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TR with or without Pulmonary HTN

 

Thank you for asking me to perform a cardiovascular of examine Mr. X, who presented with SOB.

 

The salient finding on examination was a pansystolic murmur loudest in the tricuspid region, which increased on inspiration and was associated with a JVP with large v-waves, which I believe is consistent with tricuspid regurgitation. . There was a left parasternal heave, which may represent right ventricular dilatation from TR, or pulmonary hypertension with functional TR as a manifestation.  

 

I will now present my findings in full before commenting on differentials, aetiology, severity and complications.

 

The patient was comfortable at rest with normal/increased WOB.

 

On examination of the hands, there was/was no stigmata of IE, clubbing, peripheral cyanosis, or xanthomata.

 

The pulse was ____ and regular/irregular (if irregular, consistent with atrial fibrillation).

 

The blood pressure was ____.

 

On examination of the face, there was no scleral icterus, conjunctival pallor, or xanthelasma. There was no central cyanosis. Dentition was adequate/inadequate.

 

The JVP was/was not elevated at ___ cm above the sternal notch with prominent V-waves (prominent A-waves if pulmonary hypertension). This was associated with a pulsatile liver.

 

The carotid pulse was normal character in character.

 

On inspection of the praecordium, there were/were not scars and nil obvious deformity.

 

On palpation, the apex beat was fifth intercostal space mid-clavicular line (presumably not volume or pressure loaded unless left ventricular involved). There were/were not any palpable thrills (may have thrill for TR). There was/was not a palpable P2. There was a left parasternal heave, which may represent right ventricular dilatation from TR, or hypertrophy from pulmonary hypertension.  

 

On auscultation, as aforementioned, there was a pansystolic murmur loudest in the tricuspid region, which increased on inspiration without radiation to the carotids or axilla.

 

There was a normal first and loud second heart sound (loud P2 if pulmonary HTN), with physiological/fixed/reversed splitting, with no additional third or fourth heart sound/third/fourth heart sound (RV third heart sound if RV failure).

 

On further examination, there was/was not evidence of left and right heart decompensation with sacral oedema or peripheral oedema, and vesicular breath sounds/bibasal inspiratory crackles. There was/was not a pulsatile liver, and nil gross ascites.

 

In summary:

  • My findings are consistent with tricuspid regurgitation with/without pulmonary hypertenson

 

Other differentials include:

  • Mitral regurgitation

  • Aortic stenosis

 

In terms of signs of severity:

  • Large V-waves

  • Ventricular heave

  • Soft S1

  • Pulsatile liver

  • Right sided decompensation

 

In terms of the aetiology:

  • This may be due to functional secondary TR in the context of pulmonary hypertension:

    • (Which may be secondary to left heart failure) - comment on any left sided lesions.

    • May be secondary to left to right shunts, and Eisenmenger syndrome.

  • Functional secondary to dilated cardiomyopathy

  • Primary:

    • IE

    • Rheumatic

    • Congenital - Ebstein’s anomaly

    • RV papillary muscle infarction

 

I would proceed from here by:

  • Confirming my diagnosis with an echocardiogram

 

What are the aetiologies?

  • Functional - from RV failure and pHTN

  • Rheumatic - rarely isolated however

  • IE

  • Congenital (Ebstein’s anomaly)

  • RV papillary muscle infarction

  • Tricuspid valve prolapse

 

What is the aetiology of pulmonary hypertension?

  • 1 = PAH, connective tissue disease

  • 2 = left heart failure

  • 3 = chronic lung disease

  • 4 = chronic thromboembolic disease

  • 5 = other

 

What does the parasternal heave represent?

  • A sustained systolic left parasternal lift is most frequently appreciated in the presence of significant right ventricular hypertrophy. Long-standing, severe pulmonary arterial hypertension, whether precapillary (eg, idiopathic pulmonary arterial hypertension or pulmonary valve stenosis) or postcapillary (eg, mitral stenosis, cardiomyopathy), produces right ventricular hypertrophy and a sustained lower left parasternal lift.

  • A hyperdynamic but not sustained left parasternal systolic impulse may be palpable when right ventricular volume is increased, as with an atrial septal defect or tricuspid regurgitation. The left parasternal impulse becomes sustained during systole when pulmonary arterial hypertension is also present

 

What are the indications for surgery?

  • Rarely if functional, unless getting open cardiac surgery otherwise

  • Class 1 = severe and getting left sided surgery regardless

  • Class 2a if right side failure and primary severe TR

 

Working out the JVP:

  • Single large clear upstroke - going to be A-wave or V-wave

  • If followed by two troughs, think A-wave

  • If followed by one trough, think V-wave

  • A-wave quickly followed (the trough/descent part afterwards) by S1

  • Take a guess

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