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HMS Homeostasis I > Pericardial Disease > Flashcards

Pericardial Disease Flashcards

1
Q

Pericardial pressure cycles

A

In the healthy heart, intrapericardial pressure varies during the respiratory cycle from −5 mm Hg (during inspiration) to +5 mm Hg (during expiration) and nearly equals the pressure within the pleural space.

However, pathologic changes in pericardial stiffness, or the accumulation of fluid within the pericardial sac, may profoundly increase this pressure.

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2
Q

Idiopathic pericarditis

A

Most pericarditis is of idiopathic origin, however serology has demonstrated these episodes are likely viral in origin. Particularly implicated viridae are echovirus and coxsackievirus group B, with other common viruses rarely causing pericarditis.

The exception to this is in AIDS patients. Pericarditis is the most common cardiovascular disease manifestation in AIDS patients and usually arises due to HIV itself or due to superimposed tuberculosis.

Usually self-limited, running its course in 1-3 weeks.

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3
Q

Tuberculosis pericarditis

A

Incidence in US is low, but it is an important cause of pericarditis in immunosuppressed patients.

Tuberculous pericarditis arises from reactivation of the organism in mediastinal lymph nodes, with spread into the pericardium via lymph or hematogenous dissemination.

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4
Q

Purulent pericarditis

A

A catchall for ‘nontuberculosis bacterial pericarditis’. (As if TB pericarditis isn’t purulent enough?). Also mostly immunocompromised patients.

Most commonly pneumococci or staphylococci. May arrive from 1) perforating trauma of chest, 2) contamination during chest surgery, 3) extension of intracardiac infection, 4) extension of pneumonia or subdiaphragmatic infection, 5) hematogenous spread from anywhere

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5
Q

Pericarditis following MI

A

Two types:

  1. Occurs within first few days, likely extension of inflammation from myocardium. Occurs more in patients w/ transmural infarcts. Does not affect prognosis, but is a nuisance in that it can be hard to dinstinguish pericardial pain from recurring angina.
  2. Dressler syndrome: May develop 2 weeks to several months post-MI. Thought to be autoimmune in origin, maybe triggered against antigens released during the MI.
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6
Q

Post-pericardiotomy pericarditis

A

Syndrome that is clinically similar to Dressler syndrome, but occurs weeks to months following heart surgery rather than post-MI.

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7
Q

Uremic Pericarditis

A

Pericarditis is a serious complication of chronic renal failure, but its pathogenesis in this setting is unknown. May even develop in patients during the first few months of dialysis therapy.

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8
Q

Neoplastic pericarditis

A

Tumor involvement of the pericardium most commonly results from metastatic spread or local invasion by cancer of the lung, breast, or lymphoma. Primary tumors of the pericardium are very rare.

Neoplastic effusions are usually large and hemorrhagic and frequently lead to cardiac tamponade.

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9
Q

Radiation-induced pericarditis

A

Radiation-induced damage causes a local inflammatory response that can result in pericardial effusions and ultimately fibrosis.

Cytologic examination of the pericardial fluid helps to distinguish radiation-induced pericardial damage from that of tumor invasion.

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10
Q

Pericarditis Associated with Connective Tissue Diseases

A

Pericardial involvement is common in many connective tissue diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis, and progressive systemic sclerosis.

Customary treatment of the underlying connective tissue disease usually ameliorates the pericarditis as well.

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11
Q

Drug-Induced Pericarditis

A

Several pharmaceutical agents have been reported to cause pericarditis as a side effect, often by inducing a systemic lupus-like syndrome.

hese drugs include the antiarrhythmic procainamide and the vasodilator hydralazine. Drug-induced pericarditis usually abates when the causative agent is discontinued.

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12
Q

Stages of pericarditis

A
  1. Vasodilation and transudation
  2. Increased vascular permeability
  3. Exudation with leukocytic infiltrate
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13
Q

Serous pericarditis

A

Characterized by scant polymorphonuclear leukocytes, lymphocytes, and histiocytes. The exudate is a thin fluid secreted by the mesothelial cells lining the serosal surface of the pericardium.

This likely represents the early inflammatory response common to all types of acute pericarditis.

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14
Q

Serofibrinous pericarditis

A

Most commonly observed morphologic pattern in patients with pericarditis.

The pericardial exudate contains plasma proteins, including fibrinogen, yielding a grossly rough and shaggy appearance (termed “bread and butter” pericarditis). Portions of the visceral and parietal pericardium may become thickened and fused.

