Causes of Asphyxia
List of causes of Asphyxia
Following is a list of causes or underlying conditions
(see also Misdiagnosis of underlying causes of Asphyxia)
that could possibly cause Asphyxia includes:
Longer list of causes of Choking:
see full list of causes for Choking
Asphyxia Causes: Book Excerpts
Asphyxia as a complication of other conditions:
Other conditions that might have
Asphyxia as a complication may,
potentially, be an underlying cause of Asphyxia.
Our database lists the following as having
Asphyxia as a complication of that condition:
Related information on causes of Asphyxia:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Asphyxia may be found in:
Causes of Asphyxia: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Asphyxia.
Dyspnea:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Asthma
–Classic triad of chronic cough, dyspnea, and wheezing
COPD; chronic bronchitis Pulmonary edema (acute or chronic)
–Cardiogenic pulmonary edema: LV failure (e.g., MI, cardiomyopathy), valve disease, high-output states (e.g., thyrotoxicosis), volume overload, hypertensive emergency
–Noncardiac pulmonary edema: Sepsis, inhalation injury, drugs (e.g., narcotics), renal failure, high altitude, aspiration, pancreatitis, seizure, trauma, emboli (fat, air, amniotic fluid), CNS injury, airway obstruction (e.g., croup, foreign body)
-
Coronary artery disease
–May present without chest pain (“anginal equivalent”)
-
Pneumonia
-
Pleural effusion
–Common causes: CHF, pneumonia, cancer, pulmonary embolus, connective tissue disease (e.g., SLE, rheumatoid arthritis), pancreatitis, and renal or liver disease
-
Pulmonary embolism
–Risk factors (Virchow's triad) present in 90% of cases: Venous stasis (e.g., immobility, pedal edema), endothelial damage (e.g., recent trauma or surgery, burns, indwelling catheters, IV drug use), hypercoagulability (e.g., malignancy, obesity, pregnancy, HRT/OCP)
-
Pneumothorax
-
Interstitial lung disease
–A group of disorders characterized by inflammation and fibrosis of alveolar walls and the interstitium -
Pulmonary hypertension
–Primary pulmonary HTN: No identifiable cause
–Secondary pulmonary HTN: Due to underlying disease (e.g., mitral stenosis, PE, COPD)
-
Less common etiologies (“zebras”) include pericardial disease, chest wall abnormality, tracheal obstruction, neuromuscular diseases, and psychogenic
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Orthopnea:
Differential Diagnosis
(In a Page: Signs and Symptoms)
-
Congestive heart failure is the most common cause of orthopnea
–Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
-
Aortic regurgitation
–Most commonly due to rheumatic fever
-
Cardiomyopathies
-
Pleural effusion
–Common causes: CHF, pneumonia, cancer, pulmonary embolus, connective tissue disease (e.g., SLE, rheumatoid arthritis), pancreatitis, renal or liver disease
-
Aortic stenosis
–Associated with angina, syncope, and CHF - Mitral stenosis
–Usually secondary to rheumatic heart disease (after 15–40 years)
–Advanced cases result in pulmonary hypertension and right heart failure
–Dyspnea is the most significant symptom
–Classic triad: Diastolic rumble, opening
snap, and loud first heart sound
-
Congenital heart disease
–May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
-
Severe COPD and asthma
-
Severe bilateral apical lung disease
-
Bilateral diaphragmatic paralysis
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Paroxysmal Nocturnal Dyspnea:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- CHF is the most common cause
–Etiologies include uncontrolled HTN, pulmonary embolus, endocarditis, hyperthyroidism, pericardial disease, endocardial disease (e.g., valvular stenosis, insufficiency, rupture, endocarditis), and myocardial disease (e.g., MI, ischemia, arrhythmias)
- Mitral stenosis
–Almost always secondary to rheumatic heart disease (after 15–40 years)
–Advanced cases result in pulmonary hypertension and right heart failure
–Dyspnea is the most significant symptom
–Classic triad: Diastolic rumble, opening
snap, and loud first heart sound
-
Aortic regurgitation
–Most commonly due to rheumatic fever -
Cardiomyopathies
–Abnormal myocardium, resulting in
impaired cardiac output and CHF -
Aortic stenosis
–Due to senile valve degeneration, rheumatic
disease, or congenital
–Associated with angina, syncope, and CHF
-
Congenital heart disease
–May see failure to thrive, progressive CHF symptoms, cyanosis, and/or murmur
- “Cardiac asthma”
–Bronchospasm secondary to pulmonary congestion and interstitial edema that compresses small airways
–Standing decreases lung congestion
-
Anxiety
-
Severe COPD and emphysema
-
Asthma
-
Obstructive sleep apnea
-
Obesity/hypoventilation
-
Tropical pulmonary eosinophilia (filariasis)
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Stridor & Wheezing:
Differential Diagnosis
(In a Page: Signs and Symptoms)
Stridor (inspiratory)
- Croup (laryngotracheobronchitis)
–Viral infection with tracheal narrowing due
to airway edema
–“Bark-like” cough, hoarseness
- Epiglottitis
–Airway emergency most commonly due to Haemophilus influenzae or group A streptococcus infection
–Abrupt onset of high fevers, sore throat, hoarseness, dysphagia, respiratory distress
-
Foreign body lodged in the upper airway
-
Allergic reaction/anaphylaxis
–May have urticaria and angioedema (subcutaneous or mucosal swelling, often of the lips)
-
Trauma
-
Postendotracheal intubation
-
Psychogenic (e.g., paroxysmal vocal cord dyskinesia)
Stridor (expiratory)
-
COPD (expiratory vocalization to prolong time to airway closure and avoid air trapping)
-
Cardiac failure (expiratory vocalization to prolong increased intrathoracic pressure and unload left ventricle)
Wheezing
-
Asthma
–Triad of chronic cough, dyspnea, wheezing
–Wheezing may be absent in cases of severe
obstruction (insufficient air movement)
-
Pulmonary edema
–Leakage of fluid into the interstitium and alveoli due to elevated capillary pressure (cardiogenic) or abnormal capillary permeability (noncardiogenic)
COPD
GERD
Respiratory infection
–Upper respiratory infection
–Bronchiolitis
–“Atypical” pneumonia
-
Aspirated foreign body
–Abrupt onset of unilateral wheezing or stridor (if lodged in the upper airway), cough, and decreased breath sounds
Allergic reaction/anaphylaxis
–Urticaria, throat swelling (angioedema), and lip/tongue edema may be present
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Apnea:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Much apnea is physiologic and normal
–Post-sigh apnea is normal
–Newborns, especially premature babies, may
have irregular breathing as their respiratory control center matures
–Periodic breathing at high altitude
-
Prolonged apnea is respiratory arrest, and inadequate ventilation is respiratory failure, and both require immediate intervention
-
Apnea may be divided into central, obstructive, and mixed apnea; etiologies vary by age
-
Central apnea in infants
–Apnea of prematurity
–Congenital central hypoventilation syndrome
(CCHS, or Ondine curse)
–CNS depression (sepsis, shock, drug effect, RSV, seizure or postictal state)
–Respiratory muscle failure (e.g., myotonia, infantile botulism)
- Obstructive apnea in infants
–Upper airway obstruction (severe laryngomalacia, choanal atresia, macroglossia, micrognathia, subglottic stenosis or web, laryngospasm)
–Lower airway: Rarely causes obstructive apnea (tracheal stenosis, rings, slings)
- Central apnea in children
–CNS (drug-induced CNS depression, CCHS, abnormal CNS brainstem anatomy and function, sepsis/septic shock)
–Respiratory muscle failure (muscular dystrophy, myotonia, myasthenia gravis) - Obstructive apnea in children
–Upper airway obstruction, obstructive sleep apnea syndrome (OSAS), tonsillar and adenoidal hypertrophy, macroglossia, micrognathia, subglottic stenosis, laryngospasm
- Mixed apnea
–CNS depression and decreased upper airway tone
–Gastroesophageal reflux leading to increased parasympathetic activity and/or laryngospasm
–Respiratory muscle failure and adenoidal hypertrophy
-
Apparent life-threatening events (ALTE)
-
Trauma may cause apnea at any age
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Dyspnea:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
- Dyspnea is driven by an aberration in the mechanics of breathing; consider the pathway taken by oxygen to the tissues, and the mechanics of getting it there
- Hypoxia
–Low O2 delivery to tissues increases effort to deliver it, including increased respiratory effort
–Any cause of hypoxia will lead to dyspnea (decreased availability, V/Q mismatch due to pneumonia or other lung disease)
- Obstructive disease causes increased effort to move air
–Upper airway: Nasal congestion, choanal atresia, FB, tonsils, adenoids, macroglossia, decreased tone, retropharyngeal abscess, laryngomalacia, VCD/paralysis, laryngeal web or polyp, subglottic stenosis
–Lower airway: Asthma, BALT, bronchiolitis obliterans, tracheobronchomalacia, bronchial atresia, bronchiectasis, bronchitis, CF, PCD, hemangioma, polyps, TEF
-
Restrictive disease
–Small or stiff lungs, chest wall disease (e.g., obesity, kyphoscoliosis, chest deformity), respiratory muscle weakness (Duchenne muscular dystrophy, paralysis)
-
Parenchymal disease
–Pneumonia, congenital lesions
-
Vascular disease
–Pulmonary hypertension, sequestered lung
-
Cardiac disease
–Congenital cyanotic heart disease (e.g., TOF,
TAPVR, TGA)
–Pericarditis
–Myocarditis
-
Compression of the lung
–Pneumothorax
–Tumors (e.g., cyst, teratoma)
–Elevated diaphragm
–Effusions (e.g., empyema, hemothorax)
-
Pulmonary embolism (rare)
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Stridor:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
Nasal cavity and nasopharynx
-
Congenital
–Piriform aperture stenosis
–Choanal atresia
–Lacrimal duct cyst
–Craniofacial anomaly
–Nasopharyngeal mass (teratoma)
-
Inflammatory/infectious
–Rhinosinusitis
–Adenoid hypertrophy
Oral cavity, oropharynx, and hypopharynx
-
Congenital
–Macroglossia
–Glossoptosis
–Vallecular cyst
-
Inflammatory/infectious
–Tonsillar hypertrophy
-
Tumors
–Lingual thyroid
–Dermoid
–Lymphovascular malformation
-
Foreign body
Laryngeal
- Congenital
–Laryngomalacia (#1 cause in infants); usual onset is in the first 2 weeks of life, typically positional; most resolve spontaneously by age 1
–Saccular cyst
–Webs
–Clefts
–Vocal cord paralysis
-
Inflammatory/infectious
–Epiglottitis
–Laryngotracheitis (croup)
–Gastroesophageal reflux
-
Tumors
–Papillomas
–Hemangiomas
-
Trauma
–Subglottic stenosis
–Foreign bodies
–Laryngeal fracture
–Caustic ingestion
Tracheobronchial
-
Congenital
–Tracheomalacia
–Vascular rings
–Tracheoesophageal fistula
-
Inflammatory
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Apnea:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
❑ Airway obstruction. Occlusion or compression of the trachea, central airways, or smaller airways can cause sudden apnea by blocking the patient’s airflow and producing acute respiratory failure.
❑ Brain stem dysfunction. Primary or secondary brain stem dysfunction can cause apnea by destroying the brain stem’s ability to initiate respirations. Apnea may arise suddenly (as in trauma, hemorrhage, or infarction) or gradually (as in degenerative disease or tumor). Apnea may be preceded by a decreased LOC and by various motor and sensory deficits.
❑ Neuromuscular failure. Trauma or disease can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury or respiratory weakness or paralysis from acute or degenerative disease.
❑ Parenchymatous lung disease. An accumulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange and producing acute respiratory failure. Apnea may arise suddenly, as in near drowning and acute pulmonary edema, or gradually, as in emphysema. Apnea may also be preceded by crackles and labored respirations with accessory muscle use.
❑ Pleural pressure gradient disruption. Conversion of normal negative pleural air pressure to positive pressure by chest wall injuries (such as flail chest) causes lung collapse, producing respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest wall and asymmetrical or paradoxical respirations.
❑ Pulmonary capillary perfusion decrease. Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or lack of circulatory patency. It occurs suddenly in cardiac arrest, massive pulmonary embolism, and most cases of severe shock. In contrast, it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension, tachycardia, and edema.
Other causes
❑ Drugs. Central nervous system (CNS) depressants may cause hypoventilation and apnea. Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients.
Neuromuscular blockers — such as curariform drugs and anticholinesterases — may produce sudden apnea because of respiratory muscle paralysis.
❑ Sleep-related apneas. These repetitive apneas occur during sleep from airflow obstruction or brain stem dysfunction.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Bradypnea:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
❑ Diabetic ketoacidosis. Bradypnea occurs late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may experience Kussmaul's respirations. Associated signs and symptoms include a decreased LOC, fatigue, weakness, a fruity breath odor, and oliguria.
❑ Hepatic failure. Occurring with end-stage hepatic failure, bradypnea may be accompanied by coma, hyperactive reflexes, asterixis, a positive Babinski's sign, fetor hepaticus, and other signs.
❑ Increased intracranial pressure (ICP). A late sign of increased ICP, a life-threatening condition, bradypnea is preceded by a decreased LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late medullary strangulation.
