History

Fact Explanation
Fatigue and exercise intolerance Tricuspid Regurgitation(TR) can occur according to the following mechanisms: secondary to pulmonary hypertension, anatomical abnormalities. In a patient with pulmonary hypertension, the walls of pulmonary vasculature becomes thicker. The resistance to the flow is increased[2].During exercise,inadequate pulmonary circulation results in hypoxia.This reduces aerobic metabolism in the tissues and the patient describes this as fatigue.In an isolated tricuspid regurgitation due to anatomical defect, above symptoms are due to reduced right sided cardiac output to the pulmonary circulation.[1]
Dyspnoea Dyspnoea is defined as labored breathing.This is due to hypoxia resulted by restricted pulmonary circulation,that creates a ventilation perfusion mismatch.Hypoxia stimulates respiratory center in medulla oblongata, increasing the rate and respiratory effort.[1]
Palpitations This is related to atrial arrhythmias ( atrial fibrillation/flutter).These arrhythmias are secondary to alteration in conduction circuits in atrial walls that occurs due to atrial dilation. There are two mechanisms which may result in this: conditions such as mitral stenosis gives rise to both left atrial dilation and pulmonary hypertension(secondary tricuspid regurgitation, the regurgitant flow of blood can dilate right atrium.[1]
Peripheral edema This can manifest as ankle edema or hydrocele.In tricuspid regurgitation, the increased pressure (due to regurgitant flow) in right atrium is transmitted back to venous system(Inferior vena cava).The pressure gradient at the venular end increases and transudation occurs. [1]
Abdominal distension Ascites can present as abdominal distension as a result of chronic severe TR which is from chronic congestion or fibrosis of liver (cardiac cirrhosis) resulting from reduced cardiac output from right-sided heart failure.[1]
Early satiety, dyspepsia, or indigestion Symptoms are due to congestion and resultant transudation in the stomach and intestinal walls.
Right hypochondrial pain Transudate accumulates beneath the hepatic capsule.Stretching of the capsule which is pain sensitive, causes pain.
History of a aetiology in secondary TR. Pathological TR is often secondary.The annular dilatation and increased leaflet tethering are the results of pressure or volume overload.Pressure overload is due to left sided heart diseases or cor pulmonale. Volume overload is due to intrinsic valve disease or an atrial septal defect.[4]
References
  1. ROGERS Jason H. BOLLING Steven F. The Tricuspid Valve-Current Perspective and Evolving Management of Tricuspid Regurgitation. Circulation-American Heart Association 2009 [Online].vol119. pg 2718-2725.[viewed 18 April 2014] DOI: 10.1161/CIRCULATIONAHA.108.842773
  2. GALIE Nazzareno et al. Guidelines for the diagnosis and treatment of pulmonary hypertension. European Heart Journal [Online] (2009) 30, 2493–2537. doi:10.1093/eurheartj/ehp297
  3. GIBSON D.G. Valve disease. WARREL, David A. et al ed. Oxford Textbook of Medicine. 4th edition. London.Oxford University Press. 2003
  4. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109

