Pericardial tamponade

My DDU point form notes on pericardial tamponade…

The rest of my DDU notes are here.

Effusion size

separation seen only in systole = normal or trivial effusion
present in systole and diastole >50ml (small)

end diastolic measurements are more predictive if the effusion is circumferential

adapted from Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013;26:965–1012.e15

Pericardium

sac surrounding heart, great arteries, pulmonary veins and vena cavae

2 layers

outer layer

fibrous

merges with adventitia of aorta, pulmonary artery

attached to vertebra, diaphragm and sternum

inner layer

serous

1 layer of mesothelial cells on top of epicardial fat

forms parietal and visceral pericardium

reflections → sinuses

blind ending

oblique sinus

behind LA

boundaries

upper: pericardial reflection to upper pulmonary veins

left and right: pericardial reflections to left and right pulmonary veins (and vena cavae)

transverse sinus

above pulmonary vein reflection

boundaries

anterior: great arteries

posterior: LA roof

pericardial fluid

10-50 ml
ultrafiltrate of plasma
usually drains to thoracic duct and R lymphatic duct

lymphatic blockage or ↑ CVP → pericardial fluid accumulates

normally small capacitance → small ↑ volume tolerated then ↑ pressure

cf chronic volume overload → ↑ capacitance markedly

roles of pericardium

stops spread of infection / malignancy
↓ friction
mediates ventricular interaction

e. g. (in dogs) fluid loading → ↑ RV volume → ↓ LV compliance – abolished by pericardiectomy

Echo of pericardium

covers whole heart so seen in all windows

PLAX usually adequate except postoperatively

normally space not seen, except in posterior pericardial space during systole
pericardial thickening better defined on CT / MRI

protocol

full 2D examination initially re ASD, RV hypertrophy etc (modifies signs of tamponade)
location, volume, characteristics e.g. strands, adhesions, slow moving contrast of pericardial fluid

in postoperative patients, detailed search including localized chamber compression

long loops (covering respiratory cycle) of

2D and M-mode of

RA and RV free walls

IVC (with sniff also)

PWD of

tricuspid and mitral inflow

pulmonary and hepatic veins

TDI (S’, E’, A’) of mitral annulus (medial and lateral)

effusion

causes

neoplasia: 2° or 1°
trauma / surgery
infection: bacterial, viral, fungal, parasitic
systemic inflammation: RA, SLE, systemic sclerosis, Reiter’s
metabolic: renal failure, ↓ T₄, Addison’s
radiation, asbestosis

echo features

1st seen in oblique sinus posterior to LV (PLAX best)
circumferential at ~100 mL

↑ echogenicity → suggest inflammation
d/dx ≥ 5% of patients have anterior and posterior echo free space

L pleural effusion: behind DAo

epicardial fat: prominent anteriorly, speckled not anechoic, moves with heart, commoner in elderly, obese female diabetics

Tamponade: key findings

effusion

↑ IVC diameter

seen in >90% of cases, but nonspecific
IVC > 2.1 cm with <50% inspiratory collapse

↑ hepatic vein diameter

↓ LV end-diastolic and end-systolic dimensions

since LV mass unchanged, appears “hypertrophied”

↓ SV and ↓ CO on Doppler

cf lesser findings…

Chamber collapse during relaxation phase

precedes pulsus paradoxus, M mode ideal, absence of collapse has >90% NPV for clinical tamponade, loculated collection may affect L chambers first

RA

near peak of R wave (systolic)
> 1/3 of cardiac cycle ~100% sensitive and specific for clinical tamponade

cf brief inversion can be normal

RV

after end of T wave (early diastole)
initially seen only during inspiration (lowers R heart pressures) then throughout cycle
longer collapse → more severe
usually precedes BP ↓

collapse not seen when ↑ R heart pressures prior to tamponade

RVH, severe pulmonary HT, severe LV failure

cf collapses earlier in course if hypovolaemic

Respiratory variation

not a standalone criterion – changes below are seen with inspiration (opposite in expiration):

↑ RV and ↓ LV size

→ inspiratory bulge or “bounce” of IVS into LV

confirmatory only as seen in other conditions with pulsus paradoxus eg. marked dyspnoea, COPD, PE

not seen if LVH, pre-existing ↑ LV filling pressures

Doppler velocities

↑ tricuspid and pulmonary

>60% respiratory variation in tricuspid = diagnostic

↓ mitral and aortic

cf normal Δ in peak mitral E ~5%

> 30% inspiratory ↓ on first beat of inspiration considered diagnostic – for example from Bonita – confirmed in Klein et al:

if transmitral E velocity on the first beat of inspiration is 65 cm/s and 95 cm/s on the first beat of expiration

% Δ

=(1st expiration – 1st inspiration) / 1st expiration

= (95 – 65) / 95

= 30%

cf for transtricuspid, same calculation but result is -ve

can use CWD instead of PWD if cardiac motion troublesome

↑ IVRT as well

low hepatic vein velocities…

normal: 50cm/s, S > D, both increasing with inspiration
effusion: ↓ velocities (~20-40 cm/s), S even > D

because D parallels E cf S relates to ventricular descent which “makes room” in atria

moderate tamponade: often no D except on inspiration
marked tamponade: no D at all
prearrest: no S or D except on inspiration

with large expiratory reversals

D wave flow reversed

constriction vs restriction tricky! See Ch 28 in The Practice of Clinical Echocardiography 4th Ed (Otto et al)

Cover image: Pericardial fluid drainage from kiwicardiology.com