DDx: Dyspnea Flashcards Preview

10 PULMONARY AND CRITICAL CARE MEDICINE > DDx: Dyspnea > Flashcards

Flashcards in DDx: Dyspnea Deck (36):
1

Differential Diagnosis of Acute "Dyspnea"Pulmonary Causes:

"Subjective SOB"

Anaphylaxis

Asthma (may also present as chronic dyspnea)

Pneumonia

Pneumothorax

Pleural effusion/hemothorax

Pulmonary embolism

Aspiration

2

Anaphylaxis

Allergen exposure

Urticaria, facial edema, wheezing

3

Asthma

Episodic cough, chest tightness, related to exercise, nocturnal symptoms

Wheezing

History of rhinitis and eczema...intermittent dyspnea and coughing.

Rx: Aspirin is a common trigger for bronchoconstriction in patients with asthma, especially those with concurrent chronic rhinitis andnasal polyps.  Nonselective beta blockers (eg, propranolol, nadolol, sotalol, timolol) act on β1 and β2 receptors and often triggerbronchoconstriction in patients with underlying asthma. 

4

Pneumonia

Fever, cough, sputum; pleuritic chest pain (acute)

Fever, crackles, dullness to percussion

5

Pneumothorax

History of trauma, pleuritic chest pain

Absent breath sounds, deviated trachea (tension pneumothorax)

6

Pleural effusion/hemothorax

History of trauma or pneumonia

Dullness to percussion, absent breath sounds

7

Pulmonary embolism

Sudden-onset dyspnea, nonproductive cough, tachycardia, and mild hypoxia is highly suggestive of acute pulmonary embolism (PE). 

Tx: Early, effective anticoagulation decreases the mortality risk of acute PE and should be considered in patients without absolute contraindications (eg, hemorrhagic stroke, massive gastrointestinal bleed).

Modified Wells score 

 +3 points

Clinical signs of DVT

Alternate diagnosis less likely than PE

 +1.5 points

Previous PE or DVT

Heart rate >100

Recent surgery or immobilization

+1 point

Hemoptysis

Cancer

Total score for clinical probability
≤4 = PE unlikely
>4 = PE likely

Dx: Given clinically stablity (normotensive, mild hypoxemia) with no evidence of distress, the diagnosis of PE can be confirmed with CT angiography (CTA).  If CTA confirms PE, clinical judgment can dictate whether anticoagulation is initiated or other options are pursued (eg, inferior vena cava filter placement) based on the estimated risk of bleeding from the peptic ulcer.

8

Aspiration

Observed aspiration, symptoms start during or shortly after eating or vomiting. Patient with altered mental status or abnormal gag reflex at baseline

Unilateral, and sometimes bilateral, crackles, more commonly on the right, fever

9

Differential Diagnosis of Chronic Dyspnea: Cardiovascular Causes​

Aortic stenosis

Mitral stenosis

Mitral regurgitation

Chronic constrictive pericarditis

Cor Pulmonale

Hypertrophic Cardiomyopathy

10

Aortic stenosis

History of heart murmur, chest pain, syncope, dyspnea; history of rheumatic fever; history of aortic coarctation

Crescendo-decrescendo systolic murmur at right upper sternal border cardiac base with radiation to carotid arteries

11

Mitral stenosis

History of rheumatic fever, heart murmur

Opening snap followed by diastolic murmur with presystolic accentuation

12

Mitral regurgitation

History of heart murmur, mitral valve prolapse, or myocardial infarction

Holosystolic murmur at cardiac base

13

Chronic constrictive pericarditis

Hx: History of pericarditis, possible chest pain; recognized potential complication after coronary artery bypass surgery.

Px: Evidence of elevated right ventricular heart pressure (jugular venous distention, hepatojugular reflux, pedal edema), clear lungs, edema, tricuspid regurgitation, pulsatile liver

Kussmaul sign (jugular vein engorgement with inspiration)

Dx: Echocardiographic findings of restrictive filling and ventricular interdependence (ie, diastolic filling of one ventricular chamber that impedes that of the other, as may be manifested by a to-and-fro diastolic motion of the ventricular septum).

Cardiac computed tomography or cardiac magnetic resonance imaging would likely show pericardial thickening.

 

14

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is typically asymptomatic in childhood and adolescence.