Examination

Fact Explanation
Pulse- Rhythm Regular or Irregularly irregular This is due to atrial arrhythmias ( atrial fibrilation/flutter).These Arrhythmias are secondary to alteration in conduction circuits in atrial walls that are results of atrial dilation. The mechanisms of this phenomenon are: conditions such as mitral stenosis gives rise to both left atrial dilation and pulmonary hypertension(secondary tricuspid regurgitation, the regurgitant flow of blood can dilate right atrium.[2][3]
Peripheral edema(ankle edema,hydrocele) In TR, the increased pressure (due to regurgitant flow) in right atrium is transmitted back to venous system(Inferior vena cava).The pressure gradient at the venular end increases(Starling's Forces) and transudation occurs.[1]
Elevated jugular venous pressure with a prominent 'c and v' Waves. The 'c' wave occurs as the right ventricular systolic pressure is transmitted to right atrium before the closure of tricuspid valve.[4] Then backward pressure wave is transmitted along the internal jugular vein. The 'v' wave occurs during the venous return to right atrium[4].There is a regurgitant flow due to TR that increase the total volume in the right atrium.This becomes a vicious cycle that leads to dilation of the right atrium.Eventually the backward pressure wave is transmitted along the internal jugular vein.
Precordial bulging In a patient with pulmonary hypertension (due to either a cardiac or pulmonary cause), the resistance in the pulmonary circulation causes right ventricular hypertrophy. With time changes in shape of the thoracic wall can be observed.
Para sternal heave The hypertrophied right ventricle creates pressure on the precordium,[4] that is palpated in the form of para sternal heave[5].
Pan systolic murmur at left lower sternum which increases in intensity on inspiration. (Carvallo’s sign). The murmur is generated by turbulent flow. In TR increased blood flow and regurgitation across the tricuspid valve causes the turbulence of flow.[1],[2],[3],[4],[5]
Third heart sound (S3) A third heart sound (S3) is heard in rapid ventricular filling.Due to the regurgitant flow, there is an increase the total volume in the right atrium.The increased volume produces S3.This is common in patients with heart failure.[5]
Loud second heart sound in the pulmonary area (P2) This is audible in patients with pulmonary hypertension.[5]
Pulsatile, tender hepatomegaly In Tricuspid Regurgitation, the increased pressure (due to regurgitant flow) in right atrium is transmitted back to venous system(Inferior vena cava).The pressure gradient at venular end increases and transudation occurs.The transudate accumulates and stretches the pain sensitive hepatic capsule. The back pressure causes congestion of blood in hepatic venous system.This also contributes to the hepatomegaly.[5]
Ascitis Ascites can present as abdominal distension as a result of chronic severe TR which is from chronic congestion or fibrosis of liver (cardiac cirrhosis) resulting from reduced cardiac output from right-sided heart failure.[1],[2]
Signs of aetiology in secondary TR Pathological TR is often secondary.The annular dilatation and increased leaflet tethering are the results of pressure or volume overload. Pressure overload is due to left sided heart diseases such as mitral stenosis or cor pulmonale. Volume overload is due to intrinsic valve disease or atrial septal defects.[6]
References
  1. GIBSON D.G. Valve disease. WARREL, David A. et al ed. Oxford Textbook of Medicine. 4th edition. London.Oxford University Press. 2003
  2. ROGERS Jason H. BOLLING Steven F. The Tricuspid Valve-Current Perspective and Evolving Management of Tricuspid Regurgitation. Circulation-American Heart Association 2009 [Online].vol119. pg 2718-2725.[viewed 18 April 2014] DOI: 10.1161/CIRCULATIONAHA.108.842773
  3. EAGLE Kim A, BALIGA RR. Practical Cardiology: Evaluation and Treatment of Common Cardiovascular. 2nd edition. Philadelphia. Lippincott Williams & Wilkins. 2008.
  4. CAMM AJ. BUNCE NH. Cardiovascular Disease. KUMAR, Parveen, CLARK Michael ed. Kumar & Clark's Clinical Medicine. 8th edition. London. Saunders Elsevier. 2012.
  5. GALIE Nazzareno et al. Guidelines for the diagnosis and treatment of pulmonary hypertension. European Heart Journal [Online] (2009) 30, 2493–2537. doi:10.1093/eurheartj/ehp297
  6. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109

Differential Diagnoses

Fact Explanation
Atrial septal defect The patient may present with similar presentation due to secondary TR.For the differentiation, Following symptoms, signs may be useful. The murmur is usually results from flow across the pulmonic valve and audible in the left upper parasternal region. Instead of holosystoli, it's much softer, mid or ejection systolic c, and wide fixed split second heart sound may be seen [1] Usually this is diagnosed and treated in the childhood.If untreated, it's likely to presented with complications (Eisenmenger syndrome) [2]
Parent ductus arteriosus Usually diagnosed in neonates( specially in preterms).Associated with a bounding pulse continuous murmur at the base of the heart.[1] likely to present with complications (Eisenmenger syndrome cyanosis,clubbing and polycythemia) if the patient is untreated.[2]
Mitral regurgitation Presents with left sided heart failure symptoms (exertional dyspnoea, orthopnoea). Following signs are useful in differentiation: a displaced apex beat, soft first heart sound, and a pan systolic murmur most prominent at the mitral area that radiates to the axilla.[1],[2],[3]
Pulmonic stenosis This is commonly diagnosed neonates.In milder forms, symptoms and signs are of right heart failure, but a soft P2 ,harsh mid systolic ejection murmur and a thrill at the pulmonary area are differentiating signs.[1],[2]
Tetralogy of Fallot Typically neonates/infants who are cyanosed with a heart murmur. There maybe a antenatal diagnosis on fetal echocardiogram. Cyanosis or hypercyanotic spells will present at later stages.The patient may be diagnosed with genetic syndromes such as DiGeorge syndrome. Physical examination may reveal significant tachypnoea and cyanosis in severe cases, a single second heart sound, a parasternal heave and harsh ejection systolic murmur best heard at the left sternal border.[1],[2]
References
  1. CAMM AJ. BUNCE NH. Cardiovascular Disease. KUMAR, Parveen, CLARK Michael ed. Kumar & Clark's Clinical Medicine. 8th edition. London. Saunders Elsevier. 2012.
  2. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109

