Introduction

Pericardial disease is potentially

curable
Pericardial diseases Spectrum of the disease is determined
by epidemiological setting of patient
Western countries largely idiopathic
Developing countries tuberculous
But there are a large number of
diseases that can cause it.

What is it? Where is it?

Fibrous sac surrounding heart-

heart-dense Surrounds the heart
network of collagen fibres
Continuous with the great arteries and
Serous membrane two continuous layers
the diaphragm
separated by a small amount of fluid
lubricant (10-
(10-20mls straw coloured)
Layers are called visceral and parietal
Visceral is inner layer (epicardium)
Parietal is continuous with diaphragm and outer
walls of great arteries

What is its function? Pericardial Physiology

Stabilises the position of the heart not needed to sustain life

within the chest physiologic functions
Prevents friction between the moving limit cardiac dilatation
heart and adjacent structures maintain normal ventricular compliance
Allows for small acute changes in size reduce friction to cardiac movement
and shape but limits ventricular filling barrier to inflammation
(not the case in chronic setting) limit cardiac displacement

1
 Pericardial disease

May be primary and acute

or
Acute pericarditis
Chronic
- Constrictive
- Effusive
- Or constrictive-
constrictive-effusive

Review of aetiology, incidence and

Causes
pathogenesis of pericarditis
Aetiology Incid Pathogenesis
Acute pericarditis is either dry, fibrinous or effusive,
independent from its aetiology. (%)
Idiopathic (idio and pathy) 86% Infectious Multiplication and spread of
Infective (viral or bacterial) 7% pericarditis the causative agent and
Following a myocardial infarction or cardiac surgery Viral (Coxsackie 3050 release of toxic substances
(Dresslers syndrome) A9, B1-4, Echo in pericardial tissue cause
Radiation therapy 8, Mumps, EBV, serous, serofibrinous or
Neoplastic disease (commonly lung or breast) 6% CMV, Varicella, haemorrhagic (bacterial,
Rubella, HIV, viral, tuberculous, fungal) or
Connective tissue disease
Parvo B19...) purulent inflammation
(bacterial).

Review of aetiology, incidence and

Review of aetiology, incidence and
pathogenesis of pericarditis
pathogenesis of pericarditis
Aetiology Incid. Pathogenesis
Aetiology Incid. Pathogenesis %
%
Infectious Multiplication and spread
Infectious Multiplication and spread pericarditis of the causative agent and
pericarditis of the causative agent and release of toxic substances
Fungal (Candida, Rare
Bacterial (Pneumo- 510 release of toxic substances in pericardial tissue cause
Histoplasma...)
, Meningo-, in pericardial tissue cause serous, serofibrinous or
serous, serofibrinous or Parasitary Rare
Gonococcosis, haemorrhagic (bacterial,
haemorrhagic (bacterial, (Entameba
Hemophilus, T. histolytica, viral, tuberculous, fungal)
pallidum,Borreliosi viral, tuberculous, fungal) or purulent inflammation
or purulent inflammation Echinococcus,
s, Chlamydia, (bacterial).
(bacterial). Toxoplasma...)
Tuberculosis...)

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Review of aetiology, incidence and Review of aetiology, incidence and
pathogenesis of pericarditis pathogenesis of pericarditis
Aetiology % Pathogenesis Aetiology % Pathogenesis
Pericarditis in systemic Cardiac manifestations of the Type 2 (auto)immune Secondary, after
autoimmune dis. basic disease, often clinically process infection/surgery
Systemic LE mild or silent. Rheumatic fever Mostly in acute phase
30 2050
Rheumatoid arthritis Postcardiotomy syndrome 20 1014 days after surgery
30
Spondylitis ankylosans Postmyocardial infarction 15 DDg P. epistenocardica
1 syndrome
Systemic sclerosis
> 50 Autoreactive (chronic)
Dermatomyositis 23.1 Common form
Rare pericarditis
Periarteritis nodosa
Rare
Reiters syndrome
2
Familial Medit. fever
0.7