❑ Renal failure. Occurring with end-stage renal failure, bradypnea may be accompanied by convulsions, a decreased LOC, GI bleeding, hypotension or hypertension, uremic frost, and diverse other signs.
❑ Respiratory failure. Bradypnea occurs with end-stage respiratory failure along with cyanosis, diminished breath sounds, tachycardia, mildly increased blood pressure, and a decreased LOC.
Other causes
❑ Drugs. Overdose with an opioid analgesic or, less commonly, a sedative, barbiturate, phenothiazine, or other CNS depressant can cause bradypnea. The use of any of these drugs with alcohol can also cause bradypnea.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Dyspnea:
Other causes
(Handbook of Signs & Symptoms (Third Edition))
Chemical irritants.
Dysuria may result from irritating substances, such as bubble bath salts and feminine deodorants; it's usually most intense at the end of voiding. Spermicides may cause dysuria in both sexes. Other findings include urinary frequency and urgency, a diminished urine stream and, possibly, hematuria.
Drugs.
Dysuria can result from monoamine oxidase inhibitors. Metyrosine can also cause transient dysuria.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Hyperpnea:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Head injury
Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle’s sign; an absent doll’s eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and a widening pulse pressure.
Hyperventilation syndrome
Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia
Many pulmonary disorders that cause hypoxemia — for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax — may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia Other effects include dyspnea, a cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis
Alcoholic ketoacidosis (occurring most commonly in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting
Kussmaul’s respirations begin abruptly and are accompanied by vomiting for several days, a fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul’s respirations
The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may or may not have a history of diabetes mellitus. Other clinical features include a fruity breath odor; orthostatic hypotension; a rapid, thready pulse; generalized weakness; a decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul’s respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, a decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure
Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul’s respirations Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin
Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymoses. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include an altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis
A severe infection may cause lactic acidosis, resulting in Kussmaul’s respirations
Other findings include tachycardia, a fever or a low temperature, chills, a headache, lethargy, profuse diaphoresis, anorexia, a cough, wound drainage, burning on urination, confusion or a change in mental status, and other signs of local infection.
Shock
Potentially life-threatening metabolic acidosis produces Kussmaul’s respirations, hypotension, tachycardia, narrowed pulse pressure, a weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain or arrhythmias and signs of heart failure (in cardiogenic shock); a high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). The onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs
Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul’s respirations So can ingestion of methanol and ethylene glycol, found in antifreeze solutions.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Orthopnea:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Chronic obstructive pulmonary disease (COPD)
COPD typically produces orthopnea and other dyspneic complaints, accompanied by accessory muscle use, tachypnea, tachycardia, and paradoxical pulse. Auscultation may reveal diminished breath sounds, rhonchi, crackles, and wheezing. The patient may also exhibit a dry or productive cough with copious sputum. Other features include anorexia, weight loss, and edema. Barrel chest, cyanosis, and clubbing are usually late signs.
Left-sided heart failure
Orthopnea occurs late in left-sided heart failure. If heart failure is acute, orthopnea may begin suddenly; if chronic, it may become constant. The earliest symptom of this disorder is progressively severe dyspnea. Other common early symptoms include Cheyne-Stokes respirations, paroxysmal nocturnal dyspnea, fatigue, weakness, and a cough that may occasionally produce clear or blood-tinged sputum. Tachycardia, tachypnea, and crackles may also occur.
Other late findings include cyanosis, clubbing, a ventricular gallop, and hemoptysis. Left-sided heart failure may also lead to signs of shock, such as hypotension, a thready pulse, and cold, clammy skin.
Mediastinal tumor
Orthopnea is an early sign of a mediastinal tumor, resulting from pressure of the tumor against the trachea, bronchus, or lung when the patient lies down. However, he may be asymptomatic until the tumor enlarges. Then it produces retrosternal chest pain, a dry cough, hoarseness, dysphagia, stertorous respirations, palpitations, and cyanosis. Examination reveals suprasternal retractions on inspiration, bulging of the chest wall, tracheal deviation, dilated jugular and superficial chest veins, and face, neck, and arm edema.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Stridor:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Airway trauma
Local trauma to the upper airway commonly causes acute obstruction, resulting in the sudden onset of stridor. Accompanying this sign are dysphonia, dysphagia, hemoptysis, cyanosis, accessory muscle use, intercostal retractions, nasal flaring, tachypnea, progressive dyspnea, and shallow respirations. Palpation may reveal subcutaneous crepitation in the neck or upper chest.
Anaphylaxis
With a severe allergic reaction, upper airway edema and laryngospasm cause stridor and other signs and symptoms of respiratory distress: nasal flaring, wheezing, accessory muscle use, intercostal retractions, and dyspnea. The patient may also develop nasal congestion and profuse, watery rhinorrhea. Typically, these respiratory effects are preceded by a feeling of impending doom or fear, weakness, diaphoresis, sneezing, nasal pruritus, urticaria, erythema, and angioedema. Common associated findings include chest or throat tightness, dysphagia and, possibly, signs of shock, such as hypotension, tachycardia, and cool, clammy skin.
Anthrax (inhalation)
Initial signs and symptoms are flulike and include a fever, chills, weakness, a cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial symptoms. The second stage develops abruptly with rapid deterioration marked by stridor, a fever, dyspnea, and hypotension generally leading to death within 24 hours. Radiologic findings include mediastinitis and symmetric mediastinal widening.
Aspiration of a foreign body
Sudden stridor is characteristic in foreign body aspiration, a life-threatening situation. Related findings include an abrupt onset of dry, paroxysmal coughing; gagging or choking; hoarseness; tachycardia; wheezing; dyspnea; tachypnea; intercostal muscle retractions; diminished breath sounds; cyanosis; and shallow respirations. The patient typically appears anxious and distressed.
Hypocalcemia
With hypocalcemia, laryngospasm can cause stridor. Other findings include paresthesia, carpopedal spasm, and positive Chvostek’s and Trousseau’s signs.
Inhalation injury
Within 48 hours after inhalation of smoke or noxious fumes, the patient may develop laryngeal edema and bronchospasms, resulting in stridor. Associated signs and symptoms include singed nasal hairs, orofacial burns, coughing, hoarseness, sooty sputum, crackles, rhonchi, wheezes, and other signs and symptoms of respiratory distress, such as dyspnea, accessory muscle use, intercostal retractions, and nasal flaring.
Mediastinal tumor
Commonly producing no symptoms at first, a mediastinal tumor may eventually compress the trachea and bronchi, resulting in stridor. Its other effects include hoarseness, a brassy cough, a tracheal shift or tug, dilated neck veins, swelling of the face and neck, stertorous respirations, and suprasternal retractions on inspiration. The patient may also report dyspnea, dysphagia, and pain in the chest, shoulder, or arm.
Retrosternal thyroid
Retrosternal thyroid is an anatomic abnormality that causes stridor, dysphagia, a cough, hoarseness, and tracheal deviation. It can also cause signs of thyrotoxicosis.
Other causes
Diagnostic tests
Bronchoscopy or laryngoscopy may precipitate laryngospasm and stridor.
Treatments
After prolonged intubation, the patient may exhibit laryngeal edema and stridor when the tube is removed. Aerosol therapy with epinephrine may reduce stridor. Reintubation may be necessary in some cases. Neck surgery, such as thyroidectomy, may cause laryngeal paralysis and stridor.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Paroxysmal nocturnal dyspnea:
Medical causes
(Handbook of Signs & Symptoms (Third Edition))
Left-sided heart failure
Dyspnea — on exertion, during sleep, and eventually even at rest — is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-
Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient’s condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.
With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, a weak pulse, and cold, clammy skin.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Signs & Symptoms (Third Edition), 2006
Apnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Airway obstruction
Occlusion or compression of the trachea, central airways, or smaller airways can cause sudden apnea by blocking the patient’s airflow and producing acute respiratory failure.
Brain stem dysfunction
Primary or secondary brain stem dysfunction can cause apnea by destroying the brain stem’s ability to initiate respirations. Apnea may arise suddenly (as in trauma, hemorrhage, or infarction) or gradually (as in degenerative disease or tumor). Apnea may be preceded by decreased LOC and various motor and sensory deficits.
Neuromuscular failure
Trauma or disease can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury, or respiratory weakness or paralysis from acute or degenerative disease.
Parenchymatous lung disease
An accumulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange and producing acute respiratory failure. Apnea may arise suddenly, as in near drowning and acute pulmonary edema, or gradually, as in emphysema. Apnea also may be preceded by crackles and labored respirations with accessory muscle use.
Pleural pressure gradient disruption
Conversion of normal negative pleural air pressure to positive pressure by chest wall injuries (such as flail chest) causes lung collapse, producing respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest wall and asymmetrical or paradoxical respirations.
Pulmonary capillary perfusion decrease
Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or lack of circulatory patency. It occurs suddenly in cardiac arrest, massive pulmonary embolism, and most cases of severe shock; it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension, tachycardia, and edema.
Other causes
Drugs
Central nervous system (CNS) depressants may cause hypoventilation and apnea. Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients.
Neuromuscular blockers—such as curariform drugs and anticholinesterases— may produce sudden apnea due to respiratory muscle paralysis.
Sleep-related apneas
These repetitive apneas occur during sleep from airflow obstruction or brain stem dysfunction.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Bradypnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Diabetic ketoacidosis
Bradypnea occurs late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may experience Kussmaul’s respirations. Associated signs and symptoms include decreased LOC, fatigue, weakness, fruity breath odor, and oliguria.
Hepatic failure
Occurring in end-stage hepatic failure, bradypnea may be accompanied by coma, hyperactive reflexes, asterixis, a positive Babinski’s reflex, fetor hepaticus, and other signs.
Increased intracranial pressure (ICP)
A late sign of increased ICP—a life-threatening condition—bradypnea is preceded by decreased LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late medullary strangulation.
Renal failure
Occurring in end-stage renal failure, bradypnea may be accompanied by seizures, decreased LOC, GI bleeding, hypotension or hypertension, uremic frost, and diverse other signs.
Respiratory failure
Bradypnea occurs in end-stage respiratory failure along with cyanosis, diminished breath sounds, tachycardia, mildly increased blood pressure, and decreased LOC.
Other causes
Drugs
An overdose of an opioid analgesic or, less commonly, a sedative, barbiturate, phenothiazine, or another CNS depressant can cause bradypnea. Use of any of these drugs with alcohol can also cause bradypnea.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Dyspnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Acute espiratory distress syndrome (ARDS)
This life-threatening form of noncardiogenic pulmonary edema usually produces acute dyspnea as the first complaint. As respiratory distress progresses, the patient develops restlessness, anxiety, decreased mental acuity, tachycardia, and crackles and rhonchi in both lung fields. Other findings include cyanosis, tachypnea, motor dysfunction, and intercostal and suprasternal retractions. Severe ARDS can produce signs of shock, such as hypotension and cool, clammy skin.
Amyotrophic lateral sclerosis
Also known as Lou Gehrig’s disease, this disorder causes slow onset of dyspnea that worsens with time. Other features include dysphagia, dysarthria, muscle weakness and atrophy, fasciculations, shallow respirations, tachypnea, and emotional lability.
Anemia
Dyspnea usually develops gradually in anemia, which commonly causes fatigue, weakness, and syncope; severe anemia may also cause tachycardia, tachypnea, restlessness, anxiety, and thirst.
Anthrax, inhalation
Anthrax is an acute infectious disease that’s caused by the gram-positive, spore-forming bacterium Bacillus anthracis. Although the disease most commonly occurs in wild and domestic grazing animals, such as cattle, sheep, and goats, the spores can live in the soil for many years. The disease can occur in humans exposed to infected animals, tissue from infected animals, or biological agents. Most natural cases occur in agricultural regions worldwide. Anthrax may occur in cutaneous, inhalation, or GI forms.
Inhalation anthrax is caused by inhalation of aerosolized spores. The disease generally occurs in two stages with a period of recovery after the initial signs and symptoms. Dyspnea is a symptom of the second stage of this disorder along with fever, stridor and hypotension; the patient usually dies within 24 hours. Initial signs and symptoms are flulike and include fever, chills, weakness, cough, and chest pain.
Aspiration of a foreign body
Acute dyspnea marks this life-threatening condition, along with paroxysmal intercostal, suprasternal, and substernal retractions. The patient may also display accessory muscle use, inspiratory stridor, tachypnea, decreased or absent breath sounds, asymmetrical chest expansion, anxiety, cyanosis, diaphoresis, and hypotension.
Asthma
Acute dyspneic attacks occur in this chronic disorder along with audible wheezing, a dry cough, accessory muscle use, nasal flaring, intercostal and supraclavicular retractions, tachypnea, tachycardia, diaphoresis, prolonged expiration, flushing or cyanosis, and apprehension. Medications that block beta receptors can exacerbate asthma attacks.
Avian influenza
These potentially life-threatening viruses are spread to humans through contact with infected poultry or surfaces contaminated with infected bird excretions. Within 1 to 5 days of exposure to avian influenza, the patient typically develops flulike symptoms, such as fever, sore throat, cough, and muscle aches. Those with severe forms of the virus may develop dyspnea caused by acute respiratory distress or pneumonia. To date, the most virulent strain of this virus has not yet surfaced in humans in the United States, but a recent outbreak in Asian countries has had a mortality rate of about 50% among infected humans.
