CRIT BIT CORNER

When Infection Becomes a Structural Heart Problem

In endocarditis, the bedside concern is not only that an infection is present.

The bigger question is:

What is the infection doing to the valve?

Once organisms attach to valve tissue or prosthetic material, they can change the structure and function of the heart itself.

That can create several major problems:

• The valve may stop closing correctly, causing acute regurgitation.
• Blood may begin flowing backward instead of forward.
• Filling pressures can rise, leading to pulmonary edema and worsening oxygenation.
• Forward flow can fall, causing hypotension, shock, rising lactate, or worsening kidney perfusion.
• Pieces of vegetation can break off and embolize to the brain, kidneys, spleen, lungs, coronary arteries, or extremities.
• Infection can extend into nearby tissue and irritate the conduction system, causing new PR prolongation, AV block, or complete heart block.

That is why a new murmur, worsening oxygenation, changing hemodynamics, subtle neurologic changes, or new conduction abnormalities should not be brushed off. In endocarditis, those changes may be the first bedside clue that the infection has become a structural heart problem.

What Is Endocarditis?

Infective endocarditis is an infection of the endocardial surface of the heart.

In practice, this usually means infection involving:

• A native heart valve
• A prosthetic heart valve
• An intracardiac device
• Nearby cardiac tissue

The classic lesion is a vegetation.

A vegetation is not just a clump of bacteria sitting on a valve. It is a mixture of organisms, fibrin, platelets, inflammatory debris, and thrombotic material attached to the valve surface or prosthetic material.

Think of it as an infected clot stuck to a moving valve.

That creates three major problems:

• The infection can persist. Organisms inside the vegetation are partly protected from immune cells and harder for antibiotics to reach.
• The valve can become damaged. Infection can interfere with valve closure, destroy valve tissue, or worsen regurgitation. This can lead to acute heart failure, pulmonary edema, shock, or worsening oxygenation.
• Pieces can break off and embolize. Infected material can travel to other organs, including the brain, kidneys, spleen, lungs, coronary arteries, or extremities.

That is why endocarditis is not just an infectious disease problem.

It is also a structural heart problem.

Once infection attaches to the valve, the question becomes:

Can the valve still do its job?

How Does Endocarditis Start?

Endocarditis usually needs two things:

1. A surface organisms can stick to
2. Organisms in the bloodstream

A healthy endocardial surface is relatively resistant to infection. The problem starts when that surface is damaged or abnormal.

This can happen with:

• Turbulent blood flow
• Abnormal native valves
• Prosthetic valves
• Prior valve repair
• Intracardiac devices
• Indwelling lines
• Repeated bloodstream exposure from procedures, injections, or infection

When the valve surface is injured, platelets and fibrin can collect along the damaged area.

At first, this layer may be sterile. Think of it as a sticky landing pad.

Then bacteremia or fungemia gives organisms the opportunity to reach that surface. The organisms may come from:

• Skin or line sources
• Dental or oral sources
• GI/GU sources
• Surgical or procedural sources
• Injection drug use
• Another active infection

Once organisms attach, they become embedded in the platelet-fibrin material.

The vegetation then begins to grow.

More fibrin and platelets collect around the organisms, which helps protect the infection from the immune system and makes antibiotic penetration more difficult.

That is one reason endocarditis is hard to treat.

The organisms are not just floating freely in the bloodstream.

They are buried inside a protected infected structure attached to a moving valve.

Endocarditis Is a Structural Infection

Endocarditis is not just bacteremia.

Endocarditis means organisms have attached to cardiac tissue or prosthetic material and created a protected infected structure.

That difference matters.

With bacteremia, the main question is:

How do we clear the bloodstream infection?

With endocarditis, the question becomes bigger:

What has the infection done to the heart?

The team has to think through several layers:

• What organism is causing the infection?
• Have the blood cultures cleared?
• Is there a vegetation?
• Is the valve still opening and closing normally?
• Is there new or worsening regurgitation?
• Has the infection extended beyond the valve?
• Is there an abscess?
• Are there embolic complications?
• Is the patient developing heart failure or shock?
• Does the patient need surgery?

That is why bedside assessment matters so much.

A new murmur, worsening crackles, increasing oxygen needs, new heart block, persistent fever, recurrent positive cultures, new stroke symptoms, worsening renal function, or new abdominal pain can all be clues that the infection is no longer contained.

In endocarditis, those changes may mean the problem has moved from “infection in the blood” to “infection changing the structure and function of the heart.”

Why Murmurs Matter in Endocarditis

A murmur is the sound of turbulent blood flow.

In endocarditis, that turbulence may be the bedside clue that infection has changed the valve.