Review of aetiology, incidence and Review of aetiology, incidence and

pathogenesis of pericarditis pathogenesis of pericarditis
Aetiology % Pathogenesis Aetiology % Pathogenesis
Pericarditis and PE in Pericarditis in
diseases of surrounding metabolic disorders
organs
Renal insufficiency Frequent Viral/toxic/autoimmune
Acute MI
520 15 days after transmural (uraemia) Serous, cholesterol rich PE
(P.Epistenocardica)
30 MI Myxedema 30 Membranous leak?
Myocarditis
Rare Accompanying Addisons disease Rare
Aortic aneurysm
Lung infarction Rare epimyocarditis Diabetic ketoacidosis Rare
Pneumonia Rare Dissection: haemorrhagic Cholesterol pericarditis Very rare Transudation of
Oesophageal diseases Rare PE cholesterol (sterile
Hydropericardium in CHF Rare serofibrinous PE)
Paraneoplastic pericarditis Frequent No direct neoplastic infiltrate

Review of aetiology, incidence and Review of aetiology, incidence and

pathogenesis of pericarditis pathogenesis of pericarditis
Aetiology % Pathogenesis Aetiology % Pathogen.
Traumatic pericarditis Neoplastic pericardial disease
Direct injury (penetrating Rare Primary tumours Rare
thoracic injury, oesophageal Secondary metastatic tumours Frequent
40 Serous or
Lung carcinoma
perforation, foreign bodies) Less frequent after fibrinous,
Breast carcinoma 22
Indirect injury (Non- Rare introduction of Accomp. dis. during the infiltr. of malign. cells frequently
penetrating thoracic injury, topical convergent Gastric and colon 3 haemorrhagic
mediastinal irradiation) irradiation Other carcinoma 6 effusion
Leukemia and lymphoma 15
Melanoma 3
Sarcoma 4
7
Other tumours

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Review of aetiology, incidence and
pathogenesis of pericarditis
Aetiology % Pathogenesis
Idiopathic 3.5, Serous or fibrinous,
in other frequently haemorrhagic
series >50 effusion
Serous, fibrinous,
sometimes haemorrhagic
PE with suspect viral or
autoimmune secondary
immunopathogenesis
Pericardial Inflammation
pathogenesis
Contiguous spread
lungs, pleura, mediastinal lymph nodes,
myocardium, aorta, esophagus, liver
Hematogenous spread
septicemia, toxins, neoplasm, metabolic
Lymphangetic spread
Traumatic or irradiation

Pathophysiology Pathophysiology
Significantly increased intrapericardial Normal difference in diastolic
pressure impedes diastolic filling of the
ventricles pressures between RV and LV is lost
Therefore in order for the ventricles to fill As the pericardial effusion worsens the
the end-
end-diastolic pressure must exceed the
pericardial pressure EDP cannot raise significantly to
Global effusion pericardial pressure is maintain cardiac output
equal around heart
Therefore both ventricles have to increase
EDP to same amount for ventricles to fill

Pericardial Inflammation Signs, Symptoms and

pathology Investigations
inflammation provokes a fibrinous Think about how an inflamed, thickened
exudate with or without serous pericardium might affect the hearts
effusion function how can we diagnose this?
the normal transparent and glistening Clinical examination
pericardium is turned into a dull, Auscultation
opaque, and sandy sac Chest x-
x-ray
can cause pericardial scarring with ECG
adhesions and fibrosis
Echo
Catheter laboratory investigations

4

Clinical Examination
pericarditis vs infarction
Retrosternal or left precordial chest pain (radiates
to the trapezius ridge, can be pleuritic or simulate
ischaemia, and varies with posture)
Retrosternal chest pain sharp worse on insp and
lying flat
Non-productive cough
Shortness of breath.
Friction rub (high pitched scratching noise)
Raised jugular venous pressure
Chest Pain History
Common characteristics
retrosternl or precordial with radiation to
the neck, back, left shoulder or arm
Special characteristics (pericarditis)
pericarditis)
more likely to be sharp and pleuritic
with coughing, inspiration, swallowing
worse by lying supine, relieved by sitting
and leaning forward

Heart sounds of Clinical signs differential

Pericarditis diagnosis - pleurisy
Pericardial friction rub is pathognomic Pleuritic pain has similar sharp quality
for pericarditis but is usually more specific in location
scratching or grating sound Pleural rub is heard over the area
Classically three components:
components: where the pain occurs
presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after A2P2)

ECG (acute pericarditis)

Convexly elevated J-ST segment and PR depression

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 Acute Pericarditis ECG differential diagnosis
ECG features - MI
ST-
ST-segment elevation What leads is the ST elevation in?
reflecting epicardial inflammation What shape is the elevation?
leads I, II, aVL,
aVL, and V3-
V3-V6
lead aVR usually shows ST depression
Are there Q waves?
ST concave upward Do the ST T changes evolve with time?
ST in AMI concave downward like a dome History of the patient
PR segment depression (early stage) Cardiac enzymes etc
T-wave inversion But remember that you can get more than
occurs after the ST returns to baseline one pathology at the same time!

