashHala Ayyash
(1)
Respiratory Failure Respiratory Failure (RF)(RF)
Hala Ayyash
Respiratory Failure (RF)Respiratory Failure (RF)
• Definition
• Classification of RF
• Distinction between Acute and Chronic RF
• Diagnosis of RF
• Causes
• Clinical presentation
• Investigations
• Management of RF
• Complications of ARF
Definitions RFDefinitions RF
• Definition
• Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O2 from atmosphere to blood and remove CO2 from blood.
• Clinically
• Respiratory failure is defined as PaO2 <60 mmHg while breathing air, or a PaCO2 >50 mmHg.-Acute and chronic
Hala Ayyash
Classification of RFClassification of RF
Hala Ayyash
Classification of RFClassification of RF
– Type 1• Hypoxemic RF **
• PaO2 < 60 mmHg with normal or ↓ PaCO2
Associated with acute diseases of the lung
Pulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse
– Type 2• Hypercapnic RF
• PaCO2 > 45 mmHg
• Hypoxemia is common
• Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthma
Hala Ayyash
Distinction between Acute and Distinction between Acute and Chronic RFChronic RF
• Acute RF
• Develops over minutes to hours
• ↓ pH quickly to <7.2
• Example; Pneumonia
• Chronic RF
• Develops over days
• ↑ in HCO3
• ↓ pH slightly
• Polycythemia, Corpulmonale
• Example; COPD
Hala Ayyash
Diagnosis of RFDiagnosis of RF1 – Clinical (symptoms, signs)1 – Clinical (symptoms, signs)
• Hypoxemia• Dyspnea, Cyanosis• Confusion, somnolence, fits• Tachycardia, arrhythmia• Tachypnea (good sign)• Use of accessory ms• Nasal flaring• Recession of intercostal ms• Polycythemia• Pulmonary HTN,
Corpulmonale, Rt. HF
• Hypercapnia• ↑Cerebral blood flow, and
CSF Pressure• Headache• Asterixis• Papilloedema• Warm extremities,
collapsing pulse • Acidosis (respiratory, and
metabolic)• ↓pH, ↑ lactic acid
Hala Ayyash
Diagnosis of RFDiagnosis of RF 2 – Causes2 – Causes
• 1 – CNS
• Depression of the neural
drive to breath
• Brain stem tumors or vascular abnormality
• Overdose of a narcotic, sedative
Myxedema, chronic metabolic
alkalosis
• Acute or chronic hypoventilation
and hypercapniaHala Ayyash
Diagnosis of RFDiagnosis of RF2 – Causes2 – Causes
• 2 - Disorders of peripheral
nervous system, Respiratory ms, and Chest wall
• Inability to maintain a level of minute ventilation appropriate for the rate of CO2 production
• Guillian-Barre syndrome, muscular dystrophy, myasthenia gravis, morbid obesity
• Hypoxemia and hypercapnia
Hala Ayyash
Diagnosis of RFDiagnosis of RF2 – Causes2 – Causes
• 3 - Abnormities of the airways
• Upper airways
– Acute epiglotitis
– Tracheal tumors
• Lower airway
– COPD, Asthma, cystic fibrosis
• Acute and chronic hypercapnia
Hala Ayyash
Diagnosis of RFDiagnosis of RF2 – Causes2 – Causes
• 4 - Abnormities of the alveoli
• Diffuse alveolar filling
• hypoxemic RF
– Cardiogenic and noncardiogenic pulmonary edema
– Aspiration pneumonia
– Pulmonary hemorrhage
• Associate with Intrapulmonary shunt and increase work of breathing
Hala Ayyash
Diagnosis of RFDiagnosis of RF3 – Common causes3 – Common causes
Hypoxemic RFHypoxemic RF
Chronic bronchitis, emphysema
Pneumonia, pulmonary edema
Pulmonary fibrosis
Asthma, pneumothorax
Pulmonary embolism,
Pulmonary hypertension
Bronchiectasis, ARDS
Fat embolism, Obesity
Cyanotic congenital heart disease
Granulomatous lung disease
Hypercapnic RFHypercapnic RF
Chronic bronchitis,emphysema
Severe asthma, drug overdose
Poisonings, Myasthenia gravis
Polyneuropathy, Poliomyelitis
Primary ms disorders
1ry alveolar hypoventilation
Obesity hypoventilation synd.