Blast lung injury
The result of a forceful percussive wave following an explosive detonation, blast lung injury is commonly characterized by dyspnea and hypoxia. Worldwide terrorist activity has recently increased the incidence of this condition, which may also cause cyanosis, chest pain, wheezing, and hemopytsis. Chest X-ray, the primary diagnostic tool, reveals a characteristic “butterfly” pattern. Many of these patients suffer concomitant injuries and require complex management, usually in an intensive care setting.
Cardiac arrhythmias
Acute or gradual dyspnea can result from decreased cardiac output in a patient with arrhythmias. The pulse rate may be rapid, slow, or irregular, with frequent premature or escape beats. Alternating pulse may be present. Other symptoms include palpitations, chest pain, diaphoresis, light-headedness, weakness, and vertigo.
Cor pulmonale
Chronic dyspnea begins gradually with exertion and progressively worsens until it occurs even at rest. Most patients with cor pulmonale have an underlying cardiac or pulmonary disease. Other findings may include a chronic productive cough, wheezing, tachypnea, jugular vein distention, dependent edema, hepatomegaly, increasing fatigue, weakness, and light-headedness.
Emphysema
This chronic disorder gradually causes progressive exertional dyspnea as well as barrel chest, accessory muscle hypertrophy, diminished breath sounds, anorexia, weight loss, malaise, peripheral cyanosis, tachypnea, pursed-lip breathing, prolonged expiration and, possibly, a chronic productive cough. Clubbing is a late sign. The patient may have a history of smoking, an alpha1-antitrypsin deficiency, or exposure to an occupational irritant.
Flail chest
In this condition, dyspnea results suddenly from multiple rib fractures and is accompanied by paradoxical chest movement, severe chest pain, hypotension, tachypnea, tachycardia, and cyanosis. Bruising and decreased or absent breath sounds occur over the affected side.
Guillain-Barré syndrome
This syndrome, which usually follows a fever and upper respiratory tract infection, causes slowly worsening dyspnea along with fatigue, ascending muscle weakness and, eventually, paralysis.
Heart failure
Dyspnea usually develops gradually in patients with heart failure. Chronic paroxysmal nocturnal dyspnea, orthopnea, tachypnea, tachycardia, palpitations, ventricular gallop, fatigue, dependent peripheral edema, hepatomegaly, dry cough, weight gain, and loss of mental acuity may occur. With acute onset, heart failure may produce jugular vein distention, bibasilar crackles, oliguria, and hypotension.
Interstitial fibrosis
Besides dyspnea, this disorder causes chest pain, a dry cough, crackles, weight loss and, possibly, cyanosis and pleural friction rub.
Lung cancer
Dyspnea develops slowly and worsens progressively in late-stage lung cancer. Other findings include fever, hemoptysis, a productive cough, wheezing, clubbing, chest pain, and pleural friction rub.
Monkeypox
Dyspnea is one of the less common symptoms of this rare viral disease. Infected individuals may also experience fever, muscle aches, sore throat, chills, and lymphadenopathy. A papular rash appears 1 to 3 days after the fever begins. The virus is similar to smallpox; however, the symptoms are milder and the disease is rarely fatal in developed countries.
Myasthenia gravis
This neuromuscular disorder causes bouts of dyspnea as the respiratory muscles weaken. In myasthenic crisis, acute respiratory distress may occur, with shallow respirations and tachypnea.
Myocardial infarction
Sudden dyspnea occurs with crushing substernal chest pain that may radiate to the back, neck, jaw, and arms. Other signs and symptoms include nausea, vomiting, diaphoresis, vertigo, hypertension or hypotension, tachycardia, anxiety, and pale, cool, clammy skin.
Plague
Caused by Yersinia pestis, plague is one of the most virulent and, if untreated, most lethal bacterial infections known. Clinical forms include bubonic (the most common), septicemic, and pneumonic plagues. The pneumonic form can be contracted by inhaling respiratory droplets from an infected person or inhaling the organism that has been dispersed in the air through biological warfare. Among the symptoms of the pneumonic form are dyspnea, a productive cough, chest pain, tachypnea, hemoptysis, increasing respiratory distress, and cardiopulmonary insufficiency.
Pleural effusion
Dyspnea develops slowly and worsens progressively in this disorder. Initial findings include a pleural friction rub accompanied by pleuritic pain that worsens with coughing or deep breathing. Other findings include a dry cough; dullness on percussion; egophony, bronchophony, and whispered pectoriloquy; tachycardia; tachypnea; weight loss; and decreased breath sounds, chest motion, and tactile fremitus. Fever may occur if infection is present.
Pneumonia
Dyspnea occurs suddenly in pneumonia and is usually accompanied by fever, shaking chills, pleuritic chest pain that worsens with deep inspiration, and a productive cough. Fatigue, headache, myalgia, anorexia, abdominal pain, crackles, rhonchi, tachycardia, tachypnea, cyanosis, decreased breath sounds, and diaphoresis may also occur.
Pneumothorax
This life-threatening disorder causes acute dyspnea unrelated to the severity of pain. Sudden, stabbing chest pain may radiate to the arms, face, back, or abdomen. Other signs and symptoms include anxiety, restlessness, dry cough, cyanosis, decreased vocal fremitus, tachypnea, tympany, decreased or absent breath sounds on the affected side, asymmetrical chest expansion, splinting, and accessory muscle use. In patients with tension pneumothorax, tracheal deviation occurs in addition to these typical findings. Decreased blood pressure and tachycardia may also occur.
Poliomyelitis (bulbar)
Dyspnea develops gradually in this disorder and worsens progressively. Additional signs and symptoms include fever, facial weakness, dysphasia, hypoactive deep tendon reflexes, decreased mental acuity, dysphagia, nasal regurgitation, and hypopnea.
Pulmonary edema
Commonly preceded by signs of heart failure, such as jugular vein distention and orthopnea, this life-threatening disorder causes acute dyspnea. Other features include tachycardia, tachypnea, crackles in both lung fields, a ventricular gallop (third heart sound [S3]), oliguria, thready pulse, hypotension, diaphoresis, cyanosis, and marked anxiety. The patient’s cough may be dry or may produce copious amounts of pink, frothy sputum.
Pulmonary embolism
This life-threatening disorder is characterized by acute dyspnea that’s usually accompanied by sudden pleuritic chest pain. Related findings include tachycardia, low-grade fever, tachypnea, a nonproductive cough or a productive cough with blood-tinged sputum, pleural friction rub, crackles, diffuse wheezing, dullness on percussion, decreased breath sounds, diaphoresis, restlessness, and acute anxiety. A massive embolism may cause signs of shock, such as hypotension and cool, clammy skin.
Sepsis
This potentially fatal disorder gradually causes dyspnea along with chills and sudden fever. As dyspnea worsens, it may be accompanied by tachycardia, tachypnea, restlessness, anxiety, decreased mental acuity, and warm, flushed, dry skin. Late findings include hypotension; oliguria; cool, clammy skin; and rapid, thready pulse.
Severe acute respiratory syndrome (SARS)
SARS is an acute infectious disease of unknown etiology; however, a novel coronavirus has been implicated as a possible cause. Although most cases have been reported in Asia (China, Vietnam, Singapore, Thailand), cases have cropped up in Europe and North America. After an incubation period of 2 to 7 days, the illness generally begins with a fever (usually greater than 100.4° F [38° C]). Other symptoms include headache, malaise, a nonproductive cough, and dyspnea. The severity of the illness is highly variable, ranging from mild illness to pneumonia and, in some cases, progressing to respiratory failure and death.
Shock
Dyspnea arises suddenly and worsens progressively in this life-threatening disorder. Related findings include severe hypotension, tachypnea, tachycardia, decreased peripheral pulses, decreased mental acuity, restlessness, anxiety, and cool, clammy skin,
Tuberculosis
Dyspnea commonly occurs with chest pain, crackles, and a productive cough. Other findings are night sweats, fever, anorexia and weight loss, vague dyspepsia, palpitations on mild exertion, and dullness on percussion.
Tularemia
Also known as “rabbit fever,” this infectious disease causes dyspnea along with fever, chills, headache, generalized myalgia, a nonproductive cough, pleuritic chest pain, and empyema.
Other causes
Inhalation injury
Dyspnea may develop suddenly or over several hours after inhalation of chemicals or hot gases. Increasing hoarseness, a persistent cough, sooty or bloody sputum, and oropharyngeal edema may also be present. The patient may also exhibit thermal burns, singed nasal hairs, and orofacial burns as well as crackles, rhonchi, wheezing, and signs of respiratory distress.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Hyperpnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Head injury
Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation. Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle’s sign; an absent doll’s eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and widening pulse pressure.
Hyperventilation syndrome
Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia
Many pulmonary disorders that cause hypoxemia—for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax—may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis
Alcoholic ketoacidosis (occurring most often in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul’s respirations begin abruptly and are accompanied by vomiting for several days, fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul’s respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may have a history of diabetes mellitus. Other clinical features include fruity breath odor; orthostatic hypotension; rapid, thready pulse; generalized weakness; decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul’s respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure
Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul’s respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymosis. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis
A severe infection may cause lactic acidosis, resulting in Kussmaul’s respirations. Other findings include tachycardia, fever or a low temperature, chills, headache, lethargy, profuse diaphoresis, anorexia, cough, wound drainage, burning on urination, confusion or change in mental status, and other signs of local infection.
Shock
Potentially life-threatening metabolic acidosis produces Kussmaul’s respirations, hypotension, tachycardia, narrowed pulse pressure, weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain, arrhythmias, and signs of heart failure (in cardiogenic shock); high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). Onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs
Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul’s respirations. So can ingestion of methanol or ethylene glycol, found in antifreeze solutions.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Orthopnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Chronic obstructive pulmonary disease
This disorder typically produces orthopnea and other dyspneic complaints, accompanied by accessory muscle use, tachypnea, tachycardia, and paradoxical pulse. Auscultation may reveal diminished breath sounds, rhonchi, crackles, and wheezing. The patient may also exhibit a dry or productive cough with copious sputum. Other features include anorexia, weight loss, and edema. Barrel chest, cyanosis, and clubbing are usually late signs.
Left-sided heart failure
Orthopnea occurs late in this disorder. If heart failure is acute, orthopnea may begin suddenly; if chronic, it may become constant. The earliest symptom of this disorder is progressively severe dyspnea. Other common early symptoms include Cheyne-Stokes respirations, paroxysmal nocturnal dyspnea, fatigue, weakness, and a cough that may occasionally produce clear or blood-tinged sputum. Tachycardia, tachypnea, and crackles may also occur.
Other late findings include cyanosis, clubbing, ventricular gallop, and hemoptysis. Left-sided heart failure may also lead to signs of shock, such as hypotension, thready pulse, and cold, clammy skin.
Mediastinal tumor
Orthopnea is an early sign of this disorder, resulting from pressure of the tumor against the trachea, bronchus, or lung when the patient lies down. However, many patients are asymptomatic until the tumor enlarges. Then, it produces retrosternal chest pain, dry cough, hoarseness, dysphagia, stertorous respirations, palpitations, and cyanosis. Examination reveals suprasternal retractions on inspiration, bulging of the chest wall, tracheal deviation, dilated jugular and superficial chest veins, and edema of the face, neck, and arms.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Stridor:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Airway trauma
Local trauma to the upper airway commonly causes acute obstruction, resulting in the sudden onset of stridor. Accompanying this sign are dysphonia, dysphagia, hemoptysis, cyanosis, accessory muscle use, intercostal retractions, nasal flaring, tachypnea, progressive dyspnea, and shallow respirations. Palpation may reveal subcutaneous crepitation in the neck or upper chest.
Anaphylaxis
With a severe allergic reaction, upper airway edema and laryngospasm cause stridor and other signs and symptoms of respiratory distress: nasal flaring, wheezing, accessory muscle use, intercostal retractions, and dyspnea. The patient may also develop nasal congestion and profuse, watery rhinorrhea. Typically, these respiratory effects are preceded by a feeling of impending doom or fear, weakness, diaphoresis, sneezing, nasal pruritus, urticaria, erythema, and angioedema. Common associated findings include chest or throat tightness, dysphagia and, possibly, signs of shock, such as hypotension, tachycardia, and cool, clammy skin.
Anthrax, inhalation
Initial signs and symptoms are flulike and include fever, chills, weakness, cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial symptoms. The second stage develops abruptly with rapid deterioration marked by stridor, fever, dyspnea, and hypotension generally leading to death within 24 hours. Radiologic findings include mediastinitis and symmetric mediastinal widening.
Aspiration of a foreign body
Sudden stridor is characteristic in this life-threatening situation. Related findings include abrupt onset of dry, paroxysmal coughing, gagging or choking, hoarseness, tachycardia, wheezing, dyspnea, tachypnea, intercostal muscle retractions, diminished breath sounds, cyanosis, and shallow respirations. The patient typically appears anxious and distressed.
Epiglottiditis
With this inflammatory condition, stridor is caused by an erythematous, edematous epiglottis that obstructs the upper airway. Stridor occurs along with fever, sore throat, and a croupy cough.
Hypocalcemia
With this disorder, laryngospasm can cause stridor. Other findings include paresthesia, carpopedal spasm, and positive Chvostek’s and Trousseau’s signs.
