17R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach, DOI 10.1007/978-81-322-0535-7_2, © Springer India 2012

Case scenario 1

A 30-year-old male patient presented with acute onset of breathlessness, dry cough, fever, myalgia, and malaise for 4 days. On examination, he was found to be febrile and restless, with respiratory rate of 46/min and pulse rate of 124/min. His oxygen saturation was 80% on room air, and chest skiagram showed bilateral parenchymal in fi ltrate.

Case scenario 2

A 60-year-old male patient with chronic obstructive airway disease presented with increasing shortness of breath, cough, and expectoration for 5 days and drowsiness with confusion for 1 day. On examination, he was found to be drowsy, cyanosed with respiratory rate of 30/min, tachycardia, and fl apping tremors. His oxygen saturation was 80% on initial evaluation, and a chest radiograph showed hyperin fl ated lung fi elds and right lower zone in fi ltrates.

Case scenario 3

A 30-year-old female patient with anxiety disorder presented to the emergency department in a comatosed condition with history of ingestion of some unknown tablets. On examination, she was found to be E2M4V1, with pulse rate of 64/min, respiratory rate of 14/min, and blood pressure of 90/60 mmHg.

R. Guleria , M.D., D.M. (*) • J. Kumar , M.D. Department of Pulmonary Medicine , All India Institute of Medical Sciences , New Delhi , India e-mail: randeepg@hotmail.com

2 Acute Respiratory Failure

Randeep Guleria and Jaya Kumar

18 R. Guleria and J. Kumar

Acute respiratory failure results from the failure of respiratory system in one or both of its gas exchange functions—oxygenation and carbon dioxide elimination. It is a major cause of morbidity and mortality in intensive care units (ICUs). There are two types—type 1 hypoxic respiratory failure and type 2 hypercapnic respiratory failure.

Step 1: Initiate cardiopulmonary resuscitation All patients should be resuscitated as mentioned in Chap. 78 .

• Airway : In all patients with altered sensorium, a secure airway should be the fi rst priority. This includes clearing the upper airway and keeping it patent. If the patient cannot maintain an airway, endotracheal intubation should be performed to keep the airway patent. • Breathing : Once the airway is patent, the breathing has to be assessed. If it does not result in adequate gas exchange, oxygen supplementation and assisted venti-lation may be required. • Circulation : An intravenous access should be established and intravenous fl uids should be started.

Step 2: Clinical assessment including history and detailed physical examination Take appropriate history and do detailed examination to distinguish whether the • etiology is pulmonary or extrapulmonary and to know whether it is type 1 or type 2 respiratory failure (Tables 2.1 and 2.2 ). Assess the severity and fi nd out the underlying cause and/or precipitating cause. Speci fi c focus should be on the following:

A detailed respiratory system and neurological assessment. – Look for clinical features of hypoxia and hypercapnia (Tables – 2.1 and 2.2 ). Signs of pulmonary hypertension and right ventricular failure. – Clinical features of drug overdose. – Chest wall deformity, obesity. –

Step 3: Check pulse oximetry and do arterial blood gas analysis Pulse oximetry and arterial blood gases are the mainstay of diagnosis and essential to decide on the therapeutic intervention.

Oximetry is a rapid technique to know if there is signi fi cant hypoxia, but it gives • no clue about the presence or absence of hypercapnia. Also, the severity of hypoxia on pulse oximetery should be interpreted cautiously if the patient is already on oxygen.

Restlessness, anxiety Irritability, impaired intellectual functioning, and consciousness Cyanosis Tachycardia, hypertension Bradycardia, arrhythmia Shock, hypotension Convulsions, coma, death

Table 2.1 Hypoxia-related clinical features

192 Acute Respiratory Failure

Arterial blood gas analysis is essential for both diagnostic and therapeutic • decisions.

Type 1 respiratory failure is recognized by hypoxemia (PaO –2 < 60 mmHg).

With or without widening of alveolar-arterial oxygen gradient, PaCO 2 is either

low or normal. Type 2 respiratory failure is diagnosed when a PaO –

2 of less than 60 mmHg is

associated with a PaCO 2 of more than 45 mmHg and respiratory acidosis.

This needs to be followed by an assessment of the pH and HCO • 3 to decide

whether the type 2 respiratory failure is acute, acute on chronic, or chronic. Type II acute respiratory failure presents with low pH, high PaCO •

2 , and normal

HCO 3 ; acute on chronic presents with low pH, high PaCO

2 , and high HCO

3 ;

while chronic respiratory failure presents with normal pH along with raised PaCO

2 and HCO

3 .

This should be followed by an assessment of alveolar-arterial oxygen gradient, • which helps to narrow down the cause of respiratory failure (see appendix 2).

2 2 2PaO PiO PaCO / R= -

Step 4: Differentiate between type 1 and type 2 respiratory failures Type 1 respiratory failure occurs when the gas exchange is inadequate at rest or dur-ing exercise, leading to hypoxemia, and PaO

2 is less than 60 mmHg (Table 2.3 ).

Type 2 respiratory failure occurs as a result of alveolar hypoventilation, which can be due to a pulmonary or extrapulmonary cause. Chronic obstructive pulmo-nary disease is the commonest cause of type 2 respiratory failure, but various other conditions listed below can also lead to hypercapnia and respiratory failure (Table 2.4 ).

An approach to a patient with acute hypoxemic respiratory failure is summarized in Fig. 2.1 .

