Definition, Types, Clinical Features & Diagnostic studies
Watch Free Online Medical Video Lecture on Cardiac Tamponade
What is Cardiac Tamponade?
It is a condition in which fluid is accumulated in the pericardial sac exerting pressure on the heart.
Pericardium exerts so much pressure on the cardiac chambers that it obstructs the inflow of blood to the heart. Eventually cardiac filling is compromised, cardiac output will drop and the patient becomes hemodynamically unstable.
Most of the time, the patient having pericardial effusion, but isn’t exerting pressure on cardiac walls to strangulate the heart, then it is not called tamponade.
Cardiac tamponade is a medical emergency, so its diagnosis should be rapid and correct.
The mechanism and development of cardiac tamponade mainly depend upon the following factors:
Amount of fluid.
Rapidity, with which fluid is accumulated.
Compliance of pericardium. If pericardium is very stiff, then small amount of fluid can produce the tamponade.
These three factors increase intra-pericardial pressure. If it is more than 15mmHg, it definitely can lead to cardiac tamponade. Actually, this pressure (>15mmHg) is more than the filling pressure of the heart.
Types of cardiac tamponade
1. Acute cardiac tamponade (rapid accumulation of fluid, 100-200 ml fluid)
Chest trauma leading to rupture the free wall of the heart.
2. Subacute/Chronic cardiac tamponade (slow accumulation of fluid, up to 2000 ml fluid)
Other causes of cardiac tamponade:
Use of anticoagulants in acute pericarditis.
Uremic pericarditis (Renal failure)
Clinical presentation of Cardiac Tamponade
In acute cardiac tamponade, patients usually have Beck’s triad:
Increased JVP and changed the JVP wave pattern (sharp x-descent and absence of y-descent)
Low blood pressure.
Muffled heart sound, soft heart sound, absent heart sound.
Normal JVP wave pattern
Jugular venous pressure/pulse reflects the pressure changes in the right atrium. When atria contract, pressure goes up and a-wave is produced. After atrial systole, tricuspid valve opens, atria start relaxing, pressure will go down, then suddenly ventricular contraction starts and tricuspid valve are closed, producing a little jerk in a wave pattern, this little jerk represents c-wave.
After closure of the tricuspid valve, atrium relaxes, pressure will come down, and this is called x-descent. Now more blood comes to the atrium and tricuspid valve is still closed, so the accumulation of blood will take the pressure up producing V-wave. After opening of the tricuspid valve, ventricular filling (atrial emptying) starts producing y-descent.
Increased JVP in cardiac tamponade
In cardiac tamponade, the heart is strangulated and blood will pool behind, this will raise JVP leads to distension of the neck veins, so this is also called Jugular Venous Distention (JVD).
Lost of y-descent
When the tricuspid valve opens, pressure goes down, atria start emptying and ventricles start filling leads to produce y-descent. In cardiac tamponade as cardiac chamber is strangulated, even after the opening of tricuspid valve, blood cannot rapidly fall down due to high pressure in ventricles so y-descent is lost.
Relaxing of atria produces x-descent, this x-descent becomes sharp and deeper because high blood pressure in JVP system eventually fills the atrium when it is relaxing.
Note: JVP changes are the most sensitive sign in cardiac tamponade.
Muffled heart sounds (soft heart sound, absent heart sound)
There is a lot of fluid around the heart and you cannot hear the heart sounds. Secondly, as the heart is compressed, it really beats hard.
Decreased blood pressure
As the heart is strangulated, ventricular filling is decreased, leading to less end diastolic volume (low end diastolic pressure). This condition causes decrease in the stretch and contraction in myocardium, stroke volume, cardiac output, leading towards a decrease in systolic blood pressure.
Due to low blood pressure, the patient may have clinical manifestations of shock, i.e., cold and clammy hand.
Development of Tachycardia
When blood pressure falls, sympathetic overflow occurs and tachycardia is developed.
When there is no tachycardia, there is no cardiac tamponade, except in these conditions:
Patient of cardiac tamponade, who have pericardial effusion as a result of myxedema due to hypothyroidism.
Uremia, because uremia produces bradycardia and heart blocks.
The patient taking beta-blockers.
The patient at terminal stage.
Clinical features like heart failure
In chronic tamponade, features of cardiac tamponade may not be very pronounced, but features like heart failure may exist.
Due to slow compression of right heart for a long time and elevated central venous pressure, there is back pressure in the liver leading to hepatomegaly, ascites and oedema.
If left heart is unable to receive the blood, it can lead to congestion of vessels in the lungs, causing the dyspnea, cough, orthopnea and tachypnea etc.
Other clinical features
Patients may have clinical features of underlying causes like:
Tuberculosis: weight loss, night sweats, low-grade fever and anorexia etc.
Uremia: Features of renal failure.
Patients may have clinical features of acute pericarditis like chest pain, pericardial rub etc.