Inhalation injury
Within 48 hours after inhalation of smoke or noxious fumes, the patient may develop laryngeal edema and bronchospasms, resulting in stridor. Associated signs and symptoms include singed nasal hairs, orofacial burns, coughing, hoarseness, sooty sputum, crackles, rhonchi, wheezes, and other signs and symptoms of respiratory distress, such as dyspnea, accessory muscle use, intercostal retractions, and nasal flaring.
Laryngeal tumor
Stridor is a late sign and may be accompanied by dysphagia, dyspnea, enlarged cervical nodes, and pain that radiates to the ear. Typically, stridor is preceded by hoarseness, minor throat pain, and a mild, dry cough.
Laryngitis (acute)
This disorder may cause severe laryngeal edema, resulting in stridor and dyspnea. Its chief sign, however, is mild to severe hoarseness, perhaps with transient voice loss. Other findings include sore throat, dysphagia, dry cough, malaise, and fever.
Mediastinal tumor
Commonly producing no symptoms at first, this type of tumor may eventually compress the trachea and bronchi, resulting in stridor. Its other effects include hoarseness, brassy cough, tracheal shift or tug, dilated neck veins, swelling of the face and neck, stertorous respirations, and suprasternal retractions on inspiration. The patient may also report dyspnea, dysphagia, and pain in the chest, shoulder, or arm.
Retrosternal thyroid
This anatomic abnormality causes stridor, dysphagia, cough, hoarseness, and tracheal deviation. It can also cause signs of thyrotoxicosis.
Thoracic aortic aneurysm
If this aneurysm compresses the trachea, it may cause stridor accompanied by dyspnea, wheezing, and a brassy cough. Other findings include hoarseness or complete voice loss, dysphagia, jugular vein distention, prominent chest veins, tracheal tug, paresthesia or neuralgia, and edema of the face, neck, and arms. The patient may also complain of substernal, lower back, abdominal, or shoulder pain.
Other causes
Diagnostic tests
Bronchoscopy or laryngoscopy may precipitate laryngospasm and stridor.
Treatments
After prolonged intubation, the patient may exhibit laryngeal edema and stridor when the tube is removed. Aerosol therapy with epinephrine may reduce stridor. Reintubation may be necessary in some cases. Neck surgery, such as thyroidectomy, may cause laryngeal paralysis and stridor.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Paroxysmal nocturnal dyspnea:
Medical causes
(Professional Guide to Signs & Symptoms (Fifth Edition))
Left-sided heart failure
Dyspnea—on exertion, during sleep, and eventually even at rest—is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient’s condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.
With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, weak pulse, and cold, clammy skin.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Acute Dyspnea:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Asthma
❑ COPD exacerbation
❑ Left heart failure
❑ Pneumonia
❑ Pulmonary embolism
❑ Pneumothorax
❑ Hyperventilation
❑ Pleural effusion
❑ Pericardial tamponade
❑ Upper airway obstruction
❑ Pulmonary hypertension
❑ Lung cancer
❑ Noncardiogenic pulmonary edema
❑ Bilateral diaphragmatic paralysis
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Source: Field Guide to Bedside Diagnosis, 2007
Chronic Dyspnea:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Chronic obstructive pulmonary disease
❑ Congestive heart failure
❑ Asthma
❑ Recurrent pulmonary embolism
❑ Interstitial lung disease
❑ Lung cancer
❑ Chronic pleural effusion
❑ Primary pulmonary hypertension
❑ Cystic fibrosis
❑ Kyphoscoliosis
❑ Myasthenia gravis
❑ Tracheal stenosis
❑ Mitral stenosis
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Source: Field Guide to Bedside Diagnosis, 2007
Asphyxia:
Causes
(Handbook of Diseases)
Asphyxia results from any condition or substance that inhibits respiration:
hypoventilation as a result of narcotic abuse, medullary disease or hemorrhage, pneumothorax, respiratory muscle paralysis, or cardiopulmonary arrest
intrapulmonary obstruction, as in airway obstruction, severe asthma, foreign-body aspiration, pulmonary edema, pneumonia, and near drowning
extrapulmonary obstruction, as in tracheal compression from a tumor, strangulation, trauma, or suffocation
inhalation of toxic agents, as in carbon monoxide poisoning, smoke inhalation, and excessive oxygen inhalation.
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Source: Handbook of Diseases, 2003
Apnea:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Airway obstruction
Occlusion or compression of the trachea, central airways, or smaller airways can cause sudden apnea by blocking the patient’s airflow and producing acute respiratory failure.
Brain stem dysfunction
Primary or secondary brain stem dysfunction can cause apnea by destroying the brain stem’s ability to initiate respirations. Apnea may arise suddenly (as in trauma, hemorrhage, or infarction) or gradually (as in degenerative disease or a tumor). Apnea may be preceded by a decreased LOC and by various motor and sensory deficits.
Neuromuscular failure
Trauma or disease can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury, or respiratory weakness or paralysis from acute or degenerative disease.
Parenchymatous lung disease
An accumulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange and producing acute respiratory failure. Apnea may arise suddenly, as in near drowning and acute pulmonary edema, or gradually, as in emphysema. Apnea also may be preceded by crackles and labored respirations with accessory muscle use.
Pleural pressure gradient disruption
Conversion of normal negative pleural air pressure to positive pressure by chest wall injuries, such as flail chest, causes lung collapse, producing respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest wall and asymmetrical or paradoxical respirations.
Pulmonary capillary perfusion decrease
Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or lack of circulatory patency. It occurs suddenly in cardiac arrest, massive pulmonary embolism, and most cases of severe shock. In contrast, it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension, tachycardia, and edema.
Other causes
Drugs
CNS depressants may cause hypoventilation and apnea. Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients.
Neuromuscular blockers
These medications, such as curariform drugs and anticholinesterases, may produce sudden apnea because of respiratory muscle paralysis.
Sleep-related apnea
These repetitive apneas occur during sleep from airflow obstruction or brain stem dysfunction.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Bradypnea:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Diabetic ketoacidosis
Bradypnea occurs late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may experience Kussmaul’s respirations. Associated signs and symptoms include decreased LOC, fatigue, weakness, fruity breath odor, and oliguria.
Hepatic failure
Occurring with end-stage hepatic failure, bradypnea may be accompanied by coma, hyperactive reflexes, asterixis, a positive Babinski’s sign, fetor hepaticus, and other signs.
Increased intracranial pressure (ICP)
A late sign of increased ICP — a life-threatening condition — bradypnea is preceded by decreased LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late medullary strangulation.
Renal failure
Occurring with end-stage renal failure, bradypnea may be accompanied by convulsions, decreased LOC, GI bleeding, hypotension or hypertension, uremic frost, and diverse other signs.
Respiratory failure
Bradypnea occurs with end-stage respiratory failure along with cyanosis, diminished breath sounds, tachycardia, mildly increased blood pressure, and decreased LOC.
Other causes
Drugs
Overdose with an opioid analgesic or, less commonly, a sedative, barbiturate, phenothiazine, or other CNS depressant can cause bradypnea. Use of any of these drugs with alcohol can also cause bradypnea.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Dyspnea:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
See Dyspnea: Causes and associated findings, pages 122 to 125.
Acute respiratory distress syndrome (ARDS)
ARDS is a life-threatening form of noncardiogenic pulmonary edema that usually produces acute dyspnea as the first complaint. Progressive respiratory distress then develops with restlessness, anxiety, decreased mental acuity, tachycardia, and crackles and rhonchi in both lung fields. Other findings include cyanosis, tachypnea, motor dysfunction, and intercostal and suprasternal retractions. Severe ARDS can produce signs of shock, such as hypotension and cool, clammy skin.
Amyotrophic lateral sclerosis (ALS).
Also known as Lou Gehrig disease, ALS causes slow onset of dyspnea that worsens with time. Other features include dysphagia, dysarthria, muscle weakness and atrophy, fasciculations, shallow respirations, tachypnea, and emotional lability.
Anemia
Dyspnea usually develops gradually with anemia. Anemia commonly causes fatigue, weakness, and syncope; if severe, it may also cause tachycardia, tachypnea, restlessness, anxiety, and thirst.
Anthrax (inhalation).
Dyspnea is a symptom of the second stage of this inhalation anthrax, along with fever, stridor, and hypotension (the patient usually dies within 24 hours). Initial symptoms of this disorder, which are due to the inhalation of aerosolized spores (from infected animals or a result of bioterrorism) from the bacterium Bacillus anthracis, are flulike and include fever, chills, weakness, cough, and chest pain.
Aspiration of a foreign body.
Acute dyspnea marks aspiration of a foreign body — a life-threatening condition — along with paroxysmal intercostal, suprasternal, and substernal retractions. The patient may also display accessory muscle use, inspiratory stridor, tachypnea, decreased or absent breath sounds, possibly asymmetrical chest expansion, anxiety, cyanosis, diaphoresis, and hypotension.
Asthma
Acute dyspneic attacks occur with this asthma — a chronic disorder — along with audible wheezing, dry cough, accessory muscle use, nasal flaring, intercostal and supraclavicular retractions, tachypnea, tachycardia, diaphoresis, prolonged expiration, flushing or cyanosis, and apprehension. Medications that block beta receptors can exacerbate asthma attacks.
Cardiac arrhythmia
In a patient with arrhythmias, acute or gradual dyspnea can result from decreased cardiac output. The pulse rate may be rapid, slow, or irregular, with frequent premature or escape beats. Alternating pulse may be present. Other symptoms include palpitations, chest pain, diaphoresis, light-headedness, weakness, or vertigo.
Cor pulmonale
Chronic dyspnea begins gradually with exertion and progressively worsens until it occurs even at rest. Underlying cardiac or pulmonary disease is usually present. The patient may have a chronic productive cough, wheezing, tachypnea, jugular vein distention, dependent edema, and hepatomegaly. He may also experience increasing fatigue, weakness, and light-headedness.
Emphysema
Emphysema is a chronic disorder that gradually causes progressive exertional dyspnea. A history of smoking, an alpha1-antitrypsin deficiency, or exposure to an occupational irritant usually accompanies barrel chest, accessory muscle hypertrophy, diminished breath sounds, anorexia, weight loss, malaise, peripheral cyanosis, tachypnea, pursed-lip breathing, prolonged expiration and, possibly, a chronic productive cough. Clubbing is a late sign.
Flail chest
Sudden dyspnea results from multiple rib fractures and is accompanied by paradoxical chest movement, severe chest pain, hypotension, tachypnea, tachycardia, and cyanosis. Bruising and decreased or absent breath sounds occur over the affected side.
Guillain-Barré syndrome
Usually following a fever and upper respiratory tract infection, Guillain-Barré syndrome causes slowly worsening dyspnea along with fatigue, ascending muscle weakness and, eventually, paralysis.
Heart failure
Dyspnea usually develops gradually in patients with heart failure. Chronic paroxysmal nocturnal dyspnea, orthopnea, tachypnea, tachycardia, palpitations, ventricular gallop, fatigue, dependent peripheral edema, hepatomegaly, dry cough, weight gain, and loss of mental acuity may occur. With acute onset, heart failure may produce jugular vein distention, bibasilar rates, oliguria, and hypotension.
Inhalation injury
Dyspnea may develop suddenly or gradually over several hours after inhalation of chemicals or hot gases. Increasing hoarseness, persistent cough, sooty or bloody sputum, and oropharyngeal edema may also be present. The patient may also exhibit thermal burns, singed nasal hairs, and orofacial burns as well as crackles, rhonchi, wheezing, and signs of respiratory distress.
Interstitial fibrosis.
Besides dyspnea, interstitial fibrosis causes chest pain, dry cough, crackles, weight loss and, possibly, cyanosis and pleural friction rub.
Lung cancer
Dyspnea that develops slowly and progressively worsens occurs with late-stage lung cancer. Other findings include fever, hemoptysis, productive cough, wheezing, clubbing, chest pain, and pleural friction rub.
Myasthenia gravis
Myasthenia gravis is a neuromuscular disorder that causes bouts of dyspnea as the respiratory muscles weaken. With myasthenic crisis, acute respiratory distress may occur, with shallow respirations and tachypnea.
Myocardial infarction
Sudden dyspnea occurs with crushing substernal chest pain that may radiate to the back, neck, jaw, and arms. Other signs and symptoms include nausea, vomiting, diaphoresis, vertigo, hypertension or hypotension, tachycardia, anxiety, and pale, cool, clammy skin.
Plague
(Yersinia pestis). Among the symptoms of the pneumonic form of plague are dyspnea, a productive cough, chest pain, tachypnea, hemoptysis, increasing respiratory distress, and cardiopulmonary insufficiency. The onset of this virulent infection is usually sudden and includes such signs and symptoms as chills, fever, headache, and myalgias. If untreated, plague is one of the most potentially lethal diseases known.
Pleural effusion
Dyspnea develops slowly and becomes progressively worse with pleural effusion. Initial findings include a pleural friction rub accompanied by pleuritic pain that worsens with coughing or deep breathing. Other findings include dry cough; dullness on percussion; egophony, bronchophony, and whispered pectoriloquy; tachycardia; tachypnea; weight loss; and decreased chest motion, tactile fremitus, and decreased breath sounds. With infection, fever may occur.
