Cardiac Tamponade

Introduction to Cardiac Tamponade

Cardiac tamponade is pressure on the heart due to fluid build-up in the pericardium. The heart’s ventricles aren’t able to fully expand, so the heart cannot supply enough blood to the body.

The pericardium is the sac surrounding the heart.

The three main causes of cardiac tamponade are:

1. Pericarditis
2. Beck’s Triad, pulsus paradoxus
3. Decreased cardiac output caused by right heart failure

Related Video – Cardiac Tamponade

Pericarditis

The most common etiology of cardiac tamponade is pericarditis, an inflammation of the pericardium. Inflammation is typically caused by a bacteria, virus, fungus, or another pathogen, and the inflammation produces fluid between the visceral pericardium and the parietal pericardium. 

Other causes of pericarditis include heart attacks, wounds to the heart, end-stage lung cancer, and cardiac tumors. Cardiac tumors may also push on the myocardium and compress the heart, leading to cardiac tamponade.

There is fluid between the visceral pericardium and the parietal pericardium.

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Beck’s Triad and Pulsus Paradoxus

This section explains Beck’s triad and pulsus paradoxus.

Becks’ Triad

Beck’s triad has, appropriately, three symptoms: 

1. Hypotension
2. Muffled heart sounds
3. Increased jugular vein distention (JVD)

The jugular veins are located at the neck.

Related Video – Understanding the Adult Cardiac Arrest Algorithm

Pulsus Paradoxus

Pulsus paradoxus is a sharp decrease in systolic blood pressure by at least 10 mm Hg during inspiration. When a patient breathes in, the clinician will see blood pressure drop by more than 10 mm Hg. 

All the fluid accumulated inside the pericardial space between the pericardial layers pushes and compresses on the heart. When the patient breathes in, the lungs expand and momentarily sequester the blood in the chest, ultimately decreasing the cardiac output. 

When the patient breathes out, the heart moderately expands, improving cardiac output and blood pressure. There is at least a 10 mm Hg difference between inspiration and expiration.

Pathophysiology: Decreased Cardiac Output and Right-sided Heart Failure

Right heart failure can be a cause of cardiac tamponade or a result of it. The right side of the heart is preload-dependent. If it doesn’t get the requisite volume needed to stretch and contract the atrium and ventricle, it will fail. Blood begins to back up due to right heart failure and can leak into the pericardial space. The compressed heart isn’t able to accept the venous return coming back to the heart, causing further heart failure.

Patients will exhibit hypotension due to decreased cardiac output. The excess fluid in the pericardial space compresses the heart, decreasing stroke volume and impairing the diastolic filling of the ventricles. Compressed ventricles decrease stroke volume and cardiac output, causing hypotension.

The equation for cardiac output and blood pressure:

Blood pressure = cardiac output × systemic vascular resistance

Cardiac output = heart rate × stroke volume

Patients will exhibit jugular vein distension (JVD), a sign of right-sided heart failure. There is a decrease in preload, or venous return, due to the compression of the heart. The return does not completely fill the ventricles, so the blood can’t get in. Blood backs up into the neck and peripheral systemic circulation, evidenced by the distention of the jugular veins.

Patients will also exhibit muffled heart sounds. The surrounding built-up fluids muffle heartbeats.

Pulsus paradoxus may be present as well.

Care for Patients with Cardiac Tamponade

Clinicians should direct care towards interventions and assessments to help manage decreased cardiac output — the main consequence of cardiac tamponade. Clinicians should also direct interventions toward right-sided heart failure.

Clinicians should monitor the patient’s airway and breathing. If cardiac output is so diminished that the patient’s brain is not getting perfused, the patient may have mental status issues, confusion, or be somnolent or lethargic. They may not be able to protect their airway.

Clinicians should monitor heart rate and blood pressure frequently during the acute phase. These patients have the potential to become very hypotensive and go into a shock state.

The clinician positions the patient upright to facilitate lung expansion because the lungs are not fully perfused due to decreased cardiac output. Clinicians should monitor the electrocardiogram (ECG ) because dysrhythmias can result.

During the acute phase, clinicians should perform hourly measurements of fluid intake and fluid output. . If the kidneys aren’t perfused, they won’t put out any urine. If there’s a large urine decrease from hour to hour, the patient either needs more fluid or they’re entering an early phase of cardiac failure from cardiac tamponade.

Physicians should monitor arterial blood gases (ABGs) to make sure the acid-base balance is not affected. Clinicians will deliver oxygen as necessary.

Monitor the patient’s vitals and symptoms until the patient can receive a pericardiocentesis.

Patients with cardiac tamponade require frequent assessment and close monitoring for potential complications. 

Pericardiocentesis is a critical intervention. During pericardiocentesis, the clinician drains the fluid out of the patient’s pericardial space, allowing the heart to expand. Occasionally, physicians may also order dobutamine or other positive inotropic drugs to help the heart contract more efficiently and increase cardiac output.

Related Video – Understanding the Adult Immediate Post-Cardiac Arrest Care Algorithm

Summary

Cardiac tamponade is pressure on the heart due to fluid build-up in the pericardium. Clinicians must care for patients until a pericardiocentesis is performed. The three main causes of cardiac tamponade are pericarditis, Beck’s triad or pulsus paradoxus, and decreased cardiac output due to right heart failure.