MEDICINE III

DR. SILAHIS ROSARIO

TOPIC: PERICARDITIS & MYOCARDITIS
DATE: SEPTEMBER 30, 2022

OUTLINE PAGE ACUTE PERICARDITIS

The Case 1 •
Acute Pericarditis 1 by typical chest pain, a pathognomonic pericardial friction rub
Classification of Pericarditis 2 and specific ECG changes
Cardiac Tamponade 2 •
Constrictive Pericarditis 3
FOUR PRINCIPAL DIAGNOSTIC FEATURES:
Tuberculous Pericardial Disease 5
Myocarditis 6
Cardiomyopathies 6
THE CASE
C.R. 29-year-old female
CC: fever and dyspnea
HPI:
• 2 weeks PTA - flu-like symptoms and fever relieved
temporarily with paracetamol
• 1 week PTA - exertional dyspnea, palpitation, occasional
chest pain, tiredness, insomnia
• 3 days PTA - progression of dyspnea, associated with
fatigue, pallor, chest pain and 4-pillow orthopnea
• The day of admission - anemia with hemoglobin of 7,4 gm%
and hematocrit of 23.3%, 1.0mg/dl creatinine and 0.66
mIU/L TSH, respectively
PE:
She was awake, conscious, pale-looking, oriented to time and place,
ambulatory, febrile, and in slight respiratory distress.
BP = 110/70 PR = 104 RR = 24 Temp = 38.4
Skin: good turgor, no lesions
HEENT: pale palpebral conjunctiva, anicteric sclera, no naso-aural
discharges, no tonsillopharyngeal congestion.
Neck: supple, no NVE, no masses
C/L: equal chest expansion, clear breath sounds
CVS: adynamic precordium, PMI at 5th LICS, MCL, S1S2 distinct,
tachycardia, regular rhythm, grade 2/6 holosystolic murmur at the
apex, scratchy sound at the LLSB
Abdomen: flat, NABS, no tenderness, no organomegaly
Chest x-ray = clear lungs with slight cardiomegaly
ECG = Sinus tachycardia, nonspecific ST-T wave changes
2D echocardiogram: Normal left ventricular geometry, with
hypokinesia of the anterior IVS and anterior LV free wall from base to
apex with ejection fraction of 40%, dilated left atrium; moderate
mitral, tricuspid and pulmonic regurgitations; thickened pericardium
with moderate pericardial effusion.
Anatomically there was chamber enlargement of the left atrium.
Physiologic regurgitation of mitral, tricuspid, and pulmonic. Mildly
Reduced EF (40-50%). Functional class III.
Acute fibrinous or dry pericarditis is a syndrome characterized
Inflammation or irritation of the pericardium
1. CHEST PAIN
o Important but not variable symptom in various forms of acute
pericarditis
o Usually present in the acute infectious types and in many of
the forms presumed to be related to hypersensitivity and
autoimmunity
o Often absent in slowly developing tuberculosis, post-
irradiation, neoplastic, and uremic pericarditis
o Often severe, retrosternal and left precordial, and referred to
the neck, arms, or left shoulder
o Often the pain is pleuritic, consequent to accompanying
pleural inflammation (i.e., sharp and aggravated by
inspiration and coughing)
o It is steady, constricting pain that radiates into either arm or
both arms and resembles that of myocardial ischemia
2. PERICARDIAL FRICTION RUB
o audible in about 85% of these patients
o may have three components per cardiac cycle
o high-pitched, and is described as rasping, scratching, or
grating
o it can be elicited sometimes when the diaphragm of the
stethoscope is applied firmly to the chest wall at the left lower
sternal border
o heard most frequently at end expiration with the patient
upright and leaning forward
o pericardial rub is heard throughout the respiratory cycle,
whereas a pleural rub disappears when respiration is
suspended
3. ELECTROCARDIOGRAM
o changes secondary to acute subepicardial inflammation
o typically evolves through four stages:
▪ stage 1, there is widespread elevation of the ST
segments, often with upward concavity, involving two
or three standard limb leads and V2 to V6, with
reciprocal depressions only in aVR and sometimes V1,
as well as depression of the PR segment below the TP
segment reflecting atrial involvement. Usually there
are no significant changes in QRS complexes.
▪ Stage 2, after several days, the ST segments return to
normal
▪ Stage 3, T waves become inverted
▪ Stage 4, Ultimately, weeks or months after the onset
of acute pericarditis, the ECG returns to normal

