ICL 5.6: Clinical Pericardial Diseases

Question 1

what are the two layer of the pericardial sac?

Answer 1

rigid, avascular fibrous sac made of 2 layers?

1. outermost fibrous pericardium
2. inner serous pericardium (parietal and visceral layers)

Question 2

what is the function of the pericardium?

Answer 2

1. a barrier to infection
2. limits distention of cardiac chambers
3. fluid between the pericardial layers reduces the friction between the myocardium and surrounding structures

Question 3

how much fluid is in the pericardium?

Answer 3

15-50 mL

Question 4

what are the causes of acute pericarditis?

Answer 4

1. infectious
2. radiation
3. injury
4. drugs/toxins
5. metabolic
6. malignancy
7. collagen vascular disease
8. immune mediated

Question 5

what is the clinical presentation of acute pericarditis?

Answer 5

1. “flu like” or GI symptoms early on
2. sharp, pleuritic chest pain – worst by laying flat and relieved by leaning forward
3. EKG changes
4. friction rub at left sternal border
5. pericardial effusion

Question 6

what helps with the pain seen with pericarditis? why?

Answer 6

sharp pain that’s worst by laying flat and relieved by leaning forward

inflammation of the nerves that supply the pericardium and with gravity, the inflammation and gravity is placed on the nerves which are posteriorly located

when the person sits forward, some of the pressure/inflammation is taken off the pericardial space

Question 7

how do you differentiate between a pleural vs. pericardial friction rub?

Answer 7

ask the patient to hold their breath

pleural friction rub will stop because they’re not breathing and lungs aren’t causing friction

pericardial friction rub will persist

Question 8

what EKG changes are consistent with acute pericarditis?

Answer 8

ST elevation diffusely in all leads

also PR depression early in the course of pericarditis

but the one exception is aVR has PR elevation and ST depression

in later stages the ST normalizes and there’s T wave inversions

Question 9

what are the PE findings during routine evaluation of acute pericarditis?

Answer 9

1. pericardial rub
2. diffuse ST elevation and PR depression
3. pericardial effusion with or without tamponade on echo
4. CXR is usually normal but you may see cardiomegaly “water bottle” heart shadow indicative of pleural effusions
5. inflammatory marker elevation = ESR, CRP, WBC
6. markers of myocardial necrosis* = troponin and CKMB

Question 10

how do you diagnose acute pericarditis?

Answer 10

2+ criteria:

1. characteristic chest discomfort = persistent, pleuritic and positional
2. suggestive EKG changes
3. pericardial friction rub
4. new or worsening pericardial effusion

Question 11

what would indicate that acute pericarditis needs to be treated in hospital?

Answer 11

most cases can be managed in the outpatient setting but sometimes hospitalization is needed if:

2. high fever
3. subacute onset
4. large pericardial effusion
5. signs of tamponade
6. signs of myocarditis
7. immunosuppressed patient because infection can spread

Question 12

how do you treat acute pericarditis?

Answer 12

symptom relief and decrease inflammation via:

1. NSAIDs/salicylates – add aspirin if underlying CAD
2. colchicine (3 months) – great anti-inflammatory properties and also big reduction in recurrent pericarditis which is a significant problem with acute pericarditis

AVOID glucocorticoids and pericardioectomy –> avoid steroids early on because they have lower rates of recurrent pericarditis

Question 13

what are the potential causes of hemorrhagic pericardial effusion?

Answer 13

1. malignancy
2. surgery/procedure complication
3. post-pericardiotomy syndrome
4. complications of MI
5. idiopathic
6. aortic dissection
7. infection (TB)

Question 14

what is the biggest risk factor of an effusion causing cardiac tamponade?

Answer 14

the rate of fluid accumulation

if a small effusion accumulates in minutes that can lead to tamponade very quickly as opposed to a large effusion that has gradually accumulated over weeks or months

this is because when there’s fluid around the chambers, it can cause pressure; the pericardium has a degree of elasticity and it has a limit; once you reach the limit there’s the potential for tamponade and chamber compression –> depending on how fast you ask the pericardium to stretch you may get tamponade immediately or later on if it’s an effusion that happens over time

Question 15

what are the symptoms of cardiac tamponade?

Answer 15

1. dyspnea
2. chest discofort or fullness
3. peripheral edema
4. fatiguability
5. sinus tachycardia
6. JVD
7. pulsus paradoxus
8. instant heart sounds
9. clear lung fields
10. hypotension

Question 16

what are the EKG changes seen with pericardial effusions?

