Pericarditis: Clinical sciences

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Pericarditis: Clinical sciences

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Introduction to the cardiovascular system
Introduction to the lymphatic system
Cardiovascular system anatomy and physiology
Coronary circulation
Lymphatic system anatomy and physiology
Abnormal heart sounds
Normal heart sounds
Baroreceptors
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Renin-angiotensin-aldosterone system
Cardiac cycle
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Changes in pressure-volume loops
Pressure-volume loops
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac afterload
Cardiac contractility
Cardiac preload
Frank-Starling relationship
Law of Laplace
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Cardiac conduction velocity
Cardiac conduction system
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Control of blood flow circulation
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Compliance of blood vessels
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Pressures in the cardiovascular system
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Action potentials in myocytes
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Excitability and refractory periods
Adrenergic antagonists: Beta blockers
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
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Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
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Long QT syndrome and Torsade de pointes
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Pericarditis and pericardial effusion
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Acyanotic congenital heart defects: Pathology review
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Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
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Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
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Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Arteriole, venule and capillary histology
Artery and vein histology
Cardiac muscle histology
Development of the cardiovascular system
Fetal circulation
Anatomy of the coronary circulation
Anatomy of the heart
Anatomy of the inferior mediastinum
Anatomy of the superior mediastinum
Anatomy clinical correlates: Heart
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Introduction to pharmacology
Chest X-ray interpretation: Clinical sciences
Electrolyte disturbances: Pathology review
Anatomy clinical correlates: Breast
Anticoagulants: Heparin
Thrombolytics
Congestive heart failure: Clinical sciences
Approach to ascites: Clinical sciences
Approach to dyspnea: Clinical sciences
Approach to lower limb edema: Clinical sciences
Coronary artery disease: Clinical sciences
Chronic obstructive pulmonary disease: Clinical sciences
Tobacco use: Clinical sciences
Approach to chest pain: Clinical sciences
Approach to hypertension: Clinical sciences
Acute coronary syndrome: Clinical sciences
Carotid artery stenosis screening: Clinical sciences
Diabetes mellitus (Type 1): Clinical sciences
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Essential hypertension: Clinical sciences
Peripheral arterial disease and ulcers: Clinical sciences
Abdominal aortic aneurysm: Clinical sciences
Aortic dissection: Clinical sciences
Approach to bradycardia: Clinical sciences
Approach to postoperative hypotension: Clinical sciences
Approach to tachycardia: Clinical sciences
Atrioventricular block: Clinical sciences
Cardiac tamponade: Clinical sciences
Central line-associated bloodstream infection: Clinical sciences
Hypovolemic shock: Clinical sciences
Infectious endocarditis: Clinical sciences
Pericarditis: Clinical sciences
Ventricular tachycardia: Clinical sciences

Decision-Making Tree

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Pericarditis is inflammation of pericardium, sometimes associated with the accumulation of fluid, known as a pericardial effusion. The underlying inflammation might be due to viral infection, uremia, autoimmune disease, or after trauma, but regardless of cause, is associated with severe chest pain due to the pericardium’s abundant nerve supply.

Additionally, pericarditis may lead to the development of dangerous complications, such as pericardial effusion, which is characterized by accumulation of fluid around the heart; as well as cardiac tamponade, where the accumulated fluid compresses the heart.

So, if you suspect pericarditis or one of its complications, first you should perform an ABCDE assessment, to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation, which typically requires obtaining IV access and intubating the patient if you need to secure the airway.

Next, perform a focused history and physical examination. On physical exam be on the lookout for Beck triad, which includes hypotension, jugular venous distension, and muffled heart sounds. Additionally, a physical exam might reveal pulsus paradoxus, which is when the systolic blood pressure drops with inspiration, and no audible pericardial friction rub.

All of these findings should lead you to suspect that a large pericardial effusion has resulted in cardiac tamponade, so your next step is to order an ECG and chest x-ray immediately to evaluate your suspicions. Alternatively, if available, perform point of care ultrasound, or POCUS for short.

ECG typically shows sinus tachycardia with low QRS voltage and electrical alternans, defined as beat-to-beat variation in the QRS amplitude. This occurs as a result of swinging of the heart in the pericardial fluid, which can be seen with a large pericardial effusion. On the other hand, chest x-ray might show an enlarged cardiac silhouette with clear lung fields. Finally, you can use POCUS to directly visualize pericardial effusion and detect collapse of the right sided cardiac chambers. These findings confirm the diagnosis of pericardial effusion and cardiac tamponade. On the flip side, if you do not find any evidence of effusion or cardiac tamponade, then consider an alternate diagnosis.

Once you’ve confirmed that there’s a large pericardial effusion causing cardiac tamponade, provide treatment as quickly as possible. Emergent treatment involves drainage of the pericardial effusion, either by pericardiocentesis, which can be performed at the bedside and guided by the use of POCUS, or the creation of a pericardial window, in which case you’ll call the surgical team for a consultation.

Now, here’s a clinical pearl! A large pericardial effusion resulting in cardiac tamponade ultimately impairs filling of the heart chambers such that cardiac output drops, causing obstructive shock. So, in this case, use IV fluid administration with careful judgment, because you might increase preload and precipitate cardiovascular collapse. Similarly, mechanical ventilation can increase intrathoracic pressure, further preventing the heart chambers from filling. Therefore, the definitive treatment is to drain the effusion, allowing the heart to fill normally and the cardiac output to improve.

Next, let’s go back to the ABCDE assessment and take a look at stable patients. If your patient is stable, proceed with a focused history and physical examination, and order ECG and echocardiography. Next, use your findings to calculate a clinical criteria score that will help you confirm the diagnosis. The first clinical criteria that a patient will likely report is severe pleuritic chest pain, meaning it worsens with deep inspiration. Additionally, they might report that pain is positional, usually improved by sitting up and worsened by lying down.

The second clinical criteria, which you’ll find on auscultation of the chest, is a pericardial friction rub. This is a scratchy or squeaking sound best heard at the left sternal border when your patient leans forward. The third one is the presence of ECG findings classic for pericarditis, which include diffuse ST segment elevations with or without associated PR segment depressions. Finally, the last one includes echocardiography findings that reveal a new or worsening pericardial effusion.

If none or only one of these criteria is met, then consider an alternative diagnosis. On the other hand, 2 or more criteria confirm the diagnosis of pericarditis. While not needed to make the diagnosis of pericarditis, there are some laboratory and imaging studies that can provide supporting evidence and help guide clinical decisions. Helpful lab studies include CBC and inflammatory markers, like ESR and CRP, while important imaging studies include a chest x-ray and transthoracic echocardiography, or TTE. Elevated WBC count, ESR and CRP suggest an underlying systemic inflammatory condition.

Sources

  1. "Evaluation and Treatment of Pericarditis: A Systematic Review" JAMA (2016)
  2. "American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography" J Am Soc Echocardiogr (2013)
  3. "Management of Acute and Recurrent Pericarditis: JACC State-of-the-Art Review" J Am Coll Cardiol (2020)
  4. "Pericardial disease" Circulation (2006)
  5. "Acute pericarditis: diagnosis and management" Am Fam Physician (2014)