Murmurs may occur because:

• A vegetation prevents a valve from closing properly.
• Infection destroys or perforates a valve leaflet.
• Chordae or supporting structures are damaged.
• A prosthetic valve becomes unstable or dehisced.
• Severe regurgitation creates volume overload and high-flow turbulence.
• Infection extends into surrounding tissue and changes how the valve functions.

The key question is not just:

Do I hear a murmur?

The better question is:

What is this murmur telling me about blood flow?

A murmur means blood is moving turbulently, and turbulent flow usually comes from one of two problems:

• Stenosis: Blood is having trouble moving forward through a narrowed valve opening.
• Regurgitation: Blood is leaking backward through a valve that should be closed.

Endocarditis can cause either problem, but it becomes especially dangerous when it causes acute regurgitation.

That means the valve can no longer close correctly.

When that happens, blood moves the wrong direction:

• Aortic regurgitation sends blood backward from the aorta into the left ventricle during diastole.
• Mitral regurgitation sends blood backward from the left ventricle into the left atrium during systole.
• Tricuspid regurgitation sends blood backward from the right ventricle into the right atrium during systole.
• Pulmonic regurgitation sends blood backward from the pulmonary artery into the right ventricle during diastole.

Acute regurgitation can rapidly increase filling pressures, worsen pulmonary edema, decrease forward flow, and contribute to shock.

So the murmur is not just a sound.

It is a clue about the direction blood is moving — and whether the valve is still doing its job.

Timing: The First Step in Understanding Murmurs

Before trying to memorize every murmur, anchor yourself to timing.

The first question is:

When do I hear it?

A murmur can happen during systole or diastole.

Systolic Murmurs

Systolic murmurs happen between S1 and S2.

S1 is the sound of the mitral and tricuspid valves closing. It marks the start of systole, when the ventricles begin to contract.

S2 is the sound of the aortic and pulmonic valves closing. It marks the end of systole and the beginning of diastole.

If the murmur happens during systole, ask:

Is blood having trouble getting out, or is blood leaking backward while the ventricle contracts?

Systolic murmurs usually come from one of two patterns:

• Forward flow obstruction: Blood is trying to leave the ventricle through a narrowed valve.
• Backward regurgitant flow: Blood is leaking backward through an AV valve while the ventricle contracts.

Common systolic murmurs include:

• Aortic stenosis
• Pulmonic stenosis
• Mitral regurgitation
• Tricuspid regurgitation
• Ventricular septal defect

Diastolic Murmurs

Diastolic murmurs happen after S2.

In adults, diastolic murmurs are not considered innocent. They usually reflect abnormal valve function.

If the murmur happens during diastole, ask:

Is blood leaking backward from the great vessels, or is blood struggling to move into the ventricle?

Diastolic murmurs usually come from one of two patterns:

• Backward regurgitant flow: Blood leaks backward from the aorta or pulmonary artery after the semilunar valve should be closed.
• Impaired ventricular filling: Blood has trouble moving through a narrowed mitral or tricuspid valve during diastole.

Common diastolic murmurs include:

• Aortic regurgitation
• Pulmonic regurgitation
• Mitral stenosis
• Tricuspid stenosis

In this case, the patient had a blowing diastolic murmur.

That timing and quality fit with aortic regurgitation, where blood leaks backward from the aorta into the left ventricle after the aortic valve should be closed.

Mitral Regurgitation

Mitral regurgitation means the mitral valve does not close properly during systole. When the LV contracts, some blood goes forward into the aorta, but some leaks backward into the left atrium.

In endocarditis, this can happen when infection affects the mitral valve structure.

The infection may:

• Damage the mitral leaflet
• Cause leaflet perforation
• Involve the chordae
• Disrupt valve closure
• Create severe valve dysfunction

Mitral regurgitation can also be functional.

That means the valve leaflets themselves may not be directly infected or destroyed, but the valve still does not close correctly because the surrounding heart geometry has changed.

Functional mitral regurgitation can occur with:

• LV dilation
• Annular dilation
• Ischemia
• Papillary muscle dysfunction
• Altered ventricular geometry

Either way, the problem is the same:

• The mitral valve is not sealing during systole.
• Blood is moving backward into the left atrium when it should be moving forward into the aorta.

What It Sounds Like

Chronic mitral regurgitation is classically:

• Holosystolic
• High-pitched
• Blowing

It usually starts with S1 and continues through systole.

Acute severe mitral regurgitation can be harder to recognize.

It may be:

• Early systolic
• Shorter than expected
• Decrescendo
• Softer than expected

This happens because the left atrium has not had time to stretch or adapt. Pressure rises quickly, and left atrial pressure can begin to equalize with LV pressure during systole.

That means the murmur may not sound as dramatic as the physiology actually is.