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 ETIOLOGIC CLASSIFICATION
• Infectious pericarditis
o Viral (coxsackievirus A and B, echovirus, mumps,
adenovirus, hepatitis, HIV)
o Pyogenic (pneumococcus, streptococcus, staphylococcus,
Neisseria, Legionella)
o Tuberculous
o Fungal (histoplasmosis, coccidioidomycosis, Candida,
blastomycosis)
• widespread elevation of the ST segments, often with upward o Other infections (syphilitic, protozoal, parasitic)
concavity, involving two or three standard limb leads and V2 to • Noninfectious pericarditis
V6, o Acute myocardial infection
• reciprocal depressions only in aVR and sometimes V1 o Uremia
• depression of the PR segment below the TP segment o Neoplasia
reflecting atrial involvement ▪ Primary tumors (benign or malignant, mesothelioma)
• usually there are no significant changes in QRS complexes ▪ Tumors metastatic to pericardium (lung and breast
4. PERICARDIAL EFFUSION cancer, lymphoma, leukemia)
o Accumulation of transudate, exudate, or blood in the o Myxedema
pericardial sac o Cholesterol
o A common complication of pericardial disease o Chylopericardium
o should be sought in all patients with acute pericarditis o Trauma
o usually associated with pain and/or the ECG changes ▪ Penetrating chest wall
o enlargement of the cardiac silhouette ▪ Nonpenetrating
o Pericardial effusion is especially important clinically when it o Aortic dissection (with leakage into pericardial sac)
develops within a relatively short time as it may lead to o Postirradiation
cardiac tamponade o Familial Mediterranean fever
o heart sounds may be fainter with pericardial effusion o Familial pericarditis
o friction rub may disappear, and the apex impulse may vanish ▪ Mulibrey nanism
o the base of the left lung may be compressed by pericardial o Acute idiopathic
fluid, producing Ewart's sign, a patch of dullness and o Whipple’s disease
increased fremitus (and egophony) beneath the angle of the o Sarcoidosis
left scapula • Pericarditis presumably related to hypersensitivity or
o chest roentgenogram may show a "water bottle" autoimmunity
configuration of the cardiac silhouette but may be normal o Rheumatic fever
o Collagen vascular disease (SLE, rheumatoid arthritis,
ankylosing spondylitis, scleroderma, acute rheumatic fever,
Wegener’s granulomatosis)
o Drug-induced (e.g., procainamide, hydralazine, phenytoin,
isoniazid, minoxidil, anticoagulants, methysergide)
o Postcardiac injury
▪ Post myocardial infarction (Dressler’s syndrome)
▪ Post pericardiotomy
▪ Posttraumatic

CARDIAC TAMPONADE
• is a hemodynamic condition characterized by:
o equal elevation of atrial and pericardial pressures
o an exaggerated inspiratory decrease in arterial systolic
pressure >10 mmHg (pulsus paradoxus)
CLASSIFICATION OF PERICARDITIS o arterial hypotension (generally a late sign in chronic
CLINICAL CLASSIFICATION effusions)
• Acute pericarditis (<6 weeks) o Beck’s Triad: three principal features of tamponade
o Fibrinous ▪ hypotension
o Effusive (serous or sanguineous) ▪ soft or absent heart sounds
• Subacute pericarditis (6 weeks to 6 months) ▪ jugular venous distention with a prominent x descent
o Effusive-constrictive but an absent y descent
o Constrictive
• Chronic pericarditis (>6 months)
o Constrictive
o Effusive
o Adhesive (nonconstrictive)

