Pericarditis, Pericardial effusion, Cardiac Tamponade Flashcards

1
Q

wA 35-year-old male presents with pleuritic chest pain that worsens when lying supine but improves when leaning forward. The ECG is shown, what is the most likely diagnosis?

A

Acute pericarditis is inflammation of the pericardial sac, which can be an isolated finding or part of a systemic disorder.

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2
Q

What are is the most common cause of acute pericarditis?

A

Idiopathic (likely post-viral). The viral infections that are most implicated are Coxsackie virus (most common), echovirus, adenovirus, EBV, influenza, HIV, hepatitis A and B.

The other causes include: bacterial (TB), fungal, toxoplasmosis, post-MI (early or late as Dressler syndrome), uremia (commonly seen in kidney failure), connective tissue diseases (SLE, scleroderma, RA, sarcoidosis), malignancy (Hodgkin’s lymphoma, breast cancer, lung cancer), drug-induced lupus (hydralazine, procainamide), post-surgical (post-pericardiotomy), radiation, and trauma.

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3
Q

What condition is not only the leading cause of restrictive cardiomyopathy but is also associated with pericarditis?

A

Amyloidosis is the leading cause of restrictive cardiomyopathy, where the deposition of amyloid fibrils in the myocardium results in stiff ventricular walls, leading to impaired diastolic filling. Amyloidosis is also implicated in acute pericarditis, as amyloid deposits can infiltrate the pericardium, causing inflammation and symptoms associated with pericarditis.

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4
Q

A previously healthy individual develops acute pericarditis. What is the expected clinical course, and what complications should be monitored?

A

Most patients recover within 1-3 weeks, but some may have recurrent or prolonged symptoms. Complications include pericardial effusion and tamponade (up to 15% of cases).

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5
Q

A patient with a history of a viral infection presents with severe, pleuritic chest pain localized to the left pericardial region that radiates to the trapezius ridge. What is the significance of this radiation pattern?

A

Chest pain associated with acute pericarditis is the most common symptom and is often severe and pleuritic, localized to the precordial or left pericardial region, radiating to the trapezius ridge. Pain is positional, worsens when supine, with coughing, swallowing, or deep inspiration, and improves with sitting up and leaning forward.

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6
Q

A 40-year-old patient with fever, leukocytosis, and recent flu-like symptoms presents with pleuritic chest pain. What additional symptoms might be present in viral pericarditis?

A

Fever and leukocytosis (elevated ESR and CRP), preceding viral symptoms (URI or GI symptoms), nonproductive cough, and diarrhea.

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7
Q

What is the hallmark auscultatory finding in acute pericarditis (very specific), and how can it be best appreciated on physical exam?

A

Pericardial friction rub: a high-pitched, scratching sound with three components (atrial systole, ventricular systole, early diastole). Best heard in expiration with the patient sitting up. This may not be present in all patients however this finding is very specific, thus in terms of diagnostic testing, it has a low sensitivity and high specificity. Auscultatory components can have be within atrial systole, ventricular systole, or early diastole. It is best heard during expiration while the patient is sitting up.

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8
Q

An ECG shows diffuse ST-segment elevation with PR depression. What condition is most likely, and why does this ECG pattern occur?

A

Diffuse (concave) ST-segment elevation with PR depression, PR elevation in lead aVR.

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9
Q

What are the four diagnostic criteria for acute pericarditis, and how many are required for diagnosis?

A

Requires at least two of four: (1) Classic chest pain (positional component), (2) Pericardial friction rub, (3) ECG changes (diffuse ST elevation, PR depression), (4) Pericardial effusion on imaging (CXR or echo).

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10
Q

Why is echocardiography essential in evaluating pericarditis, and what findings may suggest an effusion?

A

Echo is necessary if pericarditis with effusion is suspected. Chest X-ray may show an enlarged cardiac silhouette if effusion >250 mL.

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11
Q

A patient with acute pericarditis is managed conservatively. What is the first-line treatment, and which medication can be used as adjunct therapy to reduce recurrence?

A

Most cases resolve in 2-6 weeks without intervention. Treat underlying cause. Use NSAIDs (aspirin, ibuprofen, naproxen, indomethacin) with colchicine as adjunct therapy. Glucocorticoids reserved for refractory cases due to high recurrence rates or contraindications for NSAID. Give aspirin with colchicine for patients with post-MI pericarditis. Hospitalization is needed for patients who have fever, leukocytosis, or significant pericardial effusion.

