Chest pain. Comprehensive differential diagnosis and treatment
Chest pain is one of the most common symptoms, for which patients present for medical attention. There is a variety of causes, some are serious or immediately life-threatening and others are nonemergent or "innocent" conditions that do not pose any risk for the patient. The challenge for the physician is the early diagnosis and treatment of any potential life-threatening underlying cause, or to exclude any such cause and provide treatment and reassurance to the patient.Chest pain (or chest discomfort) can occur as a result of the following categories of causes:
Cardiovascular disease (angina stable or unstable, acute myocardial infarction, aortic stenosis, acute aortic dissection, pericarditis, myocarditis).
Pulmonary or pleural disease ( pulmonary embolism, pneumonia, pneumothorax, pleuritis, pulmonary hypertension).
Esophageal or other gastrointestinal disorders (esophageal reflux, esophageal spasm, esophagitis, esophageal rupture, peptic ulcer, biliary colic, cholecystitis)
Musculoskeletal disease (Costochondritis, sternoclavicular arthritis, rib fracture, cervical disc disease.
Herpes zoster, (chest pain may appear before the rash)
Anxiety and psychiatric disorders (panic disorder, affective disorders such as depression, somatoform disorders)
Pathophysiology
Pain stimuli are transmitted by afferent nerve fibers from the heart, great vessels, lungs, and esophagus. These afferent nerve fibers enter the same thoracic dorsal root ganglia. A disease of thoracic origin can produce pain anywhere from the jaw to the epigastrium (including the arms) because dorsal segments overlap three segments above and below a level. Radiation of pain occurs because there are also somatic afferent fibers synapsing in the same dorsal root ganglia as the thoracic viscera. This can result in the central nervous system misperceiving the origin of the pain and interpreting it as pain originating from another area. ( E.g., the pain of myocardial ischemia besides being felt usually retrosternally, can also radiate to the arms).The history in the differential diagnosis of chest pain
The history is the first step in the evaluation. The history of the present illness should include the location, duration, and quality of the pain, any precipitating or triggering factors, as well as any relieving factors.
Specific factors that should be noted are the following:
Duration of the pain and if it is constant or intermittent. Chest pain of very sudden onset occurs in aortic dissection, pulmonary embolism, or pneumothorax. The pain of acute myocardial infarction also has a sudden onset, but it reaches its maximal intensity more gradually than in the above three conditions.
The duration of chest pain can also provide some useful clues. The pain of an acute myocardial infarction usually lasts from 30 minutes to many hours, whereas the pain of angina (stable or unstable), although occurring in the same location, has a smaller duration (usually <20 minutes).
Duration of the pain and if it is constant or intermittent. Chest pain of very sudden onset occurs in aortic dissection, pulmonary embolism, or pneumothorax. The pain of acute myocardial infarction also has a sudden onset, but it reaches its maximal intensity more gradually than in the above three conditions.
The duration of chest pain can also provide some useful clues. The pain of an acute myocardial infarction usually lasts from 30 minutes to many hours, whereas the pain of angina (stable or unstable), although occurring in the same location, has a smaller duration (usually <20 minutes).
If the pain is related to physical exertion, i.e. if the chest pain is present during exertion or at rest, or under conditions of psychologic stress: Pain occurring during physical exertion suggests angina due to coronary artery disease. Angina occasionally may also occur under conditions of psychologic stress (because apart from physical exertion, heart rate and contractility can increase due to stress). Retrosternal ,usually intense chest pain at rest with a rapid but relatively progressive onset is the most typical presentation of an acute myocardial infarction.
If the pain occurs or worsens with deep respiration or coughing (also called pleuritic pain: Sharp chest pain that worsens with deep inspiration or coughing can be present in pleuritis, pneumonia, pericarditis or pneumothorax.
If there is a position that relieves or exacerbates the pain: (eg, lying flat, leaning forward). A recumbent position usually exacerbates the pain of pericarditis and also the pain of reflux esophagitis. The pain of acute pericarditis may be relieved by sitting and leaning forward.
If the pain worsens with movement:
Pain reproduced by movement of the arms or trunk is suggestive of a musculoskeletal origin. Occasionally, pericarditis may also cause chest pain worsened by movement of the trunk.
Pain reproduced by movement of the arms or trunk is suggestive of a musculoskeletal origin. Occasionally, pericarditis may also cause chest pain worsened by movement of the trunk.
If the pain has a relationship to meals or if there is also difficulty in swallowing:
Pain after meals usually suggests a gastrointestinal cause.
Pain after meals usually suggests a gastrointestinal cause.
If any associated symptoms are present: Diaphoresis (sweating), palpitations, syncope, dyspnea, cough, fever, nausea or vomiting.
If there were any previous episodes and their similarity or lack of similarity to the present episode:
For example, in a patient with a documented history of coronary artery disease, if the current episode resembles previous anginal pain, assume that the pain is due to myocardial ischemia.
For example, in a patient with a documented history of coronary artery disease, if the current episode resembles previous anginal pain, assume that the pain is due to myocardial ischemia.
If there is a history of any recent trauma, thoracic procedure, or excessive physical activity:
Trauma (e.g. resulting in fractured ribs or chest wall contusions, or recent excessive physical activity can result in chest pain of musculoskeletal origin.
Past medical history should document any known potential causes or investigations suggestive of the following conditions:Trauma (e.g. resulting in fractured ribs or chest wall contusions, or recent excessive physical activity can result in chest pain of musculoskeletal origin.
A history of cardiovascular disorders /risk factors for coronary artery disease (smoking, hyperlipidemia, diabetes, hypertension, cerebrovascular or peripheral vascular disease, family history of coronary artery disease-particularly an acute coronary syndrome of a 1st-degree relative at an early age, i.e., < 55 in men and < 60 in women)
Disorders of the digestive system,
Risk factors for pulmonary embolism (eg, recent surgery, lower extremity injury, immobilization, known cancer, pregnancy).
Medications, alcohol, drug-use (e.g. cocaine use, which can cause coronary spasm)
Medications, alcohol, drug-use (e.g. cocaine use, which can cause coronary spasm)
Physical examination of the patient with chest pain
In every emergency, always assess first the ABCs. (airway, breathing, circulation). Vital signs are measured. In every situation, a quick inspection of the patient gives useful clues. The general appearance of the patient gives an initial impression if the patient looks unwell and distressed or if the patient looks comfortable. From the inspection of the patient note if pallor, diaphoresis (sweating), cyanosis or anxiety is present. Pulses are palpated in both arms and both legs and blood pressure is measured in both arms. It is also useful to check if pulsus paradoxus is present, especially in a patient with distended neck veins, if there is a suspicion of cardiac tamponade. Pulsus paradoxus refers to a drop in the systolic arterial pressure of >10 mmHg in inspiration, (which is enough to cause a noticeable difference in the strength of the pulpated pulse).
The neck is inspected for venous distention and palpated for carotid pulses. Moreover, the finding of a carotid bruit on auscultation can suggest the presence of atherosclerotic arterial disease, which can often be generalized, possibly also affecting the heart.
The lungs are percussed and auscultated for the presence and symmetry of breath sounds, signs of congestion (dry or wet rales, rhonchi), consolidation (pectoriloquy), pleural friction rubs, and effusion (decreased breath sounds, dullness to percussion).
The cardiac examination notes the intensity and timing of the 1st heart sound (S1) and 2nd heart sound (S2), the respiratory movement of the pulmonic component of S2, pericardial friction rubs, murmurs, and gallops. When murmurs are detected, the timing, duration, pitch, shape, and intensity and the response to changes of position, handgrip, and the Valsalva maneuver should be noted. When gallops are detected, differentiation should be made between the 4th heart sound (S4), which is often present with diastolic dysfunction or myocardial ischemia, and the 3rd heart sound (S3), which is present with systolic dysfunction.
The chest is inspected for skin lesions of trauma or herpes zoster infection and palpated for crepitance (suggesting subcutaneous air) and tenderness. The abdomen is palpated for tenderness, organomegaly, and masses or tenderness, particularly in the epigastric and right upper quadrant regions.
The legs are examined for arterial pulses, adequacy of perfusion, edema, varicose veins, and signs of deep venous thrombosis (eg, swelling, erythema, tenderness).
"Red flags": findings that raise suspicion of a serious etiology of chest pain:
Abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension)
Signs of hypoperfusion (eg, confusion, ashen color, diaphoresis)
Dyspnea (shortness of breath) or hypoxemia (low hemoglobin oxygen saturation on pulse oximetry)
Asymmetric breath sounds
The lungs are percussed and auscultated for the presence and symmetry of breath sounds, signs of congestion (dry or wet rales, rhonchi), consolidation (pectoriloquy), pleural friction rubs, and effusion (decreased breath sounds, dullness to percussion).