Normal respiration and arterial blood pressure.
Systolic blood pressure depends upon the cardiac output of the ventricle. When cardiac output changes, it also changes the systolic blood pressure.
During inspiration chest wall expands, the diaphragm goes down and intrathoracic pressure becomes more negative. This results in an increase in venous return to the right heart, leading to the expansion of the right ventricle and intraventricular septum are pushed toward the left side, so filling of the left ventricle is slightly under filled.
During inspiration, not only air pockets expand, but pulmonary vasculature also expands, increasing its capacity and trying to hold more blood, When the flow of blood from the lung going to left heart is less, so end diastolic volume and pressure is less, stroke volume is less, eventually leading to drop of systolic blood pressure, and reverse will occur at expiration.
The normal inspiratory fall of systolic blood pressure is less than 10 mm Hg.
In this condition, inspiratory drop in systolic blood pressure is more than 10mmHg.
Pulsus paradoxus and cardiac tamponade.
In cardiac tamponade, cardiac chambers are compressed or strangulated. There is an increased venous return to the right heart during inspiration and the free wall of the right ventricle cannot expand due to tamponade, So there will be too much deflection of interventricular septum towards the left side and left ventricle becomes extremely under filled, it leads towards the low cardiac output and eventually there’ll be more drop in systolic blood pressure (>10mmHg)
How will you pick pulses paradoxus with
Put properly sphygmomanometer cuff, inflate it more than significantly systolic blood pressure. Now you start dropping cuff pressure slowly until you will hear the first sound (i.e. K-1) that is systolic blood pressure. K-1 sound can be heard during expiration and it will disappear during inspiration. Then continue to lower the cuff pressure at the value at which you hear Korotkoff sound with each beat; it means that you hear sounds with inspiration and expiration (i.e. K-2). The difference between K-2 and K-1 is called inspiratory drop in systolic blood pressure.
Remember, if this inspiratory drop in systolic blood pressure is more than 10mmHg, we call patient has Pulsus paradoxus.
Continue to lower the cuff pressure to the highest value at which you hear Korotkoff sounds with each beat; this means that you hear sounds with inspiration and expiration. Find the difference between the two numbers and this is the pulse. Remember, a pulse greater than 10 mm Hg is abnormal.
Pulsus paradoxus is not specific for cardiac tamponade because it can be positive in some other conditions like:
Acute or chronic obstructive airway diseases like bronchial asthma.
Sever hypovolemic shock
Normally during inspiration JVP goes down, if the JVP during inspiration fails to go down or even goes up, this is called Kussmaul sign. It has been present less often in cardiac tamponade but more often in constrictive pericarditis.
Diagnostic studies for cardiac tamponade
This is a gold standard investigation for cardiac tamponade.
There are two types of echocardiography.
i. Thoracic echocardiography
a) 2-D thoracic echocardiography:
it detects following findings:
Right atrial diastolic collapse.
Right ventricle diastolic collapse.
Abnormal motility of interventricular septum.
Dilated inferior vena cava.
b) Doppler thoracic echocardiography
Increased transvalvular velocity is a tricuspid and pulmonary valve.
Increased transvalvular velocity is a mitral and aortic valve.
ii. Transesophagus echocardiography.
It is performed when we are suspecting either there is aortic dissection or free wall rupture or tamponade after cardiac surgery.
2. Electrocardiogram (ECG).
Features of acute pericarditis on an ECG are:
ST-segment elevation with concavity upward.
Cardiac shadow will be enlarged, if pericardial effusion is more than 250ml. The cardiac shadow appears as flask-shaped or globular.
CT/MRI detects exact amount of effusion, loculated effusion, malignancies or any mass adjacent to the pericardium.
5. Cardiac catheterization.
It detects pressure in the pericardium.
Investigations for underlying causes like Tuberculosis, neoplasia, SLE, and hypothyroidism etc.
Management of Cardiac Tamponade
Acute pericarditis with pericardial effusion
Hospitalize the patient.
Monitoring: Monitor pulse, JVP, blood pressure, heart sound etc.
Pericardiocentesis is contraindicated in aortic dissection and post MI with free wall rupture.
Approach for pericardiocentesis:
Before pericardiocentesis, maintain I.V Line access then aspirates the fluid from pericardium with the needle (18-20 G).
Limited local subxiphoid thoracotomy (surgical drainage): for recurrent cardiac tamponade.
Pericardial-plerural fistula: cardiac tamponade due to neoplasia. Cardiac tamponade caused by Nepalese
Pericardiodesis: Introduction of sclerosing agents like bleomycin or tetracycline in the pericardial sac leading to sclerosis or fibrosis of the pericardium.
Introduction of small incisions in subxiphoid and you introduce a small deflated balloon into the pericardial sac and after inflation you pull it out, while it comes out, it produces a larger window in the pericardium so that fluid keeps on draining into mediastinal structure.