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13.Acute Dyspnea

a

III

INTRODUCTION. Acute dyspnea is a common cause of emergency room visits, hospital admissions, and decompen­ sation among hospitalized patients.

CAUSES OF ACUTE DYSPNEA. Dyspnea is often the chief complaint of patients with a variety of disorders, many of which can be immediately life threatening.

A. Pubnonary

1. Pneumothorax is a sudden event that is often accom­ panied by very acute dyspnea and pleuritic chest pain. This diagnosis should always be considered in a patient on a ventilator.

2. Pulmonary embolism is a difficult diagnosis to make because of the lack of sensitivity and specificity of the history and physical examination. Therefore, you should consider this possibility early in the evaluation of most patients with acute dyspnea because special­ ized testing is often required to confirm the diagnosis.

3. Bronchospasm should be suspected in patients with known obstructive lung disease, such as chronic ob­ structive pulmonary disease (COPD) or asthma. Wheezing is the hallmark physical finding; however, COPD and asthma are not the only causes of wheez­ ing. Congestive heart failure (CHF), for example, can also cause the patient to wheeze.

HO T

Not all that wheezes is asthma! K E Y

4. Aspiration should be suspected in patients with swal­ lowing dysfunction or a diminished level of con­ sciousness. Always ask family members or nurses for information.

1 02

II

Chopter 13

5. Pneumonia. Patients will usually have other symp­

toms of infection, including fever or hypothermia, chills. or a productive cough.

6. Upper airway obstruction. A very acute onset of symptoms or localized wheezing should prompt con­ sideration of this diagnosis.

7. Acute respiratory distress syndrome (ARDS). These patients are usually hospitalized with another diag­ nosis.

B. Cardiac

1. Myocardial ischemia or infarction. Dyspnea may oc­ cur in the absence of chest pain and thus may repre­ sent an anginal equivalent.

2. CHF. In hospitalized patients with CHF, acute dys­

pnea is often precipitated by fluid administration or ischemia.

3. Arrhythmias cannot be reliably diagnosed on physi­ cal examination; a 12-lead electrocardiogram (EKG) or a rhythm strip is required.

4. Pericardial tamponade is rare, but should always be

considered in a patient with right-sided heart failure and no evidence of left-sided heart failure.

C. Metabolic

1. Sepsis. Dyspnea and an acute respiratory alkalosis may be the earliest findings in a patient with a severe systemic infection.

2. Metabolic acidosis can be diagnosed on the basis of

an arterial blood gas.

D. Hematologic. Anemia can cause acute dyspnea, and can easily be missed on history and physical examination.

E. Psychiatric. Anxiety can be a primary cause of acute

dyspnea; however, a diagnosis of primary anxiety should be considered only after the more serious possibilities have been ruled out. Many patients with dyspnea of an organic cause are very anxious.

ApPROACH TO THE PATIENT. The key to evaluating a pa­ tient with acute dyspnea is to focus on recognizing the most serious disorders.

A. Patient history. There are four key areas of inquiry:

1. What was the speed of onset of the dyspnea?

2. Are there any associated symptoms (e.g., chest pain, chills)?

3. What happened immediately before the onset of

the dyspnea? What medications or fluids was the

V I I I I 1\ V I I Acute Dyspneo 103

patient receiving immediately before becoming dyspneic?

4. What are the patient's other medical problems? If already hospitalized, what is the admission diag­ nosis?

B. Physical examination. Focus on five key areas:

1. Vital signs. Markedly abnormal vital signs in an

acutely dyspneic patient may signify impending re­ spiratory failure. An oxygen saturation should be ob­ tained.

HO T

K E Y

Remember, 0 normol oxygen soturation does not ex­ clude the possibility of 0 serious disorder!

2. Lungs. Pay particular attention to the symmetry of breath sounds and the presence of wheezing or rales.

3. Heart. A complete examination should be per­

formed, focusing on the findings of right-sided and left-sided heart failure.

