Friday, April 2, 2021

Acute Pericarditis Case File

Posted By: Medical Group - 4/02/2021 Post Author : Medical Group Post Date : Friday, April 2, 2021 Post Time : 4/02/2021
Acute Pericarditis Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 9
A 23-year-old woman is evaluated in the emergency department for a 4-day history of substernal, sharp, intermittent chest pain that is aggravated by deep breaths. The pain is worse when she lies down and improves when she sits up and leans forward. She has had a 1-week history of nonproductive cough, sore throat, and myalgias. Her medical history is unremarkable and she takes no medications. On physical examination, temperature is 37.8°C (100.0°F), blood pressure is 118/54 mmHg. pulse is 90/min, and respiration rate is 22 breaths/min. Oxygen saturation on ambient air is 97%. The patient appears diaphoretic. The oropharynx is erythematous. Cardiac examination discloses a three-component scratchy rub that is loudest over the left sternal border, but no murmurs or gallops. Pulmonary auscultation reveals normal breath sounds and no crackles. There is no jugular venous distention and no chest wall tenderness. Laboratory studies show a normal cell count and normal metabolic panel. The initial set of cardiac enzymes is negative. A 12-lead electrocardiogram is shown in Figure 9-1. A chest radio graph shows no infiltrates and a normal cardiac silhouette.

c What is the most likely diagnosis?
c What is the most likely etiology for the patient’s condition?
c What is the best treatment for this patient?

12-lead ECG

Figure 9-1. A 12-lead ECG.

Answer to Case 9:
Acute Pericarditis

Summary: This 23-year-old woman presents with pleuritic chest pain, constitutional symptoms, low-grade fever, and tachycardia. Cardiac exam reveals a pericardial friction rub. A 12-lead electrocardiogram shows sinus tachycardia with diffuse, concave upward, ST segment elevation (best seen in leads II, III, and V2–V6) and PR segment depression (in most leads except aVR where PR segment elevation is noted). Lab work, including first set of cardiac enzymes, and chest radiograph are within normal limits.
  • Most likely diagnosis : Acute pericarditis.
  • Most likely et ology: Idiopathic cases, most of which are likely viral in etiology, are the most common causes of acute pericarditis.
  • Best treatment: Combination therapy with colchicine plus NSAIDs (nonsteroidal anti-inflammatory drugs).
ANALYSIS

Objectives
  1. Describe the different clinical presentations of pericardial disease: acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis.
  2. Recognize the distinct features of acute pericarditis and consider alternative potentially life-threatening causes of chest pain: acute coronary syndromes, pulmonary embolus, pneumothorax, aortic dissection, and esophageal rupture.
  3. Identify pericardial disease emergencies, including how to differentiate pericardial effusion without hemodynamic compromise from cardiac tamponade.
  4. Understand the hemodynamic consequences of pericardial disease, particularly cardiac tamponade and constrictive pericarditis.
  5. Know the common etiologies, workup, and management of the different types of pericardial disease.
Considerations
This 23-year-old woman presents to the emergency department with chest pain of a few days’ duration. The immediate priority in any patient presenting with chest pain is to rule out potentially life-threatening medical emergencies: acute coronary syndromes, pulmonary embolus, pneumothorax, aortic dissection, and esophageal rupture.

The first step is to perform a focused history, including identification of cardiac risk factors and physical examination. The chest pain of acute pericarditis is typically sharp and pleuritic, and improves by sitting up and leaning forward. The presence of a pericardial friction rub (scratchy or squeaking extra sound best heard with the diaphragm of the stethoscope and loudest over the left sternal border) on physical examination is highly specific for acute pericarditis. The second step is to perform a chest radiograph and an electrocardiogram (ECG) and to send cardiac biomarkers. Chest radiography is typically normal in acute pericarditis but may reveal cardiomegaly if accompanied by a pericardial effusion. Its value resides mainly in ruling out other causes of chest pain such as pneumothorax and aortic dissection. The ECG in acute pericarditis is characterized by diffuse ST elevation–typically concave up– along with diffuse PR segment depression (except in lead aVR, where ST segment depression and PR segment elevation are usually noted). The electrocardiographic changes in acute pericarditis differ from those in acute ST segment elevation MI (STEMI) in several ways: the typical finding in a STEMI patient is convex (domeshaped) ST elevation is characteristically limited to anatomical groupings of leads that correspond to the localized vascular area of the infarct, and has reciprocal ST segment changes (which are not seen with pericarditis except in leads aVR and V1).

