Which of the following signs and symptoms would indicate respiratory distress?

If someone around you displays signs of respiratory distress, will you know what to do? Before an emergency happens, plan for it.

Know the Signs of Respiratory Distress

Many people who suffer respiratory distress exhibit signs they’re having to work harder to breathe or not getting enough oxygen. Look out for these symptoms.

  • Increased breathing rateWhen people have trouble breathing, they may take more breaths per minute to compensate.

  • Nose flaringIf a person opens their nostrils wider with each breath, this could indicate he or she is having to work harder to breathe.

  • Color changesIf you see a bluish color around someone’s mouth, on the inside of their lips, or on the fingernails, he or she may not be getting enough oxygen. The color of the person’s face could also appear pale or gray.

  • GruntingSometimes, you may hear a person in respiratory distress make a grunting noise during each exhale. This sound is the body’s way of trying to keep air in the lungs.

  • SweatingVictims of respiratory distress may have sweat on their heads while their skin feels cool or clammy to the touch. This can happen when the breathing rate is very fast.

  • WheezingIf you hear a tight, whistling sound with each breath, this could indicate the air passages may be tighter than usual.

  • RetractionsA retraction is when a person’s chest appears to sink in under the breastbone or under the neck with each breath. This is one way the body brings more air into the lungs. It can also be seen under the rib cage or in the muscles between the ribs.

Know the Causes of Respiratory Distress

"Anything that causes lack of oxygen or impaired breathing can lead to respiratory distress. These include:

  • Asthma
  • COPD
  • Pneumonia or other lung infection
  • Pulmonary embolism
  • Collapsed lung
  • Lung cancer
  • Airway obstruction
  • Heart disease such as congestive heart failure
  • Severe allergic reaction
  • Nerve/muscle dysfunction that affects muscles used in breathing
  • Severe anemia
  • Poisoning or medication overdose
  • High altitudes."

-Dr. Irena Liang, primary care physician at Primary Care & Convenient Care - Baylor St. Luke’s Medical Group - The Woodlands, Texas

What to Do if Someone Stops Breathing

If you’re with someone who’s in respiratory distress, call 911 and a professional can assess the situation and recommend next steps. In general, you can plan on the following:

  • If the person is not making sounds, this indicates they are choking. In this instance, you can begin the Heimlich maneuver.

  • If the person is not choking but stops breathing or falls unconscious, begin administering CPR.

  • If you suspect anaphylaxis from allergies, administer epinephrine and head to the emergency room immediately.

  • If the person has a known breathing condition, help the victim take his or her prescribed inhaler or medication and head to the emergency room.

Preventing Severe Allergic & Asthmatic Attacks

“For an asthma attack, you should use your medications as prescribed. If you notice worsening of your symptoms, talk to your doctor about whether or not your medications can be optimized. Understand what triggers can worsen your asthma and try to avoid them. It is important to have an asthma ‘action plan’ and know where to go according to how bad your symptoms are (office vs. emergency room).

With allergic reactions, you need to understand that any medication or substance can potentially cause a severe allergic reaction. Know the signs of a severe allergic reaction. If you have a history of severe allergic reaction, ask your doctor about an EpiPen in case of emergency. Seek help earlier rather than later because allergic reactions can rapidly progress.”

-Dr. Irena Liang, primary care physician at Primary Care & Convenient Care - Baylor St. Luke’s Medical Group - The Woodlands, Texas

Recent Updates

Respiratory distress may be a result of disorders of the extrathoracic or intrathoracic airways (intrinsic or extrinsic compression-obstruction), alveoli, pulmonary vasculature, pleural spaces, or thorax.

From: Nelson Pediatric Symptom-Based Diagnosis, 2018

Respiratory Distress and Failure

Robert M. Kliegman MD, in Nelson Textbook of Pediatrics, 2020

Respiratory Failure

Respiratory failure occurs when oxygenation and ventilation are insufficient to meet the metabolic demands of the body. Respiratory failure may result from an abnormality in (1) lung and airways, (2) chest wall and muscles of breathing, or (3) central and peripheral chemoreceptors. Clinical manifestations depend largely on the site of pathology. Although respiratory failure is traditionally defined as respiratory dysfunction resulting in arterial partial pressure of oxygen (Pao2) <60 mm Hg when breathing room air and Paco2 >50 mm Hg resulting in acidosis, the patient's general state, respiratory effort, and potential for impending exhaustion are more important indicators than ABG values.