Pneumonia
Dyspnea occurs suddenly, usually accompanied by fever, shaking chills, pleuritic chest pain that worsens with deep inspiration, and a productive cough. Fatigue, headache, myalgia, anorexia, abdominal pain, crackles, rhonchi, tachycardia, tachypnea, cyanosis, decreased breath sounds, and diaphoresis may also occur.
Pneumothorax
Pneumothorax is a life-threatening disorder that causes acute dyspnea unrelated to the severity of pain. Sudden, stabbing chest pain may radiate to the arms, face, back, or abdomen. Other signs and symptoms include anxiety, restlessness, dry cough, cyanosis, decreased vocal fremitus, tachypnea, tympany, decreased or absent breath sounds on the affected side, asymmetrical chest expansion, splinting, and accessory muscle use. In patients with tension pneumothorax, tracheal deviation occurs in addition to these typical findings. Decreased blood pressure and tachycardia may also occur.
Poliomyelitis (bulbar)
Dyspnea develops gradually and progressively worsens. Additional signs and symptoms include fever, facial weakness, dysphasia, hypoactive deep tendon reflexes, decreased mental acuity, dysphagia, nasal regurgitation, and hypopnea.
Pulmonary edema.
Commonly preceded by signs of heart failure, such as jugular
vein distention and orthopnea, pulmonary edema — a life-threatening disorder — causes acute dyspnea. Other features include tachycardia, tachypnea, crackles in both lung fields, a third heart sound (S3 gallop), oliguria, thready pulse, hypotension, diaphoresis, cyanosis, and marked anxiety. The patient’s cough may be dry or may produce copious amounts of pink, frothy sputum.
Pulmonary embolism
Acute dyspnea that’s usually accompanied by sudden pleuritic chest pain characterizes pulmonary embolism — a life-threatening disorder. Related findings include tachycardia, low-grade fever, tachypnea, nonproductive or productive cough with blood-tinged sputum, pleural friction rub, crackles, diffuse wheezing, dullness on percussion, decreased breath sounds, diaphoresis, restlessness, and acute anxiety. A massive embolism may cause signs of shock, such as hypotension and cool, clammy skin.
Sepsis
Sepsis is a potentially fatal disorder that gradually causes dyspnea along with chills and sudden fever. As dyspnea worsens, it may be accompanied by tachycardia, tachypnea, restlessness, anxiety, decreased mental acuity, and warm, flushed, dry skin. Late findings include hypotension; oliguria; cool, clammy skin; and rapid, thready pulse.
Severe acute respiratory syndrome (SARS).
SARS is an acute infectious disease of unknown etiology; however, a novel coronavirus has been implicated as a possible cause. Although most cases have been reported in Asia (China, Vietnam, Singapore, Thailand), cases have cropped up in Europe and North America. The incubation period is 2 to 7 days, and the illness generally begins with a fever (usually greater than 100.4° F [38° C]). Other symptoms include headache, malaise, a dry nonproductive cough, and dyspnea. The severity of the illness is highly variable, ranging from mild illness to pneumonia and, in some cases, progressing to respiratory failure and death.
Shock
Dyspnea arises suddenly and worsens progressively in shock — a life-threatening disorder. Related findings include severe hypotension, tachypnea, tachycardia, decreased peripheral pulses, decreased mental acuity, restlessness, anxiety, and cool, clammy skin,
Tuberculosis
Dyspnea commonly occurs with chest pain, crackles, and productive cough. Other findings are night sweats, fever, anorexia and weight loss, vague dyspepsia, palpitations on mild exertion, and dullness on percussion.
Tularemia
Also known as rabbit fever, tularemia causes dyspnea along with fever, chills, headache, generalized myalgias, a nonproductive cough, pleuritic chest pain, and empyema.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Hyperpnea:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Head injury
Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation. Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle’s sign; an absent doll’s eye sign; and motor and sensory disturbances.
Signs of increased ICP include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and widening pulse pressure.
Hyperventilation syndrome
Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia
Many pulmonary disorders that cause hypoxemia — for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumotho-
rax — may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis
Alcoholic ketoacidosis (occurring most commonly in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul’s respirations begin abruptly and are accompanied by vomiting for several days, fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul’s respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may or may not have a history of diabetes mellitus. Other clinical features include fruity breath odor; orthostatic hypotension; rapid, thready pulse; generalized weakness; decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul’s respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure
Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul’s respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymoses. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis
A severe infection may cause lactic acidosis, resulting in Kussmaul’s respirations. Other findings include tachycardia, fever or a low temperature, chills, headache, lethargy, profuse diaphoresis, anorexia, cough, wound drainage, burning on urination, confusion or change in mental status, and other signs of local infection.
Shock
Potentially life-threatening metabolic acidosis produces Kussmaul’s respirations, hypotension, tachycardia, narrowed pulse pressure, weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain or arrhythmias and signs of heart failure (in cardiogenic shock); high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). Onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs
Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul’s respirations. So can ingestion of methanol and ethylene glycol, found in antifreeze solutions.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Stridor:
Medical causes
(Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series)
Airway trauma
Local trauma to the upper airway commonly causes acute obstruction, resulting in the sudden onset of stridor. Accompanying this sign are dysphonia, dysphagia, hemoptysis, cyanosis, accessory muscle use, intercostal retractions, nasal flaring, tachypnea, progressive dyspnea, and shallow respirations. Palpation may reveal subcutaneous crepitation in the neck or upper chest.
Anaphylaxis
With a severe allergic reaction, upper airway edema and laryngospasm cause stridor and other signs and symptoms of respiratory distress — nasal flaring, wheezing, accessory muscle use, intercostal retractions, and dyspnea. The patient may also develop nasal congestion and profuse, watery rhinorrhea. Typically, these respiratory effects are preceded by a feeling of impending doom or fear, weakness, diaphoresis, sneezing, nasal pruritus, urticaria, erythema, and angioedema. Common associated findings include chest or throat tightness, dysphagia and, possibly, signs of shock, such as hypotension, tachycardia, and cool, clammy skin.
Anthrax (inhalation)
Initial signs and symptoms of inhalation anthrax are flulike and include fever, chills, weakness, cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial symptoms. The second stage develops abruptly with rapid deterioration marked by stridor, fever, dyspnea, and hypotension generally leading to death within 24 hours. Radiologic findings include mediastinitis and symmetric mediastinal widening.
Aspiration of a foreign body
Sudden stridor is characteristic in this life-threatening situation. Related findings include an abrupt onset of dry, paroxysmal coughing, gagging or choking, hoarseness, tachycardia, wheezing, dyspnea, tachypnea, intercostal muscle retractions, diminished breath sounds, cyanosis, and shallow respirations. The patient typically appears anxious and distressed.
Epiglottiditis
With epiglottiditis, an inflammatory condition, stridor is caused by an erythematous, edematous epiglottis that obstructs the upper airway. Stridor occurs along with fever, sore throat, and a croupy cough.
Hypocalcemia
With hypocalcemia, laryngospasm can cause stridor. Other findings include paresthesia, carpopedal spasm, and positive Chvostek’s and Trousseau’s signs.
Inhalation injury
Within 48 hours after inhalation of smoke or noxious fumes, the patient may develop laryngeal edema and bronchospasms, resulting in stridor. Associated signs and symptoms include singed nasal hairs, orofacial burns, coughing, hoarseness, sooty sputum, crackles, rhonchi, wheezes, and other signs and symptoms of respiratory distress, such as dyspnea, accessory muscle use, intercostal retractions, and nasal flaring.
Laryngeal tumor
Stridor is a late sign and may be accompanied by dysphagia, dyspnea, enlarged cervical nodes, and pain that radiates to the ear. Typically, stridor is preceded by hoarseness, minor throat pain, and a mild, dry cough.
Laryngitis (acute)
Acute laryngitis may cause severe laryngeal edema, resulting in stridor and dyspnea. Its chief sign, however, is mild to severe hoarseness, perhaps with transient voice loss. Other findings include sore throat, dysphagia, dry cough, malaise, and fever.
Mediastinal tumor
Commonly producing no symptoms at first, this type of tumor may eventually compress the trachea and bronchi, resulting in stridor. Its other effects include hoarseness, brassy cough, tracheal shift or tug, jugular vein distention, face and neck swelling, stertorous respirations, and suprasternal retractions on inspiration. The patient may also report dyspnea, dysphagia, and pain in the chest, shoulder, or arm.
Retrosternal thyroid
An anatomic abnormality, retrosternal thyroid causes stridor, dysphagia, cough, hoarseness, and tracheal deviation. It can also cause signs of thyrotoxicosis.
Thoracic aortic aneurysm
If this aneurysm compresses the trachea, it may cause stridor accompanied by dyspnea, wheezing, and a brassy cough. Other findings include hoarseness or complete voice loss, dysphagia, jugular vein distention, prominent chest veins, tracheal tug, paresthesia or neuralgia, and edema of the face, neck, and arms. The patient may also complain of substernal, lower back, abdominal, or shoulder pain.
Other causes
Diagnostic tests
Bronchoscopy or laryngoscopy may precipitate laryngospasm and stridor.
Medical treatments
After prolonged intubation, the patient may exhibit laryngeal edema and stridor when the tube is removed. Aerosol therapy with epinephrine may reduce stridor. Reintubation may be necessary in some cases. Neck surgery, such as thyroidectomy, may cause laryngeal paralysis and stridor.
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Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
Bradypnea:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Diabetic ketoacidosis
Bradypnea occurs late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may experience Kussmaul’s respirations. Associated signs and symptoms include decreased LOC, fatigue, weakness, fruity breath odor, and oliguria.
Increased intracranial pressure
A late sign of increased intracranial pressure (ICP) and a life-threatening condition, bradypnea is preceded by decreased LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late medullary strangulation.
Respiratory failure
Bradypnea occurs with end-stage respiratory failure along with cyanosis, diminished breath sounds, tachycardia, and mildly increased blood pressure. The patient may also be restless, confused, irritable, or have a decreased LOC.
Other causes
Drugs
Overdose with an opioid analgesic or, less commonly, a sedative, barbiturate, phenothiazine, or other CNS depressant can cause bradypnea. Use of any of these drugs with alcohol can also cause bradypnea.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Dyspnea:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is a life-threatening form of noncardiogenic pulmonary edema that usually produces acute dyspnea as the first complaint. Progressive respiratory distress then develops with restlessness, anxiety, decreased mental acuity, tachycardia, and crackles and rhonchi in both lung fields. Other findings include cyanosis, tachypnea, motor dysfunction, and intercostal and suprasternal retractions. Severe ARDS can produce signs of shock, such as hypotension and cool, clammy skin.
Amyotrophic lateral sclerosis
Also known as Lou Gehrig disease, amyotrophic lateral sclerosis (ALS) causes slow onset of dyspnea that worsens with time. Other features include dysphagia, dysarthria, muscle weakness and atrophy, fasciculations, shallow respirations, tachypnea, and emotional lability.
Anemia
Dyspnea usually develops gradually with anemia. Anemia commonly causes fatigue, weakness, and syncope; in severe cases, it may also cause tachycardia, tachypnea, restlessness, anxiety, and thirst. In advanced stages, the patient may develop pallor, inability to concentrate, and irritability. With chronic iron deficiency, nails become spoon-shaped and brittle, the corners of the mouth crack, the tongue becomes smooth, and dysphagia may develop.
Anthrax (inhalation)
Dyspnea is a symptom of the second stage of anthrax inhalation; it’s accompanied by fever, stridor and hypotension (the patient usually dies within 24 hours). Initial symptoms of anthrax inhalation, which are caused by the inhalation of aerosolized spores (from infected animals or a result of bioterrorism) from the bacterium Bacillus anthracis, are flulike and include fever, chills, weakness, cough, and chest pain.
Aspiration of a foreign body
Aspiration of a foreign body is a life-threatening condition characterized by acute dyspnea and paroxysmal intercostal, suprasternal, and substernal retractions. The patient may also display accessory muscle use, inspiratory stridor, tachypnea, decreased or absent breath sounds, possibly asymmetrical chest expansion, anxiety, cyanosis, diaphoresis, and hypotension.
Asthma
In asthma, a chronic disorder, acute dyspneic attacks occur along with audible wheezing, dry cough, accessory muscle use, nasal flaring, intercostal and supraclavicular retractions, tachypnea, tachycardia, diaphoresis, prolonged expiration, flushing or cyanosis, and apprehension. Medications that block beta receptors can exacerbate asthma attacks.
Cardiac arrhythmia
In a patient with an arrhythmia, acute or gradual dyspnea can result from decreased cardiac output. The patient’s pulse rate may be rapid, slow, or irregular, with frequent premature or escape beats. Alternating pulse may be present. Other symptoms include palpitations, chest pain, diaphoresis, light-headedness, weakness, or vertigo.
Cor pulmonale
Chronic dyspnea begins gradually with exertion and progressively worsens until it occurs even at rest. Underlying cardiac or pulmonary disease is usually present. The patient may also have a chronic productive cough, wheezing, tachypnea, jugular vein distention, dependent edema, and hepatomegaly. He may experience increasing fatigue, weakness, and light-headedness.
Emphysema
Emphysema is a chronic disorder that gradually causes progressive exertional dyspnea. The patient may exhibit barrel chest, accessory muscle hypertrophy, diminished breath sounds, anorexia, weight loss, malaise, peripheral cyanosis, tachypnea, pursed-lip breathing, prolonged expiration and, possibly, a chronic productive cough. Clubbing is a late sign.