While serum biomarkers of myocardial injury such as cardiac troponins are usually normal in acute pericarditis, increased levels may also be noted. This usually occurs when the inflammation extends from the pericardium to involve the myocardium–such patients are considered to have myopericarditis. Since pericarditis is an inflammatory disease, laboratory signs of inflammation are common in patients with acute pericarditis. These include elevations in the white blood cell count, erythrocyte sedimentation rate, and serum C-reactive protein concentration. Once pericarditis is considered and alternative diagnoses ruled out, performing an echocardiogram is an essential part of the evaluation to look for evidence of an associated pericardial effusion and/or signs of cardiac tamponade. Most cases of acute pericarditis are idiopathic and presumed to have a viral etiology. However, other etiologies need to be considered in the appropriate clinical settings and include other infectious etiologies (bacteria, fungus, and parasites), malignancy (particularly metastatic spread of noncardiac primary tumors), autoimmune diseases, drugs, mediastinal radiation, and metabolic causes (renal failure with uremia, myxedema). Table 9-1 summarizes the major causes of pericardial disease.

In cases of pericarditis due to an identifiable cause (uremia, malignancy), management should focus on the underlying disorder. For most patients with acute idiopathic (viral) pericarditis, treatment consists of combination therapy of NSAIDs and colchicine. NSAIDs target the inflammation, and colchicine has been shown to reduce the rate of recurrences.

Approach To:
Pericardial Diseases

DEFINITIONS
Acute Pericarditis: Inflammation of the pericardial sac. It is the most common disorder of the pericardium.

Major Causes of Pericardial Disease


Peri Cardial Effusion: Accumulation of fluid (serosanguineous or blood) within the pericardial sac, typically in response to inflammation or injury.

Cardiac Tamponade: Clinical state characterized by tachycardia, relative hypotension evidence of pulsus paradoxus, and jugular venous distention. Tamponade occurs when the intrapericardial pressure exceeds right atrial and right ventricular diastolic pressure, resulting in right-sided chamber collapse and failure to provide venous return to the heart. Tamponade can occur with relatively small (200-mL) effusions if the effusion develops rapidly and the pericardium has no time to adapt by becoming more compliant. Alternatively, slowly growing effusions can exceed one liter in volume before the onset of tamponade.

Constrictive Pericarditis: Clinical state characterized by findings similar to that of tamponade but with the defining feature of discordant changes in right and left ventricular systolic pressures during respiration. Constrictive pericarditis occurs as the result of scarring and fibrosis of the pericardium following injuries such as pericarditis or radiation exposure. The fibrosed pericardium behaves like a noncompliant “tourniquet” around the heart that abruptly limits diastolic expansion and filling.


CLINICAL APPROACH
The pericardium is a fibroelastic sac surrounding the heart muscle and made up of two layers, visceral and parietal, separated by the pericardial cavity. Normally, this cavity contains 15–50 mL of an ultrafiltrate of plasma. Pericardial diseases have four clinical presentations: Diseases of the pericardium present clinically in one of four ways: (1) acute pericarditis, (2) pericardial effusion without hemodynamic compromise, (3) cardiac tamponade, and (4) constrictive pericarditis.

The diagnosis of acute pericarditis requires the presence of at least two of the following criteria: typical chest pain, pericardial friction rub, widespead s T segment elevation, and new or worsening pericardial effusion. Pericardial effusion can develop in any condition that affects the pericardium. The most critical step is to assess its hemodynamic impact, both clinically and echocardiographically, looking for evidence of cardiac tamponade, which is a medical emergency. Clinical features of cardiac tamponade include dyspnea, hypotension, tachycardia, jugular venous distention, and pulsus paradoxus of >10 mmHg. Constrictive pericarditis can complicate any pericardial disease process, most often occurring after acute pericarditis or cardiac surgery. Patients present with progressive dyspnea, edema, ascites, and/or cachexia. Typical exam findings include elevated jugular venous pressure, pulsus paradoxus, Kussmaul’s sign, and/or pericardial knock.

The major etiologies of pericardial diseases are grouped in Table 9-1. It is important
to note that any of these disease processes involving the pericardium can present
as one or more of the four clinical presentations. For example, a viral infection
may present as acute pericarditis, pericardial effusion, cardiac tamponade, and/or
constrictive pericarditis.

Clinical Presentation
Acute pericarditis: Patients with acute pericarditis typically present with a sharp pleuritic chest pain that improves when the patient sits up and leans forward. Dyspnea, palpitations, and diaphoresis may accompany the pain. In addition, symptoms and signs related to the underlying etiology may be present; for example, patients with viral pericarditis may also present with fever and “flulike” symptoms. On exam, sinus tachycardia is often present. A characteristic finding on auscultation is a pericardial friction rub, which is a scratchy sound, best heard with the diaphragm of the stethoscope, and loudest over the left sternal border.

