Symptoms and signs of heart diseases and pulmonary disturbances overlap and present diagnostic problems. These two vital organs are in the chest “married to each other”. Thus, the text also gives salient symptoms of pulmonary disorders.
EVALUATION OF CHEST PAIN
Chest pain is one of the most important and common symptoms of heart disease and must be assigned a cause quickly. The resolution of this symptom is sometimes easy, but often it presents considerable difficulty for the physician. A systematic approach is necessary; taking an accurate and relevant history is crucial to the diagnosis.
- What are the vital signs?
- Is the patient stable or unstable?
- Is the pain in the central, the left, or the right lateral chest?
- Is there associated shortness of breath and is it mild, moderate, or severe?
- If the patient is unstable, order an electrocardiogram (ECG) immediately.
- Give nitroglycerin, 0.3 mg sublingually or sublingual puffer, twice as needed (PRN); this only relieves mild angina and cannot prevent or limit size of myocardial infarction (MI). A dose of 0.4 mg is used only if the blood pressure (BP) is higher than 130 mm Hg.
- Give soft chew aspirin 75–81 mg × 3 tablets. This can prevent MI or reduce infarct size; reduces risk of death.
COMMON CAUSES OF CHEST PAIN
Cardiac pain can be life-threatening and should be assessed rapidly. The following are the three sources of cardiac pain (Box 1.1):
- The pericardium: Pericarditis
- The great vessels: Aortic dissection, pulmonary embolism and pulmonary arterial hypertension.
- Pulmonary embolism: The pain may be severe, central, or pleuritic and is often associated with acute shortness of breath; the patient is often apprehensive and may be sweaty. Pulmonary embolism should be suspected when chest pain occurs in a setting that predisposes to thromboembolism (e.g. after surgery or with sudden immobilization for >2 days). Request arterial blood gas study and ventilation-perfusion lung scan.
- Pneumothorax: Chest pain is usually associated with acute shortness of breath. Chest pain is often located in the lateral chest. Underlying causes include asthma, pneumocystis pneumonia, emphysema, tuberculosis, cystic fibrosis, interstitial pulmonary fibrosis, sarcoidosis, eosinophilic granuloma, blunt or penetrating trauma, and positive-pressure ventilation.
- Pneumonia: Shortness of breath, fever and chills are associated with pleuritic or nonpleuritic pain and cough, with or without sputum production.
Chest Wall Pain
A common cause of chest wall pain is costochondritis. Pain is usually mild to moderate; it is usually localized to a fingertip area and is often present over the second or third costochondral junction. Chest wall pain from other causes may last seconds to several hours. Pain is unrelated to exertion or activities and may seem to respond to nitroglycerin in some patients. Chest wall pain accompanies most types of heart disease, particularly ischemic heart disease and mitral valve prolapse syndrome.
Pain of Gastrointestinal Origin
- Reflux esophagitis may mimic cardiac pain and may radiate from the upper epigastrium to the substernal area, the upper chest, the throat and the arms. Pain does not radiate to the lower jaw, a feature of anginal pain. Pain lasting minutes to several hours may be mild to moderate but can be severe. Pain usually is not associated with profuse sweating or shortness of breath. The discomfort is worse on lying flat or on stooping but may start in the upright position. Pain is unrelated to exertional activities.
CHEST PAIN CAUSING A MAJOR THREAT TO LIFE
- Acute MI
- Aortic dissection
- Pulmonary embolism
- Tension pneumothorax
A patient in cardiogenic shock is usually sweaty, pale and apprehensive; there may be associated clouding of consciousness.
Does the patient look well (comfortable), sick (uncomfortable or distressed), or critical (about to die)?
If the patient is critically ill or is unstable (i.e. systolic BP is <100 mm Hg, pulse rate is <45 beats/min or >140 beats/min, or with a cardiac arrhythmia, or there is clouding of consciousness), send by ambulance to an emergency room (ER); put up IV line with dextrose to keep vein open.
Bradycardia may be caused by treatment with beta-blockers, diltiazem, or a combination of these two agents. Also, inferior MI commonly causes sinus bradycardia. Bradycardia usually requires no treatment, unless it is symptomatic
It is necessary to become familiar with the description of cardiac pain so that the diagnosis of stable angina, unstable angina, or MI can be made clinically within a few minutes. Because urgent administration of thrombolytic therapy or percutaneous coronary intervention [PCI] is crucial to reducing morbidity and mortality, it is vital to make the diagnosis of acute MI within a few minutes of assessment in the home, the physician's office, or in the ER.