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DIAGNOSIS OF CARDIAC TAMPONADE Coronary
Coronary compression in diastole
Elevated systemic venous pressure, angiography
Clinical
tachycardia, pulsus paradoxus, hypotension, No visualization of subepicardial fat along both
presentation Computer
dyspnea or tachypnea with clear lungs ventricles, which show tube-like configuration
tomography
Drugs (cyclosporine, anticoagulants, and anteriorly drawn atria
thrombolytics,etc.) recent cardiac history,
Precipitating
indwelling instrumentation, blunt chest trauma, DIAGNOSTIC PATHWAY AND SEQUENCE OF PERFORMANCE IN
factors
malignancies, connective tissue disease, renal ACUTE PERICARDITIS
failure, septicemia. TECHNIQUE CHARACTERISTIC FINDINGS
Obligatory (class I)
Can be normal or non-specifically changes (ST- Auscultation Pericardial rub
T wave), electrical alternans (QRS, rarely T). ECG Stage I: anterior and inferior concave ST-
ECG
bradycardia (end-stage), electromechanical segment deviations opposite to P polarity
dissociation) agonal phase Early Stage II: ST junctions return to the
baseline, PR deviated
Chest X-ray Enlarged cardiac silhouette with clear lungs
Late Stage II: T waves progressively flatten
Diastolic collapse of the anterior RV free wall, and invert
LA and very rarely LV collapse, increased LV Stage III: generalized T wave inversions
M-mode/2D
diastolic wall thickness “pseudohypertrophy”, Stage IV: ECG returns to prepericarditis
echocardiogram
IVC dilatation (no collapse in inspiration), state
“swinging heart” Echocardiography Effusion
1. Tricuspid flow increases, and mitral flow Signs of tamponade
decreases during inspiration (reverse in Blood analyses a. ESR, CRP, LDH, leukocytes
expiration) (inflammation markers)
Doppler
2. Systolic and diastolic flows are reduced in b. cTnI, CK-MB (markers of myocardial
systemic veins in expiration and reverse flow lesion)
with atrial contraction us increased Chest X-ray Ranging from normal to “water bottle” heart
M-mode colour Large respiratory fluctuations in mitral/tricuspid shadow.
Doppler flows Revealing additional pulmonary/mediastinal
1. Confirmation of the diagnosis and pathology
qualification of hemodynamic compromise: Mandatory in tamponade (class I), optional in large/recurrent
• RA pressure is elevated (preserved effusions or if previous tests inconclusive (class IIa), in small
systolic x descent and absent or effusions (class IIb)
diminished y descent) Pericardiocentesis Pericardial fluid cytology, and cultures,
• Intrapericardial pressure is also and drainage PCRs and histochemistry for determination
of infection or neoplasia
elevated and virtually identical to RA
pressure (both pressures fall in Optional or if previous tests inconclusive (class IIa)
inspiration) CT Effusions, peri-, and epicardium
• RV mid-diastolic pressure elevated MRI Effusions, peri-, and epicardium
and equal to the RA and pericardial Pericardioscopy, Establishing the specific etiology
pressures (no dip-and-plateau pericardial biopsy
configuration)
• pulmonary artery diastolic pressure is CONSTRICTIVE PERICARDITIS
Cardiac • Contraction of the pericardium
slightly elevated and may correspond
catheterization • Chronic inflammation
to the RV pressure
• pulmonary capillary wedge pressure • Prevents the heart from filling completely
is also elevated and nearly equal to • Profound signs and symptoms of right-heart failure and poor
intrapericardial and RA pressure cardiac output
• LV systolic and aortic pressures may • Out of proportion to any ventricular or valvular abnormalities
be normal or reduced
2. Documentation that pericardial aspiration is DIAGNOSTIC APPROACH
followed by hemodynamic improvement Clinical Severe chronic systemic venous congestion
3. Detection of the coexisting hemodynamic presentation associated with low cardiac output, including
abnormalities (LV failure, constriction, jugular venous distention, hypotension with low
pulmonary hypertension) pulse pressure, abdominal distention, edema,
4. Detection of associated cardiovascular and muscle wasting
diseases (cardiomyopathy, coronary artery ECG Can be normal, or reveal low QRS voltage,
disease) generalized T wave inversion/flattening, LA
RV/LV Atrial collapse and small hyperactive ventricular abnormalities , atrial fibrillation, atrioventricular
Angiography chambers block, intraventricular conduction defects or
rarely pseudo infarction pattern