The cardiac examination notes the intensity and timing of the 1st heart sound (S1) and 2nd heart sound (S2), the respiratory movement of the pulmonic component of S2, pericardial friction rubs, murmurs, and gallops. When murmurs are detected, the timing, duration, pitch, shape, and intensity and the response to changes of position, handgrip, and the Valsalva maneuver should be noted. When gallops are detected, differentiation should be made between the 4th heart sound (S4), which is often present with diastolic dysfunction or myocardial ischemia, and the 3rd heart sound (S3), which is present with systolic dysfunction.
The chest is inspected for skin lesions of trauma or herpes zoster infection and palpated for crepitance (suggesting subcutaneous air) and tenderness. The abdomen is palpated for tenderness, organomegaly, and masses or tenderness, particularly in the epigastric and right upper quadrant regions.
The legs are examined for arterial pulses, adequacy of perfusion, edema, varicose veins, and signs of deep venous thrombosis (eg, swelling, erythema, tenderness).
"Red flags": findings that raise suspicion of a serious etiology of chest pain:
Abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension)
Signs of hypoperfusion (eg, confusion, ashen color, diaphoresis)
Dyspnea (shortness of breath) or hypoxemia (low hemoglobin oxygen saturation on pulse oximetry)
Asymmetric breath sounds
Asymmetric pulses
New heart murmurs
Pulsus paradoxus > 10 mm Hg
New heart murmurs
Pulsus paradoxus > 10 mm Hg
Diagnostic tests
In most patients with chest pain arterial hemoglobin oxygen saturation with pulse oximetry, ECG, blood tests (complete blood count, basic biochemistry, troponin, CK-MB) and a chest X-ray are needed. More tests, such as arterial blood gases (ABG), D-dimers, echocardiography (transthoracic or transesophageal),chest computerized tomography ( CT) may be needed depending on the suspected cause. A low oxygen saturation, from pulse oximetry or ABG in the absence of an adequate explanation (pneumonia, heart failure or chronic obstructive pulmonary disease) should raise suspicion for pulmonary embolism. In the complete blood count, a low hematocrit (especially if it is ≤ 30 %) is important because it can worsen myocardial ischemia and also because a determination of the cause is required. An elevated white blood cell count can be due to pneumonia, pericarditis or myocarditis but it can also be present as a result of the acute stress in other acute conditions. The same is true for an elevated CRP (c-reactive protein). When an acute coronary syndrome (ACS) is suspected or diagnosed, serum cardiac markers such as cardiac troponin (cTn) I or T and CKMB should be obtained initially and after 8-12 hours. Troponins, cTnI or cTnT, begin to rise 2-6 hours after the onset of the symptoms of an acute myocardial infarction (MI) and return to baseline after 7-10 days and 10-15 days respectively. CK-MB begins to rise after 3-8 hours and returns to baseline after 1-3 days. The absence of troponin and CKMB elevation after 8-12 hours from symptom onset can exclude an acute MI, but cannot exclude myocardial ischemia as the cause of chest pain (they do not rise in unstable angina).
The ECG may reveal abnormalities in an acute coronary syndrome, pericarditis, or myocarditis (see below)
The chest X-ray can reveal abnormal findings in various conditions causing chest pain:
A widened mediastinum can be seen in aortic dissection or esophageal rupture
An enlarged cardiac silhouette in pericarditis (if there is a moderate to karge pericardial effusion) or congestive heart failure from various causes.
A pulmonary infiltrate in pneumonia. (The term "pulmonary infiltrate" means a substance with a higher density than air, e.g. fluid which may contain protein, leucocytes or blood, that accumulates in the lung interstitium or the alveoli. It appears as a non-homogeneous or homogeneous white shadow in the X-ray).
A pleural effusion may be present in pleuritis due to pneumonia, and in some cases of pulmonary embolism, aortic dissection or esophageal rupture.
Acute coronary syndromes are caused by an acute obstruction of a coronary artery usually due to a thrombus on the surface of a ruptured atherosclerotic plaque and infrequently due to coronary artery spasm (idiopathic or from cocaine use) or coronary arterial embolism. ( A coronary arterial embolism is rare cause and it may occur in mitral or aortic stenosis, atrial fibrillation, infective endocarditis or marantic endocarditis).
The consequences of an acute coronary aterial obstruction depend on degree and location of the obstruction and the presence or absence of collateral circulation. They range from unstable angina to NSTEMI, STEMI, and sudden cardiac death.
The ECG of a male patient, 65 years old, who complained of retrosternal pain for about half an hour, with perspiration. What is: 1) the diagnosis and 2) the proposed treatment?
2. Nitrates (if there is no hypotension), aspirin, clopidogrel loading dose (or ticagrelor loading dose),morphine, oxygen administration (particularly if the hemoglobin saturation <normal) and as soon as possible primary angioplasty (if it can be done within 90 minutes) or thrombolysis if primary angioplasty cannot be performed promptly (at most within 90 minutes). Also heparin (standard or low molecular weight heparin), a beta-blocker (if there is no bradycardia or hypotension), an ACE inhibitor (if there is no hypotension) and a statin.
A man 52 years old, with crushing substernal chest pain. What is the diagnosis and which artery is probably responsible?(the ECG is courtesy of Dr Najeebullah Sajid (facebook group CARDIOCARE)
The dissection may propagate either proximally or distally and a second tear can often occur, resulting in a free flow of blood through the false lumen. The most common site where a dissection occurs is the right lateral wall of the proximal ascending aorta (90% of all dissections), and the next most common site is just distal to the origin of the left subclavian artery. These sites are common because of the highest shear forces acting on the aortic wall at these locations. Dissection of the thoracic aorta is an uncommon but life-threatening emergency with an incidence of about 1 in 10,000 adults per year, (in men the incidence is slightly higher compared to women).
Chest pain is severe, described as tearing or ripping, has a very sudden onset and often radiates to the back. Apart from severe chest pain, aortic dissection may occasionally present with syncope.
A pain with the above characteristics in a patient with risk factors for aortic dissection or some suggestive findings from the physical examination (e.g., a sudden neurologic deficit, differences in pulses or blood pressure between the extremities) should raise the suspicion of aortic dissection. Risk factors include advanced age, hypertension, arteriosclerosis, Marfan syndrome, connective tissue disease, and Turner's syndrome.
Physical examination may reveal: hypertension, pulse deficit in an extremity or difference of blood pressure between the arms > 20 mmHg, a diastolic murmur of aortic regurgitation, neurologic deficits, signs of cardiac tamponade (hypotension, muffled heart sounds, and jugular venous distention).
Testing: The chest X-ray will usually show a widened mediastinum. A pleural effusion may also be present.
The triad of immediate and maximal tearing or ripping pain, pulse or blood pressure differential, and mediastinal widening must be regarded as highly suggestive of aortic dissection.
When aortic dissection is suspected, diagnostic tests of choice include chest computerized tomography (CT) enhanced with intravenous contrast medium, transesophageal echocardiography (TEE or TOE) or chest magnetic resonance imaging (MRI).
A left parasternal long axis echocardiographic view of the heart. The red arrow points at the aortic valve , while the blue arrow points at the flap of an aortic dissection
(1 right ventricle, 2. interventricular septum, 3 left ventricle, 4 aorta, 5 left atrium, 6 mitral valve. Note the dilated aortic root and ascending aorta and the intimal flap of aortic dissection.
Initial treatment of aortic dissection aims to decrease shearing stress on the aorta (in simple words it decreases forces acting on the aortic wall) and to relieve pain. Arrangements should be made to transfer the patient to a unit where hemodynamic monitoring can be instituted, such as an intensive care unit (ICU) or a coronary care unit (CCU) and ask for an emergency cardiac surgical or vascular surgical consultation. A reduction of shear stress on the aortic wall can be achieved by decreasing cardiac inotropy and blood pressure. In the presence of a high suspicion for aortic dissection, the administration of a beta-blocker (metoprolol, atenolol, labetalol, or esmolol) should be started immediately with a desired heart rate of 50-60 beats per minute.
Esmolol is given intravenously (IV) as a bolus of 30 mg followed by 3 mg/min. The dose can be gradually titrated to 12 mg/min.
