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Chapter 17 Dyspnea Sabina Braithwaite and Debra Perina

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Chapter 17 Dyspnea Sabina Braithwaite and Debra Perina Chapter 17 Dyspnea Sabina Braithwaite and Debra Perina ■ PERSPECTIVE Pathophysiology Dyspnea is the term applied to the sensation of breathlessness The actual mechanisms responsible for dyspnea are unknown. and the patient’s reaction to that sensation. It is an uncomfort- Normal breathing is controlled both centrally by the respira- able awareness of breathing difficulties that in the extreme tory control center in the medulla oblongata, as well as periph- manifests as “air hunger.” Dyspnea is often ill defined by erally by chemoreceptors located near the carotid bodies, and patients, who may describe the feeling as shortness of breath, mechanoreceptors in the diaphragm and skeletal muscles.3 chest tightness, or difficulty breathing. Dyspnea results Any imbalance between these sites is perceived as dyspnea. from a variety of conditions, ranging from nonurgent to life- This imbalance generally results from ventilatory demand threatening. Neither the clinical severity nor the patient’s per- being greater than capacity.4 ception correlates well with the seriousness of underlying The perception and sensation of dyspnea are believed to pathology and may be affected by emotions, behavioral and occur by one or more of the following mechanisms: increased cultural influences, and external stimuli.1,2 work of breathing, such as the increased lung resistance or The following terms may be used in the assessment of the decreased compliance that occurs with asthma or chronic dyspneic patient: obstructive pulmonary disease (COPD), or increased respira- tory drive, such as results from severe hypoxemia, acidosis, or Tachypnea: A respiratory rate greater than normal. Normal rates centrally acting stimuli (toxins, central nervous system events). range from 44 cycles/min in a newborn to 14 to 18 cycles/ Pulmonary stretch receptors also are thought to play a role. min in adults. Hyperpnea: Greater than normal minute ventilation to meet metabolic requirements. ■ DIAGNOSTIC APPROACH Hyperventilation: A minute ventilation (determined by respira- Differential Considerations tory rate and tidal volume) that exceeds metabolic demand. Arterial blood gases (ABG) characteristically show a normal Dyspnea is subjective and has many different potential causes.5 partial pressure of oxygen (Po2) with an uncompensated The differential diagnosis list can be divided into acute and respiratory alkalosis (low partial pressure of carbon dioxide chronic causes, of which many are pulmonary. Other etiologies [Pco2] and elevated pH). include cardiac, metabolic, infectious, neuromuscular, trau- Dyspnea on exertion: Dyspnea provoked by physical effort or matic, and hematologic (Table 17-1). exertion. It often is quantified in simple terms, such as the number of stairs or number of blocks a patient can manage before the onset of dyspnea. Pivotal Findings Orthopnea: Dyspnea in a recumbent position. It usually is mea- History sured in number of pillows the patient must use to lie in bed (e.g., two-pillow orthopnea). Duration of Dyspnea. Chronic or progressive dyspnea usually Paroxysmal nocturnal dyspnea: Sudden onset of dyspnea occur- denotes primary cardiac or pulmonary disease.6 Acute dys- ring while reclining at night, usually related to the presence pneic spells may result from asthma exacerbation; infection; of congestive heart failure. pulmonary embolus; intermittent cardiac dysfunction; psycho- genic causes; or inhalation of irritants, allergens, or foreign Epidemiology bodies. Onset of Dyspnea. Sudden onset of dyspnea should lead to Dyspnea is a common presenting complaint among emergency consideration of pulmonary embolism (PE) or spontaneous department patients of all ages. Causes vary widely and may pneumothorax. Dyspnea that builds slowly over hours or be due to a benign, self-limited condition or significant pathol- days may represent a flare of asthma or COPD; pneumonia; ogy that can produce long-term morbidity and premature recurrent, small pulmonary emboli; congestive heart failure; or mortality. malignancy. 