Episodes of acute respiratory failure.
The experience of dyspnea derives from interactions among multiple physiologic, psychologic, social, and environmental factors.
Pleural pain is common with pulmonary infarction caused by pulmonary embolism.
Shock and severe cerebral hypoxia.
Dyspnea is a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity.
Laughing or coughing makes pleural pain worse.
Inflammation of the costochondral junction (costochondritis) can cause chest wall pain.
Alterations in pulmonary mechanics or in the neurologic control of breathing.
Inadequate alveolar ventilation.
The amount of oxygen in the alveoli is called the Pao2.
Pulmonary disease is often classified as acute or chronic, obstructive or restrictive, and infectious or noninfectious.
Pleural pain is usually localized to a portion of the chest wall.
Small tidal volumes and rapid ventilatory rate (tachypnea).
Hypoventilation is often overlooked because breathing pattern and ventilatory rate may appear normal.
Other signs and symptoms include abnormal sputum, hemoptysis, altered breathing patterns, hypoventilation and hyperventilation, cyanosis, clubbing of the digits, and chest pain.
A pleural friction rub may be heard over the painful area.
Disorders such as pulmonary fibrosis that stiffen the lungs or chest wall and decrease compliance.
It is important to obtain blood gas analysis to determine the severity of hypercapnia.
Hypoxia is reduced oxygenation of cells in tissues.
CO2 is removed at a faster rate than it is produced, resulting in hypocapnia.
Smokers.
Loosening secretions.
The effects of inflammatory cytokines and growth factors.
Diagnosis of chest restriction is made by pulmonary function testing (reduction in forced vital capacity [FVC]), arterial blood gas measurement (hypercapnia), and radiographs.
Approximately 10% of individuals with primary pneumothorax have a significant family history linked to mutations in the folliculin gene (Birt-Hogg-Dubé syndrome).
An abnormal distribution of ventilation and perfusion.
A pulmonary embolus that impairs blood flow to a segment of the lung.
Abnormal thickness, as occurs with edema and fibrosis.
Asthma and chronic obstructive pulmonary disease.
Hypercapnia is caused by hypoventilation of the alveoli.
PaCO2 greater than 44 mmHg.
Inadequate exchange of oxygen between the alveoli and the capillaries.
The FiO2 of air at sea level is approximately 21% or 0.21.
Hypoxemia caused by hypoventilation can be corrected by improving alveolar ventilation through increases in the rate and depth of breathing.
Supplemental oxygen.
Bronchiectasis, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease.
Exertion or when recumbent.
Restriction of the chest wall or impairment of pulmonary function.
Structural and mechanical changes that impair the ability of the chest to expand normally.
The alveolocapillary barrier.
Hypercapnia and respiratory acidosis.
Edema, fibrosis, and emphysema.
The first episode of dyspnea that commonly occurs with exercise.
Opiates and serotonergic agents.
Usually bright red, has an alkaline pH, and is mixed with frothy sputum.
Strenuous exercise or metabolic acidosis.
Common causes of chest wall pain are rib fractures and excessive coughing.
Inadequate alveolar ventilation in relation to metabolic demands.
An increase in hydrogen ion in the blood due to hypercapnia.
Supplemental oxygen therapy.
If the FiO2 decreases, the Pao2 decreases.
Decreased arterial oxygenation from pulmonary diseases or pulmonary or cardiac right-to-left shunts.
Severe anemia and carbon monoxide poisoning.
Tidal volume, resulting in hypercapnia.
Lower respiratory tract infections.
People with neurologic, muscular, or bone diseases that restrict chest expansion and individuals who have COPD.
Flail chest.
Pneumothorax is diagnosed with chest radiographs, ultrasound, and CT.
Transudative effusion is watery fluid that diffuses out of the capillaries due to disorders that increase intravascular hydrostatic pressure or decrease capillary oncotic pressure. Exudative effusion is less watery and contains high concentrations of white blood cells and plasma proteins, occurring in response to inflammation, infection, or malignancy.
Cyanosis, confusion, tachycardia, edema, and decreased renal output.
Diffuse or focal disturbances of ventilation, gas exchange, or ventilation-perfusion relationships, increased work of breathing, or diseases that damage lung tissue (lung parenchyma).
By sitting in a forward-leaning posture or supporting the upper body on several pillows.