The dosage of labetalol is 10 mg IV over 2 minutes followed by 20- 80 mg every 10-15 minutes to a total dose of 300 mg. Then a maintenance dose of 2 mg/min IV infusion is administered, which can be titrated to 5-20 mg/min.
If beta-blockers are contraindicated due to severe bronchospasm, a calcium channel blocker with negative inotropic effect (diltiazem) should be administered.
For additional control of the blood pressure, nitroprusside is often administered.
For the relief of pain, morphine sulfate 3-5 mg IV can be administered every 10 minutes. Morphine treatment requires close monitoring of the respirations and blood pressure.
The decision for emergency surgical treatment or only medical management depends on the anatomic type of the dissection according to the Stanford or De Bakey classification. According to the Stanford Classification type A are dissections which involve the ascending aorta, and type B dissections, which do not involve the ascending aorta.
According to the DeBakey classification:
Type I Involves both the ascending and descending thoracic aorta
Type II Involves only the ascending aorta
Type III Involves only the descending aorta
Type IIIb is also described. This involves the descending thoracic and abdominal aorta.
Prompt (emergency) surgical treatment is required for an acute aortic dissection involving the ascending aorta (Stanford type A, or repsectively DeBakey types I and II).
Stanford type B and DeBakey type III are be treated medically and surgery is employed only if there are complications. Apart from open surgical management, endovascular repair has developed as an alternative in selected patients with aortic dissection.
In acute pericarditis, there is a sharp or burning chest pain, often of several days duration. The pain is usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. There is often a prodrome of fever and malaise. The pain becomes worse when the patient is taking deep breaths and when lying down while it is usually relieved when sitting and leaning forward.
Physical Findings: Tachycardia is a usual finding. There is often a pericardial friction rub, a coarse high pitched sound with a scratching quality, described as two pieces of leather being rubbed together. This sound is best heard at the left sternal border at end-expiration with the patient sitting and leaning forward. It can have up to three components which correspond to the movement of the heart (a systolic component, an early diastolic component corresponding to the movement of the heart due to rapid ventricular filling and a late diastolic component at atrial systole). It is present in about 85% of the patients with acute pericarditis. The rub may be intermittent.
If you click on this video you can listen to a pericardial friction rub.
Link: https://www.youtube.com/watch?v=J1R8Oxgqhfk
From: You Tube channel Rombero 123
If there is a drop in ejection fraction, one must suspect that myocardial involvement is also present and the diagnosis of concomitant inflammatory disease of the myocardium (myocarditis) is made.
An enlarged cardiac silhouette in pericarditis (if there is a moderate to karge pericardial effusion) or congestive heart failure from various causes.
A pulmonary infiltrate in pneumonia. (The term "pulmonary infiltrate" means a substance with a higher density than air, e.g. fluid which may contain protein, leucocytes or blood, that accumulates in the lung interstitium or the alveoli. It appears as a non-homogeneous or homogeneous white shadow in the X-ray).
A pleural effusion may be present in pleuritis due to pneumonia, and in some cases of pulmonary embolism, aortic dissection or esophageal rupture.
In a pulmonary embolism the chest X-ray often does not demonstrate any remarkable findings but occasionally there is a lack of vascular markings in an area of the affected lung (Westermark's sign) or a wedge-shaped opacity with its base at the pleura, due to a pulmonary infarct distal to the thrombus (Hampton's hump), atelectasis with an elevated hemidiaphragm, or a dilated central pulmonary artery (dilatation proximal to the obstruction).
Pneumothorax, the presence of air within the pleural space, may occur spontaneously, or it may be the result of trauma. Pneumothorax appears as a visceral pleural line displaced away from the chest wall, with lucency and absence of lung vascular markings peripheral to this line.
Some of the main causes of chest pain and their diagnosis and treatment
Myocardial ischemia
Myocardial ischemia is a supply of oxygen to the myocardium which is not adequate for its metabolic demands. The cause is an imbalance between myocardial oxygen requirements and myocardial oxygen supply. Myocardial oxygen consumption is elevated when there is an increased heart rate, blood pressure, or contractility. Myocardial oxygen supply is reduced when there is a stenosis (atheromatous narrowing), complete obstruction, or spasm of a coronary artery or when the oxygen content of the arterial blood is reduced. Severe ischemia with duration > 20 minutes may lead to irreversible injury of myocardial cells resulting in a myocardial infarction. Myocardial ischemia may manifest with stable angina, an acute coronary syndrome (unstable angina, non-ST elevation myocardial infarction-NSTEMI or ST-elevation myocardial infarction- STEMI) or cardiac arrhythmias, or sudden cardiac death. The pain of myocardial ischemia is usually substernal, often felt as a sensation of pressure, tightness or squeezing. Radiation can be present ( to the neck, left shoulder, left arm, or epigastrium). The ischemic pain of stable angina lasts for 2-10 minutes, is associated with activity and relieved by rest or sublingual nitroglycerin.Acute coronary syndromes are caused by an acute obstruction of a coronary artery usually due to a thrombus on the surface of a ruptured atherosclerotic plaque and infrequently due to coronary artery spasm (idiopathic or from cocaine use) or coronary arterial embolism. ( A coronary arterial embolism is rare cause and it may occur in mitral or aortic stenosis, atrial fibrillation, infective endocarditis or marantic endocarditis).
The consequences of an acute coronary aterial obstruction depend on degree and location of the obstruction and the presence or absence of collateral circulation. They range from unstable angina to NSTEMI, STEMI, and sudden cardiac death.
These categories of acute coronary syndromes (with the exception of sudden death) usually present with similar symptoms that include central chest discomfort (usually tightness or pain) with or without dyspnea, nausea, and diaphoresis (sweating). The physical examination usually does not provide diagnostic findings. Often a fourth heart sound is present. Other physical findings, such as a murmur of secondary mitral regurgitation (apical systolic murmur), basal pulmonary rales or hypotension are associated with a more severe condition of the patient, therefore they have a prognostic value. Diagnosis of an acute coronary syndrome is made by combined information derived from the clinical picture, the ECG and the presence or absence of serologic markers.
In unstable angina, the pain is similar to stable angina, but there is one of the following: Angina of recent onset at a low effort or worsening of pre-existing effort angina, also known as crescendo angina (increased severity of anginal episodes, with a higher frequency on a lower effort), or angina at rest. The pain of unstable angina usually lasts 3-20 minutes. The ECG can be normal, or with ST-segment depression, or T wave inversion or with Q waves of a previous myocardial infarction. ECG findings predictive of adverse outcomes in patients with Non ST-elevation myocardial infarction (NSTEMI) and unstable angina include ST-segment depression >0.05 mV (> 0.5 mm) and new deep T-wave inversions ≥ 0.3 mV (3 mm). Other T-wave changes are also suggestive of ischemia but less specific and of less prognostic importance.
The difference between unstable angina (UA) and NSTEMI, is that in UA there is no elevation of markers of myocardial necrosis (cardiac troponin or CKMB), whereas in NSTEMI there is. Both conditions are classified as Non-ST elevation acute coronary syndromes and their treatment is similar. Generally, the pain of acute myocardial infarction (STEMI or NSTEMI) lasts from 30 minutes to hours.
Diagnosis of ST-elevation myocardial infarction (STEMI) in patients with compatible symptoms (i.e.,in the appropriate clinical setting) is established by ECG findings of ST-segment elevation > 1 mm in two or more contiguous limb leads or precordial leads V4 to V6, or > 2 mm in two or more precordial leads V1 to V3.
In patients with typical symptoms, development of a new left bundle branch block (LBBB) should be considered as a STEMI until proved otherwise.
Another type of STEMI is a true posterior myocardial infarction (MI). True posterior MI in the acute phase presents ST depression in leads V1, V2 (and sometimes also in V3, V4). This is a mirror-image of ST elevation in the posterior leads V7-V9 and is usually caused by an acute infarction in the territory of a nondominant left circumflex (LCX) coronary artery. In case of suspicion, extending the ECG to left posterior leads V7 -V9 increases sensitivity (also with excellent specificity) for the diagnosis of acute LCX injury patterns, with the detection of ST-segment elevation in these leads.
A significant number of patients with an acute STEMI develop Q waves.
In patients with unstable angina or NSTEMI if their clinical condition is uncomplicated, emergency coronary angiography is not indicated. Then coronary angiography is usually performed within 24-48 hours from patient's admission to the hospital. In patients with unstable angina or NSTEMI with a complicated clinical condition, i.e. having high risk findings urgent or emergent coronary angiography is indicated (as soon as possible). High risk findings include heart failure, reccurent angina, a sustained ventricular arrhythmia (ventricular tachycardia with a duration of at least 30 seconds or with hemodynamic instability needing electrical cardioversion, or ventricular fibrillation), or acute ischemic ECG changes. Depending on the coronary lesions, reperfusion with PCI or CABG is usually indicated.