Flail chest
With flail chest, sudden dyspnea results from multiple rib fractures and is accompanied by paradoxical chest movement, severe chest pain, hypotension, tachypnea, tachycardia, and cyanosis. Bruising and decreased or absent breath sounds occur over the affected side.
Guillain-Barré syndrome
Usually following a fever and upper respiratory tract infection, Guillain-Barré syndrome causes slowly worsening dyspnea along with fatigue, ascending muscle weakness and, eventually, paralysis. Other clinical features include facial diplegia, dysphagia or dysarthria and, less commonly, weakness of the muscles supplied by cranial nerve XI.
Heart failure
Dyspnea usually develops gradually in patients with heart failure. Chronic paroxysmal nocturnal dyspnea, orthopnea, tachypnea, tachycardia, palpitations, ventricular gallop, fatigue, dependent peripheral edema, hepatomegaly, dry cough, weight gain, and loss of mental acuity may occur. With acute onset, heart failure may produce jugular vein distention, bibasilar rates, oliguria, and hypotension.
Inhalation injury
Dyspnea may develop suddenly or gradually over several hours after inhalation of chemicals or hot gases. Increasing hoarseness, persistent cough, sooty or bloody sputum, and oropharyngeal edema may also be present. The patient may also exhibit thermal burns, singed nasal hairs, and orofacial burns as well as crackles, rhonchi, wheezing, and signs of respiratory distress.
Lung cancer
Dyspnea that develops slowly and progressively worsens occurs with late-stage lung cancer. Other findings include fever, hemoptysis, productive cough, wheezing, clubbing, chest pain, and pleural friction rub. The patient may also report weight loss and anorexia.
CULTURAL CUE:Among indigenous Arctic populations, the incidence of lung cancer is growing faster than any other cancer. This may be a result of high smoking rates in Native Alaskan adults and children.
Myasthenia gravis
Myasthenia gravis is a neuromuscular disorder that causes bouts of dyspnea as the respiratory muscles weaken. The patient may have difficulty chewing and swallowing, which may lead to aspiration. With myasthenic crisis, acute respiratory distress may occur, with shallow respirations and tachypnea.
Myocardial infarction
With myocardial infarction, sudden dyspnea occurs with crushing substernal chest pain that may radiate to the back, neck, jaw, and arms. Other signs and symptoms include nausea, vomiting, diaphoresis, vertigo, hypertension or hypotension, tachycardia, anxiety, and pale, cool, clammy skin.
Plague
The pneumonic form of plague, caused by the bacterium Yersinia pestis, is characterized by dyspnea, a productive cough, chest pain, tachypnea, hemoptysis, increasing respiratory distress, and cardiopulmonary insufficiency. The onset of this virulent infection is usually sudden and includes such signs and symptoms as chills, fever, headache, and myalgias. If untreated, plague is one of the most potentially lethal diseases known.
Pleural effusion
Dyspnea develops slowly and becomes progressively worse with pleural effusion. Initial findings include a pleural friction rub accompanied by pleuritic pain that worsens with coughing or deep breathing. Other findings include dry cough; dullness on percussion; egophony, bronchophony, and whispered pectoriloquy; tachycardia; tachypnea; weight loss; and decreased chest motion, tactile fremitus, and decreased breath sounds. With infection, fever may occur.
Pneumonia
With pneumonia, dyspnea occurs suddenly and is usually accompanied by fever, shaking chills, pleuritic chest pain that worsens with deep inspiration, and a productive cough. Fatigue, headache, myalgia, anorexia, abdominal pain, crackles, rhonchi, tachycardia, tachypnea, cyanosis, decreased breath sounds, and diaphoresis may also occur.
Pneumothorax
Pneumothorax is a life-threatening disorder that causes acute dyspnea unrelated to the severity of pain. Sudden, stabbing chest pain may radiate to the arms, face, back, or abdomen. Other signs and symptoms include anxiety, restlessness, dry cough, cyanosis, decreased vocal fremitus, tachypnea, tympany, decreased or absent breath sounds on the affected side, asymmetrical chest expansion, splinting, and accessory muscle use. In patients with tension pneumothorax, tracheal deviation occurs in addition to these typical findings. Decreased blood pressure and tachycardia may also occur.
Pulmonary edema
Commonly preceded by signs of heart failure, such as jugular vein distention and orthopnea, pulmonary edema causes acute dyspnea. Other features include tachycardia, tachypnea, crackles in both lung fields, a third heart sound (S3 gallop), oliguria, thready pulse, hypotension, diaphoresis, cyanosis, and marked anxiety. The patient’s cough may be dry or may produce copious amounts of pink, frothy sputum.
Pulmonary embolism
Acute dyspnea that’s usually accompanied by sudden pleuritic chest pain characterizes pulmonary embolism — a life-threatening disorder. Related findings include tachycardia, low-grade fever, tachypnea, nonproductive or productive cough with blood-tinged sputum, pleural friction rub, crackles, diffuse wheezing, dullness on percussion, decreased breath sounds, diaphoresis, restlessness, and acute anxiety. A massive embolism may cause signs of shock, such as hypotension and cool, clammy skin.
Sepsis
Sepsis, a potentially fatal disorder, gradually causes dyspnea along with chills and sudden fever. As dyspnea worsens, it may be accompanied by tachycardia, tachypnea, restlessness, anxiety, decreased mental acuity, and warm, flushed, dry skin. Late findings include hypotension; oliguria; cool, clammy skin; and rapid, thready pulse.
Severe acute respiratory syndrome
Severe acute respiratory syndrome (SARS) is an infectious disease of unknown etiology that generally begins with a fever (usually greater than 100.4° F [38° C]). Other symptoms include headache; malaise; a dry, nonproductive cough; and dyspnea. The severity of the illness is highly variable, ranging from mild illness to pneumonia and, in some cases, progressing to respiratory failure and death.
CULTURAL CUE:Although most reported SARS cases have been in Asia (particularly China, Vietnam, Singapore, and Thailand), some people in Europe and North America have also been diagnosed with SARS.
Shock
Dyspnea arises suddenly and worsens progressively in a patient with shock, a life-threatening disorder. Related findings include severe hypotension, tachypnea, tachycardia, decreased peripheral pulses, decreased mental acuity, restlessness, anxiety, and cool, clammy skin.
Tuberculosis
In a patient with tuberculosis, dyspnea is commonly accompanied by chest pain, crackles, and productive cough. Other findings include night sweats, fever, anorexia and weight loss, vague dyspepsia, palpitations on mild exertion, and dullness on percussion.
Tularemia
Also known as rabbit fever, tularemia is an infectious disease that causes dyspnea along with fever, chills, headache, generalized myalgia, a nonproductive cough, pleuritic chest pain, and empyema. Other signs and symptoms include diaphoresis, weight loss, and a red spot on the skin that ultimately enlarges to an ulcer.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Hyperpnea:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Head injury
Hyperpnea can occur with severe head injury. Other clinical manifestations depend on the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle’s sign; an absent doll’s eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and widening pulse pressure.
Hyperventilation syndrome
Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia
Many pulmonary disorders that cause hypoxemia — for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax — may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis
Alcoholic ketoacidosis typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul’s respirations begin abruptly and are accompanied by vomiting for several days, fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul’s respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may or may not have a history of diabetes mellitus. Other clinical features include fruity breath odor; orthostatic hypotension; rapid, thready pulse; generalized weakness; decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul’s respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure
Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul’s respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymoses. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis
A severe infection may cause lactic acidosis, resulting in Kussmaul’s respirations. Other findings in sepsis include tachycardia, fever or a low temperature, chills, headache, lethargy, profuse diaphoresis, anorexia, cough, wound drainage, burning on urination, confusion or change in mental status, and other signs of local infection.
Shock
Potentially life-threatening metabolic acidosis produces Kussmaul’s respirations, hypotension, tachycardia, narrowed pulse pressure, weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain or arrhythmias and signs of heart failure (in cardiogenic shock); high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). Onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs
Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul’s respirations. So can ingestion of methanol and ethylene glycol, found in antifreeze solutions.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Orthopnea:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) typically produces orthopnea and other dyspneic complaints, accompanied by accessory muscle use, tachypnea, tachycardia, and paradoxical pulse. Auscultation may reveal diminished breath sounds, rhonchi, crackles, and wheezing. The patient may also exhibit a dry or productive cough with copious sputum. Other features include anorexia, weight loss, and edema. Barrel chest, cyanosis, and clubbing are usually late signs.
Left-sided heart failure
Orthopnea occurs late in left-sided heart failure. If heart failure is acute, orthopnea may begin suddenly; if chronic, it may become constant. The earliest symptom of left-sided heart failure is progressively severe dyspnea. Other common early symptoms include Cheyne-Stokes respirations, paroxysmal nocturnal dyspnea, fatigue, weakness, and a cough that may occasionally produce clear or blood-tinged sputum. Tachycardia, tachypnea, and crackles may also occur.
Other late findings include cyanosis, clubbing, ventricular gallop, and hemoptysis. Left-sided heart failure may also lead to such signs of shock as hypotension, thready pulse, and cold, clammy skin.
Mediastinal tumor
Orthopnea is an early sign of a mediastinal tumor, resulting from pressure of the tumor against the trachea, bronchus, or lung when the patient lies down. However, many patients are asymptomatic until the tumor enlarges. Then it produces retrosternal chest pain, dry cough, hoarseness, dysphagia, stertorous respirations, palpitations, and cyanosis. Examination reveals suprasternal retractions on inspiration, bulging of the chest wall, tracheal deviation, dilated jugular and superficial chest veins, and edema of the face, neck, and arms.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Stridor:
Medical causes
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Airway trauma
Local trauma to the upper airway commonly causes acute obstruction, resulting in the sudden onset of stridor. Accompanying this sign are dysphonia, dysphagia, hemoptysis, cyanosis, accessory muscle use, intercostal retractions, nasal flaring, tachypnea, progressive dyspnea, and shallow respirations. Palpation may reveal subcutaneous crepitation in the neck or upper chest.
Anaphylaxis
With a severe allergic reaction (anaphylaxis), upper airway edema and laryngospasm cause stridor and other signs and symptoms of respiratory distress: nasal flaring, wheezing, accessory muscle use, intercostal retractions, and dyspnea. The patient may also develop nasal congestion and profuse, watery rhinorrhea. Typically, these respiratory effects are preceded by a feeling of impending doom or fear, weakness, diaphoresis, sneezing, nasal pruritus, urticaria, erythema, and angioedema. Common associated findings of anaphylaxis include chest or throat tightness, dysphagia and, possibly, signs of shock, such as hypotension, tachycardia, and cool, clammy skin.
Anthrax (inhalation)
Initial signs and symptoms of inhalation anthrax are flulike and include fever, chills, weakness, cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial symptoms. The second stage develops abruptly with rapid deterioration marked by stridor, fever, dyspnea, and hypotension generally leading to death within 24 hours.
Aspiration of a foreign body
Sudden stridor is characteristic in this life-threatening situation. Related findings include abrupt onset of dry, paroxysmal coughing, gagging or choking, hoarseness, tachycardia, wheezing, dyspnea, tachypnea, intercostal muscle retractions, diminished breath sounds, cyanosis, and shallow respirations. The patient typically appears anxious and distressed.
Epiglottiditis
With epiglottiditis, a life-threatening inflammatory condition, stridor is caused by an erythematous, edematous epiglottis that obstructs the upper airway. Stridor occurs along with fever, sore throat, and a croupy cough. The cough may progress to severe respiratory distress with sternal and intercostal retractions, nasal flaring, cyanosis, and tachycardia.
Hypocalcemia
With hypocalcemia, laryngospasm can cause stridor. Other findings include paresthesia, carpopedal spasm, hyperactive deep tendon reflexes, muscle twitching and cramping, and positive Chvostek’s and Trousseau’s signs.
Inhalation injury
Within 48 hours after inhalation of smoke or noxious fumes, the patient may develop laryngeal edema and bronchospasms, resulting in stridor. Associated signs and symptoms include singed nasal hairs, orofacial burns, coughing, hoarseness, sooty sputum, crackles, rhonchi, wheezes, and other signs and symptoms of respiratory distress, such as dyspnea, accessory muscle use, intercostal retractions, and nasal flaring.
Laryngeal tumor
Stridor is a late sign of laryngeal tumor and may be accompanied by dysphagia, dyspnea, enlarged cervical nodes, and pain that radiates to the ear. Typically, stridor is preceded by hoarseness, minor throat pain, and a mild, dry cough.
Laryngitis (acute)
Acute laryngitis may cause severe laryngeal edema, resulting in stridor and dyspnea. Its chief sign, however, is mild to severe hoarseness, perhaps with transient voice loss. Other findings include sore throat, dysphagia, dry cough, malaise, and fever.
Mediastinal tumor
Commonly producing no symptoms at first, a mediastinal tumor may eventually compress the trachea and bronchi, resulting in stridor. Its other effects include hoarseness, brassy cough, tracheal shift or tug, dilated neck veins, swelling of the face and neck, stertorous respirations, and suprasternal retractions on inspiration. The patient may also report dyspnea, dysphagia, and pain in the chest, shoulder, or arm.
