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Pericardium is the sac that surrounds the heart
Made up of
- outer fibrous pericardium
- inner serous pericardium (parietal & visceral)
Pericardial fluid :
up to 50 ml of clear plasma ultra filtrate between the two
layers of the serous pericardium
The Normal Pericardium
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Functions
1.Stabilization of the heart within the thoracic cavity by virtue
of its ligamentous attachments -- limiting the hearts motion.
2. Protection of the heart from mechanical trauma and infection
from adjoining structures.
3. The pericardial fluid functions as a lubricant and decreases
friction of cardiac surface during systole and diastole.
4. Prevention of excessive dilation of heart especially during
sudden rise in intra-cardiac volume (e.g. acute aortic or mitral
regurgitation).
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Etiological classification
T = Trauma, Tumour
U = Uremia
M = Myocardial infarction (acute, post)
Medications (hydralazine)
O = Other infections (viral,bacterial, fungal, TB)
R = Rheumatoid, autoimmune disorder
Radiation
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Clinical features- Symptoms
Preceded by fever, malaise and myalgia
Common characteristics of pain
retrosternal or precordial with radiation to the
trapezius ridge, neck, back, left shoulder or arm
Special characteristics of pericardial pain
more likely to be sharp
with coughing, inspiration, swallowing
worse by lying supine, relieved by sitting and
leaning forward
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Clinical features- Signs
Triphasic friction rub is pathognomonic;
scratching or grating sound; evanescent
Best heard in the lower LSB with the patient
sitting and leaning forward
Pericardial rub Pleural rub
Can be heard even after
cessation of breathing
Can be heard only during
inspiration and expiration
Heard mostly over the
sternum or sternal borders
Heard mostly over the
lateral parts of the chest
Intensity doesnt increase
with increased pressure of
the steth
Intensity of rub increases
with increased pressure of
the steth over the chest
wall
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ECG CHANGES
Pericarditis MI Early Repolarisation
ST elevations Concave, Not restricted
to arterial territory.
return to normal within
hours
Convex
Not restricted to arterial
territory.
return to normal within
days
Concave
Not restricted to arterial
territory. ; never return to
normal
ST depression
(Reciprocal)
in avR /V1 More prominent Not present
PR segment
depression
present Not present Not present
QRS changes No such changes Q waves, as well as
notching and loss of R-
wave amplitude)
No such changes
T-wave inversions after ST segment
becomes isoelectric.
usually seen within
hours before the ST
segments have become
isoelectric.
Not present; Tall T wave
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Pericarditis after AMI
Early
Occurs - 1 to 3 days (no more
than a week
due to transmural necrosis
with pericardial inflammation
40% of patients with large, Q-
wave MIs have pericarditis
Benign
aspirin doses (650 mg orally
three or four times per day
for 2 to 5 days) or
acetaminophen is usually
effective
Late (Dressler's Syndrome)
Occurs - 1 week to a few
months after AMI .
autoimmune etiology
3% to 4%.
Polyserositis with pericardial
or pleural effusions
Aspirin , Colchicine .
Prednisone, 40 to 60 mg /d
with a 7- to 10-day taper(If
not responding to treatment
or for recurrent symptoms)
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Etiology- CCP
Idiopathic or viral 42 to 49 %
Post cardiac surgery 11 to 37 %
Post radiation therapy 9 to 31 %
Connective tissue disorder 3 to 7 %
Post infectious (tuberculous or purulent
pericarditis) 3 to 6 %
Miscellaneous causes (malignancy, trauma,
drug-induced, asbestosis, sarcoidosis, uremic
pericarditis) 1 to 10 %
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CCP -Pathophysiology
Consequence of impaired ventricular filling
causes fatigue, muscle wasting, and weight loss
2. Reduced cardiac output : Hypotension/shock, Reflex tachycardia
Riased JVP; Hepatic congestion, peripheral edema, ascites ,
anasarca, and cardiac cirrhosis.
