Pericardial Physiology + Congenital Heart Diseases

Front 1

Two main components of Pericardium -

Innervation of pericardium

Back 1

Visceral pericardium

Parietal pericardium

Well innervated

Front 2

Visceral pericardium fxn-

Back 2

mesothelial monolayer facilitate fluid and ion exchange

Front 3

Parietal pericardium characteristic -

Back 3

fibrocollagenous tissue

Front 4

Pericardial fluid and it's drainage (important - objective)

Back 4

15 - 50 ml of clear plasma ultrafiltrate.

Drainage occurs both by the thoracic duct via the parietal pericardium and by the right lymphatic duct via the right pleural space.

Front 5

Ligamentous attachment of pericardium -

Back 5

to the sternum, vertebral column, diaphragm

Front 6

Pericardial physiology -

Back 6

-limit cardiac dilatation
-maintain normal ventricular compliance
-reduce friction to cardiac movement
-barrier to inflammation
-limit cardiac displacement

not needed to sustain life !

Front 7

Causes of Acute pericarditis -

Back 7

Idiopathic
Infections (mcc-viral, tuberculosis, fungal)
Uremia
Acute myocardial infarction (acute, delayed)
Neoplasm
Post-cardiac injury syndrome (trauma, CT Surgery)

Systemic autoimmune disease (systemic lupus erythematosus, rheumatoid arthritis, ankylosing sponduylitis, periarteritis nodosa, Reiter’s syndrome)

After mediastinal radiation

Front 8

Dx of acute pericarditis -

Back 8

History - sudden onset of anterior chest pain that is pleuritic and substernal

Physical exam - two or three component rub

ECG - most imp!!!!!

Front 9

Distinguis chest pain from pericarditis vs infarction -

Back 9

Common characteristics
retrosternal or precordial with radiation to the neck, back, left shoulder or arm

Special characteristics (pericarditis)
more likely to be sharp and pleuritic

INCREASE with coughing, inspiration, swallowing

worse by lying supine, relieved by sitting and leaning forward

Front 10

Pericardial friction rub is pathognomic for

Back 10

pericarditis

Front 11

3 components of pericardial friction rub -

Back 11

presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after A2P2)

Front 12

Acute pericarditis ECG features -

Back 12

Diffused ST elevation, PR depression

Front 13

Tx of acute pericarditis -

Back 13

Tx underlying causes
Analgesic agents
Anti inflammatory agents

Corticosteroids - sx improve, but AVOIDED as increased probability of relapse

Front 14

Chronic Relapsing Pericarditis -

Back 14

occurs in a small % of patients with acute idiopathic pericarditis
steroid dependency requiring gradual tapering over 3-12 months; NSAIDs, analgesics, and colchicine may be beneficial
pericardiectomy for relief of symptoms is not always effective

Front 15

What is Dressler's syndrome?

Back 15

fever, pericarditis, pleuritis(typically with a low grade fever and a pericardial friction rub)


occurs in the first few days to several weeks following MI or heart surgery
incidence of 6-25%
treat with high-dose aspirin

Front 16

Bacterial pericarditis -

Back 16

Rare


Typically arises from contiguous spread of intrathoracic infection (pneumonia, empyema, mediastinitis, endocarditis, trauma, surgery)
Usually fatal without adequate treatment
Diagnosis frequently missed
Often lacks characteristic features of acute pericarditis

Front 17

TB Pericarditis -

Back 17

Physical findings: fever, pericardial friction rub, hepatomegaly
TB skin test usually positive
Fluid smear for TB often negative
Pericardial biopsy more definitive

Front 18

Different types of pericardial effusive fluids -

Back 18

Serous
Suppurative
Hemorrhagic
Serosanguinous

Front 19

Serous effusive fluid -

Back 19

transudative - heart failure

Front 20

Suppurative effusive fluid

Back 20

pyogenic infection with cellular debris and large number of leukocytes

Front 21

Hemorrhagic effusive fluid

Back 21

occurs with any type of pericarditis
especially with infections and malignancies

Front 22

What is std for dx Pericardial effusion -

Back 22

Echocardiography

Front 23

Pericardial effusion echocardiography findings -

Back 23

a posterior echo-free space present only during systolic phase
echo-free space persist throughout the cardiac cycle (> 25 cc)
large effusion with a “swinging” heart

Front 24

What happens to Intrapericardial pressure as a result of pericardial effusion?

Back 24

Increase in pericardial effusion fluid volume increases the Intrapericardial pressure

Front 25

Beck's triad - 3 features of acute tamponade -

Back 25

Decline in systemic arterial pressure
Elevation in systemic venous pressure (e.g. distended neck vein)
A small, quiet heart

Front 26

Cardiac Tamponade pathophysiology

Back 26

fluid accumulation within the pericardial space resulting in
increased intracardiac pressure
progressive limitation of ventricular diastolic filling
reduction of stroke volume and cardiac output

Front 27

Cardiac tamponade clinical features -

Back 27

Sx - dyspnea, fatigue, agitation and restlessness, syncope, shock, anuria

Physical examination - pulsus paradoxus!!!!!!
tachycardia
increased jugular venous pressure
hypotension

Front 28

When to tx pericardial effusion?