Occasionally, this process leads to a dense scar that restricts movement and diastolic filling of the cardiac chambers (decreased preload).

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15
Q

Suppurative (or purulent) pericarditis

A

Intense inflammatory response associated most commonly with bacterial infection. The serosal surfaces are erythematous and coated with purulent exudate.

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16
Q

Hemorrhagic pericarditis

A

A grossly bloody form of pericardial inflammation and is most often caused by tuberculosis or malignancy.

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17
Q

Most frequent clinical symptoms of pericarditis

A
  • Chest pain
    • Localized retrosternally and to the left precordium
    • May radiate to back and ridge of left trapezius
    • Sharp, pleuritic, and positional
  • Fever
  • Dyspnea (may be secondary to pleuritic pain)
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18
Q

Pleuritic pain

A

Aggravated by inspiration and coughing

Not necessarily relating to pleura specifically

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19
Q

Positional pain

A

Changing position lessens the discomfort

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20
Q

If a young, otherwise healthy individual presents with pericarditis, it is probably ___.

A

If a young, otherwise healthy individual presents with pericarditis, it is probably viral.

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21
Q

Physical exam findings

A
  • Pleuritic, positional chest pain
  • Friction rub on cardiac auscultation
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22
Q

Pericarditis ECG

A

Diffuse ST segment elevation is present, reflecting inflammation of the adjacent myocardium, with the exception of aVR and V1 (top middle two, makes it look like a sack or bag).

Also notice depression of the PR segment (arrow).

23
Q

Pericarditis studies

A
  • ECG
  • Elevated ESR/CRP
  • Leukocytosis
  • Sometimes elevated troponin, suggesting inflammation of neighboring myocardium
  • Echo can show pericardial effusion
  • PPD test for TB
  • Serology for ANA and RF
  • Careful search for malignancy
  • Pericardiocentesis
24
Q

Treatment for pericarditis

A
  • Treat underlying cause
  • Rest (reduce HR, reduce the kicking around of the pericardium)
  • Pain relief (usually NSAIDs)
  • Colchicine sometimes useful
  • Oral corticoteroids, but only in uncomplicated cases
  • Purulent pericarditis and TB pericarditis warrant drainage and intensive antibiotics, multidrug for TB
25
Q

Causes of noninflammatory, serous pericardial effusion

A
  • Increased capillary permeability (e.g., hypothyroidism)
  • Increased capillary hydrostatic pressure (e.g., congestive heart failure)
  • Decreased plasma oncotic pressure (e.g., liver failure or nephrotic syndrome)
26
Q

Pericardial PV relationship

A

Pericardium is not very stretchy at baseline (A), but with chronic effusion it gradually becomes more compliant over time (B).

27
Q

Three factors that determine whether pericardial effusion remains silent or whether tamponade ensues

A
  1. Volume of fluid
  2. Rate of fluid accumulation
  3. Compliance of the pericardium
28
Q

Other symptoms sometimes associated with pericardial enlargement due to anatomic relationships

A
  • dysphagia (difficult swallowing because of esophageal compression)
  • dyspnea (shortness of breath resulting from lung compression)
  • hoarseness (due to recurrent laryngeal nerve compression)
  • hiccups (resulting from phrenic nerve stimulation)
29
Q

Ewart sign

A

ullness to percussion of the left lung over the angle of the scapula owing to compressive atelectasis by the enlarged pericardial sac.

30
Q

Pericardial effusion ECG

A

“Electrical alternans”

Reduced voltage of the complexes with height of the QRS complex may vary from beat to beat, a result of a constantly changing electrical axis as the heart swings from side to side within the large pericardial volume

31
Q

Pericardial effusion echo

A
32
Q

Treating pericardial effusion

A
  • If cause is known, treat underlying cause
  • If unknown and patient is unstable, pericardiocentesis should be performed immediately and fluid analyzed
33
Q

Cardiac tamponade

A

Pericardial fluid accumulates under high pressure, compresses the cardiac chambers, and severely limits filling of the heart (decreased preload). May lead to hypotensive shock and death.

Diastolic pressure within each chamber becomes elevated and equal to the pericardial pressure.

