Myocardial and pericardial disorders Flashcards
Normal Pericardium Definition
- double-walled sac
- surrounds the heart and great vessels origin
Normal Pericardium Components
Two layers
- Fibrous Parietal layer (2 mm thick, accelular)
- Serous Visceral layer = epicardium- contact with mioyocardium
- Pericardial cavity
- Pericardial fluid → 15 –50 ml (serous fluid- plasma ultrafiltrate)
→ secreted / absorbed continuously
→ 800 ml/day
! well Innervated → inflammation may produce severe pain
→ trigger vagus mediated reflexes
PHYSIOLOGY OF THE PERICARDIUM
PERICARDIUM ROLES
- Fixes the heart to the mediastinum (ligamentous attachments to the diaphragm, sternum, and other structures)
- Limits friction between the heart and surrounding structures
- prevents displacement of the heart and kinking of the great vessels
- Provides lubrication for the heart
- Protection against extension of mediastinal infections
- Delaying extension of infections / malignancy
- HEMODYNAMIC Role → distribution of the hydrostatic forces
- Coupling of ventricular diastolic pressures
- Facilitating atrial filling in ventricular systole
- Increasing blood volume in ventricular systole
- Preventing acute dilations of heart
Classical pericardial syndromes
- Pericarditis (Inflammatory Diseases)
- Pericardial effusion
- Cardiac tamponade
- Constrictive pericarditis
- Other
• Congenital absence of pericardium
• Tumors
Acute pericarditis Definition
Syndrome due to Pericardial Inflammation
- without pericardial effusion
- with pericardial effusion
Not causing compression
Causing compression
ESC Classification
- Acute pericarditis : New-onset pericarditis
- Incessant : Lasting for >4–6 Weeks but <3
Months without remission - Chronic Pericarditis : lasting for >3 Months
- Recurrent Reccurence of pericarditis after a documented first episode of acute pericarditis and a
symptom-free interval of 4–6 Weeks or longer
Pericarditis- Etiologic Classification
1.Infectious Pericarditis
2.Non - Infectious Pericarditis
3. Pericarditis most likely related to hypersensitivity or
autoimmunity
Infectious Pericarditis
- Viral (coxsackievirus A and B, echovirus, mumps, adenovirus, HIV)
- Bacterial → Pyogenic (pneumococcus, streptococcus, staphylococcus, etc)
- Tuberculous
- Fungal
- Other infections (syphilitic, protozoal, parasitic)
Non- Infectious Pericarditis
- Acute myocardial infarction
- Uremia
- Neoplasia
a) Primary tumors (benign or malignant, mesothelioma)
b) Tumors metastatic to pericardium (lung and breast cancer, lymphoma, leukemia) - Myxedema
- Chylopericardium
- Trauma
a) Penetrating chest wall
b) Nonpenetrating - Aortic dissection (with leakage into pericardial sac)
- Postirradiation
- Familial Mediterranean fever
10.Acute idiopathic
11.Whipple’s disease
12.Sarcoidosis
III. Pericarditis most
Pericarditis most likely related to hypersensitivity or
autoimmunity
- Rheumatic fever
- Collagen vascular disease (systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, granulomatosis with polyangiitis (Wegener’s)
- Drug-induced (e.g., hydralazine, phenytoin, Isoniazide, anticoagulants)
- Post-cardiac injury
a) Postmyocardial infarction (Dressler’s syndrome)
b) Postpericardiotomy
c) Posttraumatic
Pericarditis
Clinical diagnosis
At least 2 out of 4 following criteria:
(1) Pericarditic Chest Pain
(2) Pericardial Rubs
(3) Dynamic Ecg changes (New widespread ST-
elevation or PR depression)
(4) Evidence of Pericardial effusion (new or worsening)
Additional supporting findings: - ↑ marker of inflammation CRP, erythrocyte sedimentation rate, and WBC - Evidence of pericardial inflammation (imaging technique: CT, CMR)
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
CLINICAL aspect
- Symptoms suggestive for etiology (ex.: fever, myalgia)
- Typical features
- Nerves compression / iritation
Symptoms
Dyspnea Cough
Dysphagia Hiccup
Dysphonia Nausea
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
(1) CHEST PAIN characteristics
- Localization Retrosternal
- Left precordial area