4. Extremities. Look for edema (unilateral versus bilat­

eral) and cyanosis.

5. Mental status. Evaluating the patient's mental status is crucial for two reasons:

a. A markedly depressed level of consciousness may necessitate intubation for airway protection.

b. The finding of altered mental status as a result of the dyspnea suggests a significant homeo­ static insult.

C. Diagnostic studies. Four studies should be routinely per-

formed when the patient is acutely dyspneic.

a. 12-Lead EKG

b. Arterial blood gas analysis

c. Chest radiograph

d. Complete blood count (CEC)

II

TREATMENT

1 04 Chapter 1 3

should b e administered supplemental oxygen. A history of COPD or carbon dioxide retention should not prevent oxygen therapy for hypoxemic patients; however, pa­ tients at risk for carbon dioxide retention should be closely monitored.

B. Diuretics. Any process associated with excess lung water

(e.g., pulmonary edema, ARDS. aspiration. pneumonia) may improve with diuresis.

C.

f1

Agonists. Regardless of the cause, wheezing will likely

unprove somewhat with nebulized f3 agonist therapy.

D. Mechanical ventilation. The need for immediate or po­

tential intubation should be assessed. Indications for me­ chanical ventilation include:

1. Refractory hypoxemia (Pa02 < 60 mm Hg despite maximal oxygen therapy)

2. Ventilatory failure (generally manifested by an in­

creasing Paco2 despite therapy) 3. Inability to protect the airway

4. Impending upper airway obstruction

V I I I I 1\ V I I

14.Massive Hemoptysis

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III

INTRODUCTION. Hemoptysis, defined as the expectoration

of blood, can be an insignificant symptom of a benign illness, a first manifestation of serious malignancy, or a fatal process in and of itself. Hemoptysis is usually classified as either

massive or nonmassive.

A. Massive hemoptysis is usually defined as > 200 ml blood/ 24 hours and requires immediate evaluation: it is the focus of this chapter.

B. Nonmassive hemoptysis, usually defined as < 200 ml blood/24 hours. accounts for more than 90% of cases but usually does not necessitate admission of the patient to the hospital. Patients with massive hemoptysis have a higher mortality rate than those with nonmassive hemop­ tysis, but patients expectorating small amounts of blood warrant close attention, because they may "open up" (i.e., develop massive hemoptysis in an unpredictable fashion).

CAUSES OF HEMOPTYSIS. The list of differential diagno­ ses is long. The following mnemonic may help you to remem­ ber the many causes of hemoptysis-think of soldiers in a "BATTLE CAMP" coughing up blood.

Causes of Hemoptysis ("BATIlE CAMP") Bronchiectosis· or Bronchitis Asperg illoma' Tumor" Tuberculosis' Lung abscess' Emboli Coagulopothy

Arteriovenous molformation, Arteritis, or Alve· oIar hemorrhoge

Mitral stenosis

Pneumonia

* Most common causes of massive hemoptysis

1 06 Chopter 1 4 A. Bronchitis is the most common cause of hemoptysis but

rarely causes massive bleeding.

B. Bronchiectasis is relatively rare because the number of

cases of tuberculosis and untreated pneumonia has de­ clined: however, bronchiectasis is still seen commonly in patients with cystic fibrosis.

C. Aspergilloma. Any cavitary fungal lesion can cause he­ moptysis, but the "fungus ball" caused by Aspergillus Jumigatus is most common.

D. Tuberculosis. Hemoptysis in patients with tuberculosis is often caused by the rupture of Rasmussen's aneurysms (i.e., dilated segments of pulmonary arteries that traverse pulmonary cavities).

E. Emboli. Bland or septic emboli can cause lung infarction.

F. Coagulopathy is often associated with hemoptysis but is

not causative in and of itself. An underlying lesion should be sought.

G. Arteriovenous malformation is usually congenital and is often associated with hereditary hemorrhagic telangiec­ tasia (Osler-Weber-Rendu syndrome).