Symptoms that develop in HCM include angina, dyspnea, palpitations, fatigue, dizziness, and syncope. Symptoms may be caused by diastolic dysfunction, myocardial ischemia, outflow obstruction with or without associated mitral regurgitation, or atrial fibrillation. The most common pattern of hypertrophy is asymmetric septal hypertrophy. In this type, a midsystolic murmur caused by left ventricular outflow tract obstruction may be evident. Maneuvers that decrease preload (Valsalva maneuver) enhance the murmur, and those that augment venous return (leg elevation) diminish the murmur.

Patients with symptoms (eg, syncope, heart failure, angina) should be treated with negative inotropic agents (eg, beta blockers, verapamil, disopyramide) as the initial medical therapy.  Beta blockers (eg, metoprolol, atenolol) are the most commonly used agents for initial monotherapy. 

15

Differential Diagnosis of Chronic Dyspnea: Pulmonary Causes

COPD

Interstitial lung disease

Pulmonary hypertension

Pleural effusion/hemothorax

Hepatopulmonary syndrome

16

COPD

Hx: Smoking history, cough, sputum

Px: Diminished breath sounds, wheezing, prolonged expiration, large chest

Dx: Increased residual volume and increased total lung capacity.

Tx: Low-dose (20 mg) extended-release morphine given daily has been used to relieve dyspnea in patients with advanced COPD.

17

Interstitial lung disease

Hx: Possible exposure history (silica, asbestos, smoking); collagen vascular disease (scleroderma)

Px: Possible clubbing (pulmonary fibrosis), dry crackles (pulmonary fibrosis)

Dx: Associated with a reduction in both total lung capacity and residual volume.

18

Pulmonary hypertension

May be idiopathic or related to other disease, such as interstitial lung disease (ILD), chronic thromboembolic disease, other causes (scleroderma, sarcoidosis), or cardiac shunts (atrial septal defect)

Hx: Right ventricular failure develops late in the disease and manifests with right ventricular heave, jugular venous distension, tender hepatomegaly, ascites, edema, etc. 

Px: Loud P2, fixed split S2, right-sided S3, pansystolic tricuspid regurgitant murmur, clear lungs or crackles depending on cause.

Dx: CRX shows enlargement of the pulmonary arteries with rapid tapering of the distal vessels (pruning) and enlargement of the right ventricle.  An EKG may show right axis deviation, which is secondary to right ventricular strain and hypertrophy due to pulmonary hypertension.  Diagnosis can only be confirmed by right heart catheterization.

Untreated pulmonary hypertension would eventually lead to Cor pulmonale.

 

 

19

Pleural effusion/hemothorax

History of cancer, possible chest pain

Dullness to percussion, absent breath sounds

20

Hepatopulmonary syndrome

Cirrhosis, platypnea (dyspnea sitting up, relieved lying down)

Findings of chronic liver disease, normal pulmonary examination

21

Differential Diagnosis of Chronic Dyspnea: Other Causes

Anemia

Thyrotoxicosis

Neuromuscular disease

Deconditioning

22

Anemia

History of blood loss or hemolytic disease

Conjunctival pallor

23

Thyrotoxicosis

Heat intolerance, weight loss, nervousness

Possible goiter

24

Neuromuscular disease

Dx: Normal cardiac and pulmonary examinations.

Pulmonary function tests show a restrictive pattern without evidence of obstruction and with increased residual volume. Residual volume is increased because of the patient's inability to exhale fully.

25

Deconditioning

Situations leading to decreased exercise tolerance

Normal cardiac and pulmonary examinations

26

Differential Diagnosis of Acute Dyspnea: Cardiovascular Causes:

Heart failure (acute)

Myocardial infarction

Pericardial tamponade

27

Heart failure (acute)

I (asymptomatic) 5%-10% Mortality

II (symptomatic; slight limitation of physical activity) 15%-30% Mortality

IIIa (symptomatic; marked limitation of physical activity) 15%-30% Mortality

IIIa (symptomatic; marked limitation of physical activity) 15%-30% Mortality

IV (inability to perform any physical activity without symptoms) 50%-60% Mortality

Hx: Cardiovascular risk factors, paroxysmal nocturnal dyspnea

Px: Jugular venous distention 0.92 (specificity), S3 gallop 0.99, Pulmonary crackles 0.78, Hepatojugular reflux  0.96, Ascites 0.97, Edema 0.78.