Cough that has persisted for more than 3 weeks, although some researchers suggest 7 or 8 weeks as a more appropriate timeframe.
Cancer and pulmonary infarction.
Dyspnea may induce secondary physiologic and behavioral responses.
Pulmonary pain can be central chest pain that is pronounced after coughing.
Sighing respirations consist of irregular breathing characterized by frequent, deep sighing inspirations, often caused by anxiety.
Ventilatory support, such as with a bag-valve mask, noninvasive positive pressure ventilation, or intubation and placement on mechanical ventilation.
The Pao2 is dependent on the presence of adequate oxygen content of the inspired air and the amount of alveolar minute ventilation.
Limited cardiac reserve, chronic renal failure, chronic hepatic disease, and infection.
The selective bulbous enlargement of the end (distal segment) of a digit (finger or toe).
The work of breathing is increased and ventilation may be compromised due to a decrease in tidal volume.
Pneumothorax is the presence of air or gas in the pleural space caused by a rupture in the visceral pleura or the parietal pleura and chest wall.
Chest expansion because of pain.
Clinical manifestations of spontaneous or secondary pneumothorax begin with sudden pleural pain, tachypnea, and possibly mild dyspnea. Manifestations depend on the size of the pneumothorax.
Tension pneumothorax may be complicated by severe hypoxemia, tracheal deviation away from the affected lung, and hypotension.
Decreased tidal volume.
Exudative effusion occurs in response to inflammation, infection, or malignancy and involves inflammatory processes that increase capillary permeability.
High altitude, low oxygen content of gas mixture, and enclosed breathing spaces (suffocation).
Supercostal retractions.
Skillful and knowledgeable care plays a major role in decreasing respiratory morbidity and mortality.
The most common signs and symptoms of pulmonary disease are dyspnea and cough.
High blood pressure in the pulmonary circulation (pulmonary hypertension) can cause pain during exercise.
Any condition that slows blood flow to the brainstem or neurologic impairment above the brainstem.
Hypoxemia is reduced oxygenation of arterial blood.
Alveolar ventilation that exceeds metabolic demands.
Procedures involving the central nervous system, thorax, or upper abdomen.
Poor circulation resulting from intense peripheral vasoconstriction.
Many conditions.
Dyspnea on exertion that can progress to respiratory failure.
Primary (spontaneous) pneumothorax occurs unexpectedly in healthy individuals, usually men between ages 20 and 40 years, and is most often caused by the spontaneous rupture of blebs on the visceral pleura.
0.8 to 0.9.
Pneumothorax is treated with the insertion of a chest tube attached to a water-seal drainage system with suction. After the pneumothorax is evacuated and the pleural rupture is healed, the chest tube is removed.
The source of the fluid in pleural effusion is usually blood vessels or lymphatic vessels lying beneath either pleura, but occasionally an abscess or other lesion may drain into the pleural space.
Organ infarction.
Intracardiac defects and intrapulmonary arteriovenous malformations.
Dyspnea that occurs when an individual lies flat and is common in individuals with heart failure.
Cough that resolves within 2 to 3 weeks of the onset of illness or with treatment of the underlying condition.
Dark, has an acidic pH, and is mixed with food particles.
A slightly increased ventilatory rate, very large tidal volume, and no expiratory pause.
A clinician with a clear understanding of the pathophysiology of common respiratory problems can greatly affect the outcome for each individual.
Dyspnea is often described as breathlessness, air hunger, shortness of breath, increased work of breathing, chest tightness, and preoccupation with breathing.
Pleural pain emanates from the area around the infarction.
Chest wall pain can often be reproduced by pressing on the sternum or ribs.
Hypoxemia can lead to tissue hypoxia.
PaCO2 less than 36 mmHg.
Hypoventilation results in an increase in Paco2 and a decrease in Pao2.
Antibiotics.
Pleural pain, which is usually sharp or stabbing in character.
Ankylosing spondylitis and pectus excavatum.
Secondary (traumatic) pneumothorax can be caused by chest trauma, such as a rib fracture, stab or bullet wounds, or a surgical procedure that tears the pleura; rupture of a bleb or bulla as occurs in COPD; or mechanical ventilation, particularly if it includes positive end-expiratory pressure (PEEP).
Low V/Q, also known as shunting.
An area where alveoli are ventilated but not perfused.
Destruction of alveoli, such as that which occurs in emphysema.
Children or adults who are thin and have poorly developed thoracic musculature.