Thoracic aortic aneurysm
If a thoracic aortic aneurysm compresses the trachea, it may cause stridor accompanied by dyspnea, wheezing, and a brassy cough. Other findings include hoarseness or complete voice loss, dysphagia, jugular vein distention, prominent chest veins, tracheal tug, paresthesia or neuralgia, and edema of the face, neck, and arms. The patient may also complain of substernal, lower back, abdominal, or shoulder pain.
Other causes
Diagnostic tests
Bronchoscopy or laryngoscopy may precipitate laryngospasm and stridor.
Treatments
After prolonged intubation, the patient may exhibit laryngeal edema and stridor when the tube is removed. Aerosol therapy with epinephrine may reduce stridor. Reintubation may be necessary in some cases. Neck surgery, such as thyroidectomy, may cause laryngeal paralysis and stridor.
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Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Respiratory Distress and Apnea:
Principal Causes of Respiratory Distress (Neonatal)
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
- Upperrespiratory tract obstruction
- Lower respiratory tract disorders
- Transienttachypnea of the newborn
- Respiratory distress syndrome (hyalinemembrane disease)
- Meconium aspiration and other aspirationsyndromes
- Pneumonia
- Pulmonary air leaks
- Pulmonary hemorrhage
- Bronchopulmonary dysplasia
- Congenital malformations of the lungs,bronchi, diaphragm, and rib cage
- Lung agenesis and aplasia
- Pulmonary hypoplasia
- Pulmonary sequestration
- Lobar emphysema
- Cystic lung lesions
- Bronchogeniccyst
- Congenital cystic adenomatoid malformation
- Intrapulmonary cysts
- Congenital pulmonary lymphangiectasia
- Chylothorax
- Bronchial malformations
- Diaphragm lesions
- Congenitaldiaphragmatic hernia
- Diaphragmatic eventration
- Diaphragmatic paralysis or paresis
- Rib cage anomalies
- Persistent fetal circulation
- Cardiac disorders
- Hematologic disorders
- Anemia
- Polycythemia
- Metabolic disorders
- Hypothermia
- Hypoglycemia
- Metabolic acidosis
- Neurologic and muscle disorders
- Braindisorders
- Spinal cord injury
- Neuromuscular disorders
- Drugs
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Stertor, Stridor, and Airway Obstruction:
Principal Causes of Airway Obstruction
(The Diagnostic Approach to Symptoms and Signs in Pediatrics)
- Noseand nasopharynx
- Congenital
- Choanal atresia
- Craniofacial anomalies
- Midline masses
- Infection/inflammation
- Rhinitis
- Adenoid hypertrophy
- Polyps
- Trauma
- Neoplasm
- Oropharynx and hypopharynx
- Congenital
- Micrognathiaand other skull base abnormalities
- Macroglossia
- Decreased pharyngeal muscle tone
- Infection/inflammation
- Tonsillarhypertrophy
- Abscess
- Foreign body
- Trauma
- Neoplasm
- Supraglottic
- Congenital
- Laryngomalacia
- Laryngeal cyst and laryngocele
- Infection/inflammation
- Supraglottitis
- Gastroesophageal reflux
- Hereditary angioedema
- Trauma
- Neoplasm
- Glottic
- Congenital
- Laryngeal web
- Laryngeal cleft
- Vocal cord paralysis
- Infection/inflammation
- Laryngitis
- Laryngeal spasm
- Foreign body
- Trauma
- Neoplasm
- Subglottic
- Congenital
- Subglottic stenosis
- Cysts
- Infection/inflammation
- Croup
- Bacterial tracheitis
- Trauma
- Neoplasm
- Tracheobronchial
- Congenital
- Tracheomalacia
- Tracheal web
- Tracheal cysts
- Tracheal stenosis
- Vascular anomalies
- Infection/inflammation
- Foreign body
- Trauma
- Neoplasm
- Tracheal
- Thyroid
- Mediastinal masses
- Psychogenic
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Source: The Diagnostic Approach to Symptoms and Signs in Pediatrics, 2006
Apnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Airway obstruction.Occlusion or compression of the trachea, central airways, or smaller airways can cause sudden apnea by blocking the patient's airflow and producing acute respiratory failure.
Brain stem dysfunction.Primary or secondary brain stem dysfunction can cause apnea by destroying the brain stem's ability to initiate respirations. Apnea may arise suddenly (as in trauma, hemorrhage, or infarction) or gradually (as in degenerative disease or tumor). Apnea may be preceded by a decreased LOC and by various motor and sensory deficits.
Neuromuscular failure.Trauma or disease can disrupt the mechanics of respiration, causing sudden or gradual apnea. Associated findings include diaphragmatic or intercostal muscle paralysis from injury or respiratory weakness or paralysis from acute or degenerative disease.
Parenchymatous lung disease.An accumulation of fluid within the alveoli produces apnea by interfering with pulmonary gas exchange and producing acute respiratory failure. Apnea may arise suddenly, as in near drowning and acute pulmonary edema, or gradually, as in emphysema. Apnea may be preceded by crackles and labored respirations with accessory muscle use.
Pleural pressure gradient disruption.Conversion of normal negative pleural air pressure to positive pressure by chest wall injuries (such as flail chest) causes lung collapse, producing respiratory distress and, if untreated, apnea. Associated signs include an asymmetrical chest wall and asymmetrical or paradoxical respirations.
Pulmonary capillary perfusion
decrease.Apnea can stem from obstructed pulmonary circulation, most commonly due to heart failure or lack of circulatory patency. It occurs suddenly in cardiac arrest, massive pulmonary embolism, and most cases of severe shock. In contrast, it occurs progressively in septic shock and pulmonary hypertension. Related findings include hypotension, tachycardia, and edema.
Other causes
Drugs.Central nervous system (CNS) depressants may cause hypoventilation and apnea. Benzodiazepines may cause respiratory depression and apnea when given I.V. along with other CNS depressants to elderly or acutely ill patients. Drug overdose can lead to respiratory depression and apnea.
Neuromuscular blockers—such as curariform drugs and anticholinesterases—may produce sudden apnea because of respiratory muscle paralysis.
Sleep-related apneas.These repetitive apneas occur during sleep from airflow obstruction or brain stem dysfunction.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Bradypnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Diabetic ketoacidosis.Bradypnea occurs late in patients with severe, uncontrolled diabetes. Patients with severe ketoacidosis may experience Kussmaul's respirations. Associated signs and symptoms include a decreased LOC, fatigue, weakness, a fruity breath odor, and oliguria.
Hepatic failure.Occurring with end-stage hepatic failure, bradypnea may be accompanied by coma, hyperactive reflexes, asterixis, a positive Babinski's sign, fetor hepaticus, and other signs.
Increased intracranial pressure (ICP).A late sign of increased ICP, a life-threatening condition, bradypnea is preceded by a decreased LOC, deteriorating motor function, and fixed, dilated pupils. The triad of bradypnea, bradycardia, and hypertension is a classic sign of late medullary strangulation.
Renal failure.Occurring with end-stage renal failure, bradypnea may be accompanied by convulsions, a decreased LOC, GI bleeding, hypotension or hypertension, uremic frost, and diverse other signs.
Respiratory failure.Bradypnea occurs with end-stage respiratory failure along with cyanosis, diminished breath sounds, tachycardia, mildly increased blood pressure, and a decreased LOC.
Other causes
Drugs.Overdose with an opioid analgesic or, less commonly, a sedative, barbiturate, phenothiazine, or other CNS depressant can cause bradypnea. The use of any of these drugs with alcohol can also cause bradypnea.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Dyspnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Acute respiratory distress syndrome (ARDS).ARDS is a life-threatening form of noncardiogenic pulmonary edema that usually produces acute dyspnea as the first complaint. Progressive respiratory distress then develops with restlessness, anxiety, decreased mental acuity, tachycardia, and crackles and rhonchi in both lung fields. Other findings include cyanosis, tachypnea, motor dysfunction, and intercostal and suprasternal retractions. Severe ARDS can produce signs of shock, such as hypotension and cool, clammy skin.
Amyotrophic lateral sclerosis (ALS).ALS causes the slow onset of dyspnea that worsens with time. Other features include dysphagia, dysarthria, muscle weakness and atrophy, fasciculations, shallow respirations, tachypnea, and emotional lability.
Anthrax (inhalation).Dyspnea is a symptom of the second stage of anthrax, along with a fever, stridor, and hypotension (the patient usually dies within 24 hours). Initial symptoms of this disorder, which are due to the inhalation of aerosolized spores (from infected animals or as a result of bioterrorism) from the bacterium Bacillus anthracis, are flulike and include a fever, chills, weakness, a cough, and chest pain.
Aspiration of a foreign body.Acute dyspnea marks this life-threatening condition, along with paroxysmal intercostal, suprasternal, and substernal retractions. The patient may also display accessory muscle use, inspiratory stridor, tachypnea, decreased or absent breath sounds, possibly asymmetrical chest expansion, anxiety, cyanosis, diaphoresis, and hypotension.
Asthma.Acute dyspneic attacks occur with asthma, along with audible wheezing, a dry cough, accessory muscle use, nasal flaring, intercostal and supraclavicular retractions, tachypnea, tachycardia, diaphoresis, prolonged expiration, flushing or cyanosis, and apprehension. Medications that block beta receptors can exacerbate asthma attacks.
Avian influenza.These potentially life-threatening viruses are spread to humans through contact with infected poultry or surfaces contaminated with infected bird excretions. Within 1 to 5 days of exposure to avian influenza, the patient typically develops flulike symptoms, such as fever, sore throat, cough, and muscle aches. Those with severe forms of the virus may develop dyspnea caused by acute respiratory distress or pneumonia.
Blast lung injury.The result of a forceful percussive wave following an explosive detonation, blast lung injury is commonly characterized by dyspnea and hypoxia. Worldwide terrorist activity has recently increased the incidence of this condition, which may also cause cyanosis, chest pain, wheezing, and hemoptysis. Chest X-ray, the primary diagnostic tool, reveals a characteristic “butterfly” pattern. Many of these patients suffer concomitant injuries and require complex management, usually in an intensive care setting.
Cor pulmonale.With cor pulmonale, chronic dyspnea begins gradually with exertion and progressively worsens until it occurs even at rest. Underlying cardiac or pulmonary disease is usually present. The patient may have a chronic productive cough, wheezing, tachypnea, jugular vein distention, dependent edema, and hepatomegaly. He may also experience increasing fatigue, weakness, and light-headedness.
Emphysema.Emphysema is a chronic disorder that gradually causes progressive exertional dyspnea. A history of smoking, an alpha1-antitrypsin deficiency, or exposure to an occupational or environmental irritant usually accompanies barrel chest, accessory muscle hypertrophy, diminished breath sounds, anorexia, weight loss, malaise, peripheral cyanosis, tachypnea, pursed-lip breathing, prolonged expiration and, possibly, a chronic productive cough. Clubbing is a late sign.
Flail chest.Sudden dyspnea results from multiple rib fractures and is accompanied by paradoxical chest movement, severe chest pain, hypotension, tachypnea, tachycardia, and cyanosis. Bruising and decreased or absent breath sounds occur over the affected side.
Heart failure.Dyspnea usually develops gradually in patients with heart failure. Chronic paroxysmal nocturnal dyspnea, orthopnea, tachypnea, tachycardia, palpitations, a ventricular gallop, fatigue, dependent peripheral edema, hepatomegaly, a dry cough, weight gain, and loss of mental acuity may occur. With acute onset, heart failure may produce jugular vein distention, bibasilar rates, oliguria, and hypotension.
Inhalation injury.Dyspnea may develop suddenly or gradually over several hours after the inhalation of chemicals or hot gases. Increasing hoarseness, a persistent cough, sooty or bloody sputum, and oropharyngeal edema may also be present. The patient may also exhibit thermal burns, singed nasal hairs, and orofacial burns as well as crackles, rhonchi, wheezing, and signs of respiratory distress.
Monkeypox.Dyspnea is one of the less common symptoms of this rare viral disease. Infected individuals may also experience fever, muscle aches, sore throat, chills, and lymphadenopathy. A papular rash appears 1 to 3 days after the fever begins. The virus is similar to smallpox; however, the symptoms are milder and the disease is rarely fatal in developed countries.
Myasthenia gravis.Myasthenia gravis causes bouts of dyspnea as the respiratory muscles weaken. With myasthenic crisis, acute respiratory distress may occur, with shallow respirations and tachypnea.
Myocardial infarction.Sudden dyspnea occurs with crushing substernal chest pain that may radiate to the back, neck, jaw, and arms. Other signs and symptoms include nausea, vomiting, diaphoresis, vertigo, hypertension or hypotension, tachycardia, anxiety, and pale, cool, clammy skin.
Plague(Yersinia pestis).Among the symptoms of the pneumonic form of plague are dyspnea, a productive cough, chest pain, tachypnea, hemoptysis, increasing respiratory distress, and cardiopulmonary insufficiency. The onset of this virulent infection is usually sudden and includes such signs and symptoms as chills, fever, headache, and myalgia. If untreated, plague is one of the most potentially lethal diseases known.
Pleural effusion.With pneumonia, yspnea develops slowly and becomes progressively worse with pleural effusion. Initial findings include a pleural friction rub accompanied by pleuritic pain that worsens with coughing or deep breathing. Other findings include a dry cough; dullness on percussion; egophony, bronchophony, and whispered pectoriloquy; tachycardia; tachypnea; weight loss; and decreased chest motion, tactile fremitus, and decreased breath sounds. With infection, a fever may occur.
