respiratory failure &ards منتدى تمريض مستشفى غزة الاوروبي

Hala Ayyash

EGH-NSG.ForumPalestine.com

Respiratory Failure (RF)

&

ARDS

10/12/2011

Hala AyyashHala Ayyash

(1)

Respiratory Failure Respiratory Failure (RF)(RF)

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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

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Classification of RFClassification of RF

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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

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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

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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

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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

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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

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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

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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

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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

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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%

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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

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Management of ARFManagement of ARF

• 4 – Mechanical ventilation• Indications

– Persistence hypoxemia despite O2supply

– Decreased level of consciousness

– Hypercapnia with severe acidosis (pH< 7.2)

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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

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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

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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

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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

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(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

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THANK YOUTHANK YOU