Test 2 - Pericardial Effusion

Purulent or Suppurative Pericarditis

1) Almost always due to infection - Direct extension (e.g lobar pneumonia) - Hematogenous seeding - Lymphatic spread - Direct introduction during cardiotomy 2) Thin to creamy purulent fluid 3) 400-500 mL 4) Acute inflammation which may organize and scar and produce constrictive pericarditis 5) Marked fever and chills!

Pathophysiology of Pericardial Effusion

1) Because the pericardium is a relatively stiff structure, the relationship between its internal volume and pressure is not linear 2) At the low volumes normally present within the pericardium, a small increase in pericardial fluid volume leads to only a small rise in pressure. 3) However, when the intrapericardial volume expands beyond a critical level , a dramatic increase in pressure occurs. At that point, even a minor increase in volume can translate into an enormous compressive force on the heart 4) Three factors determine whether a pericardial effusion remains clinically silent or whether symptoms of cardiac compression ensue: - the volume of fluid - the rate at which the fluid accumulates - the compliance characteristics of the pericardium.

Caseous Pericarditis

1) Caseation within pericardial sac From tuberculosis until proven otherwise 2) Rare 3) If untreated is most common cause of fibrocalcific chronic constrictive pericarditis

Key symptoms of Acute Pericarditis

1) Chest Pain - may mimic MI - Usually pleuritic (aggravated by inspiration) - Retrosternal - Improves when sitting up and leaning forward - Worsens when supine - Often radiates to the neck, shoulders, back, or epigastrium 2) Often have fever 3) Dyspnea is variably seen and usually due to the pleuritic chest pain 4) May have palpitations 5) May have cough or runny nose if patient has associated URI 6) May have joint swelling or pain if patient has associated rheumatologic or connective tissue disease 7) May have night sweats or weight loss if patient has associated tuberculosis

Constrictive Pericarditis

1) Heart encased in fibrous or fibrocalcific scar tissue 2) Pericardial sac obliterated by the scar tissue (concretio cordis) 3) May resemble a plaster mold 4) Any etiology of acute pericarditis can lead to this condition 5) Diastolic expansion and cardiac output impaired - Fatigue, hypotension, reflex tachycardia 6) Jugular venous distension, edema, and ascites often develop 7) May not elicit history of prior acute pericarditis 8) PE - May have Kussmaul's sign - Early diastolic "pericardial knock" may follow the second heart sound (Represents sudden ceasing of ventricular filling due to the rigid pericardial sac) 9) Treatment: pericardiectomy

A 35-year-old woman has a pericardial effusion. A tap of the effusion is obtained. 30 ml of fluid is obtained. Which of the following features is most consistent with the fluid being a transudate? 1) History of recent nasal congestion 2) Low protein content 3) Specific gravity of 1.002 4) Hypercellular fluid 5) The volume of the fluid is 30 ml

3) Specific gravity of 1.002

Review of types of acute pericarditis

Acute pericarditis (morphologic classification) - Serous pericarditis - Fibrinous and serofibrinous pericarditis - Purulent (suppurative) pericarditis - Hemorrhagic pericarditis - Caseous pericarditis

Physical Examination of Pericardial Effusion

- A large pericardial effusion "insulates" the heart from the chest wall, and the heart sounds may be muffled - In fact, a friction rub that had been present during the acute phase of pericarditis may disappear if a large effusion develops and separates the inflamed layers from one another - Dullness to percussion of the left lung over the angle of the scapula may be caused by the enlarged pericardial sac present (known as Ewart's sign) owing to compressive atelectasis)

Pericardial Effusion

- A pericardial effusion may accumulate in association with any of the forms of pericarditis previously discussed. - In addition, noninflammatory serous pericardial effusions may result from conditions of: (1) increased capillary permeability (e.g., severe hypothyroidism); (2) increased capillary hydrostatic pressure (e.g., congestive heart failure); or (3) decreased plasma oncotic pressure (e.g., cirrhosis or the nephrotic syndrome).