Pneumonia.With pneumonia, dyspnea occurs suddenly, usually accompanied by a fever, shaking chills, pleuritic chest pain that worsens with deep inspiration, and a productive cough. Fatigue, a headache, myalgia, anorexia, abdominal pain, crackles, rhonchi, tachycardia, tachypnea, cyanosis, decreased breath sounds, and diaphoresis may also occur.
Pneumothorax.Pneumothorax is a life-threatening disorder that causes acute dyspnea unrelated to the severity of the pain. Sudden, stabbing chest pain may radiate to the arms, face, back, or abdomen. Other signs and symptoms include anxiety, restlessness, a dry cough, cyanosis, decreased vocal fremitus, tachypnea, tympany, decreased or absent breath sounds on the affected side, asymmetrical chest expansion, splinting, and accessory muscle use. In patients with tension pneumothorax, tracheal deviation occurs in addition to these typical findings. Decreased blood pressure and tachycardia may also occur.
Poliomyelitis (bulbar).Dyspnea develops gradually and progressively worsens. Additional signs and symptoms include a fever, facial weakness, dysphasia, hypoactive deep tendon reflexes, decreased mental acuity, dysphagia, nasal regurgitation, and hypopnea.
Pulmonary edema.Commonly preceded by signs of heart failure, such as jugular vein distention and orthopnea, pulmonary edema—a life-threatening disorder—causes acute dyspnea. Other features include tachycardia, tachypnea, crackles in both lung fields, a third heart sound (S3 gallop), oliguria, a thready pulse, hypotension, diaphoresis, cyanosis, and marked anxiety. The patient's cough may be dry or may produce copious amounts of pink, frothy sputum.
Pulmonary embolism.Acute dyspnea that's usually accompanied by sudden pleuritic chest pain characterizes pulmonary embolism, a life-threatening disorder. Related findings include tachycardia, a low-grade fever, tachypnea, a nonproductive or productive cough with blood-tinged sputum, a pleural friction rub, crackles, diffuse wheezing, dullness on percussion, decreased breath sounds, diaphoresis, restlessness, and acute anxiety. A massive embolism may cause signs of shock, such as hypotension and cool, clammy skin.
Severe acute respiratory syndrome (SARS).SARS generally begins with a fever (usually greater than 100.4° F [38° C]). Other symptoms include a headache, malaise, a dry nonproductive cough, and dyspnea. The severity of the illness is highly variable, ranging from mild illness to pneumonia and, in some cases, progressing to respiratory failure and death.
Shock.Dyspnea arises suddenly and worsens progressively with shock, a life-threatening disorder. Related findings include severe hypotension, tachypnea, tachycardia, decreased peripheral pulses, decreased mental acuity, restlessness, anxiety, and cool, clammy skin.
Tuberculosis.Dyspnea commonly occurs with chest pain, crackles, and a productive cough. Other findings are night sweats, a fever, anorexia and weight loss, vague dyspepsia, palpitations on mild exertion, and dullness on percussion.
Tularemia.Also known as rabbit fever, tularemia causes dyspnea along with a fever, chills, a headache, generalized myalgia, a nonproductive cough, pleuritic chest pain, and empyema.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Hyperpnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Head injury.Hyperpnea that results from a severe head injury is called central neurogenic hyperventilation. Whether its onset is acute or gradual, this type of hyperpnea indicates damage to the lower midbrain or upper pons. Accompanying signs reflect the site and extent of injury and can include loss of consciousness; soft-tissue injury or bony deformity of the face, head, or neck; facial edema; clear or bloody drainage from the mouth, nose, or ears; raccoon eyes; Battle's sign; an absent doll's eye sign; and motor and sensory disturbances.
Signs of increased intracranial pressure include decreased response to painful stimulation, loss of pupillary reaction, bradycardia, increased systolic pressure, and a widening pulse pressure.
Hyperventilation syndrome.Acute anxiety triggers episodic hyperpnea, resulting in respiratory alkalosis. Other findings may include agitation, vertigo, syncope, pallor, circumoral and peripheral paresthesia, muscle twitching, carpopedal spasm, weakness, and arrhythmias.
Hypoxemia.Many pulmonary disorders that cause hypoxemia—for example, pneumonia, pulmonary edema, chronic obstructive pulmonary disease, and pneumothorax—may cause hyperpnea and episodes of hyperventilation with chest pain, dizziness, and paresthesia. Other effects include dyspnea, a cough, crackles, rhonchi, wheezing, and decreased breath sounds.
Ketoacidosis.Alcoholic ketoacidosis (occurring most commonly in females with a history of alcohol abuse) typically follows cessation of drinking after a marked increase in alcohol consumption has caused severe vomiting. Kussmaul's respirations begin abruptly and are accompanied by vomiting for several days, a fruity breath odor, slight dehydration, abdominal pain and distention, and absent bowel sounds. The patient is alert and has a normal blood glucose level, unlike the patient with diabetic ketoacidosis.
Diabetic ketoacidosis is potentially life-threatening and typically produces Kussmaul's respirations. The patient usually experiences polydipsia, polyphagia, and polyuria before the onset of acidosis; he may have a history of diabetes mellitus. Other clinical features include a fruity breath odor; orthostatic hypotension; a rapid, thready pulse; generalized weakness; a decreased LOC (lethargy to coma); nausea; vomiting; anorexia; and abdominal pain.
Starvation ketoacidosis is also potentially life-threatening and can cause Kussmaul's respirations. Its onset is gradual; typical findings include signs of cachexia and dehydration, a decreased LOC, bradycardia, and a history of severely limited food intake.
Renal failure.Acute or chronic renal failure can cause life-threatening acidosis with Kussmaul's respirations. Signs and symptoms of severe renal failure include oliguria or anuria, uremic fetor, and yellow, dry, scaly skin. Other cutaneous signs include severe pruritus, uremic frost, purpura, and ecchymoses. The patient may complain of nausea and vomiting, weakness, burning pain in the legs and feet, and diarrhea or constipation.
As acidosis progresses, corresponding clinical features include frothy sputum, pleuritic chest pain, and signs of heart failure and pleural or pericardial effusion. Neurologic signs include an altered LOC (lethargy to coma), twitching, and seizures. Hyperkalemia and hypertension, if present, require rapid intervention to prevent cardiovascular collapse.
Sepsis.A severe infection may cause lactic acidosis, resulting in Kussmaul's respirations. Other findings include tachycardia, a fever or a low temperature, chills, a headache, lethargy, profuse diaphoresis, anorexia, a cough, wound drainage, burning on urination, confusion or a change in mental status, and other signs of local infection.
Shock.Potentially life-threatening metabolic acidosis produces Kussmaul's respirations, hypotension, tachycardia, narrowed pulse pressure, a weak pulse, dyspnea, oliguria, anxiety, restlessness, stupor that can progress to coma, and cool, clammy skin. Other clinical features may include external or internal bleeding (in hypovolemic shock); chest pain or arrhythmias and signs of heart failure (in cardiogenic shock); a high fever, chills and, rarely, hypothermia (in septic shock); or stridor due to laryngeal edema (in anaphylactic shock). The onset is usually acute in hypovolemic, cardiogenic, or anaphylactic shock, but it may be gradual in septic shock.
Other causes
Drugs.Toxic levels of salicylates, ammonium chloride, acetazolamide, and other carbonic anhydrase inhibitors can cause Kussmaul's respirations. So can ingestion of methanol and ethylene glycol, found in antifreeze solutions.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Orthopnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Chronic obstructive pulmonary disease (COPD).COPD typically produces orthopnea and other dyspneic complaints, accompanied by accessory muscle use, tachypnea, tachycardia, and paradoxical pulse. Auscultation may reveal diminished breath sounds, rhonchi, crackles, and wheezing. The patient may also exhibit a dry or productive cough with copious sputum. Other features include anorexia, weight loss, and edema. Barrel chest, cyanosis, and clubbing are usually late signs.
Left-sided heart failure.Orthopnea occurs late in left-sided heart failure. If heart failure is acute, orthopnea may begin suddenly; if chronic, it may become constant. The earliest symptom of this disorder is progressively severe dyspnea. Other common early symptoms include Cheyne-Stokes respirations, paroxysmal nocturnal dyspnea, fatigue, weakness, and cough that may occasionally produce clear or blood-tinged sputum. Tachycardia, tachypnea, and crackles may also occur.
Other late findings include cyanosis, clubbing, a ventricular gallop, and hemoptysis. Left-sided heart failure may also lead to signs of shock, such as hypotension, a thready pulse, and cold, clammy skin.
Mediastinal tumor.Orthopnea is an early sign of a mediastinal tumor, resulting from pressure of the tumor against the trachea, bronchus, or lung when the patient lies down. However, he may be asymptomatic until the tumor enlarges. Then it produces retrosternal chest pain, a dry cough, hoarseness, dysphagia, stertorous respirations, palpitations, and cyanosis. Examination reveals suprasternal retractions on inspiration, bulging of the chest wall, tracheal deviation, dilated jugular and superficial chest veins, and face, neck, and arm edema.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Stridor:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Airway trauma.Local trauma to the upper airway commonly causes acute obstruction, resulting in the sudden onset of stridor. Accompanying this sign are dysphonia, dysphagia, hemoptysis, cyanosis, accessory muscle use, intercostal retractions, nasal flaring, tachypnea, progressive dyspnea, and shallow respirations. Palpation may reveal subcutaneous crepitation in the neck or upper chest.
Anaphylaxis.With a severe allergic reaction, upper airway edema and laryngospasm cause stridor and other signs and symptoms of respiratory distress: nasal flaring, wheezing, accessory muscle use, intercostal retractions, and dyspnea. The patient may also develop nasal congestion and profuse, watery rhinorrhea. Typically, these respiratory effects are preceded by a feeling of impending doom or fear, weakness, diaphoresis, sneezing, nasal pruritus, urticaria, erythema, and angioedema. Common associated findings include chest or throat tightness, dysphagia and, possibly, signs of shock, such as hypotension, tachycardia, and cool, clammy skin.
Anthrax (inhalation).Initial signs and symptoms of anthrax are flulike and include fever, chills, weakness, cough, and chest pain. The disease generally occurs in two stages with a period of recovery after the initial symptoms. The second stage develops abruptly with rapid deterioration marked by stridor, fever, dyspnea, and hypotension generally leading to death within 24 hours. Radiologic findings include mediastinitis and symmetric mediastinal widening.
Hypocalcemia.With hypocalcemia, laryngospasm can cause stridor. Other findings include paresthesia, carpopedal spasm, and positive Chvostek's and Trousseau's signs.
Inhalation injury.Within 48 hours after inhalation of smoke or noxious fumes, the patient may develop laryngeal edema and bronchospasms, resulting in stridor. Associated signs and symptoms include singed nasal hairs, orofacial burns, coughing, hoarseness, sooty sputum, crackles, rhonchi, wheezes, and other signs and symptoms of respiratory distress, such as dyspnea, accessory muscle use, intercostal retractions, and nasal flaring.
Mediastinal tumor.Commonly producing no symptoms at first, a mediastinal tumor may eventually compress the trachea and bronchi, resulting in stridor. Its other effects include hoarseness, a brassy cough, a tracheal shift or tug, dilated neck veins, swelling of the face and neck, stertorous respirations, and suprasternal retractions on inspiration. The patient may also report dyspnea, dysphagia, and pain in the chest, shoulder, or arm.
Retrosternal thyroid.Retrosternal thyroid causes stridor, dysphagia, cough, hoarseness, and tracheal deviation. It can also cause signs of thyrotoxicosis.
Other causes
Diagnostic tests.Bronchoscopy or laryngoscopy may precipitate laryngospasm and stridor.
Foreign body aspiration.Sudden stridor is characteristic in foreign body aspiration, a life-threatening situation. Related findings include an abrupt onset of dry, paroxysmal coughing; gagging or choking; hoarseness; tachycardia; wheezing; dyspnea; tachypnea; intercostal muscle retractions; diminished breath sounds; cyanosis; and shallow respirations. The patient typically appears anxious and distressed.
Treatments.After prolonged intubation, the patient may exhibit laryngeal edema and stridor when the tube is removed. Aerosol therapy with epinephrine may reduce stridor. Reintubation may be necessary in some cases. Neck surgery, such as thyroidectomy, may cause laryngeal paralysis and stridor.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
Paroxysmal nocturnal dyspnea:
Medical causes
(Nursing: Interpreting Signs and Symptoms)
Left-sided heart failure.Dyspnea—on exertion, during sleep, and eventually even at rest—is an early sign of left-sided heart failure. This sign is characteristically accompanied by Cheyne-Stokes respirations, diaphoresis, weakness, wheezing, and a persistent, nonproductive cough or a cough that produces clear or blood-tinged sputum. As the patient's condition worsens, he develops tachycardia, tachypnea, alternating pulse (commonly initiated by a premature beat), a ventricular gallop, crackles, and peripheral edema.
With advanced left-sided heart failure, the patient may also exhibit severe orthopnea, cyanosis, clubbing, hemoptysis, and cardiac arrhythmias as well as signs and symptoms of shock, such as hypotension, a weak pulse, and cold, clammy skin.
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Source: Nursing: Interpreting Signs and Symptoms, 2007
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