Pericardial effusion without hemodynamic compromise: The normal pericardium is compliant and, in cases of slowly developing effusions, it can stretch to accommodate increases in pericardial volume without significant increase in pericardial pressures. This explains how a large chronic pericardial effusion may build up without hemodynamic consequences. In that case, patients will have no symptoms or physical signs specific to the effusion, which will often be discovered incidentally.

Cardiac tamponade: With a rapidly developing effusion, the pericardium does not have the time to stretch and accommodate it. This leads to significant increases in pericardial pressures with subsequent compression of the heart chambers and serious hemodynamic consequences, resulting in a clinical picture resembling cardiogenic shock. Patients present with acute-onset chest pain, dyspnea, and/or tachypnea. A number of findings may be present on physical examination: sinus tachycardia, hypotension, elevated jugular venous pressure, and pulsus paradoxus (exaggerated inspiratory decrease in systolic blood pressure). Cardiac tamponade is a medical emergency that requires prompt intervention.     

Constrictive pericarditis: In constrictive pericarditis, the thickened, inelastic pericardium does not expand, but rather acts as a rigid box compressing the heart chambers when cardiac volume increases and thus impeding cardiac filling. Patients usually present with symptoms of fluid overload (peripheral edema, ascites, and even anasarca) and symptoms of decreased cardiac output (dyspnea, fatigue). Physical exam findings include elevated jugular venous pressure (JVP), pulsus paradoxus, Kussmaul’s sign (the lack of an inspiratory decline in JVP), a pericardial knock (an accentuated heart sound occurring slightly earlier than an S3), edema, ascites, and/or cachexia.

Diagnostic Approach
Patients with suspected pericardial disease should undergo initial evaluation with electrocardiography, chest radiography, and echocardiography.

1. Electrocardiography (ECG): Typical ECG changes in acute pericarditis consist of new widespread, typically concave up, s T elevation (due to the inflamed pericardium), and/or PR depression. In pericardial effusion and cardiac tamponade, low QRS voltage (due to the presence of fluid between the heart and ECG leads), and sometimes electrical alternans (beat-to-beat, ie, interbeat alterations in the QRS complex reflecting swinging of the heart in the pericardial fluid) are seen. There are no specific ECG findings in constrictive pericarditis, but nonspecific ST and T wave changes are common.

2. Chest Radiography (CXr ): Typically normal in acute pericarditis, and usually reveals cardiomegaly with clear lung fields if a pericardial effusion, with or without tamponade, is present. The presence of pericardial calcification is highly suggestive of constrictive pericarditis though this is not common.

3. Echocardiography: Plays an important role in the evaluation of pericardial diseases and should be performed urgently if tamponade is suspected. It is often normal in acute pericarditis unless there is an associated pericardial effusion. It plays a major role in the identification of a pericardial effusion and in assessing its hemodynamic significance (Figure 9-2). The major echocardiographic

Large pericardial effusion

Figure 9-2. Large pericardial effusion as seen on echocardiogram (LA, left atrium; LV, left ventricle;
PE, pericardial effusion; RV, right ventricle).

signs of tamponade are chamber collapse (usually right-sided chambers when intrapericardial pressure exceeds intrachamber pressure), exaggerated respiratoy  variation of cardiac and venous flows (reflecting increased ventricular interdependence, in which the hemodynamics of the left and right heart chambers are directly influenced by each other due to the constraints imposed by the compressing effusion), and inferior vena cava (iVC) plethora (dilatation and minimal reduction in the diameter of the dilated IVC during inspiration, reflecting a marked elevation in central venous pressure). Echocardiography is also helpful in the evaluation of constrictive pericarditis. While none of the findings is specific, a completely normal echocardiography virtually rules out the diagnosis of constrictive pericarditis. Features suggestive of constriction include pericardial thickening, dilatation of the inferior vena cava and hepatic veins with diminished inspiratory collapse, pronounced respiratory variation in ventricular filling, and abnormal passive filling of the ventricles during early diastole.

Additional testing is often required when constrictive pericarditis is suspected. Cardiac magnetic resonance imaging (cMRI) is increasingly used to confirm the diagnosis, because of its increased sensitivity and specificity. Characteristic cMRI features include increased pericardial thickening and dilation of the IVC.

Treatment
Acute pericarditis: For most patients with idiopathic pericarditis, treatment consists of combination therapy with NSAIDs (to decrease the inflammation) and colchicine (which has been shown to decrease recurrences). In acute pericarditis following myocardial infarction, aspirin is the recommended NSAID to use. Corticoid therapy should be reserved for autoimmune pericarditis, uremic pericarditis not responding to dialysis, and patients with contraindications to NSAID therapy.

Pericarditis effusion: The first priority is to assess its hemodynamic significance, clinically and echocardiographically, and to rule out cardiac tamponade. Treatment of asymptomatic hemodynamically stable pericardial effusion should focus on treatment of the underlying disorder; this may result in the resolution of the effusion without the need for drainage. However, sampling of the fluid may be considered for diagnostic purposes.