Acute Pericarditis Conclusion

- Acute pericarditis is most often of idiopathic or viral cause and is usually a self-limited illness. - Common findings in acute pericarditis include (a) pleuritic chest pain; (b) fever; (c) pericardial friction rub; and (d) diffuse ST segment elevation on the ECG, often accompanied by PR segment depression. - Complications of pericarditis include cardiac tamponade (accumulation of pericardial fluid under high pressure, which compresses the cardiac chambers) and constrictive pericarditis (restricted filling of the heart because of surrounding rigid pericardium).

Plasma Oncotic Pressure

- Also referred to as colloid osmotic pressure - Large plasma proteins like albumin cannot easily cross capillary walls - Albumin generates about 70-80% of the oncotic pressure in capillaries - Oncotic pressure pulls fluid into the circulatory system

Cardiac Tamponade Etiology

- Any etiology of acute pericarditis can progress to cardiac tamponade, but the most common causes are neoplastic, postviral, and uremic pericarditis. - Acute hemorrhage into the pericardium is also an important cause of tamponade, which can result from blunt or penetrating chest trauma, from rupture of the left ventricular free wall following MI, or as a complication of a dissecting aortic aneurysm.

Cardiac Tamponade Key Physical Findings

- Beck's Triad (1) jugular venous distention (2) systemic hypotension (3) a "small, quiet heart" on physical examination, a result of the insulating effects of the effusion. - Other signs include sinus tachycardia and pulsus paradoxus (described later). Dyspnea and tachypnea reflect pulmonary congestion and decreased oxygen delivery to peripheral tissues.

Hemorrhagic Pericarditis

- Blood mixed with a fibrinous or suppurative effusion - Usually due to malignant neoplasm - May also be seen in tuberculosis, other bacterial infections, and following cardiac surgery - May lead to constrictive pericarditis

Chronic Pericarditis

- Constrictive pericarditis - Adhesive pericarditis

Cardiac Tamponade Pathophysiology

- Pericardial fluid accumulates under high pressure, compresses the cardiac chambers, and severely limits filling of the heart - JVP increases - Ventricular stroke volume and cardiac output decline, potentially leading to hypotensive shock and death.

- Also called inflammatory edema - Results from the increase in blood vessel permeability that is characteristic of inflammation - Contains the cellular and chemical mediators critical to inflammation - High protein content (> 3 gm/dL) - Specific gravity > 1.020 - Contains cellular debris - Pus is an exudate rich in neutrophils, the debris of dead cells, and often microbes

Exudate

Patients with cardiac tamponade that are not having chest pain do not require any treatment. True or False

FALSE - CARDIAC TAMPONADE IS A LIFE THREATENING CONDITION

Pulsus paradoxus is pathognomonic for the diagnosis of cardiac tamponade? True or False

FALSE - MORE COMMONLY SEEN IN TAMPONADE BUT NOT PATHOGNOMONIC

ECG pattern of acute pericarditis

ECG pattern of acute pericarditis (diffuse ST elevations and subtle PR segment shifts--PR up in aVR and down inferior-laterally, opposite of ST segment). Sinus tachycardia with pericarditis pattern may be due to a number of factors including a) pain; b) pericardial effusion/tamponade; c) associated myocarditis; d) fever.

EKG findings in Acute Pericarditis

EKG is abnormal in 90% of pts with acute pericarditis - Diffuse ST Segment Elevation in most leads except aVR and V1 PR segment depression in several leads is seen in most cases ECG shows classic signs of acute pericarditis with diffuse ST elevation (ventricular current of injury from associated epicarditis) and PR changes (up in aVR/down infero-laterally)

Constrictive Pericarditis Pathogenesis

Following an episode of acute pericarditis, any pericardial effusion that has accumulated usually undergoes gradual resorption. However, in patients who later develop constrictive pericarditis, the fluid undergoes organization, with subsequent fusion of the pericardial layers, followed by fibrous scar formation. In some patients, calcification of the adherent layers ensues, further stiffening the pericardium. *Symptoms and signs of constrictive pericarditis usually develop gradually over months to years*

Constrictive Pericarditis Etiology

In the early part of the 20th century, tuberculosis was the major cause of constrictive pericarditis, but that is much less common today in industrialized societies. The most frequent cause now is "idiopathic" (i.e., months to years following presumed idiopathic or viral acute pericarditis). However, any etiology of pericarditis can lead to this complication.