Salient features of cardiac pain are as follows:
- Pain of acute MI is usually described as crushing, viselike, or a tightness or a heaviness
- The location of pain in acute MI is usually substernal across the chest, often accompanied by diaphoresis and sometimes shortness of breath.
Figure 1.1 gives the location and the radiation of cardiac pain.
The pain is unlikely to be due to MI if it can be located with one fingertip or if it is made worse by deep breathing or coughing.
If the patient is stable and the diagnosis is not yet clarified, obtain relevant information from all sources (i.e. the patient, the spouse, a relative, a chart review).
- The pain of MI usually lasts minutes to several hours
- The pain of angina is typically a retrosternal discomfort, precipitated by a particular activity, especially walking quickly up an incline or against a wind.
- Pain or discomfort disappears within seconds to minutes of stopping the precipitating activity, in keeping with the concept of oxygen supply insufficient to meet myocardial demand.Fig. 1.1: Common locations of cardiac pain.Source: Adapted from Khan M Gabriel. Heart Trouble Encyclopedia. Toronto: Stoddart; 1996.The discomfort is usually located in the lower, middle, or upper substernal area, the arm, or the lower jaw. The discomfort is usually described as tightness, squeezing, heaviness, pressure, constriction, strangulation, burning, nausea, or an indigestion-like feeling of gradual onset that disappears at rest, except with unstable anginal syndromes.
- The area of pain in MI is usually at least the size of a clenched fist and often occupies most of the central chest area. The patient uses more than two fingers, the fist, or the entire palm of the hand to indicate the site. Patients with unstable angina have pain that has changed in pattern and frequency.
- Pericardial pain is usually sharp or stabbing. It is relieved by sitting and leaning forward or standing, is made worse on lying down or on deep inspiration and does not usually radiate to the neck or arms.
- Pain of dissecting aneurysm is sudden like a gunshot; the pain is excruciating and persists with the same intensity for hours; pain may radiate to the back.
- Myocardial ischemia or infarction may cause only minimal chest discomfort for a few minutes; pain may range from causing minor distress to being severe and unbearable.
What Does the ECG Show?
Is the ECG in keeping with acute MI? Acute MI poses a threat to life; the diagnosis must be made rapidly. Thrombolytic therapy has proved effective in saving life if given within 4 hours of the onset of chest pain. It is important, however, that triage through the ER be efficient; patients presenting with chest pain caused by acute MI should receive thrombolytic therapy within 20 minutes of presentation to the ER or ambulance, if no facilities for coronary stenting is available.
Selective Physical Examination
- Assess the BP and heart rate
- Assess the cardiovascular system
- Is the patient orthopneic? Is the patient apprehensive or sweaty? Assess for elevated jugular venous pressure (JVP) or abnormal venous waves. With the bell of the stethoscope placed gently on the chest wall, listen for gallop sounds. Listen with the diaphragm of the stethoscope for murmurs and, with the patient leaning forward with the breath held in deep expiration, for an aortic diastolic murmur and pericardial friction rubs (see Chapters 11 and 15).
- Assess the respiratory system
- Assess for crackles over the lower lung fields that may indicate left ventricular failure; unilaterally decreased air entry and hyperresonance suggest a pneumothorax.
Management of the following problems is given in their respective chapters:
- Acute MI (see Chapter 7)
- Unstable angina (see Chapter 2)
- Pericarditis (see Chapter 11)
- Aortic dissection (see Chapter 12)
Intervention is necessary for symptomatic primary pneumothoraces or if the pneumothorax is more than 40%. Tension pneumothorax causes severe respiratory distress and is a medical emergency that requires urgent relief of the pressure by using a 16-gauge IV catheter. After rapid radiologic confirmation, insert a 16-gauge IV catheter as follows:
- Infiltrate the area with lidocaine and insert a 16-gauge IV catheter above the rib into the site until air is aspirated. Remove the inner needle and attach the catheter to a three-way stopcock and a 60-mL syringe to allow repeated aspirations. Aspiration is discontinued when no more air can be withdrawn, or when about 2.5 L has been removed. Occlude the catheter for about 6 hours and if the chest radiograph shows no recurrence, remove the catheter.