Pulmonary edema, ARDS
Myxedema, head and cervical cord injuryHala Ayyash
Diagnosis of RFDiagnosis of RF3 - Investigations3 - Investigations
• ABG• CBC, Hb
– Anemia → tissue hypoxemia
– Polycythemia → chronic RF • Urea, Creatinine• LFT → clues to RF or
its complications• Electrolytes (K, Mg, Ph) → Aggravate RF• ↑ CPK, ↑ Troponin 1 → MI• ↑CPK, normal Troponin 1 → Myositis • TSH → HypothyroidismHala Ayyash
Diagnosis of RFDiagnosis of RF3 - Investigations3 - Investigations
• Chest x ray → Pulmonary edema → ARDS
• Echocardiography → Cardiogenic pulmonary edema
→ ARDS
→ PAP, Rt ventricular hypertrophy in CRF
Hala Ayyash
Diagnosis of RFDiagnosis of RF3 - Investigations3 - Investigations
• ECG → cardiac cause of RF
→ Arrhythmia due to hypoxemia and severe acidosis
■ Right heart catheterization to measure
●Pulmonary capillary wedge pressure (PCWP)
● Normal → ARDS (<18 mmHg)
● Increased → Cardiogenic pulmonary edema
Hala Ayyash
Management of ARFManagement of ARF
• ICU admition
• 1 -Airway management– Endotracheal intubation:
• Indications
– Severe Hypoxemia
– Altered mental status
– Importance
• precise O2 delivery to the lungs
• remove secretion
• ensures adequate ventilationHala Ayyash
Management of ARFManagement of ARF• 2 -Correction of hypoxemia
– O2 administration via nasal prongs, face mask, intubation and Mechanical ventilation
– Goal: Adequate O2 delivery to tissues
– PaO2 = > 60 mmHg
– Arterial O2 saturation >90%
Hala Ayyash
Management of ARFManagement of ARF
• 3- Correction of hypercapnia
• Control the underlying cause
• Controlled O2 supply
• 1 -3 lit/min, titrate according O2 saturation
• O2 supply to keep the O2 saturation >90% but <93 to avoid inducing hypercapnia
• COPD-chronic bronchitis, emphysema
Hala Ayyash
Management of ARFManagement of ARF
• 4 – Mechanical ventilation• Indications
– Persistence hypoxemia despite O2supply
– Decreased level of consciousness
– Hypercapnia with severe acidosis (pH< 7.2)
Hala Ayyash
Management of ARManagement of AR
• 4 - Mechanical ventilation– Increase PaO2– Lower PaCO2– Rest respiratory ms
(respiratory ms fatigue)– Ventilator
• Assists or controls the patient breathing
– The lowest FIO2 that produces SaO2 >90% and PO2 >60 mmHg should be given to avoid O2 toxicity Hala Ayyash
Management of ARFManagement of ARF
• 5 -PEEP (positive End-Expiratory pressure
• Used with mechanical ventilation
– Increase intrathoracic pressure
– Keeps the alveoli open
– Decrease shunting
– Improve gas exchange
• Hypoxemic RF (type 1)– ARDS
– PneumoniasHala Ayyash
Management of ARFManagement of ARF• 6 - Noninvasive Ventilatory
support (IPPV)• Mild to moderate RF• Patient should have
– Intact airway, – Alert, normal airway protective
reflexes• Nasal or full face mask
– Improve oxygenation,– Reduce work of breathing– Increase cardiac output
• COPD, asthma, CHFHala Ayyash
Management of ARFManagement of ARF
• 7 - Treatment of the underlying causes
• After correction of hypoxemia, hemodynamic stability
• Antibiotics – Pneumonia– Infection
• Bronchodilators (COPD, BA)– Salbutamol
• reduce bronchospasm• airway resistance Hala Ayyash
Management of ARFManagement of ARF• 7 - Treatment of the underlying causes• Anticholinergics (COPD,BA)
– Ibratropium bromide• inhibit vagal tone
• relax smooth ms
• Theophylline (COPD, BA)– improve diaphragmatic contraction
– relax smooth ms
• Diuretics (pulmonary edema) – Frusemide, Metalzone
Hala Ayyash
Management of ARFManagement of ARF
• 7 - Treatment of the underlying causes
• Methyl prednisone (COPD, BA, acute esinophilic pn)– Reverse bronchospasm, inflammation
• Fluids and electrolytes– Maintain fluid balance and avoid fluid overload
• IV nutritional support– To restore strength, loss of ms mass– Fat, carbohydrate, protein
Hala Ayyash
Management of ARFManagement of ARF
• 7 - Treatment of the underlying causes
• Physiotherapy
– Chest percussion to loosen secretion
– Suction of airways
– Help to drain secretion
– Maintain alveolar inflation
– Prevent atelectasis, help lung expansion
Hala Ayyash
Complications of ARFComplications of ARF
• Pulmonary– Pulmonary embolism– barotrauma– pulmonary fibrosis (ARDS)– Nosocomial pneumonia