- Referred to : Neck base, left Trapeziums ridge, Left arm
- Aggravated by : Inspiration, coughing, deglutition, changes in body position, dorsal decubitus
- Relieved by : Leaning Forward, Sitting Up
Duration Hours, Days
Intensity ↑ → Infectious AP - Absent → fluid develops within long time
(neopasms, tuberculosis, uremia)
Differentiation of pericarditis from
myocardial ischemia or infarction
image slide 7
Pericarditis
Differential diagnosis
- AMI
- Aortic dissection
- Pulmonary embolism
- Pneumonia
- Mediastinitis
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
PHYSICAL EXAMINATION
Position: upright and leaning forward position
Auscultation (diagnostic feature):
(2) PERICARDIAL FRICTION RUB
- Does not respect cardiac cycle
- It’s over the cardiac sounds
- Superficial
- Inconstant
- May disappear (with great quantity of fluid)
- Characteristics : high-pitched, scratching, grating
Percution Cardiac dullness:
Normal (pericarditis without effusion or↓↓effusion) OR
Increased (pericarditis with large effusion)
Palpation: Apex beat
Interior of the dullness (if fluid +++) OR
Normal in dry pericarditis
Auscultation (other):
Cardiac sounds
Faint ( if fluid +++ ) OR
Normal ( if no fluid or ↓↓↓ fluid)
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
(3) Ecg - dynamic changes
- PR depression
- ST pattern - I. ST elevation +Twave, STE without ST
- depression, in all
(dynamic) leads, except V1 and aVR - II. Isoelectric ST segment and flattened T wave
- III. Inverted T waves later
- IV. normalisation Ecg
- ST-T Changes
- QRS ± reduction in voltage of the QRS complexes
- electrical alternans (in Cardiac Tamponade)
- Rhythm disorders: sinus tachycardia (AFi, AFl)
- Conduction disorders: usually with myocarditis
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
(4) Pericardial effusion evidence
Physical exam Echocardiography Chest Radiography ─ An increased cardiothoracic ratio occurs only with pericardial effusions > 200- 300 ml
Radioscopy
─ Diminished pulsations of the cardiac border
ECHOCARDIOGRAPHY
↑ Specificity, Sensibility →“gold standard”
has replaced other methods
• M mode detects quantity of fluid as small as 20 ml
• 2D detects circumferential / localized pericardial effusion
Detects
• Variable amount of Pericardial effusion (if present)
An ECHO-FREE space between the epicardium and
pericardium behind LV, in front of RV
( !!!! If this space is small and only in systole =
PHYSIOLOGICAL)
- If large fluid present →swinging heart
- Thickened and hyper-reflective pericardial layers
- Wall motion abnormalities in myo-pericarditis
- Normal in some patients
II. PERICARDIAL EFFUSION
Definition
- ↑ production of pericardial fluid by inflammatory processes
(exudate) - ↓ reabsorption due to a ↑systemic venous pressure (transudate)
II. PERICARDIAL EFFUSION
Classification
Onset
− Acute or subacute
− Chronic >3 months
Distribution
− Circumferential
− Loculated
Haemodynamic impact
− None
− Cardiac tamponade
− Effusive-constrictive
Size (semiquantitative echo)
− Mild (<10 mm)
− Moderate (10–20 mm)
− Large (>20 mm)
II. PERICARDIAL EFFUSION
Clinical aspect
- Acute effusive pericarditis without compression of the heart → See previous text for clinical aspect
- Pericardial effusions within specific etiologies have the clinical aspect of the basic etiology
- Cardiac tamponade → See next text
ACUTE PERICARDITIS
Fibrinous or Effusive
Without compression of the heart
(3) Ecg - dynamic changes
- PR depression
- ST pattern - I. ST elevation +Twave, STE without ST
- depression, in all
(dynamic) leads, except V1 and aVR - II. Isoelectric ST segment and flattened T wave
- III. Inverted T waves later
- IV. normalisation Ecg
- ST-T Changes
- QRS ± reduction in voltage of the QRS complexes
- electrical alternans (in Cardiac Tamponade)
- Rhythm disorders: sinus tachycardia (AFi, AFl)
- Conduction disorders: usually with myocarditis
III. CARDIAC TAMPONADE
Definition:
Large Effusive Pericarditis that compress the heart and affect ventricular diastolic filling with severe hemodynamic consequences.