The Berlin definition of ARDS was once used to describe pediatric patients with ARDS, even though the pathophysiology is different between children and adults. The current pediatric definition differs in chest imaging findings, definition of oxygenation, consideration of both noninvasive and invasive mechanical ventilation, and consideration of special populations (Table 89.7 andFig. 89.1).

Pathophysiology

Respiratory failure can be classified intohypoxic respiratory failure (failure of oxygenation) andhypercarbic respiratory failure (failure of ventilation). Systemic venous (pulmonary arterial) blood is arterialized after equilibration with alveolar gas in the pulmonary capillaries and is carried back to the heart by pulmonary veins. The ABG is influenced by the composition of inspired gas, effectiveness of alveolar ventilation, pulmonary capillary perfusion, and diffusion capacity of the alveolar capillary membrane. Abnormality in any of these steps can result in respiratory failure.Hypoxic respiratory failure results from intrapulmonary shunting and venous admixture or insufficient diffusion of oxygen from alveoli into pulmonary capillaries. This physiology can be caused by small airways obstruction, increased barriers to diffusion (e.g., interstitial edema, fibrosis), and conditions in which alveoli are collapsed or filled with fluid (e.g., ARDS, pneumonia, atelectasis, pulmonary edema). In most cases, hypoxic respiratory failure is associated with decreased functional residual capacity and can be managed by lung volume recruitment with positive pressure ventilation.Hypercarbic respiratory failure is caused by decreased minute ventilation (i.e., tidal volume multiplied by respiratory rate). This physiology can result from centrally mediated disorders of respiratory drive, increased dead space ventilation, or obstructive airways disease.Hypoxic and hypercarbic respiratory failure may coexist as a combined failure of oxygenation and ventilation.

Ventilation-Perfusion Mismatch

For exchange of O2 and CO2 to occur, alveolar gas must be exposed to blood in pulmonary capillaries. Both ventilation and perfusion are lower in nondependent areas of the lung and higher in dependent areas. The difference in perfusion (Q̇) is greater than the difference in ventilation (V̇). Perfusion in excess of ventilation results in incomplete arterialization of systemic venous (pulmonary arterial) blood and is referred to asvenous admixture. Perfusion of unventilated areas is referred to asintrapulmonary shunting of systemic venous blood to systemic arterial circulation. Conversely, ventilation that is in excess of perfusion is wasted; that is, it does not contribute to gas exchange and is referred to asdead space ventilation. Dead space ventilation results in return of greater amounts of atmospheric gas (which has not participated in gas exchange and has negligible CO2) back to the atmosphere during exhalation. The respiratory dead space is divided into the anatomic dead space and the alveolar dead space. Theanatomic dead space includes the conducting airways from the nasopharynx to the terminal bronchioles, ends at the alveoli, and has no contact with the pulmonary capillary bed. Thealveolar dead space refers to areas of the lung where alveoli are ventilated but not perfused. Under normal conditions, this physiology usually occurs in West zone I, where alveolar pressure is greater than pulmonary capillary pressure. Under clinical conditions, this physiology may result from dynamic hyperinflation, high levels of positive end-expiratory pressure (PEEP), or large tidal volume in ventilated patients. Additionally, decreased pulmonary artery perfusion from pulmonary embolism or decreased cardiac output and hypovolemia can result in alveolar dead space. The end result is a decrease in mixed expired CO2 (Peco2) and an increase in the Paco2 – Peco2 gradient. Dead space as a fraction of tidal volume (Vd/Vt) is calculated as:

Normal Vd/Vt is approximately 0.33. Venous admixture and intrapulmonary shunting predominantly affect oxygenation, resulting in a alveolar oxygen (Pao2) to Pao2 (A-ao2) gradient without elevation in Paco2. This physiology is caused by greater ventilation of perfused areas, which is sufficient to normalize Paco2 but not Pao2 because of their respective dissociation curves. The relative straight-line relationship of the hemoglobin-CO2 dissociation allows for averaging of capillary Pco2 (Pcco2) from hyperventilated and hypoventilated areas. Because the association between oxygen tension and hemoglobin saturation plateaus with increasing Pao2, the decreased hemoglobin-O2 saturation in poorly ventilated areas cannot be compensated for by well-ventilated areas where hemoglobin-O2 saturation has already reached near-maximum. This physiology results in decreased arterial oxyhemoglobin saturation (Sao2) and Pao2. Elevation of Paco2 in such situations is indicative of coincident alveolar hypoventilation. Examples of diseases leading to venous admixture include asthma and aspiration pneumonia, and those of intrapulmonary shunt include lobar pneumonia and ARDS.

