Cardiac Tamponad E: Pathophysiology and Management
Cardiac Tamponad E: Pathophysiology and Management
Cardiac Tamponad E: Pathophysiology and Management
TAMPONAD
E
PATHOPHYSIOLOGY
AND MANAGEMENT
Dr Satyam Rajvanshi
SR Cardiology, Dr. RML Hospital, New Delhi
CARDIAC TAMPONADE
Pericardial Anatomy and Physiology
Pericardial Pathology
Tamponade
Physics and Pathology
Presentation, Diagnosis and Differential
Management
PERICARDIAL ANATOMY AND
PHYSIOLOGY
Pericardial Pathology
Tamponade
Physics and Pathology
Presentation, Diagnosis and Differential
Management
PERICARDIUM - ANATOMY
• Resilient Fibro-serous sac – envelops heart and great
vessels
• 2 layers
PERICADIAL PATHOLOGY
Tamponade
Physics and Pathology
Presentation, Diagnosis and Differential
Management
PERICADIAL PATHOLOGY
Few clinicopathologic processes involve pericardium
Pericardial heart disease includes only
Pericarditis (an acute, subacute, or chronic fibrinous,
"noneffusive," or exudative process)
Complications of pericarditis - Tamponade and
Constriction (an
acute, subacute, or chronic adhesive, fibrocalcific
response)
Congenital lesions.
Despite a limited number of clinical syndromes, the
pericardium is affected by virtually every category of disease -
infectious, neoplastic, immune–inflammatory, metabolic,
iatrogenic, traumatic, and congenital etiologies.
Categories of Pericardial Disease
Idiopathic
Infectious - Viral/Bacterial/Mycobacterial/Fungal/Protozoal
Immune-inflammatory Connective tissue disease, Early post–
myocardial infarction, Dressler syndrome, Post-
cardiotomy/thoracotomy, Late post- trauma, Drug induced,
Early post–cardiac surgery and post–orthotopic heart transplantation
Hemopericardium - Trauma, Post–myocardial infarction free wall
rupture, Device and procedure related
(percutaneous coronary procedures, implantable defibrillators, pacemakers,
post–arrhythmia ablation, post–atrial septal defect closure, post–valve
repair or replacement), Dissecting aortic aneurysm
Trauma - Blunt and penetrating, Post–cardiopulmonary resuscitation
Congenital - Cysts, congenital absence
Miscellaneous - Chronic renal failure, dialysis related,
Chylopericardium,
Hypothyroidism and hyperthyroidism, Amyloidosis, Neoplastic,
Idiopathic pericarditis and any infection, neoplasm, and
autoimmune or inflammatory process that can cause
pericarditis can cause an effusion
Tamponade
Tamponade
Presentation, Diagnosis and Differential
Management
CARDIAC TAMPONADE - life-threatening, slow or rapid
compression of the heart due to the pericardial accumulation
of fluid, pus, blood, clots, or gas, as a result of effusion,
trauma, or rupture of the heart.
Pericardial compressive - Tamponade
syndromes - Constrictive Pericarditis
- Effusive-Constrictive Pericarditis
pressure
right heart.
Inspiration > reduction in intrapleural pressure that affects
all structures within the thorax, associated with a fall in
chamber pressures and pulmonary wedge pressure > The
reduction in intrapericardial pressure tends to be larger
than the fall in systemic venous pressure , and with
descent of the diaphragm, intra-abdominal pressure
increases , resulting in an increase in the pressure gradient
from extrathoracic veins to the right atrium > collectively
serve to enhance right atrial and right ventricular
filling.
Inspiration > Decrease in intrapleural pressure more
effectively transmitted to the pulmonary venous bed than to
the left ventricle > the pressure gradient from pulmonary
vein to left atrium decreases slightly > slight drop in the
transmitral pressure gradient > decrease in LV preload ,
and transmission of the negative intrathoracic pressure to
the aorta > mild decrease in systemic arterial pressure.
Inter-Ventricular Dependence/Diastolic Coupling
The right and left ventricles share the intraventricular septum and
are contained in the relatively indistensible pericardial sac
When the pericardium becomes diseased or when the heart
becomes enlarged to the pericardial limits > Enhanced
diastolic ventricular interaction
An increase in volume of one ventricle (in the setting of a
compliant septum and an intact pericardium) will affect filling and
volume of the other ventricle.
Pericardial contact pressure/pericardial restraint
Pericardial contact pressure can be estimated by
- flattened balloons in pericardial sac
- quantifying the change in the right- and left-sided heart
diastolic pressure-volume relation before and after
pericardiectomy
There is negligible pericardial restraint at low normal filling volumes,
with contact pressures in the range of 2 to 4 mm Hg at the upper
end of the normal range.
With additional filling, contact pressure rapidly increases - At left-
sided filling pressure of ∼25 mm Hg, estimated contact pressure is
∼10 mm Hg, accounting for most of the right-sided heart pressure
at
this level of filling.
