abc 2011 2012 respiratory disorders

RESPIRATORY DISORDERS

DIFFERENCE OF A CHILD’S AIRWAY ANATOMY FROM AN ADULT

The back of the head of a child is slightly larger, so positioning requires more care

The tongue is proportionately larger and more anterior in the mouth

The trachea is smaller in diameter and more flexible

The airway itself is lower and narrower

ACUTE RESPIRATORY FAILURE

ACUTE RESPIRATORY FAILURE

A clinical condition in which the pulmonary system fails to maintain adequate gas exchange

Most common organ failure in the ICU Mortality rate: 22% to 75% Results from a deficiency in the performance of the

pulmonary system Usually occurs secondary to another disorder that has

altered the normal function of the pulmonary system in such a way as to decrease the ventilatory drive, decrease muscle strength, decrease chest wall elasticity, decrease lung’s capacity for gas exchange, increase airway resistance, or increase metabolic O2 requirements

ETIOLOGY - EXTRAPULMONARY

Brain – drug overdose, brain trauma or lesion, post-op anesthesia depression

Spinal cord – Guillain-Barre syndrome, poliomyelitis, spinal cord trauma or lesion

Neuromuscular system – Myasthenia gravis, Multiple sclerosis, neuromuscular-blocking agents, organophosphate poisoning

Thorax – massive obesity, chest trauma Pleura – pleural effusion, pneumothorax Upper airways – sleep apnea, tracheal obstruction,

epiglottitis

ETIOLOGY - INTRAPULMONARY

Lower airways and alveoli – COPD, asthma, bronchiolitis, pneumonia

Pulmonary circulation – pulmomary emboli

Alveolar-capillary membrane – acute lung injury, inhalation of toxic gases, near-drowning

Extrapulmonary and intrapulmonary disorders

Insufficient oxygen to meet metabolic demands

Hypoxemia

Blood passes through alveoli that are underventilated

V/Q mismatch

Blood reaches the arterial system without participating in gas exchange

Mixing of unoxygenated and oxygenated blood

Alveolar hypoventilation

Blood passes through a portion of a lung that is not ventilated

Intrapulmonary shunting

Hypercapnia

Acidosis

ASSESSMENT AND DIAGNOSIS

Clinical manifestations are related to the development of hypoxemia, hypercapnia, and acidosis

Clinical manifestations are so varied that they considered unreliable in predicting the degree of hypoxemia or hypercapnia or the severity

ABG: PaO2 less than 60 mm Hg and the PaCO2 is greater than 45 mm Hg

Bronchoscopy, chest X-ray, thoracic CT

NURSING DIAGNOSIS PRIORITIES

Impaired gas exchange related to alveolar hypoventilation

Impaired gas exchange related to ventilation/perfusion mismatching or intrapulmonary shunting

Ineffective breathing pattern related to musculoskeletal fatigue or neuromuscular impairment

MEDICAL MANAGEMENT

Aimed at treating the underlying cause, promoting adequate gas exchange, correcting acidosis, initiating nutrition support, and preventing complications

Medical interventions to promote gas exchange are aimed at improving oxygenation and ventilation

1. OXYGENATION

Purpose is to correct hypoxemia – aim is to keep the arterial hemoglobin oxygen saturation greater than 90%

Goal is to keep the tissues’ needs satisfied but not produce hypercapnia or oxygen toxicity

Supplemental oxygenation administration is effective in treating hypoxemia related to alveolar hypoventilation and V/Q mismatching

Positive pressure is necessary when there is intrapulmonary shunting (to open collapsed alveoli) can be delivered via nasal or oronasal mask (to avoid intubation)

2. VENTILATION

Depending on the underlying cause and severity, the patient may be initially treated with noninvasive ventilation

Mechanical ventilation PEEP – positive end expiratory pressure

PEEP

Opens collapsed alveoli Stabilizes flooded alveoli Increases FRC However, Decreases cardiac output, decreasing venous

return secondary to increased intrathoracic pressure

Barotrauma, as a result of gas escaping into the surrounding spaces secondary to alveolar rupture

3. PHARMACOLOGY

Bronchodilators – Beta-agonists and antocholinergic agents

Steroids Sedation can be used to comfort the patient

and decrease the work of breathing, particularly if the patient is fighting the ventilator