Respiratory Distress

Stanley F. Malamed DDS, ... Daniel L. OrrII DDS, MS (ANES), PHD, JD, MD, in Medical Emergencies in the Dental Office (Seventh Edition), 2015

Age

Respiratory distress in younger patients (under the age of 10) most commonly is related to asthma (usually allergic asthma). Hyperventilation and heart failure are significantly less common in this age group (children with severe, uncorrected, congenital heart defects may demonstrate respiratory distress, but their medical history will have provided the doctor with this information). Hyperventilation is more likely to be the cause of respiratory distress for individuals between 12 and 40 years of age. Asthma may also occur in this age group, but in most instances patients already know that they suffer from this condition. Clinically significant heart failure is rarely seen before the age of 40 years. The peak incidence of heart failure in men is between 50 and 60 years; in women, the peak falls between 60 and 70 years.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780323171229000159

Neonatology

Basil J. Zitelli MD, in Zitelli and Davis' Atlas of Pediatric Physical Diagnosis, 2018

Respiratory Distress

The differential diagnosis and subsequent management of the infant with respiratory distress are the most frequent challenges encountered by the practitioner of newborn medicine. Problems posed by prematurity, the failure of the necessary transition to extrauterine existence, infectious complications, metabolic derangements, and various congenital and acquired abnormalities of the cardiopulmonary system may all lead to a similar presentation in the newborn period.

Infants with respiratory distress may present with tachypnea or cyanosis, or both, and varying degrees of a triad of signs, which includegrunting, flaring, andretractions. Grunting is a characteristic involuntary guttural expiratory sound made by infants as they exhale against a closed glottis in an attempt to maintain expiratory lung volume.Flaring refers to the reflexive opening of the nares during inspiration.Retractions are the result of increased respiratory effort with high negative intrathoracic pressures leading to an inward collapse of the relatively compliant chest wall of the newborn during inspiration.

Classic respiratory distress syndrome (RDS) is caused by a combination of lung immaturity secondary to preterm delivery and surfactant deficiency. The radiographic findings (Fig. 2.43) in such infants consist of low lung volumes, a ground-glass appearance (small airway and alveolar atelectasis), and “air bronchograms” (an outline of the large airways superimposed on the relatively airless lung parenchyma). Infants with RDS usually need supplemental oxygen therapy and surfactant replacement and often require mechanical ventilatory assistance.

Most infants with RDS recover without sequelae. However, a small proportion develops a chronic lung condition known asbronchopulmonary dysplasia. Histologically, this condition is characterized by varying degrees of inflammation and fibrosis (Fig. 2.44), and the chest x-rays exhibit areas of hyperinflation alternating with atelectasis (Fig. 2.45).

The most common cause of respiratory distress in term infants is transient tachypnea of the newborn (TTN). Thought to be related to the delayed removal of fetal lung fluid, this condition is more common in infants born by cesarean section. Radiographic findings may include streaky perihilar shadows caused by dilated lymphatics or visible fluid densities within the intralobar fissures (Fig. 2.46), or both. As its name implies, TTN resolves within hours to days, usually with minimal supportive care.

Unfortunately for the clinician, the early clinical and radiographic findings in infants with potentially life-threatening congenital pneumonias may mimic those seen in RDS or TTN (Fig. 2.47). This diagnostic uncertainty leads to early treatment with antibiotics until bacterial cultures, serial chest radiographs, and clinical improvements reassure the practitioner that the discontinuation of such antibiotics is warranted.

Respiratory Distress

Anjali Sharma, in Nelson Pediatric Symptom-Based Diagnosis, 2018

Summary and Red Flags

Respiratory distress may be a result of disorders of the extrathoracic or intrathoracic airways (intrinsic or extrinsic compression-obstruction), alveoli, pulmonary vasculature, pleural spaces, or thorax. The distress may be secondary to respiratory, cardiovascular, hematologic, or central nervous system diseases. The most important aspect of the evaluation of a child with respiratory distress is observation of the child's breathing pattern and a brief, directed history and physical examination. Once the cause is identified, treatment should be started quickly to avoid progression to respiratory failure.