Step 5: Send investigations Complete hemogram and biochemistry • Lung function tests (if possible) that helps to differentiate between obstructive, • restrictive, and mixed ventilatory defects Chest radiograph that may help to identify hyperin fl ation, pulmonary edema, • pneumonia, pneumothorax, neoplasm and others to give a clue to the underlying etiology Electrocardiogram to identify cardiac disorders •

Headache Drowsiness, confusion Warm extremities, fl ushing, sweating Bounding pulse, tachycardia Tremors, myoclonic jerks, asterixis, seizures Papilledema, coma

Table 2.2 Hypercapnia-related clinical features

20 R. Guleria and J. Kumar

Computed tomography (CT) or magnetic resonance imaging (MRI) if indicated • for interstitial lung disease, neoplasm, stroke, and other neurological disorders Two-dimensional echocardiography for identi fi cation of cor pulmonale, intracar-• diac shunt, patent ductus arteriosus, and pulmonary embolism

Step 6: Initiate speci fi c treatment The primary aim is to maintain oxygenation and adequate alveolar ventilation and treatment for the underlying etiology. The key principles in the management of respiratory failure are as follows:

Optimized oxygen therapy • Identi fi cation of the underlying cause and adequate treatment for the same • Clinical assessment and arterial blood gases to help decide the severity • Treatment for any precipitating cause • Appropriate pharmacological treatment • Ventilatory support—noninvasive and invasive • Oxygen therapy (see Chap. 14 )

Table 2.3 Causes of hypoxemic respiratory failure

1. Ventilation/perfusion mismatch Airways disease

Chronic obstructive pulmonary disease Asthma Cystic fi brosis Bronchiolitis obliterans

Alveolar fi lling Cardiogenic Pulmonary edema Mitral valve stenosis Acute respiratory distress syndrome Pneumonia Alveolar hemorrhage Partial atelectasis Alveolar proteinosis Transfusion related acute lung injury (TRALI) Acute interstitial pneumonia Cryptogenic organizing pneumonia Aspiration, near-drowning Pulmonary vascular disease—thromboembolism, fat embolism

2. Shunt Alveolar fi lling—see the above causes Atelectasis Intrapulmonary shunts—pulmonary AVM (Arterio Venous Malformation) Intracardiac shunt—PFO, ASD, VSD

3. Hypoventilation—refer to type 2 respiratory failure for causes of hypoventilation 4. Low inspired pressure of oxygen—high altitude

212 Acute Respiratory Failure

The primary goal is to correct the hypoxemia to maintain adequate tissue • oxygenation. Oxygen has to be given cautiously with monitoring as uncontrolled high- fl ow • oxygen can lead to respiratory depression and worsening hypercapnia in type 2 respiratory failure. Oxygen saturation around 90% should be maintained.

Table 2.4 Causes of type 2 respiratory failure

Central nervous system depression/decreased ventilatory drive Respiratory center (medulla) dysfunction Drug overdose Hypothyroidism Sleep apnea Central nervous system (CNS) causes— stroke, tumor Neuromuscular diseases Guillain–Barré syndrome Poliomyelitis Myasthenia gravis Amyotrophic lateral sclerosis Cervical cord lesions Polyneuropathies Muscle diseases like muscular dystrophy, polymyositis Chest wall/pleural diseases Kyphoscoliosis Morbid obesity Pneumothorax

V/Q mismatch

Yes

improvement with supplemental oxygen

Shunt

No

Increased A-agradient

High PaCo2

Hypoventilation

Yes

Normal A-a gradient

Low inspired O2

No

Hypoxemicrespiratory failure

Fig. 2.1 An approach to hypoxemic respiratory failure to know the etiology

22 R. Guleria and J. Kumar

Supplemental oxygen can be provided through nasal prongs at a fl ow rate of • 1–3 L/min or through a Venturi mask to deliver 24–28% oxygen in hypercapnic failure. Nasal prongs are better tolerated but provide less predictable oxygen concentra-• tion in comparison to the Venturi mask. The aim is to maintain oxygen saturation above 90%, PaO •

2 more than 60 mmHg,

and pH more than 7.35. Assisted ventilation Assisted ventilation, either noninvasive or invasive, is indicated if there is clini-• cal deterioration or if respiratory acidosis persists despite optimum oxygen and medical therapy. Refer to speci fi c Chaps. 3 and 4 for further details.

Step 7: Further management Optimum treatment for the underlying etiology must be undertaken simultaneously. •

Suggested Reading

1. Epstein SK. Acute respiratory failure. In: Bope ET, Kellerman R, Rakel RE, editors. Conn’s current therapy 2011. 1st ed. Philadelphia: Elsevier Saunders, Section 4; 2011. p. 233–8.

This chapter discusses causes and treatment strategies for acute respiratory failure. 2. Goldman L. Goldman’s Cecil medicine. 24th ed. Philadelphia: Elsevier Saunders, Chapter 104;

2011. p. 629–38. This chapter discusses the physiology and algorithmic approach for acute respiratory failure. 3. Yeow ME, Santanilla JI. Non-invasive positive pressure ventilation in the emergency depart-

ment. Emerg Med Clin North Am. 2008; 26:835–47. 4. Lellouche F. Non-invasive ventilation in patients with hypoxemic acute respiratory failure. Curr

Opin Crit Care. 2007;13(1):12–9. This article discusses the role of noninvasive ventilation in management of acute respiratory

failure. 5. Baudouin S, Blumenthal S, Cooper B, et al. Role of non-invasive ventilation in management of

acute respiratory failure in emergency department. Thorax. 2002;57:192–211. BTS standards of care committee—noninvasive ventilation in acute respiratory failure.