Dx: EKG, Labs, BNP level >100 pg/mL is 90% sensitive and 73% specific in the diagnosis of patients with heart failure in the emergency department.  Patients with chronic heart failure may have BNP levels <100 pg/mL. Other conditions that raise BNP levels include acute myocardial infarction, pulmonary embolism, chronic kidney disease, older age, and female sex. BNP is reduced by obesity.  Do not routinely measure BNP in patients with typical signs and symptoms of heart failure.

Chest radiography may be helpful in determining the cause of dyspnea. Once heart failure is diagnosed, serial chest radiographs are not sensitive to small changes in pulmonary vascular congestion and are not recommended.

Echocardiography can help identify specific causes of heart failure.  Echocardiography is necessary for distinguishing systolic heart failure from heart failure with preserved systolic function.

Coronary angiography for patients with new-onset heart failure who have angina are potential candidates for revascularization and evaluation for ischemia.

Tx: A 5-mg dose of oral morphine given four times daily has been shown to help relieve dyspnea in patients with end-stage heart failure. 

Rx: Initial therapy: 

ACE inhibitor (if ACE inhibitor is not tolerated because of cough, an ARB can be used; if ACE inhibitor is contraindicated because of hyperkalemia or renal insufficiency, combined hydralazine and isosorbide dinitrate can be used)

β-Blocker: carvedilol and extended- release metoprolol (succinate) are approved for the treatment of heart failure.  In general, β-blockers should not be initiated when a patient is acutely decompensated (hypotensive or volume overloaded), as initiation of therapy is associated with a transient decline in cardiac output. β-Blockers can be initiated and tolerated once euvolemia or near-euvolemia has been established.

Additional therapy: Diuretic as needed to maintain euvolemia [loop diuretics (eg, furosemide, bumetanide, torsemide)]

Aldosterone antagonists (spironolactone or eplerenone)

Combined hydralazine and isosorbide dinitrate (for black patients)

Digoxin is used primarily for symptom control.

Tx: Limiting dietary sodium to 2 g daily and fluid to 2 liters per day and recording daily weights results in fewer hospitalizations for patients with decompensated heart failure.

Device threapy Indications:  

Cardiac Resynchronization Therapy: Implantable Cardioverter-Defibrillator (ICD) is an internal defibrillator that senses dangerous cardiac arrhythmias and automatically converts the rhythm to sinus rhythm by either administering a high-energy shock or delivering a short series of paced beats.  

NYHA Class II or III while on optimal medical therapy AND: 

Life expectancy >1 year AND

Either of the following:

Ischemic or nonischemic cardiomyopathy with ejection fraction ≤35% (primary prevention)

History of hemodynamically significant ventricular arrhythmia or cardiac arrest (secondary prevention)

Cardiac Resynchronization Therapy: Biventricular Pacing (pacing of both the right and left ventricles that improves pump function cause by dyssynchrony because of the conduction delay)

ALL of the following:

NYHA Class III or IV

Ejection fraction ≤35%

Ventricular dyssynchrony (QRS duration >120 msec)

Cardiac transplantation improves survival, functional status, and quality of life in patients with NYHA Class III or IV heart failure. Relative contraindications to cardiac transplantation include age >65 years, end-organ damage from diabetes or vascular disease, malignancy, previous stroke, lack of psychosocial support, or active psychiatric illness.

28

Myocardial infarction

Cardiovascular risk factors, chest pain, nausea, diaphoresis

S3 and/or S4, jugular venous distention, possible mitral regurgitant murmur, pulmonary crackles

29

Pericardial tamponade

History of trauma, preceding “flu” symptoms, collagen vascular disease

Jugular venous distention, clear lungs, pulsus paradoxus, hypotension

30

Differential Diagnosis of Acute Dyspnea: Upper Airway Causes:

Tracheal stenosis, tracheomalacia

Vocal cord dysfunction

Vocal cord paralysis

Obstructive Sleep Apnea (OSA)

31

Tracheal stenosis, tracheomalacia

Injury to the trachea from chronic trauma caused by an endotracheal tube may result in inflammation, scarring, and fibrosis or loss of integrity of the tracheal structures, leading to airway narrowing and clinical symptoms. 

Hx: Prolonged mechanical ventilation and intubation

Px: Stridor, clear lungs, normal cardiac examination

Dx: Best diagnosed on pulmonary function testing, where a characteristic flattening of the curve is observed on flow-volume measurements.