1.Systemic > pulmonary venous congestion
Pericardium Rigid and Scarred > Impaired Ventricular filling-
mainly Early filling > ventricular interdependence
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Physical examination
BP, HR JVP
ascites, edema, hepatomegaly
early diastolic knock
after S2
sudden cessation of ventricular diastolic filling imposed
by rigid pericardial sac
Kussmauls sign
inspiratory increase in JVP
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Kussmauls sign
In Inspiration :
Normal :
RV Volume increases without increase in RA pressure.
In Constrictive pericarditis :
RV volume increases , as the RV cannot expand due to
thickened pericardium ,this results in increase in RA
pressure which causes Elevated JVP in inspiration.
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Evaluation/Investigation
Clinical suspicion followed by confirmation
with certain diagnostic tests
( many patients are initially seen for abdominal
symptoms)
ECG : AF in 1/3rd
of patients
flattened or inverted T waves
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Management
Medical:
Cautious diuretics and salt restriction
Sinus tachycardia is a compensatory mechanism, BB
and CCB that slow the HR should be avoided.
In patients with AF with FVR , digoxin is
recommended as initial treatment to slow the
ventricular rate before resorting to beta blockers or
calcium antagonists. In general, the rate should not
be allowed to drop 80 -90 / min
Definitive treatment : Surgical pericardiectomy
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Definition
Excessive Accumulation of fluid between the visceral
and parietal layers of serous pericardium
Quantification-
Trivial : 50 100 cc
Small : 100 cc
Moderate : 500 cc
Large : 1000 cc
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Etiology
Nature of Pericardial
Fluid
Serous
Transudative CHF , Renal
failure
Suppurative
Pyogenic infection
Hemorrhagic
occurs with any type of
pericarditis
especially with infections and
malignancies
Inciting factor
1. Inflammatory- from infection,
immunologic process.
2. Traumatic- causing bleeding in
pericardial space.
3. Physical- such as:
a. increase in hydrostatic pressure
e.g. congestive heart failure.
b. increase in capillary
permeability e.g. hypothyroidism
c. decrease in plasma oncotic
pressure e.g. cirrhosis.
4. Mechanical- Decreased drainage of
pericardial fluid due to obstruction of
thoracic duct as a result of malignancy or
damage during surgery.
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Clinical features
Usually asymptomatic
Can have symptoms of compression
- dyspnoea, dysphagia, hoarseness of voice,
hiccup, nausea
Signs : muffled heart sounds
paradoxically reduced intensity of rub
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Chest x ray
usually requires >
200 ml of fluid
cannot distinguish
between pericardial
effusion and
cardiomegaly
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Management
Depends on the etiology , presence of
hemodynamic compromise and the volume of fluid.
Medical-
No role for diuretics
Interventional-
Pericardiocentesis is not always necessary.
Pericardiocentesis if
Malignancy or Purulent pericarditis is suspected
Hemodynamic compromise present
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What is Tamponade ?
Accumulation of fluid in the pericardial space
causing increase in pressure with subsequent
cardiac compression.
Pericardial pressures > intracardiac pressures
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Aetiology
Most common causes :
Malignancy
Idiopathic pericarditis
Renal failure
Tuberculosis
Bleeding following cardiac Sx and trauma-
Hemopericardium
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Cardiac Tamponade - Pathophysiology
Most critical point occurs when an effusion
reduces the volume of the cardiac chambers such
that cardiac output begins to decline
Mainly by impeding right-sided heart filling, with
much of the effect on the left side of the heart due
to secondary under filling.
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Cardiac Tamponade - Pathophysiology
A ) Modest amounts of
rapidly accumulating
fluid can have major
effects on cardiac
function.
B) Large, slowly
accumulating effusions
are often well tolerated,
presumably because of
chronic changes in the
pericardial pressure-
volume relation
described earlier.