Microscopic Appearance of Fibrinous/Serofibrinous Pericarditis

Microscopically there is inflammation with increased lymphocytes, fibrin, and erythrocytes

Microscopic Image of Fibrinous Pericarditis

Microscopically, the pericardial surface here shows strands of pink fibrin extending outward. There is underlying inflammation. Eventually, the fibrin can be organized and cleared, though sometimes adhesions may remain.

A 25 year old man has developed acute pericarditis due to a viral upper respiratory infection. Which of these symptom pairs is he most likely to have? 1) Hemoptysis and dyspnea 2) Pleuritic chest pain relieved by lying down 3) Pleuritic chest pain and fever 4) Pulsus paradoxus and fever

Pleuritic chest pain and fever

Fibrinous Pericarditis

The epicardial surface of the heart shows a shaggy fibrinous exudate. This is another example of fibrinous pericarditis. This appearance has often been called a "bread and butter" pericarditis, but you would have to drop your buttered bread on the carpet to really get this effect. The fibrin often results in the finding on physical examination of a "friction rub" as the strands of fibrin on epicardium and pericardium rub against each other.

Hemorrhagic Pericarditis

The pericarditis here not only has fibrin, but also hemorrhage. Thus, this is called a "hemorrhagic pericarditis". It is really just fibrinous pericarditis with hemorrhage. Without inflammation, blood in the pericardial sac would be called "hemopericardium.

Diagram Depicting Fibrinous Pericarditis

This diagram depicts the appearance of a fibrinous pericarditis. The red-pink squiggly lines extending from the epicardial surface into the yellow fluid represent the strands of fibrin. This type of pericarditis is typical of uremia with renal failure, underlying myocardial infarction, and acute rheumatic carditis

Diagram Depicting Serous Pericarditis

This diagram depicts the appearance of a serous pericarditis. The amount of inflammation is minimal, so no exudation of fibrin occurs. The dark stippled dots in the yellow fluid and on the epicardial surface represent scattered inflammatory cells. Serous pericarditis is marked by fluid collection. Rarely, the fluid collection may be large enough to cause tamponade.

Picture of Purulent Pericarditis

This is a purulent pericarditis. Note the yellowish exudate that has pooled in the lower pericardial sac that has been opened here. A bacterial organism is usually implicated in this process, and the infection typically spreads from the lungs

- It is a filtrate of plasma resulting from an abnormal increase in hydrostatic pressure or decrease in plasma oncotic pressure (or colloid osmotic pressure) - Not associated with increase in vascular permeability - Low protein content (< 3 gm/dL) - Specific gravity < 1.012 - Hypocellular

Transudate

Picture of Caseous Pericarditis

Tuberculous pericarditis in a patient with pleuropulmonary tuberculosis. Axial CT scan demonstrates pericardial thickening (straight solid arrow). Pulmonary tuberculomas (curved arrows) and a right pleural effusion (open arrow) are also seen.

Pericardial Effusion Echocardiogram

Two-dimensional echocardiogram (parasternal short-axis view) of a pericardial effusion (PE) surrounding the heart. LV = Left Ventricle.