Diagnostic pathway and sequence of Diagnostic pathway and sequence of

performance in acute pericarditis (level of evidence performance in acute pericarditis (level of evidence
B for all procedures) B for all procedures)

Obligatory (indication class I) Obligatory (indication class I)

Auscultation - Pericardial rub (mono-, bi-, or triphasic) Echocardiography
ECG
Effusion types B-D (Horowitz)
Stage I: anterior and inferior concave ST segment elevation.
PR segment deviations opposite to P polarity.
Signs of tamponade
Early stage II: ST junctions return to the baseline, PR
deviated.
Late stage II: T waves progressively flatten and invert
Stage III: generalised T wave inversions
Stage IV: ECG returns to prepericarditis state.

Horowitz Cath lab-

lab- diastolic equalization of
classification of PE.
Type A, no effusion; left and right heart pressures
Type B, separation of
epicardium and pericardium
(316 ml=13 mm);
Type C 1, systolic and
diastolic separation of
epicardium and pericardium
(small effusion >15 ml 1
mm in Diastole);
Type C 2, systolic and
diastolic separation of
epicardium and pericardium
with attenuated pericardial
motion;
Type D, pronounced
separation of epicardium and
pericardium with large echo-
free space;
Type E, pericardial
thickening (>4 mm).

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High RA pressures
Diagnostic pathway and sequence of
performance in acute pericarditis (level of evidence
B for all procedures)
Obligatory (indication class I)
Chest X-ray
Ranging from normal to water bottle heart
shadow.
Revealing additional pulmonary/mediastinal
pathology.
Diagnostic pathway and sequence of
performance in acute pericarditis (level of evidence
B for all procedures)
Mandatory in tamponade (indication class I),
optional in large/recurrent effusions or if
previous tests inconclusive (indication class IIa)
in small effusions (indication class IIb)
Pericardiocentesis and drainage
PCR and histochemistry for aetiopathogenetic
classification of infection or neoplasia
Diagnostic pathway and sequence of
performance in acute pericarditis (level of evidence
B for all procedures)
Obligatory (indication class I)
Blood analyses
(a) ESR, CRP, LDH, leukocytes (inflammation
markers).
(b) Troponin I, CK-MB (markers of myocardial
lesion).
CXR
Cardiomegaly
Pleural Effusions
Analyses of pericardial
effusion
Analyses of pericardial effusion can establish
the diagnosis of viral, bacterial, tuberculous,
fungal, cholesterol, and malignant pericarditis.
Cytology and tumour markers
(carcinoembryonic antigen (CEA), a-feto protein
(AFP), carbohydrate antigens CA 125, CA 72-4,
CA 15-3, CA 19-9, CD-30, CD-25, etc.) should
be performed in suspected malignant disease.
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 Analyses of pericardial
effusion
In suspected tuberculosis acid-fast bacilli
staining, mycobacterium culture or radiometric
growth detection (e.g., BACTEC-460),
adenosine deaminase (ADA), interferon (IFN)-c,
pericardial lysozyme, and as well as PCR
analyses for tuberculosis should be performed
(indication class I, level of evidence B).
Differentiation of tuberculous and neoplastic
effusion is virtually absolute with low levels of
ADA and high levels of CEA.
Analyses of pericardial
effusion
Purulent effusions with positive cultures have
significantly lower fluid glucose levels (47.3 25.3 vs.
102.5 35.6 mg/dl) and fluid to serum ratios (0.28
0.14 vs. 0.84 0.23 mg/dl), than non-infectious
effusions.
WBC is highest in inflammatory diseases, particularly
of bacterial and rheumatologic origin.
A very low WBC count is found in myxedema.
Diagnostic pathway and sequence of
performance in acute pericarditis (level of evidence
B for all procedures)
Optional or if previous tests inconclusive
(indication class IIa)
CT - Effusions, peri-, and epicardium
MRI - Effusions, peri-, and epicardium
Pericardioscopy, pericardial biopsy -
Establishing the specific aetiology
Analyses of pericardial effusion
In suspected bacterial infection at least three cultures
of pericardial fluid for aerobes and anaerobes as well
as the blood cultures are mandatory (level of evidence
B, indication class I).
PCR analyses for cardiotropic viruses discriminate viral
from autoreactive pericarditis (indication class IIa,
level of evidence B).
Analyses of the pericardial fluid specific gravity
(>1015), protein level (>3.0 g/dl; fluid/serum ratio
>0.5), LDH (>200 mg/dL; serum/fluid >0.6), and
glucose (exudates vs. transudates = 77.941.9 vs.
96.1 50.7 mg/dl) can separate exudates from
transudates but are not directly diagnostic (class IIb).
Analyses of pericardial
effusion
Monocyte count is highest in malignant and effusions
in hypothyroidisms (79 27% and 74 26%), while
rheumatoid and bacterial effusions have the highest
proportions of neutrophils (78 20% and 69 23%).
Compared with controls, both bacterial and malignant
pericardial fluids have higher cholesterol levels (49
18 vs. 121 20 and 117 33 mg/dl).
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 Tx of Recurrent Effusions