34
Q

___ should be suspected in any patient with known pericarditis, pericardial effusion, or chest trauma who develops signs and symptoms of systemic vascular congestion and decreased cardiac output

A

Cardiac tamponade should be suspected in any patient with known pericarditis, pericardial effusion, or chest trauma who develops signs and symptoms of systemic vascular congestion and decreased cardiac output

35
Q

Key findings of cardiac tamponade

A
  1. JVD
  2. Systemic hypotension
  3. ‘Small, quiet heart’ on physical exam
  4. Pulsus paradoxus
36
Q

Measuring pulsus paradoxus

A

With your sphyngomanometer and stethoscope, find the first Korotkoff sounds beneath systolic pressure. If pressure is held here, in a patient with pulsus paradoxus, sounds will drift in and out, being audible with expiration, but absent with inspiration.

Keep going down and find the highest pressure at which the sounds are first audible in inspiration.

The difference between these two pressures is the pulsus paradoxus.

37
Q

The definitive diagnostic procedure for cardiac tamponade is . . .

A

The definitive diagnostic procedure for cardiac tamponade is cardiac catheterization with measurement of intracardiac and intrapericardial pressures, usually combined with therapeutic pericardiocentesis

38
Q

Performing pericardiocentesis

A
  • Position patient with head up at 45 degree angle to promote pooling of effusion
  • Insert needle into pericardial space through the skin, just below xiphoid process (safest place to avoid piercing a coronary artery)
39
Q

Jugular venous pressure waves in tamponade

A
40
Q

Constrictive Pericarditis

A

Often masquerades as other diseases. Occurs when pericardial effusion from pericarditis undergoes organization and fibrous scar formation, sometimes with calcification, stiffening the pericardium.

Inhibits filling during diastole. Constriction of the right ventricle causes systemic venous pressure rise and right-heart diastolic failure. Impaired filling of left ventricle causes reduced stroke volume, often leading to hypotension.

41
Q

Timecourse of constrictive pericarditis

A

Symptoms develop over months to years, resulting from 1) reduced cardiac output and 2) elevated systemic venous pressures.

Patients are often mistaken as having hepatic cirrhosis or an intraabdominal tumor due to hepatomegaly and ascites.

42
Q

Kussmaul sign

A

In a patient with constrictive pericarditis, jugular veins become more distended during inspiration, as blood is drawn into the thorax but cannot make it into the constricted right heart.

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.

43
Q

Best way to diagnose constrictive pericarditis

A

Cardiac catheterization, to reveal:

  1. Elevation and equalization of diasatolic pressure in each cardiac chamber
  2. Early diastolic ‘dip and plateau’ in LV pressure
  3. Prominent y descent in RA pressure
  4. Discordance of RV and LV systolic pressures (RV systolic pressure rises with inspiration while LV systolic pressure declines)
44
Q

The clinical and hemodynamic findings of constrictive pericarditis are often similar to those of ___

A

The clinical and hemodynamic findings of constrictive pericarditis are often similar to those of restrictive cardiomyopathy

However the prognosis is much better for constrictive pericarditis. Endomyocardial biopsy may distinguish these two.

45
Q

Treating constrictive pericarditis

A

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.

46
Q

You have a patient with pericardial tamponade. She has a blood pressure of 85/60 mm Hg and a heart rate of 120 bpm. Her JVP is elevated. You are preparing to take her to the cath lab for a pericardiocentesis, but it will be about an hour delay. Which of the following treatments would be appropriate now?

A

Administer IV fluids and a positive inotrope to try and increase blood pressure

47
Q

If pericarditis develops into pericardial effusion, ___ will disappear.

A

If pericarditis develops into pericardial effusion, the cardiac rub on auscultation will disappear.

48
Q

Exacerbation of pulsus paradoxus in cardiac tamponade

A
49
Q

Tamponade physiology diagnosis components

A
  • Elevated HR
  • Decreased BP
  • Increased Pulsus paradoxus
  • Increased venous pressures
  • Presence of pericardial effusion
50
Q

Contour of ST elevation

A

STEMI: Downward coving (tombstone)

Pericarditis: Upward coving (smiley face)

51
Q

“Concordance” between QRS and T

A

They are going in the same direction (as they should be in a healthy patient!)

52
Q

Inflammation from pericarditis may sometimes trigger. . .

A

. . . an arrhythmia, like atrial flutter.

53
Q

Most important nonpharmacologic treatment for pericarditis

A

Bed rest!!!!!

Don’t increase your heart rate, that will make it worse!

HMS Homeostasis I (62 decks)

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