A quieter or shorter murmur does not always mean a safer valve lesion.

Where To Listen

Best location:

• Apex
• Usually around the fifth intercostal space at the midclavicular line

Radiation:

• Often toward the left axilla
• May radiate toward the back or scapular region depending on the direction of the regurgitant jet

Positioning can help:

• Place the patient in the left lateral decubitus position if tolerated.
• This brings the apex closer to the chest wall.
• Use the diaphragm for the high-pitched blowing murmur.

Bedside Meaning

Severe mitral regurgitation increases pressure in the left atrium.

That pressure can back up into the:

• Pulmonary veins
• Pulmonary capillaries
• Pulmonary interstitium and alveoli

This can lead to:

• Crackles
• Pulmonary edema
• Hypoxemia
• Increased work of breathing
• Respiratory failure
• Falling forward cardiac output
• Hypotension Shock

When mitral regurgitation is acute, the left atrium has not had time to dilate and compensate.

Pressure rises fast.

That is why acute severe mitral regurgitation can deteriorate quickly into pulmonary edema, respiratory failure, and hemodynamic instability.

Other Murmurs

Our patient had severe aortic regurgitation, mitral regurgitation, and tricuspid regurgitation, so those were the main murmurs we focused on.

But at the bedside, it helps to know the other major valve sounds too.

The goal is not to become an expert cardiologist with a stethoscope.

The goal is to recognize what the murmur may be telling you about blood flow.

Pulmonic Regurgitation

Pulmonic regurgitation means the pulmonic valve does not close properly during diastole.

Blood leaks backward from the pulmonary artery into the right ventricle when the pulmonic valve should be closed.

What It Sounds Like

Pulmonic regurgitation is usually:

• Early diastolic
• Decrescendo
• Best heard at the left upper sternal border
• May become louder with inspiration

If pulmonary pressures are high, it may sound high-pitched and blowing.

If pulmonary pressures are normal, it may be softer and lower-pitched.

Bedside Meaning

Pulmonic regurgitation is a right-sided diastolic murmur.

It can contribute to RV volume overload, RV dilation, and right-sided congestion.

It is less common as the main endocarditis murmur in adult ICU patients, but it is still useful to recognize because right-sided endocarditis can involve the pulmonic valve.

Aortic Stenosis

Aortic stenosis means the aortic valve does not open well during systole.

The LV has to generate more pressure to push blood through a narrowed valve opening and out to the body.

What It Sounds Like

Aortic stenosis is usually:

• Systolic
• Harsh
• Crescendo-decrescendo
• Best heard at the right upper sternal border
• Often radiates to the carotids

Bedside Meaning

Aortic stenosis is a forward-flow obstruction.

The issue is not backward flow.

The issue is that blood has trouble leaving the LV.

Severe aortic stenosis can make patients very preload dependent and poorly tolerant of hypotension, tachycardia, or sudden drops in systemic vascular resistance.

If cardiac output falls, the murmur may become softer even though the stenosis is severe.

Pulmonic Stenosis

Pulmonic stenosis means the pulmonic valve does not open well during systole.

The RV has to push blood through a narrowed valve opening to get blood into the pulmonary artery.

What It Sounds Like

Pulmonic stenosis is usually:

• Systolic
• Crescendo-decrescendo
• Best heard at the left upper sternal border
• May become louder with inspiration

Bedside Meaning

Pulmonic stenosis is a right-sided forward-flow obstruction.

The RV has to work harder to move blood into the pulmonary circulation.

Severe pulmonic stenosis can contribute to RV hypertrophy, RV strain, reduced pulmonary blood flow, and right-sided heart failure physiology.

Mitral Stenosis

Mitral stenosis means the mitral valve does not open well during diastole.

Blood has trouble moving from the left atrium into the left ventricle.

What It Sounds Like

Mitral stenosis is usually:

• Diastolic
• Low-pitched
• Rumbling
• Best heard at the apex with the bell
• Often heard better in the left lateral decubitus position

It may have an opening snap after S2.

Bedside Meaning

Mitral stenosis is an inflow obstruction.

The left atrium has to push blood through a narrowed mitral valve into the LV.

This can increase left atrial pressure and back pressure into the pulmonary veins.

Severe mitral stenosis can contribute to pulmonary edema, pulmonary hypertension, atrial fibrillation, low LV filling, and reduced cardiac output.

Tachycardia can be especially poorly tolerated because diastolic filling time becomes shorter.

Tricuspid Stenosis

Tricuspid stenosis means the tricuspid valve does not open well during diastole.

Blood has trouble moving from the right atrium into the right ventricle.