Treatment of an acute coronary syndrome (ACS) consists of:
Bed rest
Aspirin, initially non-enteric-coated 162 -325 mg PO or chewed (preferred). Then aspirin enteric coated 80-100 mg/day.
A second antiplatelet drug (a P2Y12 inhibitor, i.e. an inhibitor of the platelet receptors for ADP) is added to aspirin. Possible choices include:
Clopidogrel, loading dose 300-600 mg followed by 75 mg/day
or
Ticagrelor,loading dose 180 mg followed by 90 mg x 2 times/day.
It is contraindicated to patients with a heart block (second or third degree).
or
Prasugrel. It can be used for post-PCI patients treated with coronary stents, of age <75 years, and weight >60 kg without any history of stroke or transient ischemic attack (TIA).
Patients unable to take aspirin (e.g. those allergic to aspirin, or with an active peptic ulcer) should receive instead of aspirin, a loading and maintenance dose of clopidogrel, ticagrelor, or prasugrel.
Nitroglycerin (NTG) sublingual 0.4 mg. It can be repeated every 5 minutes for total of three doses, then assess need for intravenous NTG. Intravenous NTG is administered if there is ongoing pain or congestive heart failure.
Nitroglycerin should be avoided in the following circumstances:
Hypotension: systolic blood pressure < 90 mm Hg or 30 mm Hg or more below baseline.
Patients who have taken a phosphodiesterase inhibitor (e.g sildenafil/ tadalafil) within the past 24 hours ( danger of severe hypotension).
MI in the distribution of the right coronary artery
Severe bradycardia (< 50 beats per minute).
Supplemental oxygen (2 -4 L/min) is administered to patients with a low arterial oxygen saturation with a goal to maintain an arterial oxygen saturation >95 % ( and in every case, at least > 90%).
In patients with a myocardial infarction(MI) the pain is relieved with morphine sulfate 2 -4 mg IV (it can be repeated, as needed, every 5-15 minutes). Morphine is a potent venous vasodilator and may cause hypotension (by reducing venous return and hence preload). Rarely, especially in high doses, it may also cause depression of the respiratory center. Then the antidote naloxone should be administered IV to reverse the action of morphine.
Apart from antiplatelet drugs, anticoagulant drugs are also administered to patients with an acute coronary syndrome. In NSTEMI or unstable angina (non ST elevation acute coronary syndrome) usually either low molecular weight heparin (LMWH) or unfractionated heparin or bivalirudin is used. Bivalirudin is used in patients with a history of heparin induced thrombocytopenia (HIT)
In STEMI undergoing primary PCI unfractionated heparin or bivalirudin are the anticoagulants of choice. Bivalirudin is preferred in those who have a high risk of bleeding and those with a history of HIT.
The usual dosage of unfractionated heparin is 70 U/kg IV(intravenously) bolus, followed by a continuous IV infusion of 15 U/kg/ hour. The dose is titrated to achieve an activated partial thromboplastin time (aPTT) 1.5-2 times the control value (usually 50-60 seconds). Some cardiologists aim for an aPTT 2-2.5 times the control value. (U = units)
Instead of unfractionated heparin, a low molecular weight heparin (LMWH) can be used. Choices include:
Enoxaparin (Lovenox/ Clexane) 1 mg/kg subcutaneously (SC) x2 times/day (1 mg/kg every 12 hours= 100 U/kg/12 hours).
Dalteparin (Fragmin) 120 U/kg SC x2 (120 U/kg every12 hr), to a maximum of 10,000 units per dose.
Treatment duration is usually for 2-8 days after patient's condition has stabilized.
For more details on the diagnosis and treatment of coronary artery disease and acute coronary syndromes please visit my free online cardiology book chapter on coronary artery disease (Link Coronary artery disease and acute coronary syndromes
In unstable angina, the pain is similar to stable angina, but there is one of the following: Angina of recent onset at a low effort or worsening of pre-existing effort angina, also known as crescendo angina (increased severity of anginal episodes, with a higher frequency on a lower effort), or angina at rest. The pain of unstable angina usually lasts 3-20 minutes. The ECG can be normal, or with ST-segment depression, or T wave inversion or with Q waves of a previous myocardial infarction. ECG findings predictive of adverse outcomes in patients with Non ST-elevation myocardial infarction (NSTEMI) and unstable angina include ST-segment depression >0.05 mV (> 0.5 mm) and new deep T-wave inversions ≥ 0.3 mV (3 mm). Other T-wave changes are also suggestive of ischemia but less specific and of less prognostic importance.
The difference between unstable angina (UA) and NSTEMI, is that in UA there is no elevation of markers of myocardial necrosis (cardiac troponin or CKMB), whereas in NSTEMI there is. Both conditions are classified as Non-ST elevation acute coronary syndromes and their treatment is similar. Generally, the pain of acute myocardial infarction (STEMI or NSTEMI) lasts from 30 minutes to hours.
Diagnosis of ST-elevation myocardial infarction (STEMI) in patients with compatible symptoms (i.e.,in the appropriate clinical setting) is established by ECG findings of ST-segment elevation > 1 mm in two or more contiguous limb leads or precordial leads V4 to V6, or > 2 mm in two or more precordial leads V1 to V3.
In patients with typical symptoms, development of a new left bundle branch block (LBBB) should be considered as a STEMI until proved otherwise.
Another type of STEMI is a true posterior myocardial infarction (MI). True posterior MI in the acute phase presents ST depression in leads V1, V2 (and sometimes also in V3, V4). This is a mirror-image of ST elevation in the posterior leads V7-V9 and is usually caused by an acute infarction in the territory of a nondominant left circumflex (LCX) coronary artery. In case of suspicion, extending the ECG to left posterior leads V7 -V9 increases sensitivity (also with excellent specificity) for the diagnosis of acute LCX injury patterns, with the detection of ST-segment elevation in these leads.
A significant number of patients with an acute STEMI develop Q waves.
Treatment
Generally, treatment of an acute coronary syndrome is with antiplatelet drugs, anticoagulants (low molecular weight heparin or unfractionated heparin), nitrates, morphine (in continuing intense pain or acute pulmonary edema),beta-blockers, a statin, an ACE inhibitor (in cases with reduced left ventricular systolic function or symptoms of heart failure without hypotension) and in every case of acute STEMI (with ST elevation, or new or presumably new LBBB, or an ECG pattern of a posterior MI) with symptom onset within the last 12 hours, prompt emergency reperfusion is indicated. Emergency reperfusion in STEMI patients is performed via primary percutaneous intervention (primary PCI), or fibrinolytic drugs, (or occasionally, coronary artery bypass graft surgery).In patients with unstable angina or NSTEMI if their clinical condition is uncomplicated, emergency coronary angiography is not indicated. Then coronary angiography is usually performed within 24-48 hours from patient's admission to the hospital. In patients with unstable angina or NSTEMI with a complicated clinical condition, i.e. having high risk findings urgent or emergent coronary angiography is indicated (as soon as possible). High risk findings include heart failure, reccurent angina, a sustained ventricular arrhythmia (ventricular tachycardia with a duration of at least 30 seconds or with hemodynamic instability needing electrical cardioversion, or ventricular fibrillation), or acute ischemic ECG changes. Depending on the coronary lesions, reperfusion with PCI or CABG is usually indicated.
Treatment of an acute coronary syndrome (ACS) consists of:
Bed rest
Aspirin, initially non-enteric-coated 162 -325 mg PO or chewed (preferred). Then aspirin enteric coated 80-100 mg/day.
A second antiplatelet drug (a P2Y12 inhibitor, i.e. an inhibitor of the platelet receptors for ADP) is added to aspirin. Possible choices include:
Clopidogrel, loading dose 300-600 mg followed by 75 mg/day
or
Ticagrelor,loading dose 180 mg followed by 90 mg x 2 times/day.
It is contraindicated to patients with a heart block (second or third degree).
or
Prasugrel. It can be used for post-PCI patients treated with coronary stents, of age <75 years, and weight >60 kg without any history of stroke or transient ischemic attack (TIA).
Patients unable to take aspirin (e.g. those allergic to aspirin, or with an active peptic ulcer) should receive instead of aspirin, a loading and maintenance dose of clopidogrel, ticagrelor, or prasugrel.