The insertion of a chest tube (tube thoracostomy) is required in patients with underlying lung disease, with respiratory compromise, or for failure of simple aspiration. A small, asymptomatic pneumothorax usually resolves spontaneously over a few days.
Esophagitis and Reflux Syndrome
The following steps need to be followed:
- Elevate the head of the patient's bed
- Give Maalox or a similar antacid, 30 mL at 1 hour and 3 hours after meals plus at bedtime
- Give lansoprazole 30 mg, omeprazole 20 mg, or similar agent 30 minutes before breakfast for 1 week and reassess.
Shortness of Breath
Shortness of breath, or dyspnea, is a common problem. Dyspnea by definition is difficult breathing. The term “dyspnea” is used synonymously with shortness of breath or breathlessness and may be expressed by individuals as follows: “I can't get enough air”; “I'm breathless or short of breath”; “I feel like I'm being smothered”; or “I'm out of breath, running after my breath”.
Because shortness of breath on exertion may be a normal phenomenon, it is necessary to make a careful assessment of the normal or altered lifestyle of the patient in relation to the degree of shortness of breath. A change from a very active lifestyle, to a few years of sedentary life, then resumption of exercise or strenuous work may be the cause of shortness of breath. Increasing body weight and advancing or intercurrent illness may be important causal factors:
- Is the shortness of breath mild, moderate, or severe?
- Did it occur suddenly and become severe within minutes?
This suggests pulmonary embolism, pneumothorax, or acute pulmonary edema.
- How long has the patient been short of breath?
- What are the vital signs?
Heart failure and pulmonary embolism are the most likely causes of acute dyspnea.
The causes of dyspnea are listed in Table 1.1. Pathophysiology of Dyspnea
Given here is a brief review of pathophysiology of dyspnea:
- An increase in the work of breathing secondary to changes in lung compliance or resistance, as occurs with interstitial pulmonary edema owing to congestive heart failure (CHF) or pulmonary fibrosis.
The respiratory center receives indirect stimuli via lung stretch (Hering-Breuer reflexes). Stretch receptors in the lung parenchyma relay information to the respiratory center, resulting directly or indirectly in dyspnea. Stretch receptors in respiratory muscles, irritant receptors and juxtacapillary (J) receptors are sensitive to congestion, vascular engorgement and mechanical stimulation.
- Shunting and other hypoxic stimulation to breathing (e.g. caused by acute respiratory distress syndrome, pneumonia, pulmonary embolism and right-to-left cardiac shunts).
- Airflow obstruction: Chronic obstructive pulmonary disease (COPD), asthma, bronchiectasis.
- Mechanical limitation to ventilation: Thoracic and neurologic abnormalities.
- Decrease in cardiac output.
- Decrease in hemoglobin (anemias).
- High altitude.
Major Threat to Life
Given below are major threats to life related to dyspnea:
- Left ventricular failure
- Pulmonary embolism.
Does the patient look sick (uncomfortable or distressed) or critical (about to die)?
- Ensure that the upper airway is clear:
- Determine the respiratory rate; if more than 20 breaths/min, consider hypoxemia, or anxiety and apprehension caused by pain and distress. Paradoxical abdominal and diaphragmatic movement during respiration indicates diaphragmatic fatigue or weakness; the presence of this sign is ominous, and some patients may require ventilator assistance.
Table 1.1 Causes of shortness of breath.CauseMeaning or associationNormal: To be expected because of relative age and lack of exercise, overweightExcessive strenuous effort precipitates symptomsElevation of the diaphragm, e.g. pregnancy, ascitesMechanical problemHeart failureIncreased pulmonary venous pressure; interstitial pulmnary edema; frank pulmonary alveolar edemaPericardial effusionRestriction to ventricular fillingAngina equivalent of chest discomfortLeft ventricular dysfunction or discomfort appreciated as breathing with difficulty or suffocationPulmonary embolismApprehension, presyncope, painPulmonary diseasesPneumonia, asthma, pneumothorax, ARDS, pleural effusion, COPD, restrictive lung disease, lymphangitis carcinomatosaLaryngeal stridorLaryngotracheal obstructionThoracic defectsNeuromuscular or bony mechanical conditionsDecreased hemoglobin or available oxygenAnemia, high altitude(ARDS: Acute respiratory distress syndrome; COPD: Chronic obstructive pulmonary disease).A respiratory rate of less than 12 breaths/min indicates a central depression of ventilation caused by drugs or overdose, narcotics, or cerebrovascular accident.