The depth of the inspiration and the degree to which the airways narrow, increasing the velocity of expiratory gas flow.
The coughing up of blood or bloody secretions.
The rate, depth, regularity, and effort of breathing.
The severity of the experience of dyspnea may not directly correlate with the severity of underlying disease.
Central chest pain can be difficult to differentiate from cardiac pain.
Alternating periods of deep and shallow breathing with apnea lasting 15 to 60 seconds followed by ventilations that increase in volume until a peak is reached, then decrease again to apnea.
Hypercapnia and the associated respiratory acidosis can result in electrolyte abnormalities, dysrhythmias, somnolence, coma, and secondary hypoxemia.
Tissue hypoxia can result from low cardiac output or cyanide poisoning.
A condition resulting from hypocapnia that can interfere with tissue function.
Atelectasis, pneumonia, pulmonary edema, and pulmonary emboli.
Conventional mechanical ventilation, high-frequency ventilation, or extracorporeal membrane oxygenation.
Infection and inflammation of the parietal pleura (pleuritis or pleurisy).
Pain from chest wall injury, surgery, or disease.
An abnormal ventilation-perfusion ratio (V/Q).
The unstable portion of the chest wall moves inward.
Pain, dyspnea, unequal chest expansion, hypoventilation, and hypoxemia.
Pleural effusion is the presence of fluid in the pleural space.
Because carbon dioxide diffuses so easily from capillary to alveolus that the individual with impaired diffusion would die from hypoxemia before hypercapnia could occur.
Lack of neurologic stimulation of the respiratory center (oversedation, drug overdose, neurologic damage), defects in chest wall mechanics (neuromuscular disease, trauma, chest deformity, air trapping), large airway obstruction (laryngospasm, foreign body aspiration, neoplasm), and increased work of breathing (emphysema, severe asthma).
Subcostal and intercostal retractions.
In the most distal bronchi and the alveoli.
Changes in the amount, consistency, color, and odor of sputum.
A short expiratory pause.
Dyspnea may be the result of pulmonary disease or many other conditions, such as pain, heart disease, trauma, and anxiety.
Pleural pain occurs during inspiration.
Effort, prolonged inspiration or expiration, stridor, and audible wheezing are typical symptoms.
Hypercapnia is an increased CO2 concentration in the arterial blood.
CO2 removal does not keep up with CO2 production, causing hypercapnia.
Somnolence or disorientation.
Respiratory failure.
When 5 g of hemoglobin is desaturated, regardless of hemoglobin concentration.
The degree of ventilatory impairment.
When air separates the visceral and parietal pleurae, it destroys the negative pressure of the pleural space, disrupting the equilibrium between the elastic recoil forces of the lung and chest wall.
Iatrogenic pneumothorax is most commonly caused by transthoracic needle aspiration.
Atelectasis, asthma due to bronchoconstriction, pulmonary edema, and pneumonia.
High V/Q, resulting in wasted ventilation.
An increase in respiratory rate.
Compensatory hyperventilation and resultant respiratory alkalosis.
Asthma, chronic bronchitis, pneumonia, acute respiratory distress syndrome, atelectasis, and pulmonary embolism.
By the use of ordinal rating scales or visual analog scales.
Centrally through the vagus nerve.
The vomiting of blood.
To minimize the work of respiratory muscles.
Causes of hypercapnia include depression of the respiratory center by drugs, diseases of the medulla, abnormalities of the spinal conducting pathways, diseases of the neuromuscular junction or respiratory muscles, thoracic cage abnormalities, large airway obstruction, and increased work of breathing or physiologic dead space.
Through blood gas analysis revealing hypercapnia.
Both ventilatory support and supplemental oxygen therapy.
A bluish discoloration of the skin and mucous membranes caused by increasing amounts of desaturated or reduced hemoglobin in the blood.
Immediate feedback about tidal volumes, encouraging deep breathing.
In the pleurae, airways, or chest wall.
Treatment for chest restriction is aimed at any reversible underlying cause, but is otherwise supportive. In severe cases, mechanical ventilation may be indicated.
Two factors: the balance between the amount of air getting into alveoli (V) and the amount of blood perfusing the capillaries around the alveoli (Q).
Instability of a portion of the chest wall, causing paradoxical movement of the chest with breathing.
Right-to-left shunt occurs, resulting in decreased systemic PaO2 and hypoxemia.