Nitroglycerin (NTG) sublingual 0.4 mg. It can be repeated every 5 minutes for total of three doses, then assess need for intravenous NTG. Intravenous NTG is administered if there is ongoing pain or congestive heart failure.
Nitroglycerin should be avoided in the following circumstances:
Hypotension: systolic blood pressure < 90 mm Hg or 30 mm Hg or more below baseline.
Patients who have taken a phosphodiesterase inhibitor (e.g sildenafil/ tadalafil) within the past 24 hours ( danger of severe hypotension).
MI in the distribution of the right coronary artery
Severe bradycardia (< 50 beats per minute).
Supplemental oxygen (2 -4 L/min) is administered to patients with a low arterial oxygen saturation with a goal to maintain an arterial oxygen saturation >95 % ( and in every case, at least > 90%).
In patients with a myocardial infarction(MI) the pain is relieved with morphine sulfate 2 -4 mg IV (it can be repeated, as needed, every 5-15 minutes). Morphine is a potent venous vasodilator and may cause hypotension (by reducing venous return and hence preload). Rarely, especially in high doses, it may also cause depression of the respiratory center. Then the antidote naloxone should be administered IV to reverse the action of morphine.
Apart from antiplatelet drugs, anticoagulant drugs are also administered to patients with an acute coronary syndrome. In NSTEMI or unstable angina (non ST elevation acute coronary syndrome) usually either low molecular weight heparin (LMWH) or unfractionated heparin or bivalirudin is used. Bivalirudin is used in patients with a history of heparin induced thrombocytopenia (HIT)
In STEMI undergoing primary PCI unfractionated heparin or bivalirudin are the anticoagulants of choice. Bivalirudin is preferred in those who have a high risk of bleeding and those with a history of HIT.
The usual dosage of unfractionated heparin is 70 U/kg IV(intravenously) bolus, followed by a continuous IV infusion of 15 U/kg/ hour. The dose is titrated to achieve an activated partial thromboplastin time (aPTT) 1.5-2 times the control value (usually 50-60 seconds). Some cardiologists aim for an aPTT 2-2.5 times the control value. (U = units)
Instead of unfractionated heparin, a low molecular weight heparin (LMWH) can be used. Choices include:
Enoxaparin (Lovenox/ Clexane) 1 mg/kg subcutaneously (SC) x2 times/day (1 mg/kg every 12 hours= 100 U/kg/12 hours).
Dalteparin (Fragmin) 120 U/kg SC x2 (120 U/kg every12 hr), to a maximum of 10,000 units per dose.
Treatment duration is usually for 2-8 days after patient's condition has stabilized.
For more details on the diagnosis and treatment of coronary artery disease and acute coronary syndromes please visit my free online cardiology book chapter on coronary artery disease (Link Coronary artery disease and acute coronary syndromes
The ECG of a male patient, 65 years old, who complained of retrosternal pain for about half an hour, with perspiration. What is: 1) the diagnosis and 2) the proposed treatment?
Answer
1.Acute anterolateral ST-elevation myocardial infarction (STEMI). Note the ST segment elevation in the anterior leads V1-V4 and the lateral leads V5, V6 and I and a mirror ST depression in leads III and aVF.2. Nitrates (if there is no hypotension), aspirin, clopidogrel loading dose (or ticagrelor loading dose),morphine, oxygen administration (particularly if the hemoglobin saturation <normal) and as soon as possible primary angioplasty (if it can be done within 90 minutes) or thrombolysis if primary angioplasty cannot be performed promptly (at most within 90 minutes). Also heparin (standard or low molecular weight heparin), a beta-blocker (if there is no bradycardia or hypotension), an ACE inhibitor (if there is no hypotension) and a statin.
A man 52 years old, with crushing substernal chest pain. What is the diagnosis and which artery is probably responsible?(the ECG is courtesy of Dr Najeebullah Sajid (facebook group CARDIOCARE)
The rhythm is sinus. There is ST elevation in the lateral leads (I, avL, V5, V6) , thus this is a lateral acute myocardial infarction (STEMI). There is also ST depression in V1 and V2 which can be attributed to an acute posterior myocardial infarction. (If we had placed an ECG lead at the patient's back, facing the posterior wall, this lead would show an ST-segment elevation). ST depression in leads III and avF is due to a mirror image of the ST elevation in the lateral leads. Often in an acute STEMI there is a mirror image of ST depression in leads having a different or opposite direction than the leads which are close to the site of the infarction. Conclusion: An acute ST-elevation myocardial infarction (STEMI) of the lateral and posterior wall (territory of the left circumflex coronary artery-LCX, which is the occluded artery in this case). Emergency reperfusion with a PCI or thrombolysis is required for this patient.
Aortic dissection
This is a tear in the intima (the inner layer of the aortic wall) with blood entering the aortic wall through that tear. This results in the presence of two lumens, the true arterial lumen through which blood continues to flow, and a false lumen within the vessel wall, which expands to some degree. Predisposing conditions for aortic dissection are cystic medial necrosis, a disorder causing weakening of the media (the central layer) of the aorta and hypertension.The dissection may propagate either proximally or distally and a second tear can often occur, resulting in a free flow of blood through the false lumen. The most common site where a dissection occurs is the right lateral wall of the proximal ascending aorta (90% of all dissections), and the next most common site is just distal to the origin of the left subclavian artery. These sites are common because of the highest shear forces acting on the aortic wall at these locations. Dissection of the thoracic aorta is an uncommon but life-threatening emergency with an incidence of about 1 in 10,000 adults per year, (in men the incidence is slightly higher compared to women).
Chest pain is severe, described as tearing or ripping, has a very sudden onset and often radiates to the back. Apart from severe chest pain, aortic dissection may occasionally present with syncope.
A pain with the above characteristics in a patient with risk factors for aortic dissection or some suggestive findings from the physical examination (e.g., a sudden neurologic deficit, differences in pulses or blood pressure between the extremities) should raise the suspicion of aortic dissection. Risk factors include advanced age, hypertension, arteriosclerosis, Marfan syndrome, connective tissue disease, and Turner's syndrome.
Physical examination may reveal: hypertension, pulse deficit in an extremity or difference of blood pressure between the arms > 20 mmHg, a diastolic murmur of aortic regurgitation, neurologic deficits, signs of cardiac tamponade (hypotension, muffled heart sounds, and jugular venous distention).
Testing: The chest X-ray will usually show a widened mediastinum. A pleural effusion may also be present.
The triad of immediate and maximal tearing or ripping pain, pulse or blood pressure differential, and mediastinal widening must be regarded as highly suggestive of aortic dissection.
When aortic dissection is suspected, diagnostic tests of choice include chest computerized tomography (CT) enhanced with intravenous contrast medium, transesophageal echocardiography (TEE or TOE) or chest magnetic resonance imaging (MRI).
(1 right ventricle, 2. interventricular septum, 3 left ventricle, 4 aorta, 5 left atrium, 6 mitral valve. Note the dilated aortic root and ascending aorta and the intimal flap of aortic dissection.
Initial treatment of aortic dissection aims to decrease shearing stress on the aorta (in simple words it decreases forces acting on the aortic wall) and to relieve pain. Arrangements should be made to transfer the patient to a unit where hemodynamic monitoring can be instituted, such as an intensive care unit (ICU) or a coronary care unit (CCU) and ask for an emergency cardiac surgical or vascular surgical consultation. A reduction of shear stress on the aortic wall can be achieved by decreasing cardiac inotropy and blood pressure. In the presence of a high suspicion for aortic dissection, the administration of a beta-blocker (metoprolol, atenolol, labetalol, or esmolol) should be started immediately with a desired heart rate of 50-60 beats per minute.
Esmolol is given intravenously (IV) as a bolus of 30 mg followed by 3 mg/min. The dose can be gradually titrated to 12 mg/min.
The dosage of labetalol is 10 mg IV over 2 minutes followed by 20- 80 mg every 10-15 minutes to a total dose of 300 mg. Then a maintenance dose of 2 mg/min IV infusion is administered, which can be titrated to 5-20 mg/min.
If beta-blockers are contraindicated due to severe bronchospasm, a calcium channel blocker with negative inotropic effect (diltiazem) should be administered.
For additional control of the blood pressure, nitroprusside is often administered.
For the relief of pain, morphine sulfate 3-5 mg IV can be administered every 10 minutes. Morphine treatment requires close monitoring of the respirations and blood pressure.