Constrictive Pericarditis And Pulsus Paradoxus

- Constrictive pericarditis results in pulsus paradoxus less frequently than cardiac tamponade. - Recall that in tamponade, this finding reflects inspiratory augmentation of RV filling, at the expense of LV filling. However, in constrictive pericarditis, the negative intrathoracic pressure generated by inspiration is not easily transmitted through the rigid pericardial shell to the right-sided heart chambers; therefore, inspiratory augmentation of RV filling is more limited. Rather, when a patient with severe pericardial constriction inhales, the negative intrathoracic pressure draws blood toward the thorax, where it cannot be accommodated by the constricted right-sided cardiac chambers. As a result, the increased venous return accumulates in the intrathoracic systemic veins, causing the jugular veins to become more distended during inspiration (Kussmaul sign). This is the opposite of normal physiology, in which inspiration results in a decline in jugular venous pressure, as venous return is drawn into the heart.

Radiologic Imaging In Cardiac Tamponade

- Echocardiography is the most useful noninvasive technique to evaluate whether pericardial effusion has led to cardiac tamponade physiology. An important indicator of high-pressure pericardial fluid is compression of the RV and right atrium during diastole. - In addition, echocardiography can differentiate between cardiac tamponade and other causes of low cardiac output, such as ventricular contractile dysfunction. - The definitive diagnostic procedure for cardiac tamponade is cardiac catheterization with measurement of intracardiac and intrapericardial pressures, usually combined with therapeutic pericardiocentesis.

Treatment of Pericardial Effusion

- If the cause of the effusion is known, therapy is directed toward the underlying disorder (e.g., intensive dialysis for uremic effusion). - If the cause is not evident, the clinical state of the patient determines whether pericardiocentesis (removal of pericardial fluid) should be undertaken. - An asymptomatic effusion, even of large volume, can be observed for long periods without specific intervention. - However, if serial examination demonstrates a precipitous rise in pericardial volume or if hemodynamic compression of the cardiac chambers becomes evident, then pericardiocentesis should be performed for therapeutic drainage and for analysis of the fluid.

EKG Findings in Pericardial Effusion

- In large effusions, the ECG may demonstrate reduced voltage of the complexes. In the presence of very large effusions, the height of the QRS complex may vary from beat to beat (electrical alternans), a result of a constantly changing electrical axis as the heart swings from side to side within the large pericardial volume - Tachycardia is also frequently present

Pericardial Fluid

- Normally there is 15 to 50 mL of thin, clear, yellow fluid in pericardial sac - The pericardial fluid is a plasma ultrafiltrate secreted by the mesothelial cells that line the serosal layer of the pericardium

Kussmaul's sign

- Normally, during inspiration, there is a decrease in the mean JVP as a result of the increased filling of the right-sided chambers associated with the decrease in intrathoracic pressure. - Kussmaul's sign denotes an inspiratory increase in the JVP, which may occur in patients with severe constrictive pericarditis when the heart is unable to freely fill and expand and blood therefore backs up. - Although Kussmaul's sign was first described in patients with constrictive pericarditis, its most common cause is severe right-sided heart failure, regardless of etiology.

Radiologic Imaging In Pericardial Effusions

- One of the most useful laboratory tests in the evaluation of an effusion is echocardiography, which can identify pericardial collections as small as 20 mL. This noninvasive technique can quantify the volume of pericardial fluid, determine whether ventricular filling is compromised, and when necessary, help direct the placement of a pericardiocentesis - May also use CT or MRI