Red flags for impending respiratory failure include sudden onset of distress (epiglottitis, foreign body aspiration), hemoptysis, severe retractions, lethargy, a sitting up–leaning forward posture, dysphagia, drooling, or aphonia. It is imperative to identify the symptoms of impending respiratory failure and not delay treatment with unnecessary clinical or radiologic studies. Epiglottitis should be recognized quickly, and treatment initiated promptly. It is also important not to miss a foreign body, which with time may produce chronic respiratory disease that is often confused with pneumonia or asthma.

Signs of a more chronic process include lack of resolution with normal therapy, chronicity of symptoms, positive family history, digital clubbing, weight loss, and/or failure to thrive. These signs should prompt further work-up and consultation with a pulmonary specialist as needed. Asthma will rarely cause digital clubbing, so its presence should raise concern for another primary lung disease process.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780323399562000030

Cyanotic Congenital Heart Disease : Evaluation of the Critically Ill Neonate With Cyanosis and Respiratory Distress

Robert M. Kliegman MD, in Nelson Textbook of Pediatrics, 2020

Differential Diagnosis

Thehyperoxia test is one method of distinguishing cyanotic CHD from pulmonary disease. Neonates with cyanotic CHD usually are unable to significantly raise their arterial blood partial pressure of oxygen (Pao2) during administration of 100% oxygen. This test is usually performed using a hood rather than nasal cannula or face mask, to best guarantee delivery of almost 100% oxygen to the patient. False-positive tests can occur if this is not done correctly. If the Pao2 rises above 150 mm Hg during 100% oxygen administration, an intracardiac right-to-left shunt can usually be excluded. This is not 100% confirmative, however, because some patients with cyanotic CHD may be able to increase their Pao2 to >150 mm Hg because of favorable intracardiac streaming patterns. In patients with pulmonary disease, Pao2 generally increases significantly with 100% oxygen as ventilation-perfusion inequalities are overcome. In infants with cyanosis from a central nervous system disorder, the Pao2 usually normalizes completely during artificial ventilation. Hypoxia in many heart lesions is profound and constant, whereas in respiratory disorders and in PPHN, Pao2 often varies with time or changes in ventilator management. Hyperventilation may improve the hypoxia in neonates with PPHN and only occasionally in those with cyanotic CHD.

Although a significant heart murmur usually suggests a cardiac basis for the cyanosis, several of the more severe cardiac defects (e.g., transposition of the great vessels) may not initially be associated with a murmur. The chest radiograph may be helpful in the differentiation of pulmonary and cardiac disease; in the latter, it indicates whether pulmonary blood flow is increased, normal, or decreased (Fig. 456.1).

Two-dimensional echocardiography with Doppler is the definitive noninvasive test to determine the presence of CHD. Cardiac catheterization is less often used for diagnostic purposes and is usually performed to examine structures that are sometime less well visualized by echocardiography, such as distal branch pulmonary arteries or aortopulmonary collateral arteries in patients with tetralogy of Fallot with pulmonary atresia (seeChapter 457.2), or coronary arteries and right ventricular sinusoids in patients with pulmonary atresia and intact ventricular septum (seeChapter 457.3). If echocardiography is not immediately available to confirm a diagnosis of cyanotic CHD, the clinician caring for a newborn with possible cyanotic CHD should not hesitate to start a prostaglandin infusion (for a possible ductal-dependent lesion). Because of the risk of hypoventilation associated with prostaglandins, a practitioner skilled in neonatal endotracheal intubation must be available.

Respiratory Distress

Stanley F. Malamed DDS, ... Daniel L. OrrII DDS, MS (ANES), PHD, JD, MD, in Medical Emergencies in the Dental Office (Seventh Edition), 2015

Management

Definitive management of respiratory distress depends on the doctor’s prompt recognition of the problem and a determination of its probable cause (Box 10-2). This chapter focuses on the basic steps common to the management of most cases of respiratory distress.