The decision for emergency surgical treatment or only medical management depends on the anatomic type of the dissection according to the Stanford or De Bakey classification. According to the Stanford Classification type A are dissections which involve the ascending aorta, and type B dissections, which do not involve the ascending aorta.
According to the DeBakey classification:
Type I Involves both the ascending and descending thoracic aorta
Type II Involves only the ascending aorta
Type III Involves only the descending aorta
Type IIIb is also described. This involves the descending thoracic and abdominal aorta.
Prompt (emergency) surgical treatment is required for an acute aortic dissection involving the ascending aorta (Stanford type A, or repsectively DeBakey types I and II).
Stanford type B and DeBakey type III are be treated medically and surgery is employed only if there are complications. Apart from open surgical management, endovascular repair has developed as an alternative in selected patients with aortic dissection.
Acute pericarditis
This is an acute inflammation of the pericardium. The most common causes are viral pericarditis (caused by a viral infection) and idiopathic pericarditis (when the cause has not been clearly identified). There are no differences in clinical features distinguishing idiopathic cases from viral pericarditis. Most cases of idiopathic pericarditis are probably undiagnosed viral infections. Other causes of pericarditis include connective tissue disease (systemic lupus erythematosus, rheumatoid arthritis), myocardial infarction, postpericardiotomy syndrome, radiation, trauma, bacterial infection, tuberculosis, uremic pericarditis, malignancy, etc. Malignancy is a cause that we should consider in the differential diagnosis, especially in patients with moderate to large pericardial effusions.In acute pericarditis, there is a sharp or burning chest pain, often of several days duration. The pain is usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. There is often a prodrome of fever and malaise. The pain becomes worse when the patient is taking deep breaths and when lying down while it is usually relieved when sitting and leaning forward.
Physical Findings: Tachycardia is a usual finding. There is often a pericardial friction rub, a coarse high pitched sound with a scratching quality, described as two pieces of leather being rubbed together. This sound is best heard at the left sternal border at end-expiration with the patient sitting and leaning forward. It can have up to three components which correspond to the movement of the heart (a systolic component, an early diastolic component corresponding to the movement of the heart due to rapid ventricular filling and a late diastolic component at atrial systole). It is present in about 85% of the patients with acute pericarditis. The rub may be intermittent.
If you click on this video you can listen to a pericardial friction rub.
Link: https://www.youtube.com/watch?v=J1R8Oxgqhfk
From: You Tube channel Rombero 123
ECG: In acute pericarditis there is a diffuse ST segment elevation (concave upward) usually present in almost all leads, except aVR and V1. PR-segment depression may be present, but in aVR there is a PR-segment elevation ( this is useful to differentiate from early repolarization and acute myocardial infarction).
Days later, ST segments return to baseline before T-wave inversion develops.
Echocardiography: often detects a pericardial effusion, which commonly (but not always) accompanies acute pericarditis.Days later, ST segments return to baseline before T-wave inversion develops.
If there is a drop in ejection fraction, one must suspect that myocardial involvement is also present and the diagnosis of concomitant inflammatory disease of the myocardium (myocarditis) is made.
Treatment of acute pericarditis
The first line therapy for acute pericarditis is the administration of non-steroidal anti-inflamatory drugs (NSAIDs):
High-dose aspirin 650 mg -1 g x 3-4 times per day, or ibuprofen 600 mg PO x 3 times per day, or indomethacin 75 mg PO x2 times per day).
Useful is the co-administration with an H2-antagonist (e.g. ranitidine) or proton pump inhibitor (e.g. pantoprazol, lansoprazol etc) to reduce the risk of gastrointestinal bleeding (which is a possible side effect of NSAIDs).
Concomitant administration of colchicine (combined with the administration of NSAIDS) can reduce the chances of recurrent
pericarditis. ( Dosage: 1-2 mg for the first day followed by 0.6–1 mg/day for 3 months).
For recurrent pericarditis, colchicine can be used with NSAIDs or instead of NSAIDs.
Colchicine side effects: It can cause gastrointestinal symptoms (in this case the lower dose may be selected). Infrequently it can cause bone marrow suppression (chronic kidney disease is a risk factor for this side effect).
In acute pericarditis, strenuous physical activity should be limited for at least 2 months.
Corticosteroids can be considered in cases of failure of NSAID and colchicine therapy. (Prednisone 0.2 - 0.5 mg/kg/day) for 4 weeks until symptoms and elevated C-reactive protein have resolved). The dose of corticosteroids is gradually reduced before discontinuation of this treatment.
A patient complaining of chest pain, worse with deep respiration, cough, and mild dyspnea. Recent surgery for a femoral fracture. What are the findings in this chest X ray?
In the lower right lung, there is a wedge-shaped consolidation with its base against the pleural surface. This radiographic sign and also the patient's history is highly suggestive of a pulmonary embolism.
In the lower right lung, there is a wedge-shaped consolidation with its base against the pleural surface. This radiographic sign and also the patient's history is highly suggestive of a pulmonary embolism.
Acute pulmonary embolism
This is an obstruction of a branch of the pulmonary artery by thrombus originating in the systemic venous system (most commonly in the lower extremity or deep pelvic veins). The thrombus travels through the venous system into the right heart chambers and from there it lodges in the pulmonary artery.Chest pain of sudden onset, accompanied by dyspnea, cough, and in some cases hemoptysis, developing in a patient who has been immobilized or bedridden or has a recent history of surgery, pelvic or lower extremity injury or cancer is suggestive of pulmonary embolism.
For more details on the diagnosis and treatment of acute pulmonary embolism click on the following chapter of this online book Pulmonary Embolism
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A patient presenting with chest pain and dyspnea of sudden onset. Diagnosis?
A right-sided pneumothorax. The border between the air in the pleural space and the collapsed right lung is seen. In this case, it is a large pneumothorax occupying the upper and lateral portion of the right hemithorax (In cases of a small pneumothorax it may occupy only the apical portion of the hemithorax). The region of the pneumothorax appears black without vascular markings and the compressed lung appears denser than the normal contralateral lung. The lack of vascular markings is a feature that differentiates free air in the pleural space from the lung. (When a small pneumothorax is suspected, it is also useful to order a chest x-ray not only in inspiration (as usual) but also in expiration. The reason is that in expiration the lung appears denser and the border between the air in the pleural space and the lung will become more visible.
A useful video link:
For analgesia usually morphine is administered, 2.5-5 mg IV with an antiemetic.
Commencement of broad-spectrum antibiotics is required such as a combination of gentamicin 5 mg/kg IV, ampicillin 1 g IV, and metronidazole 500 mg IV.
Diffuse esophageal spasm is not common but it is a motility disorder which can occasionally produce symptoms indistinguishable from angina pectoris.
It is caused by hyperdynamic contractions of the esophageal smooth muscle or elevated lower esophageal sphincter pressure. The pathophysiology is not clear but it may involve a deficiency of nitric oxide (NO) in the esophageal muscle leading to a loss of control of the esophageal peristalsis and increased intraluminal pressures. In some cases esophageal spasm is caused by gastroesophageal reflux disease (GERD).
Caylee WE. Diagnosing the Cause of Chest Pain. Am Fam Physician 2005; 72(10):2012-2021 Chest LINK https://www.aafp.org/afp/2005/1115/p2012.html
Chest pain in Haist, S, et al. Internal Medicine On Call. 2005 McGraw Hill Professional.
Fordyce CB, Newby DE, Douglas PS.Diagnostic Strategies for the Evaluation of Chest Pain: Clinical Implications From SCOT-HEART and PROMISE.
Fox KF Investigation and management of chest pain.
McConaghy JR, Oza RS Outpatient diagnosis of acute chest pain in adults.
.Am Fam Physician. 2013;87(3):177-82
A patient presenting with chest pain and dyspnea of sudden onset. Diagnosis?
A right-sided pneumothorax. The border between the air in the pleural space and the collapsed right lung is seen. In this case, it is a large pneumothorax occupying the upper and lateral portion of the right hemithorax (In cases of a small pneumothorax it may occupy only the apical portion of the hemithorax). The region of the pneumothorax appears black without vascular markings and the compressed lung appears denser than the normal contralateral lung. The lack of vascular markings is a feature that differentiates free air in the pleural space from the lung. (When a small pneumothorax is suspected, it is also useful to order a chest x-ray not only in inspiration (as usual) but also in expiration. The reason is that in expiration the lung appears denser and the border between the air in the pleural space and the lung will become more visible.