F. Arteritis. Many vasculitides can involve the lungs (e.g., Churg-Strauss syndrome, Wegener's granuloma­ tosis).

G. Alveolar hemorrhage can be caused by autoimmune pro­

cesses that also involve the kidneys [e.g., Goodpasture's syndrome, systemic lupus erythematosus (SLE)], as well as idiopathic pulmonary hemosiderosis.

H. Mitral stenosis causing pulmonary hypertension can lead to hemoptysis.

I. Pneumonia associated with hemoptysis is usually necro­

tizing (e.g., that caused by Staphylococcus aureus or Pseudomonas aeruginosa).

IIII

ApPROACH TO THE PATIENT

A. Maintain airway patency and oxygenation. Arte­ rial blood gas analysis and chest radiographs should be performed immediately to assess oxygenation and determine the extent of blood retained in the lung. Because death from massive hemoptysis usually results from alveolar flooding and hypoxemia, ensuring adequate oxygenation is the most important first step. V I I I I 1\ V I I Massive Hemoptysis 1 07 H O T K E Y

To prevent aspiration of blood into the unaffected lung in a potient with massive hemoptysis, have the potient lie in the lateral decubitus position with the bleeding side down. How do you know which lung is bleeding? Ask the patient; he or she may know.

1. If emergent intubation is indicated for airway man­ agement, hypoxemia, or hypoventilation, a large­ bore endotracheal tube (preferably � 8 mm) should be placed if possible, because the patient will most likely need urgent bronchoscopy.

2. Intubation with a double-lumen endotracheal tube allows ventilation of both lungs, while preventing aspiration of blood from one side to the other. This is a difficult technique with serious potential compli­ cations; therefore, it should be performed only by an experienced physician.

B. Identify the bleeding lesion

1. Ensure a bronchopulmonary source. It is necessary to

ensure that the patient truly has bronchopulmonary bleeding. If the source of the bleeding is not obvious, helpful techniques include the following:

a. Evaluation of the pH of the expectorated sub­ stance can provide clues-gastrointestinal con­ tents are usually acidic, whereas pulmonary ex­ pectorations are usually alkaline.

b. Examination of the pharynx and larynx may re­ veal the cause of the bleeding to be epistaxis.

2. Lung auscultation and chest radiographs can help to localize the bleeding but may not be helpful if the bleeding is diffuse or if blood has been aspirated from one lung into the other. A chest radiograph may also show a mass lesion or cavity.

3. Urinalysis and assessment of renal function may pro­ vide clues to an unsuspected vasculitis or pulmonary­

renal syndrome.

4. Computed tomography (CT) is not always useful but may reveal a space-occupying lesion (e.g., lung cancer or abscess).

1 08 Chapter 1 4

5. Early bronchoscopy is indicated for most patients for both therapeutic and diagnostic purposes. 6. Arteriography is useful for actively bleeding patients

for purposes of localization of the bleeding lesion and therapy.

C. Control the hemorrhage

1. General measures indicated for all patients with mas­ sive hemoptysis include bed rest, cough suppressants, sedatives, and stool softeners or laxatives, which help prevent sudden increases in intrathoracic pressure, thereby minimizing intravascular pressure.

2. Coagulopathies should be sought and corrected if present.

3. Intravenous vasopressin (0.2 U/min intravenously) has been used as a nonspecific vasoconstrictor but may cause ischemic complications.

4. Bronchoscopy followed by maneuvers such as iced saline irrigation, topical application of vasoconstric­ tors or thrombin, or balloon tamponade may be needed in some patients.

5. External radiation therapy may be effective for re­

ducing bleeding from tumors.

6. Definitive therapy can be achieved with angiographic arterial embolization and, if necessary, lung re­ section.

H O T

K E Y

Consult a pulmanalagist immediately if the patient pre­ sents with massive hemoptysis.

V I I I I 1\ V I I

lS.Approach to the Chest

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