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Cardiac Tamponade -- Pathophysiology
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles
SV systemicvenous pressures
CO
Hypotension/shock JVP
Reflex tachycardia hepatomegaly
ascites
peripheral edema
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Clinical features
Symptoms
acute : confusion / agitation
Signs ( Becks triad)
- hypotension
- elevated JVP
- muffled heart sounds
Pulsus paradoxus : insp drop in SBP > 10 mmhg
Pulsus paradoxus also seen in CP, COPD, asthma
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Pulsus Paradoxus- Explanation
Inspiration> Increased RV filling> Raised IPP >
leftward bulging of the IVS > RV compresses and
reduces LV volume (Ventricular Interdependence)
The normal inspiratory augmentation of RV volume
causes an exaggerated reciprocal reduction in LV
volume.
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Pulsus Paradoxus- Clinical
Demonstration
When severe, it may be detected by palpating weakness or
disappearance of the arterial pulse during inspiration.
Measured by noting the difference between the systolic
pressure at which the Korotkoff sounds are first heard
(during expiration) and the systolic pressure at which the
Korotkoff sounds are heard with each beat, independent of
respiratory phase
Between these two pressures, the sounds are heard only
intermittently (during expiration).
SYNCHRONISED FROM RESPIROPHASIC TO CARDIOPHASIC
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Take aways
Symptoms may be non cardiac
CP and PE will mimic right heart failure
In any RHF symptoms, rule out pericardial disease
Clinical suspicion is essential for diagnosis
Correct diagnosis is imperative
Potential for permanent cure
we will discuss todays topic under the following headings
To outline the pericardial anatomy- Read
Pictorial presentation of pericardium
Coming to functions..- read highlighted parts
We can broadly categorise the PERICARDIAL DISEASES into two subtypes; we will briefly summarize each of these disease entities in the subsequent slides
Lets start with Acute pericarditis
Read
From a clinical point of view , pericarditis can be--
Etiologically , mnemonic can be remembered
Ac Pericarditis clinically presents with a viral prodrome like picture with characteristics pain--
A specific clinical sign is pericardial rub which is pathognomonic- Atrial systole, ventricular systole, Ventricular diastole- protodiastole; Read--
A close d/d is MI;
Any symptoms can be described by acronym- DSO PRCA. Read
Do you have a basic idea of ECG? ECG changes are quite interesting and a target for your NEET PG MCQs; Intervals and waves
READ FOOTNOTE
Mark reciprocal STD;
Mark here no T wave inversion;
Read; For symptomatic relieve---
Just to mention a keynote regarding Pericarditis after AMI; read highlighted parts
Now lets discuss the second disease entity
Maximum cases are idiopathic, in India still TB a very common cause; data taken from western literature
The basic of haemodynamic consequences is mechanical factor. Pericardium Rigid and Scarred ; Explain negative pressure/suction ; Systolic contraction normal; Inhibits diastolic filling of both ventricles- But one at the expense of other one- ventricular interdependence
Read; Why systemic congestion more ? As during inspiration because of negative suction its RV which gets more blood that too compromising its LV counter part.
Read
A potent MCQ; read
Read
show
read
Just Show
Read
Coming to 3rd disease entity--
Defined as..
Can be enlisted as per nature..... And inciting.....; any fluid collection in body can be divided by this principle
Read
Read; associated finding in cxr like lung congestion will differenciate
5 mm in limb leads ; 10 mm in chest leads
show
read
Now coming to 3rd topic
Read- definition; mark increased pressure here unlike uncomplicated PE
read
Almost similar to CCP- There a rigid scarred pericardium, here same by pressurised fluid collection
Here Intra Cardiac Pressures- Diastolic EDP if less than IPP then tamponade starts
Read Modest amounts of rapidly vs Large, slowly accumulating
Similar to CCP
Read
Read- stress on Ventricular Interdependence
Explain by demonstration- bp and pulse simultaneous measurement
Show, QRS amplitude difference due to cardiac swinging