Pericardectomy

Pericardial-
Pericardial-peritoneal shunt

Pericardiodesis - Steroids, tetracycline,

or anti-
anti-neoplastic drugs administered
into the pericardial space sclerosis
of the pericardium

Prognosis

Pericarditis is usually a benign disorder

Diagnosis relates to underlying cause
But any cause can lead to an effusion
and tamponade which can lead to
death
Pericarditis can also progress to
pericardial constriction and heart
failure

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 Causes

Tuberculous constrictive pericarditis was

common cause of constriction pre 1960
decline in incidence.
Chronic constrictive Post-
Post-radiotherapy constriction features
pericarditis prominently today along with post-
post-surgical
causes.
Needs to be differentiated from restrictive
cardiomyopathy when making diagnosis.

Pathogenesis Pathogenesis

4 Stages in TB constrictive pericarditis

Absorptive
Do not necessarily occur in order or individually
50% of patients will reabsorb this fluid without
Dry
treatment
Inflammatory process thought secondary to
hypersensitivity reaction to tuberculoprotein Constrictive

Effusive Healing with fibrosis and calcification and

Serosangiouness fluid with leukocytes and
high protein and tubercle bacilli found in low
concentration
Pressures consistent with cardiac tamponade
are found
overall thickening of visceral pericardium
Pressures consistent with constrictive
pericarditis are found
Patients who have continued elevation of
pressures after pericardiocentesis have
effusive-
effusive-constrictive pericarditis

Pathogenesis Constrictive Pericarditis

Physical Findings
Constriction of pericardium results in elevation
and equilibrium of all 4 cardiac chambers Jugular veins
In early diastole, when intracardiac volume is prominent X and Y descent
less than stiff pericardium, diastolic filling is with inspiration (Kussmauls
(Kussmauls sign)
unimpeded and early diastolic filling abnormally Lungs - possible pleural effusion
rapidly because venous pressure is elevated. Heart - diastolic pericardial knock
Rapid early diastolic filling is abruptly halted Abdomen: ascites,
ascites, pulsatile liver
when the intracardiac volume reaches the limit Extremities: peripheral edema
set by the noncompliant pericardium.

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 Kussmauls sign
Normal subjects inspiration causes a
decrease in chest pressure. Increase in
venous return JVP falls
Constrictive pericarditis Increased
venous return cannot be
accommodated in RV because of high
EDP
So JVP rises on inspiration
CXR
Normal or mildly enlarged cardiac silhouette
Calcification of the pericardium is detected in up to
50% - not specific
A calcified pericardium is not necessarily a
constricted one.
Lateral CXR shows the atrioventricular groove &
the anterior and diaphragmatic surfaces of the
right ventricle.
Pleural effusions are present in about 60 %
Persistent unexplained pleural effusions can be the
presenting manifestation.
CT
Pericardial calcification is best
appreciated on CT
Investigations
As for acute pericarditis;
ECG may not show characteristic ST elevation
CXR may see calcification and helps to rule out
coexisting effusion
Echo to identify haemodynamic effects on heart and
coexisting effusion
Auscultation may reveal a friction rub
MRI/CT scan data about the thickness of the
pericardium. Cine CT is a new technique which also
gives info about the effects of physiology as well.
Constrictive Pericarditis
Pericardial Calcification on CXR
MRI
Normal pericardium appears curvilinear as a low
signal intensity situated between the high signal
intensity of the pericardial and epicardial fat
Normally 1 to 2 mm in thickness - a width of up to
4 mm is not necessarily pathologic.
Small quantities of pericardial fluid may be seen
normally in the superior pericardial recess
(posterior to the ascending aorta).
A pericardial thickness of greater than 4 mm is
considered evidence of constrictive pericarditis in
the appropriate clinical setting.
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 Echocardiography Doppler
mitral valve (MV)
inflow (A) and
Echocardiographic evidence is subtle hepatic vein (HV)
Pericardium, if well imaged, is thickened Doppler velocity
Ventricular cavities are small and contract recording (B) in
vigorously
Diastolic filling terminates abruptly in early diastole
constrictive
(doppler flow analysis) pericarditis.
Doppler echocardiography often shows the high E and small A
dissociation of intrathoracic and intracardiac velocities. Expir E
pressures through respiratory changes in mitral
flow velocities. velocity is 33%
E - A Reversal higher than Inspir