Pulsus paradoxus

- Pulsus paradoxus is an important physical sign in cardiac tamponade that can be recognized at the bedside using a standard blood pressure cuff. It refers to a decrease of systolic blood pressure (more than 10 mm Hg) during normal inspiration - Pulsus paradoxus is not really "paradoxical"; it is just an exaggeration of appropriate cardiac physiology. - Normally, expansion of the thorax during inspiration causes the intrathoracic pressure to become more negative compared with the expiratory phase. This facilitates systemic venous return to the chest and augments filling of the right ventricle (RV). The transient increase in RV size shifts the interventricular septum toward the left, which diminishes left ventricular filling. As a result, in normal persons, LV stroke volume and systolic blood pressure decline slightly following inspiration. - In cardiac tamponade, this situation is exaggerated because both ventricles share a reduced, fixed volume as a result of external compression by the tense pericardial fluid. In this case, the inspiratory increase of right ventricular volume and bulging of the interventricular septum toward the left have a proportionally greater effect on the limitation of LV filling. Thus, in tamponade there is a more substantial reduction of LV stroke volume (and therefore systolic blood pressure) following inspiration. - Pulsus paradoxus may also be manifested by other conditions in which inspiration is exaggerated, including severe asthma and chronic obstructive airway disease. - Measurement of Pulsus Paradoxus at the Bedside. - Pulsus paradoxus can be measured at the bedside using a manual sphygmomanometer. First, inflate the sphygmomanometer to a level greater than the patient's systolic pressure. As the cuff is slowly deflated, carefully listen for the appearance of the first Korotkoff sounds. This level marks the maximum systolic pressure and occurs during expiration. If the pressure is held at that level (i.e., if you stop deflating the cuff) in a patient with pulsus paradoxus, the Korotkoff sounds will drift in and out, audible with expiration, and absent with inspiration. That is, the systolic pressure will fall during inspiration to a level below the cuff's pressure and no sound will be heard during that time. Next, slowly deflate the cuff and continue listening. When the cuff pressure falls to the level just below the patient's systolic pressure during inspiration, the Korotkoff sounds stop drifting in and out (i.e., they are audible during both inspiration and expiration). Pulsus paradoxus is calculated as the difference between the initial systolic pressure (when the intermittent Korotkoff sounds are first heard) and this pressure (when the sounds are first audible throughout the respiratory cycle). In the presence of cardiac tamponade, this pressure difference is >10 mm Hg.

Acute Pericarditis

- Serous pericarditis - Fibrinous and serofibrinous pericarditis - Purulent (suppurative) pericarditis - Hemorrhagic pericarditis - Caseous pericarditis

Drug-Related Pericarditis

- Several pharmaceutical agents have been reported to cause pericarditis as a side effect, often by inducing a systemic lupus-like syndrome. - These drugs include the antiarrhythmic procainamide and the vasodilator hydralazine. - Drug-induced pericarditis usually abates when the causative agent is discontinued

Radiologic Imaging In Constrictive Pericarditis

- The chest radiograph in constrictive pericarditis shows a normal or mildly enlarged cardiac silhouette. Calcification of the pericardium can be detected in some patients. - Echocardiographic evidence of constriction is subtle. The pericardium, if well imaged, is thickened. The ventricular cavities are small and contract vigorously, but ventricular filling terminates abruptly in early diastole, as the chambers reach the limit imposed by the surrounding rigid shell. Aberrant diastolic motion of the interventricular septum and alterations of LV inflow velocities by Doppler also reflect the abnormal pattern of diastolic filling - Computed tomography or magnetic resonance imaging is superior to echocardiography in the assessment of pericardial anatomy and thickness. The presence of normal pericardial thickness (<2 mm) by these modalities makes constrictive pericarditis a less likely diagnosis.

Treatment Of Constrictive Pericarditis

- The only effective treatment of severe constrictive pericarditis is surgical removal of the pericardium. - Symptoms and signs of constriction may not resolve immediately because of the associated stiffness of the neighboring outer walls of the heart, but subsequent clinical improvement is the rule in patients with otherwise intact cardiac function.

Constrictive Pericarditis Pathophysiology

- The pathophysiologic abnormalities in constrictive pericarditis occur during diastole; systolic contraction of the ventricles is usually normal. - In this condition, a rigid, scarred pericardium encircles the heart and inhibits normal filling of the cardiac chambers. For example, as blood passes from the right atrium into the right ventricle during diastole, the RV size expands and quickly reaches the limit imposed by the constricting pericardium. At that point, further filling is suddenly arrested, and venous return to the right heart ceases. Thus, systemic venous pressure rises, and signs of right-sided heart failure ensue. In addition, the impaired filling of the left ventricle causes a reduction in stroke volume and cardiac output, which leads to lower blood pressure.