Transudative effusion is caused by disorders that increase intravascular hydrostatic pressure or decrease capillary oncotic pressure, such as congestive heart failure and liver or kidney disorders that cause hypoproteinemia.
As inadequate gas exchange, that is, hypoxemia (PaO2 ≤ 50 mmHg) or hypercapnia (PaCO2 ≥ 50 mmHg with a pH ≤ 7.25).
Mechanoreceptors (stretch receptors, irritant receptors, and J-receptors), upper airway receptors, and central and peripheral chemoreceptors.
A protective reflex that helps clear the airways by an explosive expiration.
Chronic bronchitis, although lung cancer must always be considered.
Bronchoscopy, combined with chest computed tomography (CT).
The major mechanisms of oxygenation that can cause hypoxemia if problematic are oxygen delivery to the alveoli, ventilation of the alveoli, diffusion of oxygen from the alveoli into the blood, and perfusion of pulmonary capillaries.
Severe anxiety, acute head injury, and conditions causing insufficient oxygenation of the blood.
Frequent turning and position changes, deep breathing exercises, and early ambulation.
It is rarely reversible with treatment of the underlying pulmonary condition.
Many individuals with chest restriction will eventually progress to hypercapnic respiratory failure.
Hypoventilation and hypercapnia, inability to remove secretions, and hypoxemia.
In open pneumothorax, air pressure in the pleural space equals barometric pressure because air is forced back out during expiration. In tension pneumothorax, the site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape during expiration.
The unstable portion of the chest wall moves outward.
Internal fixation by controlled mechanical ventilation until the chest wall has stabilized.
If the alveolocapillary membrane is thickened or the surface area available for diffusion is decreased.
Increased pressures in the pulmonary artery (pulmonary artery hypertension) and lead to right-sided heart failure and cor pulmonale.
Redistribution of body water, pressure on the diaphragm from abdominal contents, and decreased efficiency of respiratory muscles.
Upper respiratory tract infections, allergic rhinitis, acute bronchitis, pneumonia, congestive heart failure, pulmonary embolus, or aspiration.
Infection or inflammation that damages the bronchi (bronchitis, bronchiectasis) or the lung parenchyma (pneumonia, tuberculosis, lung abscess).
Whenever there is an increased work of breathing, especially if the airways are obstructed, as in chronic obstructive pulmonary disease (COPD).
Because cyanosis is not evident until severe hypoxemia is present and is an insensitive indication of respiratory failure.
Ventilation and oxygenation.
Obesity and kyphoscoliosis.
Respiratory difficulty.
The pathophysiologic effects of tension pneumothorax are life-threatening, as air pressure in the pleural space pushes against the recoiled lung, causing compression atelectasis, and against the mediastinum, compressing and displacing the heart and great vessels.
For individuals with persistent air leaks, other interventions may be needed including surgery, pleurodesis, or thoracoscopic surgical techniques.
The oxygen in the alveolar gas (PaO2) and capillary blood does not have time to equilibrate during the fraction of a second that blood remains in the capillary.
Direct injury to the lungs, airways, or chest wall or indirectly because of injury to another body system, such as the brain or liver.
Flaring of the nostrils, use of accessory muscles of respiration, and retraction of the intercostal spaces.
Inhaled particles, accumulated mucus, inflammation, or the presence of a foreign body stimulating irritant receptors in the airway.
Angiotensin-converting enzyme inhibitors for hypertension.
Rhythmic and effortless breathing with a ventilatory rate of 8 to 16 breaths per minute and tidal volume ranging from 400 to 800 ml.
An impaired sense of effort where the perceived work of breathing is greater than the actual motor response generated.
Dyspnea that occurs when individuals with heart failure or lung disease wake up at night gasping for air and must sit up or stand to relieve the dyspnea.
Postnasal drainage syndrome, nonasthmatic eosinophilic bronchitis, asthma, gastroesophageal reflux disease, or heightened cough reflex sensitivity.
The amount and duration of bleeding.
Inspiration, closure of the glottis and vocal cords, contraction of the expiratory muscles, and reopening of the glottis causing a sudden, forceful expiration.
Cellular debris or microorganisms that aid in diagnosis and choice of therapy.
Breaths that are usually 1.5 to 2 times the normal tidal volume and occur approximately 10 to 12 times per hour to help maintain normal lung function.