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12
Q

How common is it for patients with pericarditis to also have an effusion?

A

50% of the time.

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13
Q

When is a pericardiocentesis indicated for patients?

A

A pericardiocentesis is not always indicated and mainly indicated with cardiac tamponade. Fluid analysis involves protein and glucose content, cytology, cell count and differential, specific gravity, hematocrit, gram stain, acid fast stains, mycobacterial PCR, fungal smear, cultures, LDH content.

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14
Q

A patient with recent cardiac surgery presents with progressive dyspnea, edema, and ascites. The blood pressure is low and a friction rub is heard on auscultation. What condition should be suspected, and what physical exam findings support the diagnosis? What should be done acutely?

A

This patient has symptoms of fluid overload symptoms (edema, ascites, pleural effusions), low cardiac output symptoms (dyspnea on exertion, fatigue, exercise intolerance, tachypnea), secondary to restriction of effective cardiac pumping, therefore, this patient needs immediate an ECHO to evaluate for pericarditis and possible tamponade. This is managed acutely with a pericardiocentesis.

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15
Q

What is the most common cause for purulent pericarditis?

A

Staphylococcus aureus, a gram-positive cocci that grows in clusters, is the most frequently isolated organism. Staphylococcus aureus is particularly likely in patients who have portals from the skin to the bloodstream, such as a central line or dialysis catheter. S aureus is far more common in patients with end-stage renal disease who have vascular catheters. Infection could also stem from the skin directly to the pericardium due to chest injury with penetrating object or a recent cardiothoracic surgery.

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16
Q

What is the major risk factor for purulent pericarditis caused by Streptococcus pneumoniae?

A

Streptococcus pneumoniae is the most common organism in patients with adjacent pneumonia.

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17
Q

What is the major risk factor for purulent pericarditis caused by Klebsiella?

A

Klebsiella pericarditis can occasionally occur due to adjacent anaerobic lung abscess. In general, enteric bacteria, including the lactose-fermenting gram-negative bacilli (eg, Escherichia coli, Klebsiella pneumoniae, Enterobacter) are uncommon causes of purulent pericarditis.

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18
Q

What would be the risk factor for purulent pericarditis caused by Mycobacterium tuberculosis?

A

Mycobacterium tuberculosis is an acid-fast bacilli, can occasionally cause purulent pericarditis due to direct spread from the lung or a mediastinal/hilar lymph node, these patients will have risk factors associated with TB infections such as a hospital worker, prisoner, or immigrant from an endemic region.

Educational objective:
Purulent pericarditis is usually caused by hematogenous dissemination from distant infection or direct extension from an adjacent infection or chest wall trauma. Although a variety of organisms cause purulent pericarditis, Staphylococcus aureus is the most common pathogen, particularly in the setting of a portal from the skin to the bloodstream (eg,
catheter) or pericardium (eg, recent chest surgery, penetrating injury).

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19
Q

What are the risk factors associated with fungal pericarditis?

A

Candida albicans, a budding yeast that forms germ tubes, is a leading cause of fungal pericarditis, it is seen primarily in persons with significant risk factors for candidemia such as total parenteral nutrition (TPN), prolonged corticosteroid use, or immunosuppression due to malignancy.

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20
Q

Can lyme disease lead to purulent pericarditis?

A

Borrelia burgdorferi is a motile spirochete seen with silver stain. It can cause Lyme myopericarditis as a consequence of early disseminated disease, but most cases are mild and asymptomatic. In addition, an effusion caused by B burgdorferi infection would be lymphocyte (not neutrophil) predominant.

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21
Q

A purulent lymphocytic dominate aspirant from pericardiocentesis has no visual bacterial organisms on gram stain, would indicate a possible infection with … ?

A

Coxsackievirus (single-stranded RNA virus) can cause pericarditis, the pericardial fluid is usually lymphocyte predominant. This is the most common cause of pericarditis.

22
Q

A patient presents during the summer/early fall, with sharp, stabbing, lateral chest wall pain after a viral infection, involving spasms of the intercostals and elevated CK?

A

Pleurodynia, also known as Bornholm disease or “devil’s grip,” is a viral illness characterized by sudden, severe, stabbing chest or upper abdominal pain due to inflammation of the intercostal muscles and pleura. It is most commonly caused by Coxsackievirus B, a type of enterovirus.