Answer 16

1. tachycardia
2. electrical alternans = QRS complexes are small then big and they alternate every beat

the heart is shining back and forth in the large pericardial effusion and that leads to the QRS variation

Question 17

what is the pathophysiology of pericardial tamponade?

Answer 17

1. changes in systemic venous return

venous return is bimodal and peaks during systole and early diastole – compression effects cardiac volume and the venous return is shifted to systole as diastolic return decreases

2. respiratory variation in venous return

venous return increases with inspiration due to decline in thoracic pressure – if there’s a pericardial effusion that limits the amount of space the heart has to expand, the right ventricle is limited by the rigid pericardium/effusion which leads to internal building of the interventricular septum into the already underfilled LV which decreases SV and CO and BP –> this causes pulsus paradoxus

Question 18

what is the mechanism of pulsus paradoxus?

Answer 18

inspiration leads to increased venous return so the RV increases in volume which leads to bulging of the septum into the LV with decreased LV filling, decreased aortic flow, and signs of hypotension

but then during expiration, flow to the LV increases and the septum is free to go back to the middle and pressure increases which leads to a relative increase in BP

this is the mechanism of pulsus paradoxus!

Question 19

what is the clinical definition of tamponade?

Answer 19

hypotension 10+
mmHg fall between inspiration and expiration

there’s also elevated venous pressure with blunted or absent y descent

Question 20

what is Beck’s traid?

Answer 20

1. hypotension
2. muffled heart sounds
3. JVD

pathoneumonic for cardiac tamponade

Question 21

what conditions can cause pulsus parades?

Answer 21

1. respiratory
   - severe bronchial astham
   - tension pneumothorax
   - COPD
2. cardiac
   - cardiac tamponade

• constrictive pericarditis
• pericardial effusion
• restrictive cardiomyopathy

3. other
   - anaphylactic shock

• obesity

Question 22

how do you treat pericardial effusion with tamponade?

Answer 22

urgent pericardiocenesis

accomplished percutaneously rather than surgically

so use a needle guided by echo to remove fluid

IV fluids help improve CO but it’s just a temporary fix; do NOT give diuretics because it’ll decrease preload

Question 23

what is constrictive pericarditis?

Answer 23

it’s a thickened, rigid pericardium that restricts cardiac chamber enlargement

Question 24

what are the causes of constrictive pericarditis?

Answer 24

1. idiopathic
2. viral
3. post-cardiac surgery
4. post-radiation therapy
5. connective tissue disorder
6. post infectious like tuberculosis or purulent pericarditis
7. other: malignancy, trauma, drugs, asbestosis, sarcoidosis, uremic pericarditis

Question 25

what is the risk of pericarditis evolving into constrictive pericarditis?

Answer 25

tuberculosis and pericarditis are the most likely to advance to constrictive pericarditis

when a person has pericarditis caused by TB or purulent pericarditis, you need to be careful that it doesn’t progress to constrictive

Question 26

what is the clinical presentation of constrictive pericarditis?

Answer 26

related to fluid overload:
1. peripheral edema

2. anasarca

diminished CO
3. DOE

4. fatigability
5. dyspnea

PE
1. JVD

2. pulsus paradoxus
3. Kussmaul’s sign
4. pericardial knock

Question 27

what is kussmaul’s sign?

Answer 27

lack of inspiratory decline in JVP – normally your venous pressure should go down during inspiration because you’re filling the RA

seen in constrictive pericarditis

Question 28

what is pericardial knock?

Answer 28

sound earlier than S3 and with higher frequency that corresponds to the sudden cessation of ventricular filling

it’s a sign of constrictive pericarditis

Question 29

what imaging do you use for constrictive pericarditis?

Answer 29

1. CXR
2. echo/doppler

shows us exaggerated changes in hemodynamics across mitral and tricuspid valves that tell us the degree of inter ventricular filling

3. CT/MR**: this is the modality of choice

Question 30

what is the treatment of constrictive pericarditis?

Answer 30

1. diuretics

occurs over years/months and they’re more hemodynamically stable so if they have signs of HF due to diastolic dysfunction/HFpEF you can try diuretics – do NOT give diuretics to acute pericarditis

2. surgery = pericardiectomy

Question 31

what is effusive constrictive disease?

Answer 31

on presentation they have tamponade initially and once you treat them with percardiocentesis they have clinical symptoms of constriction

so effusion –> constrictive pathology