Back 28

Not an all or non response

decision to intervene requires careful consideration of the balance of risks and benefits to the patient

Front 29

What is effusive constrictive pericarditis?

Back 29

coexistence of constrictive pericarditis and tamponading fluid

Front 30

Constrictive Pericarditis -

Back 30

An uncommon post inflammatory disorder

-the encasement of the heart by a rigid, nonpliable pericardium
-characterized by a thickened, fibrotic, and frequently calcified pericardium
-rarely develop after an episode of acute idiopathic pericarditis
-more likely to develop after subacute pericarditis with effusion that evolve over several weeks

Front 31

Causes of constrictive pericarditis -

Back 31

Idiopathic
Infectious
Drugs
Radation
Chest trauma or surgery

Front 32

Clinical findings in Constrictive pericarditis -

Back 32

JVD
Diastolic pericardial knock
Ascites
Peripheral edema

Pulsus paradoxicus <10mmHg otherwise considered tamponade

Front 33

Anatomy of pericardium -

Back 33

• Visceral pericardium: directly apposed to the heart, facilitates fluid and ion exchange
• Parietal pericardium: exposed to the mediastinum
• 15 mL of ultrafiltrate of plasma separates the two layers
• Well innervated, not needed for life

Front 34

Drainage of pericardium -

Back 34

by both the thoracic duct and the right lymphatic duct

Front 35

Function of pericardium -

Back 35

limit cardiac dilatation & movement, maintain compliance, reduce friction and stop the spread of inflammation to the heart

Front 36

Normal pressure tracing of R atria -

Back 36

• a wave: R atrial contraction = “atrial kick”
• c wave: closure of tricuspid valve with ventricular contraction
• x descent: volume has fully left R atrium and it relaxes
• v wave: venous filling of R atrium and beginning contraction
• y descent: passive filling of R ventricle with opening of tricuspid valve
• h wave: continued venous filling of R atrium if heart rate is slow

Front 37

Normal pressure tracing of R ventricle -

Back 37

• Diastole
o Early rapid filling of R ventricle (correlates with y descent)
o Late filling due to R atrial kick (correlates with a wave)
• Systole
o Rapid rise in pressure (contraction)
o Rapid fall as volume leaves and relaxation begins

Front 38

Changes in atrial and ventricle tracing in constrictive pericarditis -

Back 38

• R atrial pressure changes
o Overall increase in R atrial pressure
o M or W shape: Prominent x and y descents, as a constricted R atrium does not have as much compliance
• R ventricle pressure changes
o Square root sign: dip and plateau during filling attributed to poor filling during atrial kick

Front 39

Acute pericarditis -

description
etiology-

Back 39

acute inflammation of the pericardium
• Etiology: uremia, post-MI, TB, viral (coxsackievirus), bacterial, neoplasma, post-radiation, autoimmune (Dressler’s syndrome, rheumatoid arthritis, etc), Lupus
o Differential dx: acute MI, PE, pneumonia, aortic dissection

Front 40

Presentation of acute pericarditis -

Back 40

sharp chest pain with possible radiation to neck/back/arm, exacerbated by inspiration and lying supine, relieved with leaning forward
o On exam, friction rub (scratching high pitched rub throughout all cycles)
o May have some component of pericardial effusion (see below) & myocarditis

Friction rub has 3 components:
1. During contraction of ventricles
2. During rapid filling of ventricles during early diastole
3. During atrial contraction due to atrial contraction

Diastole components grouped together to form a "to and fro" rub

Front 41

Diagnosis and treatment of acute pericarditis -

Back 41

clinical & diffuse ST elevations on ECG; signs of inflammation
• Treatment: treat underlying cause, use NSAIDs or other anti-inflammatories

Front 42

Description of pericardial effusion

Etiology
Presentation

Back 42

extra fluid between the visceral and parietal layers
• Etiology: pericarditis, transudate (CHF), suppurative (infection), hemorrhagic, neoplasm
• Presentation: chronic cases are asymptomatic; muffled heart sounds on exam
o May lead to tamponade if acute

Front 43

Diagnosis and Treatment of Pericardial effusion -

Back 43

• Diagnosis
o CXR: water jug shaped heart similar to cardiomegaly
o ECG: diffuse low voltage, electrical alternans (heart swings back/forth in fluid)
o Echo: gold standard for finding fluid
o Pericardiocentesis with biopsy to differentiate types if not clinically evident
• Treatment: treat underlying cause, drain fluid w/pericardial window or pericaridocentesis

Front 44

Pericardial tamponade description
etiology

Back 44

severe effusion that limits diastolic filling and reduces CO
• Etiology: same as effusion, trauma is a more common cause