Analgesics for pain control Methylxanthines and mucolytics are no longer

used because of their negative side effects

4. ACIDOSIS - TREATMENT

Once the patient is adequately oxygenated and ventilated, the acidosis should correct itself

Use of sodium bicarbonate has been shown to be of minimal benefit and is no longer recommended, even in the presence of severe acidosis

5. NUTRITION SUPPORT

Goals are to meet the overall nutritional needs of the patient, while avoiding overfeeding, to prevent nutrition delivery-related complications and to improve patient outcomes

The enteral route is the preferred method of nutrition administration

Parenteral nutrition for those who cannot tolerate enteral feedings or cannot receive enough nutrients enterally

6. COMPLICATIONS - TREATMENT

Maintaining oxygenation, normalizing electrolytes, and monitoring drug levels will facilitate the prevention and treatment of encephalopathy and dysrhythmias

Venous thromboembolism can be prevented by using compression stockings and low-dose unfractionated heparin or low-molecular weight heparin

GIT bleeding can be prevented through the use of histamine-2 antagonists, cytoprotective agents, or gastric proton pump inhibitors

Patient is at risk of developing complications associated with artificial airway, mechanical ventilation, enteral and parenteral nutrition, and peripheral cannulation

GUIDELINE VALUES FOR ESTIMATING FIO2 WITH LOW FLOW O2 DEVICES

100% Flow Rate (L/Min) FIO2 (%)

Nasal Cannula or Catheter123456Oxygen Mask5 - 66 - 77- 8 Mask With Reservoir Bag678910

242832364044

405060

6070809099+

NURSING MANAGEMENT

Optimizing oxygenation and ventilation Providing comfort and emotional

support Maintaining surveillance for

complications Providing patient education

1. OPTIMIZING OXYGENATION AND VENTILATION

Positioning – the goal is to place the least affected area of the affected lung in the most dependent position

– gravity normally facilitates preferential ventilation and perfusion to the dependent areas of the lungs

- the best gas exchange would take place in the dependent areas of the lungs

1. OPTIMIZING OXYGENATION AND VENTILATION

Positioning1. Patients with diffuse lung disease may benefit from

being positioned with the right lung down, because it is larger and more vascular than the left lung

2. For those with alveolar hypoventilation, a nonrecumbent position (sitting or semierect) may be beneficial

3. Semirecumbency position can help prevent aspiration and inhibit the development of hospital-associated pneumonia

4. Frequent positioning (at least every 2 hours) is beneficial in optimizing the patient’s ventilatory pattern and V/Q matching

1. OPTIMIZING OXYGENATION AND VENTILATION

Preventing desaturation – performing procedures as needed: oxygenating before suctioning, providing adequate rest and recovery time between various procedures, and minimizing oxygen consumption

Promoting secretion clearance – providing adequate systemic hydration, humidifying supplemental oxygen, coughing, and suctioning

Note: postural drainage and chest percussion and vibration have been found to be of little benefit in the critically ill patient; to facilitate breathing, the thorax should be maintained in alignment and the head of the bed elevated 30 to 45 degrees

2. PATIENT EDUCATION

Pathophysiology of the disease Specific etiology Precipitating factor modification Importance of taking medications Breathing techniques (e.g., pursed-lip

breathing diaphragmatic breathing) Energy conservation techniques

2. PATIENT EDUCATION

Measures to prevent pulmonary infections (e.g., proper nutrition, hand washing, immunization against S. pneumoniae and influenza viruses)

Signs and symptoms of pulmonary infections (e.g., sputum color change, shortness of breath, fever)

Cough enhancement techniques

COLLABORATIVE MANAGEMENT

Identify and treat underlying cause Administer oxygen therapy Intubate patient Administer medications Position patient to optimize

ventilation/perfusion matching Suction as needed

COLLABORATIVE MANAGEMENT

Provide adequate rest and recovery time between various procedures

Correct acidosis Initiate nutritional support Maintain surveillance for complications:

encephalopathy, dysrhythmias, venous thromboembolism, GI bleeding

Provide comfort and emotional support

PNEUMONIA

PNEUMONIA

An acute inflammation of the lung parenchyma that is caused by an infectious agent that can lead to alveolar consolidation