What It Sounds Like

Tricuspid stenosis is usually:

• Diastolic
• Low-pitched
• Rumbling
• Best heard along the lower left sternal border
• Often louder with inspiration

Bedside Meaning

Tricuspid stenosis is a right-sided inflow obstruction.

Blood backs up into the venous system because it cannot easily move from the right atrium into the right ventricle.

This can contribute to elevated JVP, hepatic congestion, ascites, peripheral edema, and reduced RV filling.

Like other right-sided murmurs, it may become more noticeable with inspiration because inspiration increases venous return to the right heart.

How Endocarditis Presents

Endocarditis can present dramatically, but it can also smolder.

Some patients look septic right away. Others feel vaguely unwell for days to weeks before the diagnosis becomes clear.

The presentation depends on the organism, the valve involved, the patient’s baseline cardiac structure, and whether complications have already developed.

Common findings may include:

• Fever
• Malaise
• Fatigue
• Weight loss
• Night sweats
• Myalgias or arthralgias
• New or changing murmur
• Dyspnea Heart failure symptoms
• Embolic findings
• Neurologic changes
• Back pain from vertebral osteomyelitis
• Hematuria or worsening renal function
• Petechiae or splinter hemorrhages
• Janeway lesions, Osler nodes, or Roth spots

But the absence of classic findings does not rule it out. Many of the “classic” endocarditis findings are late, uncommon, subtle, or easy to miss in a critically ill patient. In the ICU, the more important clues may be changes in physiology.

Watch for:

• Persistent bacteremia
• Persistent fever despite treatment
• Unexplained shock
• New or worsening valve dysfunction
• New or changing murmur
• Pulmonary edema
• Rising oxygen requirement
• New stroke symptoms
• Acute kidney injury
• Hematuria
• Splenic or renal infarct
• New abdominal pain
• Back pain concerning for metastatic infection
• New PR prolongation, AV block, or complete heart block

Endocarditis does not always present as a neat textbook picture. Sometimes the clue is not one dramatic finding. Sometimes it is the pattern: infection plus a valve problem, embolic finding, conduction change, or unexplained organ dysfunction.

Treatment

Antibiotics Are Necessary, But Sometimes Not Enough

Treatment depends on the valve involved, organism, susceptibilities, presence of prosthetic material, complications, and surgical candidacy. The general principles are:

Get cultures first when possible If the patient is not crashing, blood cultures should be collected before antibiotics. Start empiric therapy when indicated Empiric therapy should cover likely organisms while awaiting more information. The exact regimen depends on native vs prosthetic valve, healthcare exposure, local resistance patterns, renal function, allergies, and severity of illness. Tailor therapy to the organism Once the organism and susceptibilities are known, therapy is narrowed or adjusted. Use bactericidal therapy for a prolonged duration Endocarditis usually requires prolonged therapy because organisms inside vegetations are protected and may be metabolically less active. Monitor for complications Treatment is not just “hang antibiotics and wait.” Patients need ongoing assessment for:

• Persistent fever
• Persistent or recurrent bacteremia
• New murmur
• Worsening heart failure
• Pulmonary edema
• Embolic events
• Neurologic changes
• New conduction abnormalities
• Renal dysfunction
• Medication toxicity

Involve the team early Endocarditis care often requires infectious disease, cardiology, cardiac surgery, critical care, pharmacy, and nursing. Prosthetic valve endocarditis and fungal endocarditis are especially complex. Surgery may be needed Surgery is considered when infection causes structural or uncontrolled complications, such as:

• Acute severe valve dysfunction causing heart failure
• Cardiogenic shock from valve failure
• Paravalvular abscess
• Fistula
• Prosthetic valve dehiscence
• Persistent bacteremia or fever despite appropriate therapy
• Difficult-to-treat organisms
• Recurrent emboli
• Large/mobile vegetations with high embolic risk
• Fungal endocarditis in many cases

This is why bedside changes matter. The nurse may be the first person to notice that the “infection patient” is becoming a “valve failure patient.”

Final Bedside Takeaway

Endocarditis is not just an infection. It is an infection that can attach to the heart’s structure. Once that happens, the question becomes:

What is the infection doing to the valve?

A vegetation can block closure, destroy tissue, seed emboli, extend into the annulus, create abscess, cause heart block, and turn a slow infectious process into acute pulmonary edema, shock, stroke, renal injury, or surgical emergency. So when you hear “endocarditis,” think beyond antibiotics. Think:

• Blood cultures
• Vegetation
• Valve function
• Murmur timing
• Regurgitation vs stenosis
• Emboli
• Abscess
• Heart block
• Heart failure Surgery

The stethoscope does not replace echo. But it can help you recognize when the physiology is changing.

And in the ICU, recognizing the change is often where critical thinking starts.