Pulmonary HTN + TR 

 

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

 

The salient finding on examination were a palpable P2, left parasternal heave and loud P2 (alternatively ‘features of pulmonary hypertension’), with an associated 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 pulmonary hypertension with functional tricuspid regurgitation.

 

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 normal / 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 a palpable P2. There was a left parasternal heave.

 

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/was not an associated early diastolic murmur at the upper left sternal edge, louder during inspiration.

 

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.

• Alternatively, there was fine inspiratory crepitations throughout the lower / middle / upper lobes bilaterally with/with no added wheeze, suggesting of underlying lung disease.

 

In summary:

• My findings are consistent with pulmonary hypertension with/without functional tricuspid regurgitation +/- pulmonary regurgitation.

 

Other differentials include:

• Mitral regurgitation

• Aortic stenosis

 

In terms of aetiology:

• There were no overt signs of connective tissue disease

• There were/were not signs of congenital heart disease

• Signs of left heart failure

• There were/were not signs of chronic lung disease

 

I would proceed from here by:

• Screening for pulmonary hypertension with an echocardiogram

• Confirming with a right heart catheter

 

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

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