Tricuspid Regurgitation (TR)

Tricuspid Regurgitation is the backward flow of blood from the right ventricle (RV) into the right atrium (RA) during systole due to incomplete closure of the tricuspid valve.

It may be:

• Primary (organic) → structural abnormality of the valve apparatus
• Secondary (functional) → structurally normal valve with annular dilation/RV enlargement causing malcoaptation

Secondary/functional TR constitutes >90% of cases.

Anatomy of the Tricuspid Valve

Component	Details
Leaflets	Anterior, posterior, septal
Annulus	Saddle-shaped fibrous ring
Chordae tendineae	Attach leaflets to papillary muscles
Papillary muscles	Anterior, posterior, septal
Adjacent structures	AV node, bundle of His, RCA

Largest Cardiac Valve

• Normal area: 7–9 cm²
• Lower pressure system than mitral valve
• Highly sensitive to RV geometry and preload/afterload changes

Etiology

1. Primary (Organic) TR

Structural lesion of valve apparatus.

Causes

Cause	Mechanism
Rheumatic heart disease	Leaflet fibrosis/retraction
Infective endocarditis	Leaflet destruction
Carcinoid syndrome	Fibrous plaques on leaflets
Congenital	Ebstein anomaly
Trauma	Papillary muscle rupture
Myxomatous degeneration	Prolapse/flail leaflet
Radiation	Fibrosis
Drug-induced	Ergot drugs
Pacemaker/ICD lead	Mechanical interference
Connective tissue disease	Structural damage

2. Secondary (Functional) TR

Most common form.Valve itself normal.

Mechanism

RV or RA dilation → annular dilation → leaflet tethering → malcoaptation.

Cause	Mechanism
Left-sided heart disease	Pulmonary HTN → RV dilation
Pulmonary hypertension	RV pressure overload
RV infarction	RV dilation
Dilated cardiomyopathy	RV dysfunction
Chronic atrial fibrillation	RA enlargement
Congenital shunts	RV volume overload
Chronic lung disease	Cor pulmonale

Pathophysiology

Basic Hemodynamics

During systole:

RV contracts → blood flows:

• Forward into pulmonary artery
• Backward into RA

This causes:

• RA volume overload
• RV volume overload
• Systemic venous congestion
• Reduced forward cardiac output

Hemodynamic Consequences

Right Atrium

• RA dilation
• Elevated RA pressure
• Giant V waves
• Atrial fibrillation

Right Ventricle

• Volume overload
• Eccentric hypertrophy
• Progressive dilation
• RV failure

Venous System

Elevated venous pressure causes:

• JVP elevation
• Hepatic congestion
• Ascites
• Peripheral edema
• Pleural effusion

Severe Chronic TR

Can lead to:

• Cardiac cirrhosis
• Congestive hepatopathy
• Cardiorenal syndrome
• Cachexia
• Low cardiac output state

Causes of Functional TR — Important Concept

TR severity depends heavily on:RV geometry and Pulmonary pressures

Thus TR may worsen with:

• Fluid overload
• AF
• Pulmonary HTN
• Mechanical ventilation
• LV failure

and improve after treatment.

Acute vs Chronic TR

Feature	Acute TR	Chronic TR
RA compliance	Low	High
RA pressure	Very high	Moderately high
Symptoms	Severe	Gradual
RV adaptation	None	Present
Murmur	Soft/short	Holosystolic
Congestion	Sudden shock	Chronic edema

Clinical Features

Symptoms-Mild TR (Usually asymptomatic)

Moderate-Severe TR

Systemic Venous Congestion

• Fatigue
• Edema
• Ascites
• Abdominal distension
• Hepatic discomfort
• Early satiety
• Anasarca

Low Output Symptoms

• Weakness
• Exercise intolerance

Arrhythmias

• Palpitations
• AF/flutter

Physical Examination

• Jugular Venous Pulse –Giant CV waves / V waves(Due to systolic backflow into RA)
• Lancisi Sign-Prominent systolic neck pulsations.
• Pulsatile Liver-Systolic hepatic pulsations due to venous transmission.

Murmur

Classical Murmur

• Holosystolic/pansystolic
• Left lower sternal border
• High-pitched blowing

Carvallo Sign

Murmur intensity increases during inspiration.

Mechanism:Inspiration ↑ venous return to right heart—-Increased TR flow

This helps distinguish TR from MR.

Other Signs

Finding	Cause
RV heave	RV enlargement
Peripheral edema	Venous congestion
Ascites	Severe RHF
Hepatomegaly	Congestion
AF	RA dilation
Cyanosis	Advanced disease

Investigations

ECG May show:

• RA enlargement
• AF
• RV hypertrophy
• Right axis deviation

Chest X-ray Findings:

• Cardiomegaly
• RA enlargement
• RV enlargement
• Pleural effusion

Echocardiography (Gold Standard Investigation)

Echo Parameter	Why Important
RV size	RV overload
TAPSE	RV function
Septal flattening	RV pressure overload
IVC size/collapse	Congestion
Hepatic vein reversal	Severe TR
TR jet velocity	Severity
Pulmonary pressures	RV afterload

Jet velocity estimates pressure gradient,

NOT severity directly.

Using Bernoulli equation:

ΔP=4V2

where:V = peak TR jet velocity.