- Assess the heart rate and the BP. Hypotension suggests CHF caused by underlying cardiac disease or pulmonary embolism (check for pulsus paradoxus and cardiac tamponade; see Chapter 11).
The most common symptom of cardiac and respiratory disorders. It is often a difficult symptom to resolve, unless a clear description is obtained.
It is necessary to exclude the following conditions, which are not truly dyspnea:
- Hyperventilation states caused by anxiety: The patient refers to “feeling hungry for air”
- Sighing respirations: The patient sighs, “I feel like I need to take a deep breath”
- Splinting caused by pleuritic pain or rib or chest wall problems
- Laryngismus caused by hypocalcemia, which may occur because of hypoparathyroidism (occasionally surgically induced).
When it is determined that the patient is complaining of genuine shortness of breath, consider the following:
- Define what level of activity precipitated the shortness of breath (e.g. the number of stairs climbed, the number of steps taken, the number of blocks walked, the extent of the incline, the relation to various types of effort or exertion). Shortness of breath is abnormal when it occurs at rest or at a level of activity not expected to cause this situation.
- Duration: Seconds, minutes, hours? If the sensation lasts less than 10 seconds, it is not true dyspnea.
- Is it occurring at rest? If so, determine the duration and what makes it better or worse.
- If it occurred suddenly and with the patient at rest, is it improving or getting worse?
- Is it accompanied by cough, wheeze, chest pain, palpitations, or edema?
- Is it worse on inspiration and accompanied by tracheal or laryngeal stridor? This indicates upper respiratory tract obstruction, which can be life-threatening.
- Is it mainly with expiration? The patient has difficulty getting air out of the lungs because airflow is obstructed (a prolonged expiratory phase); this is usually due to an exacerbation of asthma or COPD.
- Is it worse only when lying down or when the trunk is immersed in water? This suggests diaphragmatic paresis or paralysis.
Shortness of breath that occurs within minutes of lying down and is relieved within a few minutes (not a few seconds) of sitting upright or dangling the legs over the bedside. This symptom is not usually accompanied by wheezing or flatulence.
Orthopnea is usually caused by severe left ventricular dysfunction, subtle left ventricular failure, or increased pulmonary venous pressure (e.g. owing to mitral stenosis). In patients with poor left ventricular function, blood returning to the heart from the lower limbs when the person is reclining is not ejected efficiently from the left ventricle. This situation results in an increase in left atrial and pulmonary venous pressures, causing increases in lung water and lung stiffness, which incite reflexes that trigger the sensation of shortness of breath. The upright position decreases venous return and improves the abnormal sensation within minutes. Orthopnea lasts 1–5 minutes and does not usually exceed 10 minutes.
Warning: Shortness of breath of more than 10 minutes’ duration while at rest is a life-threatening situation.
Paroxysmal Nocturnal Dyspnea
Shortness of breath (a suffocating feeling) that occurs after the patient has been lying in bed for more than 1 hour. The patient usually awakens several hours after retiring, typically between 1 am and 3 am, with severe shortness of breath.
- Relief is obtained only by getting out of bed, sitting in a chair, dangling the legs, or standing. In contrast to orthopnea, sitting up in bed does not cause relief in 1 or 2 minutes.
- Shortness of breath usually lasts 10–30 minutes. Paroxysmal nocturnal dyspnea is more common in patients with poor left ventricular function who have peripheral edema.
- After the patient lies down for the night, it takes 1–3 hours for edema fluid from the lower limbs to return to the heart. An extra volume of sodium and water precipitates left ventricular failure, this causes an increase in left atrial pressure (i.e. severe pulmonary venous hypertension that results in pulmonary edema).
- Cough is often associated with the feeling of suffocation and with the production of frothy, blood-tinged sputum.
In this condition, the patient takes deep inspirations, the depth of inspiration increases with each consecutive breath for 1–2 minutes, and then there is cessation of breathing for 10–30 seconds, after which the patient resumes deep breathing.
- Cheyne-Stokes respiration is usually observed in patients with cerebrovascular accidents, in patients with head injury, and in patients with severe left ventricular failure with coexisting cerebral disease.