Front 45

Pericardial tamponade presentation -

Back 45

symptoms of fatigues, dyspnea, syncope, shock
o Beck’s triad: hypotension, JVD, distant heart sounds
o Pulsus paradoxus: >10mmHg decrease in systolic blood pressure on inspiration
o Kussmaul’s sign: jugular venous pressure rises with inspiration
• Normal physiology: inspiration causes ↓intrathoracic pressure, which draws blood into the right heart → ↓jugular venous pressure

Front 46

Pericardial tamponade diagnosis and treatment -

Back 46

• Diagnosis: Echo
• Treatment: Echo guided perciardiocentesis or pericardial window

Front 47

Constrictive pericarditis -
Etiology/Presentation

Back 47

thick/fibrotic pericardium, constricting the heart leading to heart failure
• Etiology: idiopathic, post-surgical, radiotherapy, infectious
o Often develops after episode of subacute pericarditis with effusion
o Differential dx: restrictive cardiomyopathy, right heart failure, tamponade
• Presentation: symptoms of dyspnea, fatigue, edema (heart failure symptoms!)
o Exam: JVD, Kussmaul’s sign, pulsus paradoxus rare, diastolic pericardial knock

Front 48

Diagnosis and treatment of Constrictive pericarditis -

Back 48

• Diagnosis
o ECG: low voltage
o Imaging: CXR (pericardial calcification), CT/MRI (pericardial thickening)
o Hemodynamic studies: looking at pressures in the heart
• Treatment: pericardiectomy

Front 49

Tetrology of Fallot -

Back 49

1) Pulmonic stenosis, 2) RVH, 3) Overriding aorta, 4) VSD
• Mechanism: pulmonary stenosis leads to RVH, while aorta overrides the VSD draining both ventricles
o Note: degree of pulmonary stenosis determines the severity of shunt
• CXR: boot shaped heart (due to RVH)
• Presentation: “tet spells” – child suffers from cyanotic spells and squats to improve their symptoms (squatting compresses femoral arteries, thus increasing systemic resistance and reversing the R to L shunt, allowing blood to be directed towards lungs)

Front 50

Transposition of great vessels -

Back 50

aorta drains the RV and pulmonary trunk drains the LV; not compatible with life unless there is a protective shunt (VSD, PDA, PFO)
• Mechanism: failure of aorticopulmonary septum to spiral during embryology
• CXR: egg on side appearance
• Treatment: requires surgical correction

Front 51

Truncus arteriosus -

Back 51

no division between the aorta and pulmonary arteries

Front 52

Tricuspid atresia -

Back 52

no valve formation, thus no communication between RA and RV, requires multiple protective shunts (ASD/VSD & PDA)

Front 53

Total anomalous pulmonary venous return:

Back 53

pulmonary veins connect to systemic venous system rather than the L atrium, requires protective shunt (ASD, PFO)

Front 54

Ventricular septal defect (VSD) -

Back 54

most common congenital heart disease, usually in membranous portion, but defect may be in membranous or muscular septum
• Presentation: muscular defects usually close spontaneously & often asymptomatic, but if they do not, you will hear a harsh holosystolic murmur
• Association: Down’s syndrome, congenital rubella, cri du chat, Edward’s, Patau

Front 55

Atrial septal defect (ASD) -

Back 55

usually ostium secundum, may be ostium primum or foramen ovale
• Presentation: usually asymptomatic; may give paradoxical emboli; fixed split S2
• Association: Fetal alcohol syndrome, Down’s syndrome

Front 56

Patent ductus arteriosus (PDA) -

Back 56

during embryology ductus arteriosus is necessary to shunt blood from pulmonary artery to the aorta; PDA when shunt remains
• Keep it Patent with Prostaglandin E2 in those that need the shunt (ie transposition)
• Closed with indomethacin (or any other NSAID that inhibits prostaglandin formation)
• Presentation: Continuous machine like murmur, loudest at time of S2

Front 57

Eisenmenger’s syndrome:

Back 57

uncorrected L to R shunts (VSD, ASD, PDA), which leads to progressive pulmonary HTN → when pulmonary resistance is higher than systemic resistence, the shunt reverses, resulting in a R to L shunt → late cyanosis, clubbing, polycythemia

Front 58

Coarctation of aorta -

Back 58

narrowing of the aorta distal to the L subclavian artery
• Presentation
o Upper extremity HTN (elevated pressures proximal to narrowing), with risk of aortic regurgitation and berry aneurysms
o Lower extremity hypotension (decreased pressures distal), with claudication
• CXR: rib notching (intercostal arteries work as collaterals and hypertrophy)
• Infantile type: associated with Turner’s syndrome; coarctation proximal to insertion of ductus arteriosus
• Adult type: coarctation distal to ductus arteriosus

Front 59

Anomalous coronary arteries -

Back 59

defect in origin or drainage of a coronary artery
• Variable presentation and prognosis, depending on the coronary artery involved and the extent of the defect
• Consider in the differential of a young adult presenting with syncope or sudden death, or in a newborn with cyanosis and other defects are ruled out