124 125 Table 17-1 Differential Diagnoses for Acute Dyspnea Chapter Chapter 17 ORGAN SYSTEM CRITICAL DIAGNOSES EMERGENT DIAGNOSES NONEMERGENT DIAGNOSES Pulmonary Airway obstruction Spontaneous pneumothorax Pleural effusion Pulmonary embolus Asthma Neoplasm / Noncardiogenic edema Cor pulmonale Pneumonia (CAP score < = 70) Dyspnea Anaphylaxis Aspiration COPD Ventilatory failure Pneumonia Cardiac Pulmonary edema Pericarditis Congenital heart disease Myocardial infarction Valvular heart disease Cardiac tamponade Cardiomyopathy Primarily Associated with Normal or Increased Respiratory Effort Abdominal Mechanical interference Pregnancy Hypotension, sepsis from ruptured viscus, bowel Ascites obstruction, inflammatory/infectious process Obesity Psychogenic Hyperventilation syndrome Somatization disorder Panic attack Metabolic/endocrine Toxic ingestion Renal failure Fever DKA Electrolyte abnormalities Thyroid disease Metabolic acidosis Infectious Epiglottitis Pneumonia (CAP score < = 70) Pneumonia (CAP score < = 70) Traumatic Tension pneumothorax Simple pneumothorax, hemothorax Rib fractures Cardiac tamponade Diaphragmatic rupture Flail chest Hematologic Carbon monoxide poisoning Anemia Acute chest syndrome Primarily Associated with Decreased Respiratory Effort Neuromuscular CVA, intracranial insult Multiple sclerosis ALS Organophosphate poisoning Guillain-Barré syndrome Polymyositis Tick paralysis Porphyria ALS, amyotrophic lateral sclerosis; CAP, community-acquired pneumonia; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; DKA, diabetic ketoacidosis. Signs Positional Changes. Orthopnea can result from left-sided heart failure, COPD, or neuromuscular disorders. One of the earliest Physical signs in dyspneic patients may be consistent with symptoms seen in patients with diaphragmatic weakness from specific illnesses (Table 17-2). Physical findings found in neuromuscular disease is orthopnea.7 Paroxysmal nocturnal specific diseases also can be grouped as presenting patterns dyspnea is most common in patients with left-sided heart (Table 17-3). failure,6 but also can be found in COPD. Exertional dyspnea commonly is associated with COPD, but also can be seen with poor cardiac reserve and abdominal loading. Abdominal Ancillary Studies loading, caused by ascites, obesity, or pregnancy, leads to ele- vation of the diaphragm, resulting in less effective ventilation Specific findings obtained from the history and physical exam- and dyspnea. ination should be used to determine which ancillary studies Trauma. Dyspnea can result from trauma, causing fractured are needed (Table 17-4). Bedside oxygen saturation determi- ribs, flail chest, hemothorax, pneumothorax, diaphragmatic nations, or selective use of ABGs when oximetry is not reli- rupture, pericardial effusion, cardiac tamponade, or neurologic able, are useful in determining the degree of hypoxia and the injury. need for supplemental oxygen or assisted ventilation. An addi- tional resource for quickly assessing ventilatory status is non- Symptoms invasive waveform capnography. Using both the end-tidal CO2 value and the shape of the waveform itself can be helpful in Patient descriptions of dyspnea vary significantly and gener- assessing the adequacy of ventilations as well as potential ally correlate poorly with severity. Fever suggests an infectious causes of the dyspnea (See Chapter 3). An electrocardiogram cause. Anxiety may point to panic attack or psychogenic may be useful if the etiology is cardiac or suggests acute pul- dyspnea, if no organic cause can be isolated. PE or myocardial monary hypertension. infarction may present with isolated dyspnea or with associ- Serum electrolytes may suggest less common possible ated chest pain, particularly if the pain is constant, dull, or causes, such as hypokalemia, hypophosphatemia, diabetic visceral.8,9 If the pain is sharp and worsened by deep breathing ketoacidosis, or hypocalcemia. A complete blood count may but not by movement, pleural effusion and pleurisy or pleural identify severe anemia or thrombocytopenia associated with irritation from pneumonia or PE are possible. Spontaneous sepsis. The white blood cell count is not sufficiently sensitive pneumothorax also may produce sharp pain with deep breath- or specific to be of discriminatory value. Cardiac markers and ing that is not worsened by movement. D-dimer assay may be useful in pursuing etiologies such as 126 Table 17-2 Pivotal Findings in Physical Examination SIGN PHYSICAL FINDING DIAGNOSES TO CONSIDER Vital signs Tachypnea Pneumonia, pneumothorax Hypopnea Intracranial insult, drug/toxin ingestion Tachycardia PE, traumatic chest injury Hypotension Tension pneumothorax Fever Pneumonia, PE General appearance Cachexia, weight loss Malignancy, acquired immune disorder, mycobacterial infection Cardinal Presentations • Obesity Hypoventilation, sleep apnea, PE wo Pregnancy PE t Barrel chest COPD tion “Sniffing” position Epiglottitis C e “Tripoding” position COPD/asthma with severe distress S / Traumatic injury Pneumothorax (simple, tension), rib fractures, flail chest, hemothorax, pulmonary contusion Skin/nails Tobacco stains/odor COPD, malignancy, infection Clubbing Chronic hypoxia, intracardiac shunts or pulmonary vascular anomalies Pallid skin/conjunctivae Anemia Muscle wasting Neuromuscular disease Bruising Chest wall: rib fractures, pneumothorax Diffuse: thrombocytopenia, chronic steroid use, anticoagulation Subcutaneous emphysema Rib fractures, pneumothorax, tracheobronchial disruption
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