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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3055_Библиотеки_им_академика_М_И_Перельмана.pdf
204
to the emergency room. In massive PE, thrombolytic therapy
might be beneficial.
If the pretest clinical probability is low, one can order
D-dimer; if D-dimer is negative (<500 ng/mL), PE can be
ruled out. When D-dimer is positive, additional imaging is
necessary. When the pretest probability is high, the patient
needs evaluation in the emergency room (contract CT scan
or VQ scan). If the transfer and imaging studies take time,
empirical anticoagulation therapy in the absence of contra-
indication should be considered.
Diagnosis of acute airway obstruction is usually obvious
based on the history of aspiration or signs of anaphylaxis (lip
and tongue swelling, urticaria, tachycardia, and hypotension)
and stridor.
Acute-Onset Dyspnea
The most common causes in this category are congestive heart
failure (new onset or exacerbation), asthma attack, and pneumo-
nia. With history (by paying attention to risk factors and associ-
ated symptoms), physical examination, and simple tests including
chest X-ray, electrocardiogram, and BNP (brain natriuretic pep-
tide), it is usually easy to reach the correct diagnosis [4].
Congestive heart failure (CHF) is characterized by dys-
pnea, which is worsened by lying flat (orthopnea), nocturia,
weight gain, and bilateral lower extremity edema. Many
patients have cardiovascular risk factors: when those risks are
absent, acute valvular heart disease (including infective endo-
carditis (IE)) or acute myocarditis should be considered.
On physical examination, one should look for jugular
venous distension, lower extremity edema, bilateral lower
lung crackles and heart gallop, laterally displaced PMI (point
of maximal impulse), and possibly cardiac murmurs (imply-
ing the underlying valvular heart disease). Occasionally,
wheezing can be heard, and the patient may even respond to
a beta-agonist bronchodilator.
Asthma exacerbation typically presents with acute-onset
dyspnea, cough (mostly dry), and chest tightness, which is
K. Kinjo
205
worse late at night or early in the morning, often triggered by
upper respiratory infections. In many cases, wheezing can be
easily audible, but in a severe asthma attack with impending
respiratory failure, wheezing may diminish or become absent.
History of allergy (atopic dermatitis, allergic rhinitis, or con-
junctivitis) may be helpful to confirm the diagnosis.
Pneumonia is not difficult to diagnose when a patient pres-
ents with typical symptoms such as fever and cough with
purulent sputum, but the presentation can be quite variable
[5]. Many elderly may have no fever, but present with appe-
tite loss, impaired mental status, or acute decline from base-
line ADLs (activities of daily living) [6]. Atypical pneumonia
can present with GI symptoms or headache. Tachycardia or
tachypnea may be the only clue to the correct diagnosis.
Other etiologies of acute dyspnea can be identified by
history, physical examination, chest X-rays, and electrocar-
diogram in most cases.
Episodic Dyspnea
When a patient presents with recurrent episodes of dyspnea, the
common diagnoses to consider are (1) asthma, (2) panic attack,
(3) flash pulmonary edema, and (4) recurrent aspiration.
Panic attack is characterized by episodes of intense fear
accompanied by somatic complaints including dyspnea.
Although it is important to exclude other medical illnesses,
patients with typical features of panic disorders would bene-
fit from early psychiatric evaluation and treatment including
cognitive behavioral therapy.
Flash pulmonary edema presents with an acute episode of
pulmonary edema, presenting like acute CHF, but can be
caused by a non-cardiac infirmity such as bilateral renal
artery stenosis [7].
Elderly with advanced dementia or patients with underly-
ing neuromuscular disorders, may develop intermittent aspi-
ration with desaturation. Rhonchi and wheezing are often
detected when the patient becomes dyspneic.
11. Shortness of Breath
206
Table 11.2 Common causes of chronic dyspnea
Diagnosis History Physical exam Diagnostic test
CHF h/o coronary artery disease,
hypertension, valvular
disease, orthopnea, edema,
weight gain
Jugular venous
distension, lower
extremity edema,
bibasilar crackles,
gallop sound, AFib
Electrocardiogram
Chest X-ray
Echocardiography
BNP
COPD >50 y.o. with significant
smoking history, chronic
cough, sputum
Distant lung sounds,
barrel chest, wheezes
Chest X-ray
PFT
Interstitial lung disease Chronic dry cough, h/o
occupational exposure,
rheumatic disease
Bibasilar fine
crackles, clubbing
Chest X-ray
and chest CT
PFT
Asthma Episodic wheezy dyspnea,
triggered by URI, seasonal
changes
Wheezes PFT with
bronchodilator response
Anemia Dyspnea on exertion Pale conjunctiva Hemoglobin
Work up underlying
cause of anemia
Obesity/deconditioning Dyspnea on exertion,
sedentary lifestyle, obesity
Normal or obese Exclude other etiologies
K. Kinjo
207
Chronic Dyspnea
Etiology of chronic dyspnea can be divided into three catego-
ries: (1) cardiac (2) pulmonary, and (3) others. One should
always consider and thoroughly evaluate each category since
more than one cause may coexist, especially in the elderly
(e.g., COPD and coronary artery disease). When dyspnea
seems out of proportion to the severity of one disease,
another overlapping condition may be present.