A useful video link:
from the you-tube channel hammadshams
(How to diagnose pneumothorax on chest-X-ray)
Pneumothorax
The main manifestations of a large pneumothorax are shortness of breath, tachypnea and chest pain of sudden onset. A small pneumothorax can be completely asymptomatic. Pneumothorax is the presence of air in the pleural cavity between the visceral and the parietal pleura. When a large amount of air accumulates in the pleural cavity, it exerts pressure on the lung and the organs of the mediastinum.
Causes: A pneumothorax can occur as a result of spontaneous rupture of the pulmonary parenchyma at sites of blebs or bullae. This can happen to patients with a history of a pulmonary disorder, such as chronic obstructive pulmonary disease (COPD), cystic fibrosis, lung cancer or tuberculosis. It may also occur in individuals without a history of a pre-existing pulmonary disease, usually tall young men ( about 20-30 years old). Then it is called a primary spontaneous pneumothorax.
Traumatic pneumothorax occurs in chest injuries where air enters the pleural space either through a rupture of the pulmonary parenchyma (usually as a result of rib fractures which injure the underlying lung) or directly from the atmospheric air through a penetrating injury of the thoracic wall.
Iatrogenic pneumothorax occurs as a complication of certain medical procedures such as subclavian vein catheterization (e.g. to insert a pacemaker lead), thoracentesis, mechanical ventilation with high inspiratory pressures, external cardiac massage during cardiopulmonary resuscitation and thoracoscopy.
In a closed pneumothorax, the entry point of air closes, trapping air into the pleural cavity but preventing more air to accumulate. In an open pneumothorax, the entry point remains open, resulting in air entering the pleural cavity with the inspiration and exiting with expiration.
Traumatic pneumothorax occurs in chest injuries where air enters the pleural space either through a rupture of the pulmonary parenchyma (usually as a result of rib fractures which injure the underlying lung) or directly from the atmospheric air through a penetrating injury of the thoracic wall.
Iatrogenic pneumothorax occurs as a complication of certain medical procedures such as subclavian vein catheterization (e.g. to insert a pacemaker lead), thoracentesis, mechanical ventilation with high inspiratory pressures, external cardiac massage during cardiopulmonary resuscitation and thoracoscopy.
In a closed pneumothorax, the entry point of air closes, trapping air into the pleural cavity but preventing more air to accumulate. In an open pneumothorax, the entry point remains open, resulting in air entering the pleural cavity with the inspiration and exiting with expiration.
A tension pneumothorax is the most serious form because the site of air entry has such a configuration that it acts like a valve, allowing air to enter the pleural space in inspiration while preventing the air from exiting during expiration. The result is a gradual and progressive increase in the volume and pressure of air trapped in the pleural space. As the pressure increases, the ipsilateral lung collapses resulting in hypoxia and severe respiratory distress. As the pleural pressure increases further, it causes the mediastinum to shift toward the contralateral side and compress the contralateral lung. Another important feature of the pathophysiology of tension pneumothorax is the following: Due to the increased intrathoracic pressure, the large intrathoracic systemic veins are compressed and the venous return to the right atrium is impaired, causing hypotension.
In a large pneumothorax, there is a reduction in the respiratory motion of the affected hemithorax (sometimes the intercostal spaces may even appear enlarged or protruding). Auscultation reveals decreased or absent breath sounds on the affected side and percussion may reveal hyperresonance on the affected hemithorax, although this finding is not easily detected in many cases. In a tension pneumothorax, there is severe respiratory distress with tachypnea (bradypnea is a late finding), hypoxia, hypotension, the absence of breath sounds on the affected hemithorax and often jugular venous distention and a tracheal shift toward the contralateral side. If the patient is on mechanical ventilation, the airway pressure alarms are triggered. A tension pneumothorax is a life-threatening emergency.
In a large pneumothorax, there is a reduction in the respiratory motion of the affected hemithorax (sometimes the intercostal spaces may even appear enlarged or protruding). Auscultation reveals decreased or absent breath sounds on the affected side and percussion may reveal hyperresonance on the affected hemithorax, although this finding is not easily detected in many cases. In a tension pneumothorax, there is severe respiratory distress with tachypnea (bradypnea is a late finding), hypoxia, hypotension, the absence of breath sounds on the affected hemithorax and often jugular venous distention and a tracheal shift toward the contralateral side. If the patient is on mechanical ventilation, the airway pressure alarms are triggered. A tension pneumothorax is a life-threatening emergency.
The chest X-ray demonstrates a lucent (black) area in the upper and lateral portions of the hemithorax, in which the characteristic linear shades of the pulmonary vessels are completely absent. This radiolucent area is observed between the chest wall and the limits of the compressed lung. A compressed lung will have reduced volume and a dense appearance. In a tension pneumothorax, the heart and the trachea are displaced towards the contralateral side. In case of a tension pneumothorax, immediate puncture of the affected hemithorax with an angiocath needle No 16 G ( 16 gauge) into the second intercostal space at the midclavicular line can be life-saving, while the patient awaits placement of a chest tube.
A small pneumothorax, causing no significant respiratory symptoms, can usually be treated with oxygen administration (when needed) and frequent clinical and radiologic observation because the air will be spontaneously absorbed. A larger pneumothorax, e.g. involving > 20% of the lung is treated with chest tube insertion or pneumothorax catheter placement with aspiration.
A small pneumothorax, causing no significant respiratory symptoms, can usually be treated with oxygen administration (when needed) and frequent clinical and radiologic observation because the air will be spontaneously absorbed. A larger pneumothorax, e.g. involving > 20% of the lung is treated with chest tube insertion or pneumothorax catheter placement with aspiration.
Pneumonia/pleuritis.
These conditions may manifest chest pain which is typically pleuritic (worse with deep inspiration or coughing). Pneumonia is an infection of the lung parenchyma (bronchioles and alveoli). It usually manifests with fever, rigors, malaise and cough (usually productive, i.e. with sputum) and often pleuritic chest pain. There is often dyspnea, tachypnea, and tachycardia. Symptoms may be less impressive in immunocompromised states ( HIV, chronic alcoholism), in the elderly (occasionally in the elderly, pneumonia manifests only with confusion) and in diabetics.
Auscultation of the thorax in pneumonia may reveal crackles and egophony and in pleuritis, there is often a pleural friction rub. Crackles are short interrupted abnormal lung sounds perceived as discontinuous clicking or rattling sounds. Crackles can sound like salt dropped onto a hot pan or like cellophane being crumpled. In this link, you can listen to crackles https://www.easyauscultation.com/crackles-lung-sounds. Crackles can be heard in pneumonia. Bilateral crackles can be heard in congestive heart failure and in interstitial lung disease (pulmonary fibrosis).
Laboratory testing reveals leukocytosis, and an elevated erythrocyte sedimentation rate (ESR) and CRP. (ESR and CRP are usually elevated in inflammatory and infectious disease, but they are non-specific tests). The chest X-ray in pneumonia will demonstrate an infiltrate, while in pleuritis it will show a pleural effusion.
For more details on the diagnosis and treatment of pneumonia click on the following link to visit the relevant chapter of this online book: Pneumonia
For more details on the diagnosis and treatment of pneumonia click on the following link to visit the relevant chapter of this online book: Pneumonia
Esophageal rupture
This is a rare condition, but it needs prompt diagnosis and treatment because it can lead to shock. There is persistent severe chest pain (substernal, along the esophagus). The pain usually is preceded by vomiting. Factors from the history that make this diagnosis more probable are the following:
Elderly or alcoholic patient with forceful vomiting, a history of a known esophageal disease, instrumentation of the esophagus, blunt or penetrating trauma of the chest, caustic ingestion or ingestion of a foreign body. Spontaneous esophageal rupture, caused by violent vomiting is referred to as Boerhaave syndrome and produces severe chest pain and often circulatory collapse.
The pain is of abrupt onset, it is persistent and unrelieved and increases with neck flexion or swallowing.
In esophageal rupture, oral and gastric secretions leak out of the esophagus into the mediastinum or pleural cavity. This results in an inflammatory and septic process. Patients may develop circulatory shock with tachycardia, hypotension and respiratory distress, or other signs of sepsis associated with mediastinitis. Diagnostic clues are the following:
The classic triad of vomiting, lower chest pain, and subcutaneous emphysema, (although this triad is not present in many cases).
Hamon's sign may be present. This is a crunch-like sound caused by air moving within the mediastinum.
In patients with vomiting, fever, and persistent chest pain, esophageal rupture should be suspected in the differential diagnosis.