Cardiac Tamponade: Urgent drainage should be performed. Supportive care with fluid resuscitation and/or inotropes should be instituted in the interim until removal of the pericardial fluid is achieved.

Constrictive Pericarditis: Pericardiectomy (surgical removal of the pericardium) is the definitive therapy of choice for constrictive pericarditis.


COMPREHENSION QUESTIONS

9.1 A 54-year-old man is evaluated in the emergency department for a 2-day history of worsening dyspnea. He has had intermittent pleuritic chest pain for the past 7 days. On physical exam, temperature is 37.7°C (99.9°F), blood pressure is 84/46, pulse rate is 130/min, and respiratory rate is 28/min. Oxygen saturation is 91% on room air. Cardiac examination reveals muffled heart sounds. Lung auscultation discloses normal breath sounds. A 12-lead ECG shows sinus tachycardia with diffuse low voltage. A bedside echocardiogram shows a large pericardial effusion with right atrial and ventricular diastolic collapse with a normal left ventricular systolic function. 

Which of the following is the most appropriate management?
A. Cardiac catheterization
B. Spirometry
C. Urgent pericardiocentesis
D. Levofloxacin and nebulizers

9.2 A 62-year-old man is evaluated for a 7-month history of progressive dyspnea and lower extremity swelling. His medical history is significant for lymphoma treated with chest irradiation 15 years ago and currently in remission. He does not smoke or drink alcohol. On physical exam, vital signs are stable. There is jugular venous distension and jugular venous engorgement with inspiration. Cardiac exam discloses a prominent early diastolic sound but no murmurs or gallops. Lung exam reveals normal breath sounds. Abdominal examination reveals ascites, and lower extremities show 3+ pitting edema. ECG shows normal sinus rhythm with nonspecific diffuse ST-T changes. Urinalysis is normal. Chest radiography shows calcifications around the heart and clear lung fields.

Which of the following is the most likely diagnosis?
A. Cirrhosis
B. Constrictive pericarditis
C. Nephrotic syndrome
D. Ischemic cardiomyopathy

9.3 A 34-year-old woman presents to the emergency department with a 3-day history of pleuritic chest pain. She has had a recent flulike episode a week ago. On physical exam her temperature is 37.8°C (100.0°F), blood pressure is 114/54, pulse rate is 110/min, and respiration rate is 24/min. Cardiac exam reveals a pericardial friction rub. Lung exam discloses normal breath sounds. A 12-lead ECG shows sinus tachycardia and diffuse concave upward ST segment elevation. A chest radiograph shows an enlarged cardiac silhouette but no infiltrates. The first set of cardiac enzymes is negative.

What is the most appropriate next step?
A. Start antibiotics
B. Chest CT scan
C. Urgent cardiac catheterization
D. Cardiac echocardiogram


ANSWERS

9.1 C. This patient is presenting with clinical and echocardiographic evidence of cardiac tamponade. Pericardiocentesis is the appropriate immediate treatment.

9.2 B. Constrictive pericarditis is the most likely diagnosis, given the clinical presentation with signs of fluid overload (pitting edema, ascites) and low cardiac output (worsening dyspnea), the history of chest irradiation (risk factor for pericardial disease), the exam finding of a pericardial knock (prominent early diastolic sound), and the chest radiograph showing pericardial calcification.

9.3 D . This patient is presenting with signs and symptoms of acute pericarditis. The next best step is an echocardiogram to look for a pericardial effusion, which is highly likely, given the chest radiograph finding of enlarged cardiac silhouette.


CLINICAL PEARLS
C Acute pericarditis should be suspected in the setting of pleuritic chest pain, especially when a pericardial friction rub is present on exam.

C Echocardiography is essential in the evaluation of acute pericarditis to look for exidence ofan associated pleural effusion and/or signs of cardiac tamponade.

C Cardiac tamponade results in a clinical picture resembling cardiogenic shock. Patients suspected of having tamponade should be evaluated with an electrocardiogram, chest radiography, and echocardiography. Treatment is immediate removal of the pericardial fluid.

C Constrictive pericarditis presents with signs and symptoms of fluid over load and decreased cardiac output. Echocardiography is an essential diagnostic test. However, given the lack of specific findings, cardiac magnetic resonance imaging is increasingly used to confirm the diagnosis.

References

Imazio M, Bobbio M, Cecchi E, et al. Colchicine as first-choice therapy for recurrent pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial. Arch Intern Med. 2005;165:1987. 

Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005; 112:2012. 

Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med. 2004;351:2195. 

Little WC, Freeman GL. Pericardial disease. Circulation. 2006;113:1622. 

Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684.

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