Uses of TR Jet Velocity

Mainly used to estimate:

• RV systolic pressure,
• pulmonary artery systolic pressure (PASP).

PASP≈4(TRV)2+RAP

Where:

• TRV = peak TR velocity,
• RAP = right atrial pressure.

Important ICU Concept

A very high TR velocity usually suggests:

• pulmonary hypertension BUT
• severe TR itself may produce LOWER velocities because RV and RA pressures equalize quickly.

Pitfall

Severe TR may have LOW jet velocity

Because:

• RA pressure is markedly elevated,
• RV-RA gradient falls.

Thus:

low TR velocity does NOT exclude severe TR.

Severity Classification

Parameter	Mild TR	Moderate TR	Severe TR
Color jet area	Small central jet	Intermediate	Large central jet or eccentric wall-impinging jet
CW Doppler jet	Faint/parabolic	Dense	Dense triangular early peaking
Hepatic vein flow	Normal systolic dominance	Blunted systolic flow	Systolic flow reversal
RA/RV size	Normal	Mild-moderate enlargement	Marked enlargement
IVC size	Normal	Dilated	Dilated with poor collapse

Hepatic Vein Doppler

Severe TR → systolic flow reversal(Very specific finding)

Cardiac MRI

Useful for:

• RV volumes
• RV function
• Congenital disease
• Quantification

Best modality for RV assessment.

Cardiac Catheterization

Rarely needed.

May show:

• Elevated RA pressure
• Giant V waves
• Pulmonary HTN

Differential Diagnosis

Disease	Difference
Mitral regurgitation	Murmur at apex
VSD	Harsh murmur
Pulmonary regurgitation	Diastolic murmur
Constrictive pericarditis	Kussmaul sign
Restrictive cardiomyopathy	Biatrial enlargement

Management

Most mild  asymptomatic TR does not require urgent specialist evaluation.Rest all need early Cardiologist evaluation.

Main Goal

Treat:Congestion/Underlying cause

Medical therapy does NOT correct valve lesion.

Diuretics-Cornerstone.

Drugs

Drug	Role
Furosemide	Loop diuresis
Torsemide	Better bioavailability
Bumetanide	Resistant edema
Spironolactone	Adjunct

Important Concept

Aggressive diuresis may improve:

• Functional TR
• RV geometry
• Symptoms

Treat Underlying Causes

Cause	Treatment
Left HF	GDMT
Pulmonary HTN	PH therapy
AF	Rhythm/rate control
Sleep apnea	CPAP
Endocarditis	Antibiotics
Carcinoid	Somatostatin analogs

Pulmonary Hypertension Treatment

Important in secondary TR.

Reducing RV afterload may decrease TR severity.

Surgical Management Indications

• Severe symptomatic primary TR
• Severe TR during left-sided valve surgery
• Progressive RV dilation/dysfunction
• Device-related TR

Types of Surgery

1. Annuloplasty (Preferred) Most common.

Ring annuloplasty

Best outcomes.

Mechanism:

• Reduces annular diameter
• Restores leaflet coaptation

2. Valve Repair

Techniques:

• De Vega annuloplasty
• Leaflet augmentation
• Edge-to-edge repair

Repair preferred over replacement.

3. Valve Replacement

Needed when repair impossible.

Prosthesis

Type	Comments
Bioprosthetic	Preferred usually
Mechanical	Higher thrombosis risk

Why Mechanical Valves Are Less Preferred

Right-sided low-flow state predisposes to thrombosis.

Transcatheter Therapies (Rapidly Expanding)

Major modern advance.

Useful in:

• High surgical risk
• Elderly
• Advanced HF

ICU Considerations

ICU Causes of Acute/Worsening TR

ICU Condition	Mechanism
ARDS	Pulmonary HTN → RV dilation
Mechanical ventilation	Increased RV afterload
Pulmonary embolism	Acute RV pressure overload
Septic shock	RV dysfunction
RV infarction	Papillary dysfunction/dilation
Massive fluid resuscitation	Annular dilation
Pulmonary hypertension	RV remodeling
Pacemaker leads	Mechanical interference
ECMO cannulas	Valve distortion
Endocarditis	Leaflet destruction

Very important in severe TR.

Goals TO Maintain:

• Preload
• Sinus rhythm
• RV contractility

Avoid:

• Hypoxia
• Hypercarbia
• Acidosis
• Increased PVR

Preload Management

TR is:Preload dependent BUT Volume overload worsens TR

Therefore preload management is delicate.

Too Little Preload

Causes:

• Reduced RV output
• Hypotension
• Shock

Too Much Preload

Causes:

• RV dilation
• Annular dilation
• Worsening TR
• Septal shift
• Reduced LV filling

CVP Interpretation in TR

Important Pitfall

CVP is often falsely elevated in severe TR.

Thus:

• CVP poorly predicts volume responsiveness
• Giant V waves distort readings

A CVP of 18 mmHg may still coexist with intravascular depletion.

Ventilation

High intrathoracic pressure worsens:

• Venous return
• RV output

Avoid excessive PEEP.

Vasopressors

Agent	Effect
Norepinephrine	Good choice
Vasopressin	Useful in PH
Phenylephrine	May worsen RV output

Inotropes

Drug	Use
Dobutamine	RV dysfunction
Milrinone	RV failure + PH