- The patient takes deep breaths, with long inspiratory and expiratory phases, without wheezing and without the use of accessory muscles.
- The patient has no difficulty getting air into or out of the lungs and does not describe the sensation as a feeling of shortness of breath or breathlessness.
- This pattern of breathing is observed in patients with diabetic ketoacidosis, uremia and salicylate overdose.
- Metabolic acidosis stimulates the respiratory center to produce this breathing pattern, which blows carbon dioxide out of the lungs and into the atmosphere. The loss of carbon dioxide causes a compensatory adjustment in blood pH. The degree of acidosis is usually too intense to be corrected completely by ridding the lungs of carbon dioxide.
- Is the patient in distress, requiring being propped upright to ease difficult breathing?
- Is the patient using accessory muscles of respiration?
- Is cyanosis present?
Do not forget that severe hypoxia may be present with no cyanosis apparent on observation.
- Is the patient wheezing, or is the patient a known asthmatic?
Do not forget, all that wheezes is not asthma; patients with pulmonary embolism, pulmonary edema and exacerbation of chronic bronchitis may exhibit audible wheezing.
- Repeat vital signs and recheck patency of the airways. Sinus tachycardia is commonly caused by hypoxemia, pain and anxiety. If the systolic BP is less than 90 mmHg with signs of hypoperfusion, begin measures for managing cardiogenic shock.
Jugular Venous Pressure
This should be elevated to more than 3 cm above the sternal angle in patients with CHF.
Venous pressure may be markedly elevated, and the top of the blood column may be masked by the angle of the jaw. The earlobes may pulsate in patients with markedly elevated JVP and tricuspid incompetence. Look tangentially across the neck for prominent venous waves.
The JVP is elevated in the following conditions:
- Congestive heart failure
- Cardiac tamponade
A unilateral elevation of the JVP, which is nonpulsatile, is observed with superior vena cava obstruction. Watch for false elevation of the JVP in patients with an exacerbation of COPD. Venous pressure is elevated during the phase in which exhalation is difficult and it decreases during inspiration.
Listen for the Presence of Murmurs
A loud mitral systolic murmur with radiation to the left axilla or the spine may occur in patients with ruptured chordae or flail mitral valve leaflet. The murmur of aortic stenosis may be loud, but in the presence of a low cardiac output it may diminish in intensity and result in a misdiagnosis. The murmur of mitral regurgitation may be soft in patients with low cardiac output or a thick chest wall or concomitant COPD. Patients with severe aortic stenosis may die during an episode of pulmonary edema.
- Listen carefully for S3, a gallop that is commonly present if CHF is the cause of severe shortness of breath (see Chapter 8)
- Is the heart clinically enlarged?
- Cardiomegaly may be mild and may be absent in patients with aortic stenosis or pure mitral stenosis.
- Observe for abnormal pulsations, including visible gallops:
- Abnormal dyskinetic myocardium may be visible just above the apex beat, in the region of the fourth interspace, caused by recurrent MI or left ventricular aneurysm, severe valvular defects, or cardiomyopathy.
- Observe for bilateral ankle edema:
- Assess the extent of edema up to the knee and the degree of pitting. If shortness of breath was present for several days and the patient was confined to bed, check for presacral edema.
- If CHF is present, verify the underlying cause of heart disease: Valvular disease, coronary artery disease, congenital heart disease, hypertension, cardiomyopathy and cor pulmonale.
- Define a precipitating cause: Recent MI or MI and mechanical defect, ruptured chordae tendineae, flail mitral valve, worsening of valvular defect, increased salt intake and medications that precipitate CHF (beta-blockers, calcium antagonists and nonsteroidal anti-inflammatory drugs).
- Is the patient cyanotic?
- Is the trachea in the midline?
- A shift away from the side of the lesion is observed with pneumothorax and pleural effusion; a shift to the side of the lesion indicates atelectasis.
- Is there dullness to percussion?
- Stony dullness is in keeping with pleural effusion. If there is mild impairment to percussion, consider consolidation.
- Is there unilateral hyper-resonance?
- Consider pneumothorax.
- Auscultate for breath sounds:
- Air entry: If air entry is decreased or absent over an area of dullness, with decreased bronchophony, consider pleural effusion; air entry absent over a hyperresonant area is diagnostic of pneumothorax.