Cardiac catheterization
Elevation and equalization of the diastolic
pressures in all cardiac chambers
Right and left ventricular tracings show an early
diastolic "dip-
"dip-and-
and-plateau "
Right atrial pressure tracing shows a prominent Y
descent
Findings similar to restrictive cardiomyopathies,
(suggested by a right ventricular systolic BP > 60
mm Hg) and LVDP exceeding RVDP by more than
5 mm Hg
Endomyocardial biopsy can distinguish these

Catheter pressures Catheter pressures

Elevated RV diastolic pressure, dip-
dip-and-
and-plateau
waveform ("square root sign"), large P waves
(arrow)
Postoperative decreased RV diastolic pressure
normalization of dip-
dip-and-
and-plateau & P-
P-wave

The plateaued end-diastolic pressure of the right ventricle &

equalization of diastolic pressures in all cardiac chamber

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 Constrictive Pericarditis
Diagnosis
often not recognized in its early
phases by exam, x-
x-ray, ECG, echo
tendency to overlook elevated JVP

subacute chronic
diastolic knock + ++
Kussmauls + ++
paradoxical pulse ++ ++

Management Management (cont)

Chronic constrictive pericarditis is a progressive
irreversible disease
Minority survive for years with modest elevated
JVP and peripheral edema that is controlled by diet
and diuretics.
Drugs that slow HR, eg beta blockers and Ca2+
channel blockers should be avoided as mild sinus
tachycardia is a compensatory mechanism.
The majority of patients become progressively
more disabled and subsequently suffer the
complications of severe cardiac cachexia.
Treatment for constrictive pericarditis is complete
resection of the pericardium.
Attention must also be paid to the presence of
associated right atrial thrombosis, which can
partly obstruct the tricuspid valve and should be
managed with thrombectomy at the time of
pericardiectomy.
Concomitant CABG +/- +/- other
Changes in technique have included the use of
median sternotomy rather than left thoracotomy
CPB controversial

Treatment

Mortality for complete surgical

resection of the pericardium ranges
from 5-
5-16%
Symptomatic improvement in ~90%
Cardiac tamponade
5 year survival rate is 74-
74-87%
depending on co-
co-morbidities pre-
pre-op

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Cardiac tamponade
(complication of pericardial effusion)

This is a clinical diagnosis Occurs when the fluid accumulation around

- It is based upon the patients
symptoms
Investigations may be performed to
confirm the suspected cause of the
symptoms (pericardial effusion).
the heart impairs filling to such an extent that
there is haemodynamic compromise.
It is a medical emergency and must be
treated promptly.
Risk of death depends upon speed of
diagnosis, treatment and underlying cause of
the tamponade.

How much fluid is a

Cardiac Tamponade
problem?
Depends on rate of accumulation and Early stage
compliance of the pericardium mild to moderate elevation of central venous
150ml that accumulated quickly could pressure
cause a problem Advanced stage
1000ml that accumulates very slowly intrapericardial pressure
may be tolerated fairly well ventricular filling, stroke volume
hypotension
impaired organ perfusion

Cardiac Tamponade
Becks Triad
Bedside Diagnosis
Described in 1935 by thoracic surgeon
Claude S. Beck Elevated jugular venous pressure
3 features of acute tamponade Paradoxical pulse
Decline in systemic arterial pressure
Elevation in systemic venous pressure
(e.g. distended neck vein)
A small, quiet heart