23
Q

What conditions cause uremia and what is the required treatment?

A

Chronic kidney disease and renal failure can cause uremia. An associated symptom is bleeding diaphysis due to urea in the serum interfering with platelet activity. Bleeding time, PT, and PTT, will all be elevated. These patients need dialysis.

24
Q

What is constrictive pericarditis, and how does its pathophysiology lead to restrictive cardiac filling?

A

Fibrotic scarring of the pericardium leading to rigidity, thickening, and obliteration of the pericardial cavity, restricting diastolic filling.

25
Q

What are the most common causes of constrictive pericarditis?

A

Idiopathic (most cases), prior viral infection, recurrent pericarditis, uremia, radiation therapy, tuberculosis, chronic pericardial effusion, tumors, connective tissue disorders, prior cardiac surgery.

26
Q

What symptoms predominate with constrictive pericarditis?

A

Symptoms right heart failure, such as, dyspnea (shortness of breath), congestive hepatopathy (nutmeg liver), elevated JVP/JVD with a possible Kussmaul sign (an increase in JVP with a deep breath) or pericardial knock (a high-pitched sound made by the heart due to early diastole, as a ventricle does not fully fill with blood between heartbeats).

27
Q

A patient presents with Kussmaul’s sign and a pericardial knock. What diagnosis is most likely, and how does it differ from restrictive cardiomyopathy?

A

Kussmaul’s sign (increased JVP; paradoxically increases or fails to decrease on inspiration) and pericardial knock (along with ascites, and edema), are most commonly seen with constrictive pericarditis. Both constrictive pericarditis and restrictive cardiomyopathy can show elevated JVP, but Kussmaul’s sign is more prominent in constrictive pericarditis and less common in restrictive cardiomyopathy. In restrictive cardiomyopathy, there is generally a prominent y descent in JVP, but this is also a sign in both constrictive pericarditis and restrictive cardiomyopathy.

28
Q

What imaging and diagnostic tests help differentiate constrictive pericarditis from other cardiac conditions?

A
  • CXR: constrictive pericarditis may reveal calcifications.
  • ECG: Low QRS voltage, generalized T-wave flattening/inversion, left atrial abnormality/enlargement is seen in constrictive pericarditis.
  • Echo: Pericardial thickening, sharp halt in ventricular diastolic filling, biatrial enlargement. Leftward movement of the interventricular septum on inspiration.
  • CT/MRI: Pericardial thickening and calcifications.
  • Cardiac catheterization: Equalization of diastolic pressures in all chambers, rapid Y descent (dip and plateau/square root sign). In early diastole there is rapid filling, but in late diastole, filling is halted.
29
Q

Which cardiac arrhythmia is associated with constrictive pericarditis?

A

A fib is more often seen in advanced disease but overall occurs in fewer than half of all patients

30
Q

What is diagnositic for constrictive pericarditis?

A

Diagnosis is made by echocardiography revealing biatrial enlargement, normal ventricular wall thickness and cavity size, and abnormal shifting of the interventricular septum during respiration (ie, leftward during inspiration). Cardiac CT scan or MRI can aid in the diagnosis by demonstrating the extent of pericardial thickening and calcification.

31
Q

How is constrictive pericarditis treated, and when is pericardiectomy indicated?

A

Anti-inflammatory medications help slow disease progression, but definitive treatment involves pericardiectomy. Treat underlying condition, give diuretics for volume overload, and perform a pericardiectomy for definitive treatment. Often constrictive pericarditis progresses to worsening cardiac output and to hepatic or renal failure. Surgical treatment with a pericardiectomy is indicated in many cases but has a high risk of morbidity and mortality.

32
Q

What is pericardial effusion, and why are acute effusions more likely to cause tamponade compared to chronic effusions?

A

Pericardial effusion is caused by excess fluid between the heart and pericardium. Can be acute or chronic. Acute effusions are more likely to cause tamponade.

33
Q

What are the most common causes of pericardial effusion, and which underlying conditions should be ruled out?

A

Idiopathic (most common), volume overload (hypervolemia seen with congestive heart failure, cirrhosis, and nephrotic syndrome), malignancy, infections (Viral or TB), autoimmune/inflammatory conditions (SLE), and traumatic secondary to aortic dissection or post-surgical.

34
Q

A patient presents with muffled heart sounds and a soft PMI. What condition should be suspected, and what additional findings might be present?