!! A Lifethreatening cardiovascular emergency
ECHOCARDIOGRAPHY
↑ Specificity, Sensibility →“gold standard”
has replaced other methods
• M mode detects quantity of fluid as small as 20 ml
• 2D detects circumferential / localized pericardial effusion
Detects
• Variable amount of Pericardial effusion (if present)
An ECHO-FREE space between the epicardium and
pericardium behind LV, in front of RV
( !!!! If this space is small and only in systole =
PHYSIOLOGICAL)
- If large fluid present →swinging heart
- Thickened and hyper-reflective pericardial layers
- Wall motion abnormalities in myo-pericarditis
- Normal in some patients
II. PERICARDIAL EFFUSION
Definition
- ↑ production of pericardial fluid by inflammatory processes
(exudate) - ↓ reabsorption due to a ↑systemic venous pressure (transudate)
CARDIAC TAMPONADE
Beck’s Triad
suggest Diagnostic Suspicion
• ↓ arterial pressure→ hypotension
• rising systemic venous pressure ( jugular veins distension)
• heart “small and calm” (↓ intensity of the cardiac sound)
II. PERICARDIAL EFFUSION
Clinical aspect
- Acute effusive pericarditis without compression of the heart → See previous text for clinical aspect
- Pericardial effusions within specific etiologies have the clinical aspect of the basic etiology
- Cardiac tamponade → See next text
Pericarditis ≠ pericardial effusion
Pericarditis is a clinical diagnosis that cannot be made
independently by echocardiagraphy
Pericardial effusion diagnosis can be made independently by echocardiagraphy
CARDIAC TAMPONADE
“Empty” Lung (=without rales)
+ Signs /Symptoms /Ecg / Rx described previously
CARDIAC TAMPONADE
Clinical Findings determined by
- Low cardiac output
2. Hypotension
CARDIAC TAMPONADE
Diagnostic Confirmation
Echocardiography
- Echo-free space posterior to the LV > 20 mm
- Hyperkinetic heart
- RV- Diastolic collapse
- RA - systolic collapse >1⁄3 systole
- Variation with respiration of ventricular diameters
( ↓ RV in expiration )
Reciprocal respiratory changes in RV and LV volumes (septal shifting)
Reciprocal respiratory changes (>25%) in RV and LV filling
6. Reduced early-diastolic tissue Doppler velocity
7. Paradoxical septal motion
8. Severe dilation of the inferior vena cava
ALTERNATING PULSE
regular alternation of weak and strong beats
without changes in cycle length because of variation of RV debit and filling of LV
IV. CONSTRICTIVE PERICARDITIS
Etiology
- Tuberculosis (frequent)
* Other
IV. CONSTRICTIVE PERICARDITIS
CLINICAL syndrome → almost like Cardiac Tamponade
SISTEMIC CONGESTION determined by
• diastolic filling
• pressures in RV, RA, cava veins
Without a great quantity of fluid
Right Heart Failure • RHF Signs • RHF complications: - Hepatic Cirrhosis - Effusive enteropathy - Nefrotic Syndrome - Renal Veins Thrombosis
LOW CARDIAC OUTPUT Syndrome
- Fatigue
- Low BP
- Cardiac cashecsia
- Dyspnea during exertion
IV. CONSTRICTIVE PERICARDITIS
Diagnostic
Clinical Suspicion
►small heart with signs of global Heart Failure
IV. CONSTRICTIVE PERICARDITIS
Diagnostic
Characteristic elements:
- Kussmaul sign ( ↑vv with inspiration)
- Pericardial knock after S2
- Apical pulse is reduced and retracts in systole
- Paradoxical pulse (1/3 )
IV. CONSTRICTIVE PERICARDITIS
Radiology:
“small heart”, thickened pericardium
IV. CONSTRICTIVE PERICARDITIS
Jugular venous pulse:
“square root” sign ( Y)