The most common etiologies are (1) CHF, (2) COPD, (3)
interstitial lung disease, (4) asthma, (5) anemia, and (6) obe-
sity/deconditioning (Table 11.2).
Although many interstitial lung diseases are chronic, acute
interstitial pneumonia, acute eosinophilic pneumonia, pneu-
mocystis pneumonia, and dermatomyositis-associated lung
disease may present acutely or subacutely.
Other less common diagnoses to consider may include
lung cancer, pleural effusion, pulmonary hypertension, tense
ascites, neuromuscular diseases, and chest wall deformity.
When the diagnosis remains elusive after routine evalua-
tion, pulmonary or cardiology consultation should be consid-
ered. In difficult cases, cardiopulmonary exercise testing may
be helpful [8].
Treatment
Once the etiology is identified, the specific treatment can be
provided.
The stepwise asthma treatment is shown in Table 11.3 [9]. In
most cases, low-dose steroid inhaler is the preferred controller
medication. Those who have infrequent asthma symptoms (less
than twice a month, no night symptoms in 1 month, and no exac-
erbation in 1 year) can be treated only with a short-acting beta-
agonist inhaler as needed. Patients who cannot use the steroid
inhaler despite repeated instructions (e.g., cognitive impairment
or hand deformity) may use a leukotriene receptor antagonist,
although it is less effective. Patients with more frequent, more
severe symptoms should be treated with a low-dose steroid
11. Shortness of Breath
208
Table 11.3 Stepwise asthma management
Step 1 Step 2 Step 3 Step 4 Step 5
Preferred
controller
None Low-dose ICS Low-dose ICS/
LABA
Medium/high ICS/
LABA
Refer to asthma
specialist
Other
controller
choice
Consider
low-dose ICS
LTRA
Low-dose
theophylline
Medium-dose ICS
Low-dose
ICS + LTRA
Add tiotropium
High-dose
ICS + LTRA
Add low-dose
oral steroid
Reliever As needed SABA As needed SABA or low-dose ICS/formoterol
ICS inhaled corticosteroid, LABA long-acting beta2-agonist, LTRA leukotriene receptor antagonist
Modified from Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2016
K. Kinjo
209
Table 11.4 COPD management
mMRC 0–1
CAT <10
mMRC ≧2
CAT ≧ 10
Exacerbation ≧two/year
or ≧ one hospitalization
Start LAMA
⇒If further exacerbation, LAMA + LABA
or LABA + ICS
Start LAMA + LABA
⇒If further exacerbation,
LAMA + LABA + ICS
⇒If still further exacerbation,
refer to pulmonologist
0–1 exacerbation/year
and no hospitalization
Choose one from SABA, LABA, SAMA,
or LAMA
⇒If effective, continue
⇒If ineffective, stop and change to another
Start LABA or LAMA
⇒If symptoms persist,
LABA + LAMA. Consider other
cause of respiratory symptoms
1. Smoking cessation
2. Assess the symptom severity and exacerbation history and select bronchodilator treatment (see table above)
3. Treat comorbid conditions: Common comorbid conditions include cardiovascular disease, skeletal muscle dysfunc-
tion, metabolic syndrome, osteoporosis, depression, anxiety, and lung cancer. One should actively screen and treat them
appropriately in order to maximize the patient’s quality of life
4. Vaccination: Vaccinate against influenza and pneumococcus
mMRC modified MRC dyspnea scale, CAT COPD assessment test, LABA long-acting beta-agonist, SABA short-acting
beta-agonist, LAMA long-acting antimuscarinic antagonist, SAMA short-acting antimuscarinics, ICS inhaled
corticosteroid
Global Initiative for Chronic Obstructive Lung Disease Global Strategy for the Diagnosis, Management, and
Prevention of Chronic Obstructive Pulmonary Disease (2017 Report)
11. Shortness of Breath
210
inhaler and a long-acting beta-agonist (LABA). If asthma is
poorly controlled, one needs to review the diagnosis of asthma,
medication adherence (especially inhaler technique), triggering
factors (e.g., smoking, use of NSAIDs or beta blockers), and
comorbid conditions (e.g., sinusitis or GERD) and then consider
stepping up the treatment regimen. If symptoms are well con-
trolled for 3 months, consider stepping down, but it is strongly
recommended to continue the steroid inhaler.
COPD management is summarized in Table 11.4 [10].