A

Often this is asymptomatic (when fluid slowing accumulates). However, symptoms can range from nonspecific findings to impaired cardiac function along with muffled heart sounds, soft PMI, or dullness in the left lung base due to pericardial fluid compression. Pericardial friction rub may or may not be present.

35
Q

What are the initial screening tests for pericardial effusion?

A
  • CXR: water bottle appearance if >250 mL of fluid has accumulated.
  • ECG: Low QRS voltage, T-wave flattening. Electrical alternans suggests massive effusion and tamponade.
36
Q

Why is echocardiography the gold standard for diagnosing pericardial effusion, and what are the characteristic imaging findings?

A

Echo (TTE) is the most sensitive test (detects as little as 20 mL of fluid).

37
Q

What dictates the management for pericardial effusion?

A

Management depends on hemodynamic stability.

38
Q

How should a pericardial effusion be managed based on a hemodynamic stable patient?

A
  • Treat the underlying cause and observe.
  • Small effusions without tamponade require serial TTE every 1-2 weeks.
39
Q

How should a pericardial effusion be managed based on a hemodynamic unstable patient?

A

Pericardiocentesis. Perform a fluid analysis if the underlying etiology is unknown.

40
Q

What is cardiac tamponade, and why is the rate of fluid accumulation more important than the absolute volume?

A

Accumulation of pericardial fluid impairs diastolic filling of the heart due to elevation and equalized intracardiac pressures. The rate of accumulation, not volume, determines severity. Patients can literally have up to 2 L in their pericardial sac chronically. Acutely, as little as 200 mL can lead to severe symptoms. Therefore the flow matters most here. Cardiac tamponade is one of the “T’s” associated with ventricular arrhythmias and presents with signs of hemodynamic compromise, chest pain, and dyspnea. Patient will have signs of cardiogenic shock without pulmonary edema.

41
Q

What are the causes of cardiac tamponade?

A

Pericarditis, pericardial effusion, trauma (penetrating chest injury), iatrogenic (central line placement, pacemaker insertion, pericardiocentesis), post-MI free wall rupture, aortic dissection. When patients present with progressive dyspnea, chest tightness, and a **drop in systolic blood pressure >10 mm Hg with inspiration ** (ie, pulsus paradoxus), it is MOST likely a subacute cardiac tamponade. Though there are many etiologies associated with cardiac tamponade, subacute presentations are common with patients who have kidney disease. Uremia in the setting of advanced renal failure can lead to pericarditis with associated pericardial effusion and sometimes tamponade.

42
Q

A 19-year-old man, who was brought into the emergency department by his friend, suddenly collapses in the waiting room. His t-shirt is saturated in blood, and he is immediately brought to the trauma bay. Temperature is 37.0 °C (98.6
°F), pulse is 121/min, respirations are 28/min, blood pressure is 85/50 mmHg, and oxygen saturation is 96% on room air. Physical examination demonstrates a 1 cm stab wound over the left anterior chest wall, in addition to jugular venous distension. The jugular venous pulse is noted at the level of the mandible. The patient speaks in clear, complete sentences, and bilateral breath sounds are present. An ECG is performed shows electrical alternans, what is the best next step in management?

A

This patient presents with findings consistent with cardiac tamponade following penetrating chest trauma. He has jugular venous distension in addition to electrical alternans noted on telemetry. Given this patient’s unstable vital signs, he should immediately undergo transthoracic echocardiogram (TTE) and pericardiocentesis BEFORE definitive operative repair. The acute management of adult chest pain follows a stepwise approach. First, patients should be evaluated for stability-including vital sign assessment, protection of airway, and mental status. Patients should immediately receive any necessary interventions to stabilize their airway, breathing, and circulation. Patients deemed unstable should be assessed for life-threatening causes of chest pain, such as myocardial infarction, pulmonary embolism, pericardial tamponade, tension pneumothorax, aortic dissection, and Boerhaave syndrome so appropriate intervention can be performed in a timely fashion. For example, immediate TTE and pericardiocentesis is indicated in the case of cardiac tamponade, and thrombolytics are indicated in the setting of massive pulmonary embolism. Stable patients with chest pain should undergo further diagnostic workup to evaluate for more subtle presentations of a life-threatening diagnosis. All patients should receive an electrocardiogram to evaluate for ST-elevation myocardial infarction (STEMI) or signs of ischemia. Specific ECG changes that suggest a life-threatening diagnosis include electrical alternans (pericardial tamponade) or an S1QT3 pattern (pulmonary embolism - though remember, the most common ECG finding in pulmonary embolism is sinus tachycardia). Next, most patients with chest pain who have ECG changes should be further evaluated with laboratory testing using serial troponin assays to evaluate for underlying cardiac ischemia and non-ST-elevation myocardial infarction (NSTEMI). Stable patients should also have chest radiography, which can assess for the presence of a pneumothorax, mediastinal air suggestive of esophageal perforation, or a widened mediastinum suggestive of aortic dissection.