- Quality of breath sounds: If bronchial breathing is present, consider consolidation.
- Added sounds: Crackles (crepitations) over both lower lung fields associated with an increased JVP is diagnostic of CHF, but crackles may be maximal on one side.
- A chest X-ray confirms pulmonary edema or interstitial edema caused by heart failure (see Chapters 6 and 8):
- For pulmonary causes, posteroanterior and left lateral X-rays are essential: Assess for pleural effusions, diaphragmatic paralysis, emphysema, tumors and lymphangitis carcinomatosa. If emphysema or restrictive lung disease is suspected, a computed tomography scan and gas transfer assessment are recommended.
- Troponin testing in the ER helps differentiate cardiac from pulmonary causes of severe dyspnea.
- An echocardiogram helps document the degree of valvular lesions, left ventricular systolic function, ejection fraction and pericardial effusion with tamponade.
- Measures of arterial blood gases assess hypoxemia and response to therapy.
- Give furosemide 80 mg intravenously immediately, then oral furosemide 40–80 mg daily after breakfast.
- If needed, give oxygen by nasal prongs or mask 4–8 L/min until arterial blood gases show the absence of hypoxemia and the underlying cause improves or is corrected.
Causes of shortness of breath are given in Table 1.1.
Edema is an excessive accumulation of interstitial fluid in the subcutaneous tissue.
- Does the patient complain that shoes feel tighter or that sock tops leave indentations as the day progresses?
- Is the swelling more prominent at the end of the day?
- Is the swelling unilateral or bilateral?
- Is the swelling of recent onset or is it recurrent?
- Is the swelling associated with shortness of breath?
Many patients are inappropriately treated with diuretics and digitalis for edema that is noncardiac in origin. A careful history and physical examination are necessary to determine the cause accurately localization is determined mainly by gravity (Table 1.2):
- Edema of cardiac origin involves both of the feet and ankles
- It may involve the lower limbs, the trunk, the face, and the arms and may be associated with ascites and pleural effusions; this generalized edema is referred to as anasarca.
- Unilateral leg edema is typical of venous and lymphatic obstruction. Venous edema is soft, pits easily and spares the toes; lymphatic edema is firm, pits poorly and involves the toes. Patients with neurologic disease are commonly allowed to sit out of bed for prolonged periods; edema may worsen because the leg muscles are not being used.
- Edema confined to the upper limbs and face occurs with superior vena cava obstruction
- Edema of one arm may be due to venous occlusion or lymphatic obstruction (e.g. caused by breast cancer)
- Bilateral edema of the lower limbs does not usually occur until more than 7 lbs of fluid has accumulated. Weight gain of 5–10 lbs over a few days is a more reliable sign of intense sodium and water retention than is the demonstration of edema.
- Edema in patients with heart failure occurs mainly when right-sided heart failure is present for several days. Acute left ventricular failure rarely causes significant leg edema. However, the most common cause of right-sided heart failure is chronic left ventricular failure. Some degree of inappropriate shortness of breath is virtually always present when edema is caused by heart failure. Edema becomes more prominent if tricuspid regurgitation ensues.The mechanism of edema formation is threefold:
- A decrease in cardiac output causes activation of the sympathetic and renin-angiotensin-aldosterone systems, which results in sodium and water retention, and a high venous pressure. The JVP is always elevated in patients with heart failure who manifest edema. High systemic venous pressure increases the hydrostatic pressure at the venous end of capillaries, and sodium and water leak out into the subcutaneous tissue. The patient is not waterlogged but has an excess of brine (salt and water) in these tissues.
- In patients with nephrotic syndrome or cirrhosis, hypoalbuminemia causes a decrease in oncotic pressure and fluid that exudes into the interstitial tissue is not able to regain entry into the vascular compartment. Because salt and water leave the vascular compartment, the decrease in effective vascular volume causes stimulation of the renin-angiotensin-aldosterone system. This stimulation results in retention of sodium and water by the kidney, and edema worsens.
- Edema of pregnancy is caused by activation of the renin-angiotensin system, which results in sodium and water retention; this increases blood volume. Approximately 8 L of water accumulates during normal pregnancy. Normally the common iliac artery partially compresses the left common iliac vein; this increases venous pressure in the left leg. In pregnancy, and in most individuals with edema, the left limb shows edema before or of greater severity than that observed in the right leg.