Investigations - for Diagnosis

Fact Explanation
Trans thoracic echocardiography(2D/3D) and color flow doppler. Done in order to differentiate the causes (primary and secondary causes by observing structural abnormalities),asses the degree of dilation of annulus which is used to grade the severity together with pulmonary systolic pressure. [1],[2],[3] Trans esophageal echocardiography (TOE) should be considered when trans thoracic echocardiography (TTE) is of suboptimal quality or when thrombosis, prosthetic dysfunction, or endocarditis is suspected.[2]
Cardiac magnetic resonance When echocardiographic imaging is suboptimal and investigation of choice in assessing a patient with severe TR or to asses other right ventricular parameters.[1],[3]
Cardiac catheterisation This invasive procedure is only used when non invasive investigation data are suboptimal. Also this technique is used in accurate measurement of pulmonary artery pressure and pulmonary vascular resistance to identify a cause for pulmonary hypertension.[1],[3]
Chest X-Ray This investigation indicates cardiomegaly and supports the diagnosis of pulmonary hypertension.[2]
ElectroCardiogram (ECG/EKG) This is used to conform rhythm abnormalities(atrial fibrillation). It also provides additional information to suggest complications such as right bundle branch block to suggest right ventricular hypertrophy.[2]
References
  1. Guidelines for the Management of Patients with Valvular Heart Disease. ACC/AHA Practice Guidelines. American Heart Association. 2014. [viewed 18 April 2014] Available from: http://circ.ahajournals.org/content/98/18/1949.long
  2. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109
  3. BADANO Luigi P, MURARU Denisa, SARANO Maurice Enriquez. Assessment of functional tricuspid regurgitation. Eur Heart J (2013) [Online]. [viewed 18 April 2014] doi: 10.1093/eurheartj/ehs474

Investigations - Fitness for Management

Fact Explanation
Trans esophageal echocardiography Should be considered when thrombosis or endocarditis is suspected.[1]
Exercise ECG The purpose is to further assess asymptomatic patients or those with doubtful symptoms. Exercise testing will also determine the level of physical activity allowed. [1]
Exercise echocardiography Exercise echocardiography may provide additional information regarding the functional state in exertion.[1]
References
  1. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109

Investigations - Followup

Fact Explanation
Echocardiography (2D/3D) with color flow doppler. This is a non invasive, accurate and commonly performed.
References

Management - General Measures

Fact Explanation
Patient Education Patients should understand how to monitor their symptoms, weight fluctuation and restrict their sodium intake, have good compliance on medication and stay physically active. Education regarding these recommendations can significantly improve outcomes[1]
Restriction of dietary Sodium. Observational study data suggest an association between dietary sodium intake with fluid retention and risk for hospitalization. The sodium homeostasis is altered in patients with HF as opposed to healthy individuals so restriction of dietary sodium is important.[1]
Activity, Exercise Prescription, and Cardiac Rehabilitation Exercise training (or regular physical activity) is recommended.[1] Cardiac rehabilitation can be useful in clinically stable patients with HF to improve functional capacity, exercise duration, mortality[1]
References
  1. YANCY Clyde W et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure. Circulation. [Online] 2013; 128: e240-e327. [Viewed 18 April 2014]. doi: 10.1161/​CIR.0b013e31829e8776