Hydrostatic pressure

- The pressure that a fluid exerts on the walls of its container - This pressure drives fluid out of the circulatory system - Remember that normal capillaries are semipermeable (there are junctions between endothelial lining cells)

Serous Pericarditis

- Usually due to noninfectious inflammation 1. rheumatic fever 2. systemic lupus erythematosus 3. scleroderma 4. tumors 5. uremia - Exudate secreted by mesothelial cells lining the pericardium - Usually 50-200 mL of fluid which accumulates slowly - Mild inflammatory infiltrate composed of scant neutrophils, lymphocytes, and macrophages

Treatment Of Acute Pericarditis

1) Idiopathic or viral pericarditis is a self-limited disease that usually runs its course in 1 to 3 weeks. Management consists of rest, to reduce the interaction of the inflamed pericardial layers, and pain relief by analgesic and anti-inflammatory drugs (aspirin, ibuprofen, and other nonsteroidal anti-inflammatory agents). Colchicine, a drug with anti-inflammatory properties usually used to treat gout, may be useful as an additional agent in acute pericarditis. It has been shown to decrease the recurrence rate after an initial episode. Oral corticosteroids are effective for severe or recurrent pericardial pain but should not be used in uncomplicated cases because of potentially significant side effects and because even gradual withdrawal of this form of therapy often leads to recurrent symptoms of pericarditis. 2) The forms of pericarditis related to MI are treated in a similar fashion, with rest and aspirin. Other nonsteroidal anti-inflammatory agents are often avoided immediately following an MI because of experimental evidence linking them to delayed healing of the infarct. 3) Purulent pericarditis requires more aggressive treatment, including catheter drainage of the pericardium and intensive antibiotic therapy. Nevertheless, even with such therapy, the mortality rate is very high. 4) Tuberculous pericarditis requires prolonged multidrug antituberculous therapy. 5) Pericarditis in the setting of uremia often resolves following intensive dialysis. 6) Neoplastic pericardial disease usually indicates widely metastatic cancer, and therapy is unfortunately only palliative.

Laboratory Findings In Acute Pericarditis

1) Inflammation of the epicardium may cause myocyte necrosis and elevation of troponin and CK-MB levels - These elevations are usually small!! 2) Most patients have an elevated ESR (related to inflammation) 3) Other lab results often depend on underlying etiology of acute pericarditis Some Examples Include: - Elevation of white blood cell count with associated pneumonia - Elevation of BUN and creatinine with uremia and renal failure - Positive ANA in SLE

Radiologic Imaging In Acute Pericarditis

1) May see enlargement of cardiac silhouette on chest X-ray (CXR) if patient has a significant associated effusion 2) May see evidence of pneumonia on CXR if pericarditis is secondary to a pneumonia 3) May see evidence of lung mass on CXR if pericarditis is secondary to a lung cancer 4) Note: Patients with acute pericarditis should be monitored for the development of a pericardial effusion which can lead to cardiac tamponade 5) Testing in acute pericarditis often includes echocardiography (ultrasound test) to evaluate for the presence and hemodynamic significance of a pericardial effusion - May also use CT or MRI

Fibrinous/Serofibrinous Pericarditis

1) Most frequent types of pericarditis 2) Serous fluid mixed with a fibrinous exudate containing plasma proteins including fibrinogen 3) Common causes - Acute MI - Postinfarction (Dressler) syndrome - Uremia - Radiation - Rheumatic fever - Systemic lupus erythematosus - Trauma 4) Patients often develop loud pericardial friction rub - However increasing fluid may muffle and obliterate the rub