CAP – community acquired pneumonia HAP – hospital acquired pneumonia VAP – ventilator-associated pneumonia

PRECIPITATING CONDITIONS OF PNEUMONIA

Condition Etiology

Depressed epiglottal and cough reflexes

Decreased cilia activity

Increased secretions

Atelectasis

Unconsciousness, neurologic disease, endotracheal or tracheal tubes, anesthesia

Smoke inhalation, smoking history, oxygen toxicity, hypoventilation, intubation, viral infections, aging COPD

COPD, viral infections, bronchiectasis, general anesthesia, endotracheal intubation, smoking

Trauma, foreign body obstruction, tumor, splinting, shallow ventilations, general anesthesia

PRECIPITATING CONDITIONS OF PNEUMONIA

Condition Etiology

Decreased lymphatic flow

Fluid in alveoli

Abnormal phagocytosis and humoral activity

Impaired alveolar macrophages

Heart failure, tumor

Heart failure, aspiration, trauma

Neutropenia, immunocompetent disorders, patients receiving chemotherapy

Hypoxemia, metabolic acidosis, cigarette smoking history, hypoxia, alcohol use, viral infections, aging

Microorganisms/noninfectious agents

Lower airways

Loss of cough reflex, damage to cilia of the respiratory tract, impaired host defenses

Colonization of the lower respiratory tract

Release of histamine and other vasoactive chemical

mediators

Inhalation/aspiration

Vasodilation

Stage of congestion More and more exudates accumulate

Lung tissue reacts to accumulating exudates and

microorganisms

Hepatization Lung tissue attempts to

undergo healing

Stage of fibrosis

Pulmonary function impaired

Clinical manifestations

ETIOLOGY

Severe CAP – S. pneumoniae, Legionella species, H. influenzae, S. aureus, M. pneumoniae, respiratory viruses, Chlamydia pneumoniae, and P. aerugionosa

HAP – S. aureus, S. pneumoniae, P. aeruginosa, Acinetobacter baumannii, Klebsiella species, Proteus species, Serratia species, fungi, and respiratory viruses

ASSESSMENT AND DIAGNOSIS

Ineffective airway clearance related to excessive secretions or abnormal viscosity of mucus

Impaired gas exchange related to ventilatory/perfusion mismatching or intrapulmonary shunting

Risk for infection, risk factor: invasive monitoring devices

Powerlessness related to lack of control over current situation or disease progression

ASSESSMENT AND DIAGNOSIS

Chest radiograph Sputum Gram stain and culture Diagnostic bronchoscopy CBC with differential count Chemistry panel Blood cultures ABG

MEDICAL MANAGEMENT

Antibiotic therapy Oxygen therapy Fluid management Nutritional support Treatment of associated medical

problems and complications Therapeutic bronchoscopy may be

necessary in patients who have difficulty mobilizing secretions

NURSING MANAGEMENT

Optimizing oxygenation and ventilation Preventing the spread of infection Providing comfort and emotional

support Maintaining surveillance for

complications

COLLABORATIVE MANAGEMENT

Administer oxygen therapy Initiate mechanical ventilation as required Administer medications: antibiotics, bronchodilators Position patient to optimize ventilation/perfusion

matching Suction as needed Provide adequate rest and recovery time between

various procedures Maintain surveillance for complications: acute

respiratory failure Provide comfort and emotional support

PULMONARY EMBOLISM

PULMONARY EMBOLISM (PE)

Occurs when a clot (thrombotic emboli) or other matter (nonthrombotic emboli) lodges in the pulmonary arterial system, disrupting the blood flow to a region of the lungs

Majority come form the deep leg veins, particularly the iliac, femoral, and popliteal veins

Other sources: RV, the upper extremities, and the pelvic veins

Nonthrombotic emboli: fat, tumors, amniotic fluid, air, and foreign bodies

ETIOLOGY

Three predisposing factors: hypercoagulability, injury to the vascular endothelium and venous stasis (Virchow’s triad)

Venous stasis: AF, decreased CO, immobility

Injury to the vascular endothelium: local vessel injury, infection, incision, atherosclerosis

Hypercoagulability: polycythemia