Step 1: recognition of respiratory distress

Many respiratory disorders are associated with characteristic sounds, such as the wheezing of bronchospasm and the cough and crackling respirations (rales) of pulmonary edema. By contrast, hyperventilation does not usually produce a characteristic sound; however, hyperventilating patients appear—and actually are—acutely anxious and unable to control their rate of breathing.

Step 2: discontinue dental procedure

Dental treatment should cease as soon as respiratory distress is recognized. Because stress is a primary precipitating factor in most respiratory-related situations, cessation of treatment may improve the patient’s clinical signs and symptoms significantly.

Step 3: P position the patient

In conscious patients experiencing respiratory distress, positioning is based on the comfort of the patient. In the presence of near-normal or slightly elevated blood pressure (as is almost always the case in situations of respiratory distress), most persons feel more in control of their breathing in an upright (sitting or standing) position. However, patients can be maintained in this position only as long as they remain conscious.

Step 4: C → A → B (circulation-airway-breathing), basic life support, as needed

Patients in respiratory distress often experience two major problems—primary breathing difficulty initially induced by their fear of dentistry and the added problem of increased anxiety produced by their inability to breathe normally. In the unlikely event that respiratory distress leads to unconsciousness, the patient must be placed immediately into the supine position and the steps in the management of unconsciousness followed.

Step 5: D (definitive care)

Response of the victim to the steps of basic life support determines additional management.

Step 5a: monitoring of vital signs

The individual’s blood pressure, heart rate (pulse), and respiratory rate should be monitored at frequent intervals (at least every 5 minutes) throughout the episode and recorded in a permanent record.

Step 5b: definitive management of anxiety

The doctor should keep the patient as comfortable as possible and begin to manage anxiety by speaking calmly but firmly to the patient. The patient’s collar or other tight garments (that might restrict breathing) may be loosened, enabling the patient to breathe more easily (even if the “ease” in breathing is purely psychological).

Step 5c: definitive management of respiratory distress

After assessing the patient’s cardiovascular status, the doctor may begin to manage the cause of the patient’s breathing problem. (The following chapters will focus in large part on such management procedures and on the most common causes of respiratory distress.)

Step 5d: activate emergency medical services, as needed

At any time during the episode of respiratory distress, the doctor may activate emergency medical services, if indicated.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B978032317122900010X

Respiratory Distress

Juliann Lipps Kim, in Comprehensive Pediatric Hospital Medicine, 2007

INITIAL STABILIZATION

The first priority in evaluating a child with respiratory distress is to assess the airway, breathing, and circulation (ABCs). Rapid assessment and intervention can prevent the progression from respiratory compromise to respiratory failure. To assess the airway, determine whether it is patent, stable, and maintainable. If not, such an airway must be established (e.g., repositioning, instrumentation). Once these three criteria are met, the breathing process is evaluated by determining the respiratory rate, oxygen saturation, adequacy of breath sounds, and quality of respiratory effort (e.g., labored, use of accessory muscles). Determination of arterial blood gas levels may be needed if there is evidence of respiratory insufficiency or failure. If spontaneous ventilation is inadequate, assisted breathing with positive pressure, initially via a bag-mask device, is indicated. Assessment of the patient's circulation and mental status are other key aspects of the initial evaluation. Based on this rapid assessment, the clinician obtains information about the severity of the patient's condition and how rapidly interventions must be performed.

Providing supplemental oxygen is an important first step for a child presenting in distress, especially with hypoxemia demonstrated by oximetry. Oxygen can be delivered by multiple devices, and the choice depends on the child's clinical status and oxygen needs (see Chapter 38). Some of these devices can agitate a child further, worsening respiratory compromise. Allow the child to remain with the parent as much as possible, and use the least noxious form of oxygen delivery necessary. In a small number of children, airway adjuncts such as a nasopharyngeal airway, oropharyngeal airway, or assisted ventilation are needed. An oropharyngeal airway holds the tongue forward to prevent airway obstruction, so it will not be tolerated in a conscious or semiconscious patient with an intact gag reflex, and it may induce vomiting. A nasopharyngeal airway can be used in a conscious or unconscious patient but should be avoided in those with facial trauma. Continuous positive airway pressure may assist inspiratory efforts as well as provide positive end-expiratory pressure (PEEP). PEEP provides resistance to expiration, which may help expand atelectatic portions of the lung and thereby reduce ventilation-perfusion mismatch. Bilevel positive airway pressure provides inspiratory and expiratory pressure via a firmly fitting facemask, which may be uncomfortable and not well tolerated in infants or young children (see Chapter 209).