Treatment Of Cardiac Tamponade

1) Pericardiocentesis - Removal of the high-pressure pericardial fluid is the only intervention that reverses the life-threatening physiology of this condition. - Pericardiocentesis is best performed in the cardiac catheterization laboratory, where the hemodynamic effect of fluid removal can be assessed. The patient is positioned head up at a 45° angle to promote pooling of the effusion, and a needle is inserted into the pericardial space through the skin, usually just below the xiphoid process (which is the safest location to avoid piercing a coronary artery) 3) Following successful pericardiocentesis, the pericardial pressure falls to normal 4) After initial aspiration of fluid, the pericardial catheter may be left in place for 1 to 2 days to allow more complete drainage. 5) When pericardial fluid is obtained for diagnostic purposes, it should be stained and cultured for bacteria, fungi, and acid-fast bacilli (tuberculosis), and cytologic examination should be performed to evaluate for malignancy. Other common measurements of pericardial fluid include cell counts (e.g., white cell count is elevated in bacterial infections and other inflammatory conditions) and protein and lactate dehydrogenase (LDH) levels

Which of the following CT scans depicts a pericardial effusion?

B - CORRECT-BILATERAL PLEURAL EFFUSIONS ARE ALSO PRESENT

Which of the following is least likely to result in death? A. Rapid accumulation of 500 mL of pericardial fluid B.Slow accumulation of 500 mL of pericardial fluid C. Neither A or B. 500 mL of pericardial fluid is uniformly fatal

B. Slow accumulation of 500 mL of pericardial fluid

Gross Appearance of Fibrinous/Serofibrinous Pericarditis

Grossly the pericardium has a rough and shaggy appearance and contains yellow to brown fluid

A 5-year-old boy has a pericardial effusion. A tap of the effusion is obtained. 30 ml of fluid is obtained. Which of the following features is most consistent with the fluid being an exudate? 1) History of recent nasal congestion 2) Low protein content 3) Specific gravity of 1.002 4) Hypercellular fluid 5) The volume of the fluid is 30 ml

Hypercellular fluid

Which of the following has the best prognosis? 1) Idiopathic pericarditis 2) Pericarditis due to neoplastic disease 3) Purulent pericarditis 4) Cardiac tamponade

Idiopathic pericarditis

Which of the following is true about albumin? 1) Is responsible for most of the oncotic pressure within capillaries 2) Is responsible for most of the osmotic pressure within capillaries

Is responsible for most of the oncotic pressure within capillaries

Hemorrhagic pericarditis is most commonly caused by which of the following? 1) Infection 2) Motor vehicle accident 3) Uremia 4) Malignant neoplasm 5) Lupus

Malignant neoplasm

Inflammation of the pericardium

Pericarditis

A 25 year old man has developed acute pericarditis due to a viral upper respiratory infection. He has 15 ml of thin clear fluid in his pericardial sac. Does this patient have a pericardial effusion?

No

A 26 year old man has the following EKG. Does this EKG indicate acute pericarditis?

No - CORRECT-EKG IS NORMAL

Typically refers to an abnormal accumulation of fluid in the pericardial sac - The accumulation may be abnormal in either amount AND/OR composition

Pericardial Effusion

the ratio of the weight (mass) of a solution compared to the weight (mass) of an equal volume of water

Specific gravity (SG) - Specific gravity of pure water is 1.000 - More dense = higher specific gravity - Example: Maple syrup will have higher specific gravity than water

Pericardial Effusion Clinical Features

Spectrum of possible symptoms 1) May be asymptomatic 2) May complain of a dull constant ache in the chest 3) Effusion may cause symptoms resulting from compression of adjacent structures, such as dysphagia (difficult swallowing because of esophageal compression), dyspnea (shortness of breath resulting from lung compression), hoarseness (due to recurrent laryngeal nerve compression), or hiccups (resulting from phrenic nerve stimulation) May present with findings of cardiac tamponade. 4) May present with findings of cardiac tamponade.

ECG showing classic findings for acute pericarditis

The ECG shows classic findings for acute pericarditis with diffuse (leads I, II, III, aVL, aVF, V2-V6) upsloping ST segment elevations and concomitant PR segment deviations (up in aVR and down in other leads that show ST depressions).

A 55 year old woman has the following EKG. Is this EKG consistent with a large pericardial effusion?

YES-EKG SHOWS ELECTRICAL ALTERNANS