Thus, if cardiac volume or pericardial sac volume and pressure
increase above the physiologic range - Pericardial Reserve
Volume is exhausted - - acute restraint on cardiac
volume
- increasing contribution to intracavitary filling pressures, directly
because of the external contact pressure and indirectly because
Tamponade physiology
develops when the size of
the effusion becomes
sufficient to increase total
pericardial volume from the
shallow, compliant portion
of the Pericardial pressure-
volume relationship to the
steep, noncompliant
portion.
In pericardial tamponade, as intrapericardial pressure increases,
an increase in venous return (1st compensatory
mechanism) will initially serve to maintain cardiac filling and
prevent diastolic collapse of cardiac chambers.
Adrenergic stimulation causes Tachycardia (2nd compensatory
mechanism)
Further increase in pericardial pressure will lead to a
progressive impairment in atrial emptying and ventricular
filling, with blunting or disappearance of the y descent (atrial
emptying) while the x descent is typically preserved or
enhanced.
There is also loss of the early dip in minimal LV diastolic
pressure and equalization between right atrial and LV
pressure at the onset of diastole.
Enhanced Diastolic Interaction – RV and LV filling 180º out of
phase
This leads to PULSUS PARADOXUS!
As pericardial pressure continues to increase, diastolic filling
pressures will equalize across the four cardiac chambers,
eventually culminating in diastolic compression of the right
side and then the left-side cardiac chambers – Cardiogenic
Shock!
Pericardial Anatomy and Physiology
Pericardial Pathology
Tamponade : Physics and Pathology
TAMPONADE : PRESENTATION,
DIAGNOSIS AND DIFFERENTIAL
Tamponade
Management
The presentation of patients with cardiac tamponade largely
depends upon the length of time over which pericardial fluid
accumulates and the clinical situation.
Pericardial
Cardiac
Grade Volume MAP CVP HR Beck's Triad
Index
(mL)
usually not
I <200 Normal or ↑ Normal ↑ ↑
present
↑↑
III >200 ↓↓ ↓↓ (≤30–40 cm ↓ Usually present
H2O)
From Shoemaker WC, Carey SJ, Yao ST, et al: Hemodynamic monitoring for physiologic evaluation, diagnosis, and
therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973.
Acute cardiac tamponade occurs within minutes, due to
trauma, rupture of the heart or aorta, or as a complication of
an invasive diagnostic or therapeutic procedure. This
generally results in a picture resembling cardiogenic shock
that requires urgent reduction in pericardial pressure
Apprehension
Chest pain
Oppressive precordial
Positional
Dyspnea
Dry Cough
Hoarseness
Dysphagia
Singultus
Early Satiety, Nausea, Abdominal Pain
Clinical Signs
Clinical Signs – More specific
General
Anxious
Apprehensive
Ashen gray facies
Cool perspiration
Tachypnea
Tachycardia - Exceptions include patients with bradycardia during uremia and
patients with hypothyroidism
Tachypnea
Jugular venous distension
Quiet precordium with both inspection and palpation, Impure muffled heart
sounds
Rub
Peripheral Cyanosis
Bamberger-Pins-Ewart sign
Variable dullness and bronchial breathing at one or both bases most
frequently
Physical findings in 56 patients diagnosed with Cardiac Tamponade at the bedside.
Circulation. 1981: 64, 633-9
Pulsus Paradoxus – Key diagnostic finding
Electrical Alternans 76 - 93 % 8 - 33 %
Doppler
Exaggerated respiratory variation in mitral and
tricuspid inflow velocities
Phasic variation in right ventricular outflow
tract/left
ventricular outflow tract flow
Exaggerated respiratory variation in inferior vena
cava flow
RV Diastolic Collapse
Most commonly involves the RV outflow tract (more
compressible area of RV)
When collapse extends form outflow tract to the body of the right
ventricle, this is evidence that intrapericardial pressure is
elevated more substantially
Early Diastole
Late Diastole
Parasternal long axis view
M-mode
Beginning of systole
ES DC
Short axis view
TAMPONADE : MANAGEMENT
Acute Cadiac Tamponade
The treatment of cardiac tamponade is drainage of the
pericardial contents, preferably by needle paracentesis, with
the use of echocardiographic or another type of imaging,
such as fluoroscopy or CT.
Medical treatment of acute cardiac tamponade, including
inotropic support with or without vasodilators, is relatively
controversial, no specific guideline.
Aimed at supporting compensatory mechanisms to reduce the
elevated vascular resistance. Thus, dobutamine,
administered to reverse the hypotension, is theoretically
ideal.
During tamponade, however, endogenous inotropic stimulation
of the heart is often already maximal.
Increasing the volume may help only in patients with
hypovolemia, since in patients with normovolemia and
hypervolemia, volume infusion may increase intracardiac
pressures as well as heart size, which in turn increases
pericardial pressure, further reducing or eliminating the low
transmural myocardial pressures supporting the circulation.
Fluid overload with intravenous administration of 500 mL of
normal saline over 10 minutes. Cardiac index increased by
>10% in (47%), remained unchanged in (22%), and
decreased in (31%). No patient developed clinical
complications. Predictors of this favorable response were
systolic blood pressure <100 mm Hg and low cardiac index.
Circulation.2008; 117: 1545-
1549