Careful reevaluation after every intervention is critical to the care of a child with respiratory compromise. This confirms proper application of the intervention and monitors the patient's response.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780323030045500491

Malaria

Arjen M. Dondorp, Lorenz Von Seidlein, in Infectious Diseases (Fourth Edition), 2017

Respiratory Distress

Respiratory distress manifesting as deep breathing or tachypnea is associated with poor outcome in children with severe malaria.44 There may be intercostal recession, use of the accessory muscles of respiration and flaring of the alae nasi. Respiratory distress is often present as respiratory compensation for a profound metabolic acidosis, but can also be caused by the presence of severe anemia or a concomitant lung infection. Pulmonary edema is rare in children. Respiratory depression can be caused by an overuse of anticonvulsants, particularly phenobarbital in combination with benzodiazepines. Identification of these different causes of respiratory distress is important as each requires a different treatment modality.

In adults with severe falciparum malaria, but occasionally in severe vivax infections, ARDS with increased pulmonary capillary permeability can develop, which has a high mortality rate. Pregnant women are especially prone to this complication. Overhydration aggravates the condition, but is not the cause of the respiratory distress; the pulmonary capillary wedge pressure is usually normal.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780702062858001179

Medical and Surgical Interventions for Respiratory Distress and Airway Management

Jonathan F. Bean MD, ... Namasivayam Ambalavanan MBBS, MD, in Assisted Ventilation of the Neonate (Sixth Edition), 2017

Surgical Management of the Neonatal Airway

Respiratory distress in the neonate has a variety of causes (Box 36-1), and pediatric surgeons and otolaryngologists are increasingly becoming involved in the care of these patients. The ability to intubate, mechanically ventilate, and thereby prolong the lives of children with neonatal asphyxia, congenital anomalies, or other causes of respiratory distress redefines the role of the surgeon as part of the neonatal management team.

The role of the surgeon is twofold: (1) as a diagnostician and therapist for those infants who manifest respiratory distress from an anatomic problem or who present with congenital airway obstruction (i.e., congenital stridor [Box 36-2]) and (2) as a consultant for neonates undergoing medical treatment requiring long-term intubation of their airways.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780323390064000363

Chest and Abdominal Trauma

Peggy Tseng MD, Emily Rose MD, FAAP, FAAEM, FACEP, in Urgent Care Medicine Secrets, 2018

10 What are the red flag physical exam findings after chest and abdominal trauma?

Respiratory distress in a child after trauma is a red flag for serious injury and potential for decompensation. Chest pain with neck discomfort is concerning for mediastinal free air; and distended neck veins are associated with pericardial tamponade. Children should be transferred to the emergency department for further evaluation with any abnormalities of lung auscultation, respiratory rate, chest rise pattern, and oxygen saturation.

In abdominal trauma, focal tenderness, distension, vomiting, and bruising are red flags for injury. Any sign of rigidity or rebound tenderness is a late finding and concerning for severe abdominal injury.

Read full chapter

URL: https://www.sciencedirect.com/science/article/pii/B9780323462150000276

Which is the major symptom of respiratory distress syndrome?

The first symptom of ARDS is usually shortness of breath. Other symptoms of ARDS are low blood oxygen, rapid breathing, and clicking, bubbling, or rattling sounds in the lungs when breathing. ARDS can develop at any age.

What are 5 causes of respiratory distress?

Causes.
Sepsis. The most common cause of ARDS is sepsis, a serious and widespread infection of the bloodstream..
Inhalation of harmful substances. ... .
Severe pneumonia. ... .
Head, chest or other major injury. ... .
Coronavirus disease 2019 (COVID-19). ... .
Others..

Which of the following signs indicate respiratory failure?

Symptoms include shortness of breath or feeling like you can't get enough air, extreme tiredness, an inability to exercise as you did before, and sleepiness.

Which of the following signs is indicative of respiratory distress in infants?

Signs and Symptoms Fast breathing very soon after birth. Grunting “ugh” sound with each breath. Changes in color of lips, fingers and toes. Widening (flaring) of the nostrils with each breath.