Constrictive pericarditis Flashcards
Pathophys of pericardial dz
constrictive or restrictive
o Impaired cardiac filling
o ↑ atrial pressures
- Constrictive physiology: ↑atrial pressure with steep X and Y descent on pressure waveforms
- Usually, these disease processes will lead to R sided CHF
o Systemic capillaries will leak at 10-15mmHg
o Pulmonary capillaries will leak at 30mmHg
Hemodynamic criteria for constrictive pericardial dz
o Equalization of ventricular pressure
o Abrupt cessation of ventricular filling in early diastole
o Restriction of further filliing → plateau of diastolic L/RVP
Etiology constrictive pericarditis
- Parietal/visceral pericardium fused or fibrosed
o ↓ compliance
o Constriction is uniform → all chambers involved equally
↓ diastolic volume
↑ atrial and ventricular filling P
Pressure waveform: RA and LA
- ↑RAP and PCWP (LAP)
o Magnitude of ↑ determined by degree of constriction
Moderate 12-15mmHg
Severe 20-25mmHg
o RAP = PCWP in pure constriction
If significant MR: PCWP > RAP
Equalization of PCWP, RAP, LAP, PAP, RVP, LVP, - Atrial pressure waveform: W shape
o Rapid filling in early diastole
Steep Y descent
o Atrial contraction → ↓ atrial volume
Steep X descent
Pressure waveform RV
Dip and plateau = square root sign
o Rapid, normal early ventricular filling
o Abrupt cessation in mi diastole when limit of ventricular distensibility is reached
Plateau: little additional volume expansion occurs
Respiratory pressure variation
o Inspiratory ↓ R sided pressure does not occur
↓ or absent flow in Ca/CrVC
Non compliant pericardium limit transmission of intrathoracic pressures to the heart
What is Kussmaul’s sign
Inspiratory ↑ in RAP/venous pressures (normally decreases)
DDX for kussmaul sign
- RV infarction
- R sided CHF
- Cardiac tumors
- TV stenosis
- Pulmonary embolism
What is pulsus paradoxus
Exaggeration of physiologic phenomenon
↑ pulse pressure in expiration
Why does pulsus paradoxus happen
o Exaggeration of physiologic phenomenon
Manifestation of ventricular interdependence → ↑RV filling in inspiration impairs LV filling since fixed intracardiac volume
o ↑ pulse pressure in expiration due to ↑ LV filling
o >10% or >10mmHg fall in inspiratory pulse pressure
Pulse may disappear for several beats during inspiration
DDX pulsus paradoxus
Pulmonary: embolism, pneumothorax, asthma, COPD
Non-pulmonary/cardiac: anaphylactic shock, hypovolemia, CrVC obstruction, pregnancy, obesity
Hemodynamic changes with constrictive pericarditis
Pulsus paradoxus
Repsiratory pressure variation
Dip and plateau RV waveform
W RA waveform
Incr RA and PCWP
Decr SV
Pathophys effusive constrictive pericarditis
- Constriction of the heart by pericardium + pericardial fluid accumulation btw visceral and parietal pericardium
o Small volume of effusion → dramatic ↑ in intrapericardial P - Progressive phenomenon as fluid accumulates
o ↑ intrapericardial P will equilibrate RV filling pressures → R sided tamponade
↓CO
↑venous systemic pressures (resistance to venous return)
o Further ↑ will equilibrate LV filling pressures → L sided tamponade
Hemodynamic findings tamponade
o Hemodynamic compromise is proportional to intrapericardial pressure
Pressure rise with fluid accumulation depend on
Volume
Rate of fluid accumulation
* Slow fluid accumulation → ↓CO and systemic congestion
o Can accommodate larger amount of fluid
* Sudden fluid accumulation → can develop acute cardiogenic shock
o Small volume can cause c/s
Physical nature of pericardium
* Normally holds 2.5-15ml
* Can accommodate 50-150ml w/o significant change in P