43
Q

A trauma patient presents with hypotension, distended neck veins, and muffled heart sounds. What is the most likely diagnosis, and what emergency intervention is required?

A
  • Cardiac tamponade. A medical emergency!
    1) Perform ABCDE
    2) Do an emergent TTE
    3) Pericardiocentesis (Emergency Procedure)
    4) Give IV fluids
44
Q

If a patient has a high index of suspicion for cardiac tamponade, even if the said patient is hemodynamically unstable, what is performed BEFORE pericardiocentesis?

A

TTE! This confirms the effusion and will help guide the emergency procedure.

45
Q

What is Beck’s triad, pulsus paradoxus, and a narrow pulse pressure, and how do they aid in diagnosing cardiac tamponade?

A
  • Beck’s triad, pulsus paradoxus, and a narrowed pulse pressure are all accompanying signs of cardiac tamponade.
  • Beck’s triad: Hypotension, muffled heart sounds, elevated JVP.
  • Pulsus paradoxus: Exaggerated (>10 mmHg) drop in systolic BP during inspiration.
  • Narrow pulse pressure: Small difference between systolic (top) and diastolic (bottom) blood pressure readings.
  • Engorged inferior vena cava.

vvvvvvvvvvvvvv

Tamponade classically presents with Beck’s triad of hypotension (often less prominent with subacute compared to acute tamponade), distant heart sounds, and jugular venous distension. Normally, a pressure gradient exists between the vena cava and the right side of the heart, allowing blood to fill the right atrium during diastole. With inspiration, a reduction in intrathoracic pressure pulls additional blood into the right side of the heart and the pulmonary circulation, causing normal inspiratory collapse of the inferior vena cava (IVC). With cardiac tamponade, increasing pericardial pressure begins to compress the relatively low-pressure, right-sided heart chambers and restrict diastolic filling. The increased right-sided pressures are transmitted backward to the vena cava, causing engorgement of the IVC with decreased inspiratory collapse that can be seen on echocardiography. In addition, because the right ventricle is compressed and unable to expand during diastole, the increase in right-sided blood flow during inspiration causes the ventricular septum to bow into the left ventricle; this reduces left ventricular stroke volume during inspiration and is responsible for the observed >10 mm Hg drop in systolic blood pressure. As tamponade progresses, impaired right-sided filling causes the left ventricle to receive less blood, resulting in decreased cardiac output and obstructive shock. Because the obstruction to blood flow is primarily right sided, there is no pulmonary edema and the lungs remain clear to auscultation.

46
Q

Is pulsus paradoxus seen in constrictive cardiomyopathy or restrictive cardiomyopathy?

A

No. This is a sign of cardiac tamponade (also COPD, asthma, hypovolemic shock, and tension pneumothorax).

47
Q

Is Kussmaul sign seen in cardiac tamponade?

A

No. This is a sign of constrictive pericarditis and restrictive cardiomyopathy, not cardiac tamponade.

48
Q

How does an echocardiogram confirm the diagnosis of cardiac tamponade, and what are the key findings?

A
  • Echo is the test of choice: shows pericardial effusion with right atrial and right ventricular collapse during diastole.
  • ECG: Electrical alternans.
49
Q

What will be seen on JVP when a patient has cardiac tamponade?

A

Absent Y descent

50
Q

what conditions also see an absent Y descent?

A

Cardiac Tamponade (Classic Association) and Severe Right Ventricular Dysfunction.

51
Q

What will be seen on catheterization in a patient with cardiac tamponade?

A

Equalization of intracardiac pressures.

52
Q

How is cardiac tamponade managed?

A

Hemodynamically stable: Monitor closely. Dialysis is preferred in uremic tamponade.
Unstable: Perform emergent pericardiocentesis. If secondary to trauma, surgical repair is required, and pericardiocentesis is only a temporizing measure. Surgical repair is usually indicated for hemorrhagic tamponade.