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Pulsus
Paradoxus Pulsus Paradoxus
tamponade without pulsus
an exaggerated atrial septal defect
drop in blood aortic insufficiency
pressure with LVH with LVEDP
inspiration
pulsus without tamponade
(>10mmHg)
COPD, RV infarct, pulmonary embolism

Clinical presentation Precipitating factors

Elevated systemic venous pressure Drugs (cyclosporine, anticoagulants,

Tachycardia thrombolytics, etc.), recent cardiac
Pulsus paradoxus surgery, indwelling instrumentation,
blunt chest trauma, malignancies,
Hypotension connective tissue disease, renal
Dyspnoea or tachypnoea with clear failure, septicaemiae
lungs

Electrical alternans
ECG The QRS axis alternates between beats. In this example it is best seen in the
chest leads where the QRS points in different directions!

Can be normal or non-specifically

changed (ST-T wave)
Electrical alternans (QRS, rarely T)
Bradycardia (end-stage)
Electromechanical dissociation (agonal
phase)

15
 Chest X-ray M mode/2D echocardiogram

globular heart Diastolic collapse of the anterior RV-

Enlarged cardiac silhouette with free wall
clear lungs RA collapse, LA and very rarely LV
collapse
increased LV diastolic wall thickness
pseudohypertrophy,
VCI dilatation (no collapse in
inspirium)
swinging heart

Swinging of the heart

Doppler

Tricuspid flow increases and mitral

Large pericardial effusion with swinging of the heart
and collapse of the RA and LA in end diastole (A,
arrows) and diastolic collapse of the RV (B, arrows),
which was consistent with pericardial tamponade.
tamponade.
flow decreases during inspiration
(reverse in expiration)
Systolic and diastolic flows are
reduced in systemic veins in expirium
and reverse flow with atrial contraction
is increased

M-mode colour Doppler Cardiac catheterisation

(1) Confirmation of the diagnosis and quantification of
Large respiratory fluctuations in
mitral/tricuspid flows
the haemodynamic compromise
RA pressure is elevated (preserved systolic x descent and
absent or diminished diastolic y descent)
Intrapericardial pressure is also elevated and virtually
identical to RA pressure (both pressures fall in inspiration)
RV mid-diastolic pressure elevated and equal to the RA and
pericardial pressures (no dip-and plateau configuration)
Pulmonary artery diastolic pressure is slightly elevated and
may correspond to the RV pressure
Pulmonary capillary wedge pressure is also elevated and
nearly equal to intrapericardial and right atrial pressure
LV systolic and aortic pressures may be normal or reduced

16
 Near
equalization
(w/in 5 mm Hg) Cardiac catheterisation
of the RA, RV,
PCWP, RV
diastolic, & LV (2) Documenting that pericardial aspiration is
diastolic followed by haemodynamic improvementg
pressures (3) Detection of the coexisting haemodynamic
RA pressure abnormalities (LV failure, constriction,
tracings show pulmonary hypertension)
diminshed (4) Detection of associated cardiovascular
systolic y diseases (cardiomyopathy, coronary artery
descent disease)

FA-femoral artery

RV/LV angiography
Atrial collapse and small hyperactive Treatment
ventricular chambers
Medical emergency intensive care
Coronary angiography environment needed.
Coronary compression in diastole Oxygen
Volume expansion
Computer Tomography Bed rest with leg elevation
Inotropic drugs if necessary
No visualisation of subepicardial fat along both
ventricles, which show tube-like configuration
and anteriorly drawn atrias

17
Pericardiocentesis Pericardiocentesis

Pericardiocentesis is the definitive

therapy to remove the excessive fluid
Commonly performed in the cath lab
but may be done blind in an intensive
care environment

US Guided-
How is it done?
Pericardiocentesis
Subcostal approach Patient lies on the table with the upper body
Traditional approach
elevated to a 60 degree angle. Limb ECG
leads attached.
Blind
Xyphisternum puncture site is cleaned with
Increased risk of injury to liver, heart
an antiseptic solution and local anaesthetic
Echo guided is injected to numb area.
Left parasternal preferred for needle entry or Patient is instructed to remain still
Largest area of fluid collection adjacent to the Physician inserts a large needle with syringe
chest wall attached into chest wall until pericardial sac
is reached

The needle is then pushed through the

tough pericardial sac (patient may
experience some pain/pressure at this
point)
A guidewire is inserted through the needle
and the needle withdrawn
A catheter can then be passed over the
guidewire and into the pericardial space
This can be used for continuous drainage.

18