Management - Specific Treatments

Fact Explanation
Diuretics Following are commonly used diuretics[1] in managing symptomatic patients. Bumetanide, furosemide, and torsemide inhibit Na+ absorption in thick ascending limb of the loop of Henle (thus, the term loop diuretics)[2] and they are the more preferred group. Thiazides inhibit transport of Na+ in Proximal Convoluted Tubules(PCT). [2] Aldesterone receptor antagonists such as spironolactone antagonize the effect of Aldesterone at the collecting tubules.[2] Sodium is the significant osmotically active ion that retains water. These drugs increase urinary sodium excretion and decrease physical signs of fluid retention in patients with heart failure.[1]
Angiotensin Converting Enzyme Inhibitors (ACEI) Drugs such as Captopril or Enalapril inhibit the conversion of angiotensin I to angiotensin II.It reduces the effect of angiotensin II and there by produce vasodilation, reduce peripheral resistance and reduces afterload. It also reduces Aldesterone secretion and eventually reduce salt and water retention.[3] ACEI reduce morbidity and mortality in heart failure.[1]
Angiotensin Receptor Blockers (ARB) They inhibit the action of angiotensin II on AT1 receptors found on the vasculature.The effect is similar to that of ACEI these are used as an alternative to ACEI in patients intolerant to ACEIs. [3]
Beta Blockers (bisoprolol, carvedilol, and sustained release metoprolol succinate) These drugs competitively inhibit the action of catecholamines on beta receptors on the myocardium exerting a negative inotropic effect.These are a prognostically beneficial class of drugs. [3]
Digoxin Used treat atrial fibrillation. This cardiac glycoside increases the intracellular free calcium level and increase contractility and reduces heart rate.This is only beneficial symptomatically.[3]
Anticoagulants The selection of an anticoagulant agent for permanent/persistent/paroxysmal AF should be individualized.The action of Warfarin is that,it blocks gamma carboxylation of glutamate residues of clotting factors II, VII, IX and X. This means that they stay in an inactive form. This is used in the treatment of chronic atrial fibrillation.[4]
Sildenafil Causes vasodilation in pulmonary vasculature in patients with pulmonary hypertension and relives dyspnoea. However the precipitant cause must be managed optimally.[5]
Surgical valve replacement Surgery is indicated in patients with severe TR. If it is technically feasible valve repair is preferable to valve replacement and surgery should be carried out early enough to avoid irreversible right ventricular dysfunction. Surgery limited to the tricuspid valve is recommended in symptomatic patients with severe primary TR. Though these patients respond well to diuretic therapy, delaying surgery is likely to result in irreversible RV damage, organ failure. [1],[6]
Endocarditis Prophylaxis Antibiotic prophylaxis should be considered for high-risk procedures in high-risk patients such as those with prosthetic heart valves or patients with previous endocarditis.[6]
References
  1. YANCY Clyde W et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure. Circulation. [Online] 2013; 128: e240-e327. [Viewed 18 April 2014]. doi: 10.1161/​CIR.0b013e31829e8776
  2. IVES Harlan E. Diuretic Agents. KATZUNG Bertram G, MASTERS Susan B, TREVOR Anthony J ed. Basic & Clinical Pharmacology.12th edition. New York. McGraw-Hill. 2012.
  3. KATZUNG Bertram G. Drugs used in heart failure. KATZUNG Bertram G, MASTERS Susan B, TREVOR Anthony J ed. Basic & Clinical Pharmacology.12th edition. New York. McGraw-Hill. 2012.
  4. ZENDER James L. Drugs used in disorders of coagulation. KATZUNG Bertram G, MASTERS Susan B, TREVOR, Anthony J ed. Basic & Clinical Pharmacology.12th edition. New York. McGraw-Hill.2012.
  5. GALIE Nazzareno et al. Guidelines for the diagnosis and treatment of pulmonary hypertension. European Heart Journal [Online] (2009) 30, 2493–2537. doi:10.1093/eurheartj/ehp297
  6. VAHANIAN Alec et al. Guidelines on the management of Valvular Heart Diseases. European Heart Journal [Online] (2012) 33, 2451–2496. doi:10.1093/eurheartj/ehs109