32

Vocal cord dysfunction

Previous normal spirometry results, history of immediate improvement following intubation

Stridor, clear lungs, normal cardiac examination

33

Vocal cord paralysis

History of thyroid or neck surgery

Single frequency wheezing localized to throat, dysphonia

34

Obstructive Sleep Apnea (OSA)

OSA is defined by upper airway narrowing or collapse that results in cessation (apnea) or reduction (hypopnea) in airflow despite ongoing efforts to breathe. 

Hx: Loud snoring, gasping, and pauses in breathing are commonly observed by a bed partner.  Subjective symptoms include frequent awakenings, snorting, and nonrestorative sleep. The most important risk factor for OSA is obesity, particularly in patients with prominent distribution of adipose tissue in the trunk and neck. Less important risk factors include male sex, postmenopausal state, family history of OSA, and race. Some possible mechanisms by which obesity can cause OSA include increased upper airway fat deposition, leading to a decrease in airway size and muscle tone as well as reduced lung volume. Central obesity (larger waist-hip ratio) is more important than general obesity. Other risk factors for OSA are larger neck circumference (>17 inches in men; >16 inches in women), nasal narrowing or congestion, large tongue, low-lying soft palate, enlarged tonsils and adenoids, abnormalities of the face or jaw that contribute to airway narrowing, use of muscle relaxants, smoking and alcohol use, and primary medical disorders (acromegaly, androgen therapy, neuromuscular disorders, and stroke).

Dx: Polysomnography (PSG) is the gold standard for diagnosis of OSA. During PSG monitoring, upper airway events are classified as apneas (characterized by complete cessation of airflow) or hypopneas (reductions in airflow), collectively known as disordered breathing events. The apnea-hypopnea index (AHI) is the number of disordered breathing events per hour of sleep and is the standard for measuring the severity of OSA. An AHI of 5 to 15 indicates mild OSA; an AHI of 16 to 30 indicates moderate OSA, and an AHI of more than 30 indicates severe OSA.

Tx: CPAP should be considered first-line therapy in any patient who has OSA and associated symptoms, particularly excessive daytime sleepiness.  Optimal positive airway pressure therapy may have salutary effects on cardiovascular diseases that are associated with OSA.

35

Differential Diagnosis of Acute Dyspnea: Psychiatric Causes:

Panic attack

Rapid onset of chest pain, dyspnea that resolve without specific treatment

Normal cardiac and pulmonary examinations

36

Cor pulmonale

Right-sided heart failure (RHF) from pulmonary hypertension (PH). 

May be idiopathic or due to chronic obstructive pulmonary disease (COPD), interstitial lung disease (eg, idiopathic pulmonary fibrosis), obstructive sleep apnea, pulmonary vascular disease (eg, thromboembolic), or chest wall disorders (eg, kyphoscoliosis).  COPD is the most common cause of cor pulmonale in the United States, with nearly 25% of COPD patients developing this disorder.

Cor pulmonale typically has a gradual onset but can present acutely due to a sudden increase in pulmonary artery pressures (eg, pulmonary embolism).  Patients often develop exertional symptoms (eg, dyspnea, angina, syncope). 

Physical examination may show loud P2 (pulmonic component of the 2nd heart sound), tricuspid regurgitation murmur (holosystolic at the left lower sternal border), elevated jugular venous pressure (JVP), peripheral edema, hepatomegaly due to hepatic congestion, and possible ascites.  COPD patients usually have distant heart sounds due to hyperinflated lungs.  End-stage cor pulmonale may present with hypotension, tachycardia, and other signs of cardiogenic shock due to decreased stroke volume.

Chest x-ray may show enlarged central pulmonary arteries and loss of retrosternal air space due to right ventricular hypertrophy.  Electrocardiogram usually shows right axis deviation, right bundle branch block, right ventricular hypertrophy, and right atrial enlargement.  Right heart catheterization is the gold standard for diagnosis and typically shows elevated central venous pressure, right ventricular end-diastolic pressure, and mean pulmonary artery pressure (>25 mm Hg at rest) without left heart disease. 

Treatment involves optimizing right ventricular dynamics (preload, afterload, and contractility) with supplemental oxygen, diuretics, treatment of underlying etiology, and intravenous inotropes for severe decompensation.