FEV1 value is important to establish the diagnosis of COPD
(post bronchodilator FEV1/FVC <70%), but the medication
choice is strongly influenced by the degree of symptoms and
the history of exacerbation. LAMA (long-acting antimuscar-
nic antagonists) is the preferred choice in many patients; it is
shown to improve symptoms and quality of life and reduce
exacerbation and hospitalizations and has little systemic side
effects. None of the pharmacologic therapies are shown to
slow the decline of the lung functions; smoking cessation is the
only definitive treatment of COPD. A detailed discussion of
COPD therapy is beyond the scope of this chapter.
Comanagement with a pulmonary specialist may be indicated
in patients with advanced COPD. Newer therapies including
pulmonary rehabilitation and lung reduction surgery may be
appropriate to consider. Comorbid conditions such as cardio-
vascular disease are very common in patients with COPD;
screening and treatment of comorbidity is important.
Management of heart failure is summarized in Fig. 11.2
[11]. While cardiologists may provide many aspects of spe-
cialized care, the primary care providers should work in con-
junction with cardiologists and manage comorbid conditions
such as obesity, smoking, hypertension, and diabetes.
In patients with chronic heart or lung disease, the symp-
tom of dyspnea can be challenging to manage; physical ther-
apy may be beneficial in some cases. Oxygen therapy can be
considered in select hypoxic patients. Those with advanced
end-stage illness may suffer from refractory dyspnea; opiates
should be considered in these situations [12].
K. Kinjo
211
Avoid
Life style modification
Treat comorbidity
HFpEF
(EF^50%)
HFrEF
(EF%40%)
Heart failure
Stage A
At risk for HF
but without
structural
disease or
symptoms
Stage B
With structural
heart disease
but without
signs or
symptoms
Stage C
With structural
heart disease
with prior or
current
symptoms
Stage D
Refractory
HF requiring
specialized
interventions
Treat comorbidity
ACEI or ARB
+
beta blockers
ACEI or ARB
+
beta blockers
+
Diuretics
+
Aldosterone
antagonist
ACEI or ARB
+
beta blockers
+
Aldosterone
antagonist
+
Diuretics
Digitalis in select
patients
Consider inotropes
Consider palliative
care
• NSAIDs
• Exercise
• HTN • HTN
• CAD• CAD
• DM • DM
• Lipid
• CKD
• CKD
• Hyperthyroidism
• Anemia
• Sleep apnea
• Smoking
cessation
• Obesity management
• Smoking cessation
• Alcohol, illicit drug
• Salt, fluid restriction
• Thiazolidinediones
• Most antiarrhythmics
• verapamil, diltiazem
+
+
Cardiology Consultation
• Revascularization
• Valve repair
• Biventricular pacing
• Arrhythmia treatment, ICD
• LVAD, transplant
+
Fig. 11.2 Heart failure management. Stage A: Patients at high risk
for heart failure but without structural disease or symptoms. Stage
B: Patients with structural heart disease but without signs or symp-
toms. Stage C: Patients with structural heart disease with prior or
current symptoms. Stage D: Patients with refractory heart failure
requiring specialized interventions. (1) HFpEF heart failure with
preserved ejection fraction (EF ≧ 50%). (2) HFrEF heart failure
with reduced ejection fraction (EF ≦40%). (3) HTN hypertension,
CAD coronary artery disease, DM diabetes mellitus, CKD chronic
kidney disease. (4) ACEI angiotensin-converting enzyme inhibitor,
ARB angiotensin receptor blocker. (5) ICD implantable cardio-
verter defibrillator. (6) LVAD left ventricular assist device. (7)
NSAIDs nonsteroidal anti-inflammatory drugs. 2013 ACCF/AHA
guideline for the management of heart failure: executive summary:
a report of the American College of Cardiology Foundation/
American Heart Association Task Force on practice guidelines.
Modified from Yancy CW, Jessup M, Bozkurt B et al. Circulation
2013; 128: 1810–52
11. Shortness of Breath
212
Clinical Pearls
When the routine history and physical examination are not
revealing, carefully watch how the patient walks and with
what pace while monitoring pulse rate and oxygen saturation
by pulse oximetry. This way the provider can get a sense of
the patient’s exercise capacity.
Don’t Miss This!
• Viral myocarditis may present with malaise, low-grade
fever, and nausea with little classical CHF symptoms; it
can be misdiagnosed as viral gastroenteritis but the
patient’s general appearance is usually quite ill.
• Patients with angina may describe vague chest symptoms
as dyspnea on exertion. Careful attention to the symptoms
of chest tightness (which may or may not be typical squeez-
ing in nature), nausea, and diaphoresis is important espe-
cially in patients with cardiovascular risk factors. If acute
coronary syndrome is deemed likely, patients would be best
evaluated in the emergency room.
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11. Shortness of Breath