- Lymphatic obstruction may be caused by inflammatory, parasitic, or neoplastic processes, resulting in unilateral or bilateral lower or upper limb edema.
- Confirm that edema is unilateral or bilateral.
- Test for pitting:
- Using two finger pads held about 1 cm apart, apply firm pressure to the lower tibial area. Press firmly for about 10 seconds. Edema leaves two pits, 0.5–2 cm deep, with a ridge in between. Observe the extent of edema—ankles only, to below the knee, or above the knee (presacral edema).
- Is there associated swelling of the eyelids?
- Assess the JVP; JVP elevated to more than 3 cm bilaterally indicates CHF.
- Edema occurring weeks after the onset of ascites in a patient with an elevated JVP suggests constrictive pericarditis. If the JVP is not elevated, consider cirrhosis.
- Is generalized edema (i.e. anasarca) present?
- Anasarca often occurs in patients with nephrotic syndrome but can occur with severe chronic CHF.
Management involves treatment of the underlying cause. Symptomatic relief is obtained as follows:
- Use a diuretic: Furosemide 40–80 mg daily for a few days, then 40 mg daily for maintenance
- If CHF is the cause, treat with furosemide, angiotensin-converting enzyme (ACE) inhibitor and digoxin
- Treat the underlying cause of CHF
- If edema is chronic, furosemide may not cause complete clearing of edema. The addition of an aldosterone antagonist (e.g. amiloride 5 mg, spironolactone 25 mg, or eplerenone 25–50 mg daily) is advisable if more than 40 mg furosemide is needed.
- Furosemide, large doses, stimulates the renin-angiotensin-aldosterone system and is best used with eplerenone, amiloride, or an ACE inhibitor.
Cough is a common symptom of patients with cardiopulmonary disease. Cough is a defense mechanism that helps to protect the airways from the effects of irritant substances and to clear the airways of unwanted secretions.
- Is the cough productive or nonproductive?
- If productive, is the sputum blood-tinged or mucopurulent?
- Is there associated shortness of breath or wheezing?
- Is the patient's temperature elevated?
If cough is associated with hemoptysis and shortness of breath, consider left ventricular failure and mitral stenosis. A “brassy” cough may indicate a thoracic aortic aneurysm:
- Cough can be caused by reflux [gastroesophageal reflux (GER)], occurring mainly at nights. But unnoticeable reflux can cause sufficient irritation of the laryngotracheal area. The irritated nerve fibers in that small irritated spot triggers cough, which can be like a dog barking. This can occur day or night without a sensation of reflux and may last several weeks to months.
Salient Features of Cough
- Episodes lasting several minutes suggest an irritating phenomenon, mechanical or chemical (e.g. related to an allergic response or inhalation of smoke).
- Episodes lasting several days with associated fever and evidence of upper respiratory tract infection suggest virus or laryngotracheobronchitis.
- Coughing related to smoking suggests chronic bronchitis.
- A change in character or pattern suggests carcinoma of the lung.
- Weight loss, fever and night sweats suggest tuberculosis.
- Paroxysmal coughing, at night or with exercise, with or without wheezing, suggests asthma.
- Coughing precipitated by exercise or sexual intercourse may suggest tight mitral stenosis.
- Paroxysmal brassy cough, often with stridor, suggests tracheal obstruction produced by an aortic aneurysm.
- Productive of sputum:
- Purulent sputum associated with acute illness and fever suggests inflammatory conditions.
- Purulent and chronic sputum, occurring especially in the early morning, suggests bronchiectasis.
- Foul-smelling sputum suggests bronchoalveolar carcinoma.
- Pink, foamy and voluminous sputum with shortness of breath is typical of pulmonary edema.
- Rusty prune juice sputum with fever and chills is diagnostic of pneumonia.
- This may result from a hyperactive cough reflex that responds to ordinary innocuous stimuli.
- Several diseases may cause nonproductive cough, depending on the phase of the disease, notably cancer of the lung.
- Sarcoidosis may cause cough with dyspnea and can be complicated by conduction disturbances, including complete heart block.
- Medications, including ACE inhibitors, amiodarone and methotrexate, may be implicated.
- Barking or croupy owing to laryngeal disease.
- Paroxysmal with whoops typical of whooping cough.
- Brassy from major airways.