The chest X-ray may demonstrate a widened mediastinum, pneumomediastinum (detection of air within the mediastinal shadow), and a pleural effusion or a pneumothorax. Diagnosis is made with esophageal fluoroscopy using water soluble
contrast ( water soluble contrast esophagram). For critically ill patients who cannot tolerate a fluoroscopic study, a chest CT may show air in the mediastinum and/or paraesophageal fluid.
Management of esophageal rupture includes IV fluid resuscitation, IV analgesia, IV antibiotics and early surgical consultation, for surgical correction.For analgesia usually morphine is administered, 2.5-5 mg IV with an antiemetic.
Commencement of broad-spectrum antibiotics is required such as a combination of gentamicin 5 mg/kg IV, ampicillin 1 g IV, and metronidazole 500 mg IV.
Gastroesophageal reflux disease (GERD)
It is a common esophageal disorder that occurs when the reflux of contents of the stomach into the esophagus causes symptoms or complications. It is caused by an incompetence (reduced function) of the lower esophageal sphincter. Risk factors that increase the probability of a person to develop GERD include central obesity, increased consumption of caffeine, alcohol and tobacco, increasing age and a family history of GERD (a genetic component may also be present). The classic symptoms of GERD include heartburn (a burning retrosternal sensation or burning pain) and acid regurgitation, whereas occasionally chest pain or dysphagia occurs. Some patients may have cough, laryngitis or erosions of the teeth. Symptoms of GERD often occur when the patient lies flat after a meal. Symptoms are alleviated by drinking water or milk, and they are mostly alleviated by the ingestion of antiacid medications.
GERD can lead to the development of:
Rarely GERD may lead to the development of:
Treatment of GERD consists of drugs that lower gastric acid secretion such as proton pump inhibitors (e. g. omeprazole 20 mg, esomeprazole 40 mg, pantoprazole 40 mg, lansoprazole 30 mg x 1 time/day) or ranitidine 150 mg before sleep. Other measures include avoidance of eating a large meal within 3 hours before sleeping, elevation of the head of the bed by about 15 cm, reducing caffeine, alcohol and tobacco and weight loss for overweight individuals. Surgery is reserved for more serious cases with esophagitis, esophageal strictures etc.
Kandulski A, Malfertheiner P. GERD in 2010: diagnosis, novel mechanisms of disease
and promising agents. Nat Rev Gastroenterol Hepatol 2011; 8:73-74.
Esophagitis can manifest with odynophagia (pain with swallowing), dysphagia (difficulty in swallowing such as a sensation of obstruction during the passage of food), or chest pain.
Diagnosis is by endoscopy. Thus, when there is a clinical suspicion of esophagitis, the patient should be referred to a gastroenterologist for the diagnosis and appropriate treatment, which depends on the etiology.
Diffuse Esophageal Spasm
(Spastic Pseudodiverticulosis; Rosary Bead or Corkscrew Esophagus)
GERD can lead to the development of:
- Esophagitis (inflammation of the esophageal mucosa) which may manifest with odynophagia (pain with swallowing) or even esophageal hemorrhage
- A peptic esophageal ulcer (which can manifest with pain similar to the pain of a gastric ulcer, with the difference that the location of pain is in the xiphoid or substernal area)
Rarely GERD may lead to the development of:
- An esophageal stricture (a narrowing of the esophageal lumen due to the development of scar tissue),
- Barret's esophagus (where the esophageal epithelium changes from the normal stratified squamous epithelium to a simple columnar epithelium, resembling the epithelium of the small intestine) This condition predisposes to the later development of esophageal cancer
- An esophageal adenocarcinoma
Treatment of GERD consists of drugs that lower gastric acid secretion such as proton pump inhibitors (e. g. omeprazole 20 mg, esomeprazole 40 mg, pantoprazole 40 mg, lansoprazole 30 mg x 1 time/day) or ranitidine 150 mg before sleep. Other measures include avoidance of eating a large meal within 3 hours before sleeping, elevation of the head of the bed by about 15 cm, reducing caffeine, alcohol and tobacco and weight loss for overweight individuals. Surgery is reserved for more serious cases with esophagitis, esophageal strictures etc.
Kandulski A, Malfertheiner P. GERD in 2010: diagnosis, novel mechanisms of disease
and promising agents. Nat Rev Gastroenterol Hepatol 2011; 8:73-74.
Esophagitis
It is an inflammation of the esophageal mucosa. Possible causes include GERD, some medications, eosinophilic esophagitis (this condition is attributed to an allergic-immunologic reaction, but eosinophilic infiltration of the esophageal mucosa may also occur in esophagitis caused by GERD) or infection. Esophageal infection ( often from Candida but also from Herpes simplex virus, Cytomegalovirus or Mycobacterium tuberculosis) can occur in immunocompromised (e/g HIV infection/chemotherapy) or debilitated patients.Esophagitis can manifest with odynophagia (pain with swallowing), dysphagia (difficulty in swallowing such as a sensation of obstruction during the passage of food), or chest pain.
Diagnosis is by endoscopy. Thus, when there is a clinical suspicion of esophagitis, the patient should be referred to a gastroenterologist for the diagnosis and appropriate treatment, which depends on the etiology.
Diffuse Esophageal Spasm
(Spastic Pseudodiverticulosis; Rosary Bead or Corkscrew Esophagus)
Diffuse esophageal spasm is not common but it is a motility disorder which can occasionally produce symptoms indistinguishable from angina pectoris.
It is caused by hyperdynamic contractions of the esophageal smooth muscle or elevated lower esophageal sphincter pressure. The pathophysiology is not clear but it may involve a deficiency of nitric oxide (NO) in the esophageal muscle leading to a loss of control of the esophageal peristalsis and increased intraluminal pressures. In some cases esophageal spasm is caused by gastroesophageal reflux disease (GERD).
Usually, it manifests with substernal squeezing chest pain which may be aggravated by the ingestion of very hot or cold liquids. It is often accompanied by dysphagia (difficulty in swallowing) for both liquids and solid food. Occasionally the pain may also occur with exercise (like angina pectoris). The pain is relieved by nitrates or calcium channel blockers because these are drugs that relax smooth muscle.
Diagnosis: Often myocardial ischemia will need to be excluded with tests such as the ECG, an ECG exercise test or other tests (e.g. a myocardial perfusion scan-SPECT).
Tests that can aid in the diagnosis of esophageal spasm include:
Treatment is with calcium channel blockers. Other treatment options include nitrates, sildenafil (50 mg orally), or low-dose tricyclic antidepressants (e.g., imipramine, 10 to 50 mg before bedtime).
Diagnosis: Often myocardial ischemia will need to be excluded with tests such as the ECG, an ECG exercise test or other tests (e.g. a myocardial perfusion scan-SPECT).
Tests that can aid in the diagnosis of esophageal spasm include:
- A barium swallow which typically will show a "corkscrew esophagus" with multiple simultaneous contractions that obliterate the lumen and
- Esophageal manometry.
Treatment is with calcium channel blockers. Other treatment options include nitrates, sildenafil (50 mg orally), or low-dose tricyclic antidepressants (e.g., imipramine, 10 to 50 mg before bedtime).
GO BACK TO THE TABLE OF CONTENTS
LINK: Emergency medicine book-Table of contents
Bibliography and links
LINK: Emergency medicine book-Table of contents
Bibliography and links
Caylee WE. Diagnosing the Cause of Chest Pain. Am Fam Physician 2005; 72(10):2012-2021 Chest LINK https://www.aafp.org/afp/2005/1115/p2012.html
Chest pain in Haist, S, et al. Internal Medicine On Call. 2005 McGraw Hill Professional.
Fordyce CB, Newby DE, Douglas PS.Diagnostic Strategies for the Evaluation of Chest Pain: Clinical Implications From SCOT-HEART and PROMISE.
J Am Coll Cardiol. 2016; 67(7):843-52.
The MSD manual: Chest pain
Heart. 2005 ;91(1):105-10.
McConaghy JR, Oza RS Outpatient diagnosis of acute chest pain in adults.
.Am Fam Physician. 2013;87(3):177-82
LINK https://www.aafp.org/afp/2013/0201/p177.html
A video
A presentation by dr Anastasia Anthi LINK Pulmonary embolism (website Livemedia) From the site you can download the presentation (showing chest Xray images and CT images of pulmonary embolism cases) in PDF.
A video
Pulmonary infarct LINK: Pulmonary embolism (infarct) Hampton's hump on chest X ray and Chest CT
from you tube channel:
A presentation by dr Anastasia Anthi LINK Pulmonary embolism (website Livemedia) From the site you can download the presentation (showing chest Xray images and CT images of pulmonary embolism cases) in PDF.
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