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 Chest X-ray Pericardial calcifications, pleural effusions Cardiac “dip and plateau” or “dip and plateau”,
M-mode/2D Pericardial thickening and calcifications as well catheterization “square root sign” RVEDP and
echocardiogram as the indirect signs of constriction: LVEDP often>5 mmHg LVDEP usually
- RA and LA enlargement with normal greater than RVEDP, but equal,
appearance of the ventricles, and normal may be identical, RV inspiration:
systolic function systolic pressure >50 increase in RV
- Early pathological outward and inward mmHg, RVEDP <1/3 systolic pressure.
movement of the interventricular septum (dip- RVSP Decrease in lv
plateau phenomenon) systolic pressure,
- Flattering waves at the LV posterior wall with expiration,
- LV diameter is not increasing after rapid filling opposite
phase
- IVC and the hepatic veins are dilated with EMB May reveal specific May be normal or
restricted respiratory fluctuations cause of restrictive show nonspecific
Doppler Restricted filling of both ventricles with cardiomyopathy hypertrophy or
respiratory variation >25% over the AV-valves fibrosis
TEE Measurement of the pericardial thickness
CT/MRI Thickened and/or calcified pericardium, tube- CT/MRI Pericardium usually Pericardium must
like configuration of one or both ventricles, normal be thickened or
enlargement of one or both atria, narrowing of calcified
one or both atrio-ventricular grooves,
congestion of the canal veins Features That Distinguish Cardiac Tamponade From Constrictive
Cardiac “dip and plateau “or “square root” sign in the Pericarditis And Similar Clinical Disorders
catheterization pressure curve of the right and/or left ventricle Characteristics Tampona Constrictive Restrictiv RVMI
Equalization of the LV/RV end-diastolic de pericarditis e cardio
pressures in the range of 5mmHg or less myopathy
RV/LV The reduction of RV & LV size and increase in Clinical
angiography RA & LA size Pulsus paradoxus Common Usually Rare Rare
absent
During diastole a rapid early filling with stop of
Jugular veins
further enlargement (“dip-plateau”
Prominent y descent Absent Usually Rare Rare
Coronary In all patients over 35 years and in patients with present
angiography a history of mediastinal irradiation, regardless Prominent x descent Present Usually Present Rare
of the age present
Kussmaul’s sign Absent Present Present Present
CONSTRICTIVE PERICARDITIS VS RESTRICTIVE
CARDIOMYOPATHY Third heart sound Absent Absent Rare Maybe
Method Restrictive Constrictive present
cardiomyopathy pericarditis Pericardial knock Absent Often present Absent Absent
Physical findings Kussmaul’s sign +/-, Kussmaul’s sign Electrocardiogram
apical impulse +++, +, apical impulse - Low ECG voltage May be May be May be Absent
present present present
S3 (advanced), , pericardial knock
Electrical alternans May be Absent Absent Absent
S4(early disease), +, regurgitant present
regurgitant murmurs +++ murmurs -
Echocardiography
ECG Low voltage, Low voltage Thickened Absent Present Absent Absent
pseudoinfarction, left (<50%) pericardium
axis deviation, AF, Pericardial Absent Often present Absent Absent
conduction disturbances calcification
Chest radiography No calcifications Calcifications may Pericardial effusion Present Absent Absent Absent
be present (low RV size Usually Usually Usually Enlarge
diagnostic small normal normal d
accuracy) Myocardial Normal Normal Usually Normal
thickness increased
2D Small lv cavity with large Normal wall Right atrial collapse Present Absent Absent Absent
& RVDC
Echocardiography atria. Increased wall thickness
Increased early Absent Present Present May be
thickness sometimes Pericardial filling, ↑mitral flow present
present (especially thickening, velocity
thickened interatrial prominent early Exaggerated Present Present Absent Absent
septum in amyloidosis) diastolic filling respiratory variation
thickened valves and with abrupt in flow
granular sparkling displacement of CT/MRI
(amyloidosis) IVS Thickened/calcified Absent Present Absent Absent
pericardium