- Time relationships:
- Nighttime, nonproductive, chronic, paroxysmal cough with wheeze suggests asthma.
- Nighttime cough, with orthopnea or paroxysmal nocturnal dyspnea, with or without wheeze, is typical of CHF.
- Cough occurring with meals and in bed may indicate GER or diverticulum; details on GER causing cough was mentioned earlier.
- Cough on awakening or with change of posture is a hallmark of bronchiectasis; on awakening in a smoker, cough suggests chronic bronchitis or bronchogenic carcinoma.
- Intractable, chronic, but nonproductive cough suggests medications (especially ACE inhibitors and amiodarone).
- Paroxysmal wheezing strongly suggests asthma.
- Fever, chills, and rigors suggest pneumonia.
- Stridor is a hallmark of involvement of the pharynx, larynx, extrathoracic trachea by foreign body, branchial cyst, acute epiglottitis, diphtheritic infection, or laryngeal edema caused by allergic reaction to drugs, such as ACE inhibitors, or other causes of angioneurotic edema.
- Orthopnea suggests heart failure.
- Weight loss, weakness and night sweats suggest tuberculosis or carcinoma.
- With particular occupations, consider restrictive lung disease.
- Pleuritic chest pain: Pneumonia, pulmonary embolism.
- Central chest pain suggests pulmonary embolism.
- Conditions that cause an increase in left atrial pressure: Pulmonary venous hypertension that results in interstitial or pulmonary edema, left ventricular failure due to all causes, mitral stenosis, and left atrial myxoma.
- Pulmonary embolism.
- Compression of the tracheobronchial tree, as with aortic aneurysm.
- Compression of the recurrent laryngeal nerve caused by an aortic aneurysm, a greatly enlarged left atrium, or pulmonary artery, which can cause cough and hoarseness.
- Congenital cyanotic heart disease, in particular Eisenmenger's syndrome.
Determine if the sputum is:
- Pink, frothy, voluminous and associated with acute shortness of breath: These are hallmarks of pulmonary edema.
- Rusty, “prune juice” with fever and chills: These are typical of pneumonia.
- Rank blood, bright red or dark, suggests the following in the differential diagnosis: Bronchogenic carcinoma, pulmonary embolism, aortic aneurysm, arteriovenous fistula, mitral stenosis, Goodpasture's syndrome, blood dyscrasias and hereditary telangiectasia.
Determine whether the episodes of hemoptysis are associated with the following:
- Early-morning cough or cough with change in posture: This suggests bronchiectasis, chronic bronchitis and bronchogenic carcinoma.
- Dyspnea at rest, during effort, or during pregnancy: In this situation, small amounts of rusty sputum or small amounts of bright red blood suggest mitral stenosis. Sudden increase in left atrial pressure during effort or pregnancy may cause rupture of small bronchopulmonary anastomosing veins. Severe dyspnea and blood-tinged sputum are typical of pulmonary edema caused by mitral stenosis or left ventricular failure.
- Weight loss and night sweats: These suggest tuberculosis.
- Pleuritic pain: This suggests pulmonary embolism.
- Congenital heart disease and cyanosis: These suggest Eisenmenger's syndrome.
- Assess vital signs.
- Examine for the presence of left ventricular failure: Crackles over the lower lung fields, gallop rhythm and increased JVP; valvular lesions, in particular mitral stenosis (see Chapter 15). Assess for consolidation caused by pneumonia.
Treat the underlying problem:
- Drugs-causing cough: Consider discontinuing drugs that cause cough, in particular ACE inhibitors, rarely angiotensin receptor blockers [ARBs] and amiodarone.
Cough suppressants: Cough suppressants are not recommended without considerable thought. Treatment of the underlying condition is recommended; if cough persists and is bothersome and is preventing sleep, give a trial of dextromethorphan 15 mg at bedtime: but this is not advisable if the cough is productive of sputum.
Cough expectorants: Cough expectorants are not recommended because they are ineffective. It is virtually impossible to liquefy thick, tenacious sputum. Ensure that the patient is well hydrated and improve the humidity of the inspired air.
- Farkouh ME, Douglas PS. The management of acute chest pain: what lies beyond the emergency department doors? J Am Coll Cardiol. 2016;67(1):27–8.
- Khan MG. Cardiac Drug Therapy, 8e. New York: Humana Press. Springer Science+Business Media New York; 2015.