• Cardiovascular– Hypotension, – Arrhythmia– MI, pericarditis
• GIT– Stress ulcer, ileus, diarrhea,
hemorrhage
• Infections– Nosocomial infection– Pneumonia, UTI,
catheter related sepsis• Renal
– ARF (hypoperfusion, nephrotoxic drugs)
– Poor prognosis• Nutritional
– Malnutrition, diarrhea hypoglycemia, electrolyte disturbances
Hala Ayyash
(2)ARDS
ARDSAlso 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
Memory Jogger
• Assault to the pulmonary system
• Respiratory distress
• Decreased lung compliance
• Severe respiratory failure
Direct Causes (Inflammatory process is involved in all)
• Pneumonia*
• Aspiration of gastric contents*
• Pulmonary contusion
• Near drowning
• Inhalation injury
Indirect Causes (Inflammatory process is involved)
Sepsis* (most common) gm -
• Severe trauma with shock state that requires multiple blood transfusions*
• Drug overdose
• Acute pancreatitis
Pathophysiology of ARDSPathophysiology 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
Pathophysiologic Stages in Pathophysiologic Stages in ARDSARDS
• 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 pulmonary hypertension
occurs
• Fibrotic-2-3 week after– Diffuse scarring and fibrosis, decreased surface area,
decreased compliance and pulmonary hypertension
The essential disturbances The essential disturbances of ARDSof ARDS
**interstitial and alveolar edema and atelectasis
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
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
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
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)
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
Chest X-Ray of ARDSChest X-Ray of ARDS
Clinical Manifestations
• If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue
Nursing Diagnoses
• Ineffective airway clearance
• Ineffective breathing pattern
• Risk for fluid volume imbalance
• Anxiety
• Impaired gas exchange
• Imbalanced nutrition: Less than body requirements
Planning
• Following recovery
– PaO2 within normal limits or at baseline
– SaO2 > 90%
– Patent airway
– Clear lungs or auscultation
Dyspnea and Tachypnea
The Auscultation Assistant - Breath Sounds
Nursing Assessment
• Lung sounds• ABG’s• CXR• Capillary refill• Neuro assessment• Vital signs• O2 sats• Hemodynamic monitoring values
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
Severe ARDSSevere ARDS
*Goal of Treatment for ARDS
Maintain adequate ventilation and respirations.
Prevent injury
Manage anxiety
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• 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
Cont.
• Crystalloids versus colloids
• Mild fluid restriction and diuretics
Proning
• Proning typically reserved for refractory hypoxemia not responding to other therapies
– Plan for immediate repositioning for cardiopulmonary resuscitation
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
Effect of prone position on ventilation distribution. In the supine position, the distribution of ventilation is preferentially distributed to the ventral regions. When the patient is prone, the stiffness of the dorsal chest wall favors the distribution of ventilation to the dorsal regions, facilitating reinflation in this area.
Prone DeviceProne Device
• *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 mortalityNo benefit in mortality
Benefits to Proning
Before proning After proning
Positioning
• Other positioning strategies – Continuous lateral rotation therapy
Continuous Lateral Rotation
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
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
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
Medical Supportive TherapyMedical Supportive Therapy
• Maintenance of cardiac output and tissue perfusion
– Continuous hemodynamic monitoring
– Continuous BP measurement via arterial catheter
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
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
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
MedicationsMedications
• Inhaled Nitric Oxide
• Surfactant therapy
• corticosteroids
Hala Ayyash
THANK YOUTHANK YOU