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Cardiac catheterization PERICARDIOCENTESIS
Equalization of Usually Usually Usually Absent Indications for pericardiocentesis
diastolic pressures present present absent or Class I
present • Cardiac tamponade
Cardiac biopsy No No Sometime No
• Effusions >20mm in echocardiography (diastole)
helpful? s
• Suspected purulent or tuberculous pericardial effusion
Class IIa
• Effusions 20-30mm in echocardiography in diastole for
diagnostic purposes other than purulent pericarditis or
tuberculosis (pericardial fluid and tissue analyses,
pericardioscopy, and epicardial/pericardial biopsy)
• Suspected neoplastic pericardial effusion
Class IIb
• Effusions <10 mm in echocardiography in diastole for
diagnostic purposes other than purulent, neoplastic, or
tuberculous pericarditis (pericardial fluid and tissue
analyses, pericardioscopy, and epicardial/pericardial
biopsy). In symptomatic patients diagnostic pericardial
puncture should be reserved for dedicated centers
Contraindications
• Aortic dissection
• Relative contraindications include uncorrected
coagulopathy, anticoagulant therapy, thrombocytopenia
<50,000/ mm3, small, posterior and loculated effusions
SYMPTOMATIC MANAGEMENT
• Pericardiocentesis is not necessary when the diagnosis
● Exercise restriction
can be made otherwise or the effusions are small and
● Hospitalization is warranted to determine the etiology and
resolving under anti-inflammatory treatment.
observe for tamponade as well as the effect of treatment
● Pain management
TUBERCULOUS PERICARDIAL DISEASE
○ NSAID are the mainstay
● Chronic infection, a common cause of chronic pericardial
○ Ibuprofen- preferred due to its rare side-effects, favorable
effusion
impact on the coronary flow; 300-800 mg every 6-8 hours,
● Common in Africa, Asia, the Middle East, and other parts of the
days to weeks or until effusion has disappeared
developing world where active tuberculosis is endemic
○ Aspirin- alternative regimen, 30-600 mg every 4-6 hours
● Clinical picture: a chronic, systemic illness in a patient with
○ Indomethacin- should be avoided in elderlyy patients due
pericardial effusion
to its flow reduction in the coronary artery.Gastrointestinal
● Consider this diagnosis in a patient with known tuberculosis, with
protection must be provided
HIV, and with fever, chest pain, weight loss, and enlargement of
TREATMENT AND PREVENTION OF RECURRENCES the cardiac silhouette of undetermined origin
● Colchicine – 0.5 mg bid, added to NSAID as monotherapy for ● Pericardial biopsy if chronic pericardial fluid analysis is obscure
the initial attack and prevention of recurrences ● Antituberculous chemotherapy is indicated if definitive evidence
● Percutaneous balloon pericardiotomy – in cases resistant to is still lacking but the specimen shows granulomas with
medical treatment caseation
● Corticosteroids – should be used only in patients with poor ● Biopsy specimen shows a thickened pericardium,
general condition or in frequent crises. Prednisone 1-1.5 mg/kg pericardiectomy should be carried out to prevent the
for at least one month; should be tapered over a three-month development of constriction
period ● Tubercular cardiac constriction should be treated surgically while
● Pericardiectomy – indicated in frequent and highly symptomatic the patient is receiving antituberculous chemotherapy.
recurrences resistant to medical treatment.
CARDIOMYOPATHIES AND MYOCARDITIS
● Dilated cardiomyopathy
● Hypertrophic cardiomyopathy
● Restrictive cardiomyopathy
● Myocarditis -causes

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 MYOCARDITIS
● An inflammatory process, most commonly attributed to infectious
organisms
● Invade the myocardium directly, produce cardiotoxins, and
trigger chronic inflammatory responses
● Infective myocarditis has been reported with almost all types of
infectious agents, but is most commonly associated with viral
infections, the protozoan Trypanosoma cruzi in South
America, and endomyocardial fibrosis in equatorial Africa.
● Often presents with symptoms and signs of heart failure
• Some patients present with chest pain suggestive of pericarditis
or acute myocardial infarction
• Occasionally, the presentation is dominated by atrial or
ventricular tachyarrhythmias, or by pulmonary or systemic
emboli from intracardiac thrombi
• Electrocardiographic or echocardiographic abnormalities may
also be detected incidentally during evaluation for other
diagnoses
• The typical patient with presumed viral myocarditis is a young to Patient with Myocarditis
middle-aged adult who develops progressive dyspnea and • You start by stabilizing hemodynamics, you give your diuretics,
weakness within a few days to weeks after a viral syndrome that vasodilators. If stable, you can do remodeling therapy (treatment
was accompanied by fever and myalgias for your heart failure) like your ACEi/ARB, Beta blockers,
• A small number of patients present with fulminant myocarditis, Aldosterone antagonists. If px remains stable, you can follow up
with rapid progression from a severe febrile respiratory px with repeat echo, CMR, and continue pharmaco treatment. If
syndrome to cardiogenic shock that may involve multiple organ LVEF persists <35%, may consider AICD indiv
systems, leading to renal failure, hepatic failure, and • If unstable, you can give hemodynamic support like inotropic
coagulopathy. agents, If hypotensive you can do your balloon pump, VAD). If
px continues to be unstable, you can do your immune therapy
Laboratory Evaluation for Myocarditis
like steroids/azathioprine, interferons, immune adsorption. Still
• ECG, an echocardiogram, and serum levels of troponin and unstable, cardiac transplantation and mechanical assist
creatinine phosphokinase fractions
• Magnetic resonance imaging CARDIOMYOPATHIES
• Endomyocardial biopsy is not often indicated for the initial • Disease of the heart muscle
evaluation of suspected viral myocarditis unless ventricular • Accounts for 5-10% of the 5-6 million patients already diagnosed
tachyarrhythmias suggest possible etiologies of sarcoidosis or with heart failure in United States
giant cell myocarditis
• Exclude cardiac dysfunction that results from other structural
• First line therapy for all patients with myocarditis and heart heart disease, such as coronary artery disease, primary valve
failure: supportive care disease (like aortic stenosis can produce hypertrophy...
• Very small proportion of patients will require hemodynamic thickened myocardium, similar to hypertrophic cardiomyopathy)
support • Also in hypertension, it would cause an increase in left
o Vasopressors ventricular mass so it will have a thickened myocardium. It would
o Intra-aortic balloon pump look like hypertrophic cardiomyopathy. Exclude always
o Ventricular assist device hypertrophic cardiomyopathy.
• Specific guidelines for myocarditis management • Non-ischemic cardiomyopathy is from other causes, so it is a
o Japanese Circulatory Society heterogeneous group of diseases of the myocardium associated
o European Society of Cardiology with mechanical and electrical dysfunction. Usually, it exhibits
o American College of Cardiology/American Heart Association inappropriate ventricular hypertrophy or dilatation due to a
▪ Acute DCM/Dilated Cardiomyopathy and a syndrome variety of causes that frequently are genetic.
of Heart Failure

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• This is a table that shows the difference between dilated,
restrictive, and hypertrophic based on your ejection fraction. If it
is dilated, cardiomyopathy the heart is big, it’s >60 mm, and
usually has a reduced ejection fraction of <30%.
• Usually, for restrictive and hypertrophic, they have a reserved
ejection fraction.
• For hypertrophic, they have a markedly increased left ventricular
wall thickness.
• For restrictive, they present more as right-sided heart failure.
• Common arrhythmia for all is atrial fibrillation.
COURSE IN THE WARD
• The patient was admitted and 2 units of packed RBC
were transfused.
• She was given furosemide 20 mg IV, trimetazidine 35
mg twice daily and isosorbide mononitrate 30 mg
daily.
• There was slight improvement of dyspnea but still felt
weak and had episodes of moderate to high-grade
fever.
• She was referred to a cardiologist the day after.
• She was given ibuprofen 400 mg capsule twice daily
and colchicine 0.5 mg daily.
• She became febrile on the third hospital day, the
friction rub was no longer appreciated, and she had
improved symptoms.
• She was discharged on the 6th hospital day.
Question:
What other medications would you like to give the patient to prevent
remodeling?
Answer:
• 4 pillars to prevent remodeling:
o Spironolactone
o ACE inhibitor
o Beta-blocker
▪ Calcium-channel blocker – in patients who have
dilated cardiomyopathy, you have to be careful in using
CCBs because it will push more to heart failure.
▪ What class
o SGLT
▪ Usually given in diabetic patients, but can also be
given in non-diabetic with reduced ejection fraction.
▪ Empagliflozin & Dapagliflozin – only approved SGLT
And what kind of CCB are you going to give? You have ACE or ARNI,
BB, MRA (Aldosterone Receptor Antagonist) or spironolactone and
SGLT2 (usually given to diabetic patients). There are only 2 approved
– epaglucacin and tapamucocin (not sure but according to Google,
there are 3 approved by FDA – canagliflozin, dapagliflozin,
empagliflozin).
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