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Rare cause of desaturation in a patient with decompensated chronic heart failure

Session Poster Session 4

Speaker Alexander Valerievitch Nossikoff

Event : Heart Failure 2019

  • Topic : valvular, myocardial, pericardial, pulmonary, congenital heart disease
  • Sub-topic : Pulmonary Embolism
  • Session type : Poster Session

Authors : A Nossikoff (Sofia,BG), K Angeloff (Sofia,BG), N Koleva (Sofia,BG), D Evrev (Sofia,BG), T Donova (Sofia,BG)

Authors:
A Nossikoff1 , K Angeloff1 , N Koleva1 , D Evrev2 , T Donova2 , 1University Hospital "Lozenets", Cardiology - Sofia - Bulgaria , 2University Hospital "Lozenets", Cardiac and vascular surgery - Sofia - Bulgaria ,

Citation:

Clinical presentation. 78-year old male was admitted to our institution due to progressive shortness of breath. He had known LV dysfunction and congestive heart failure and recent hospitalisation for a previous decompensation. On admission he appeared to be drifting away, while desaturating down to 67% on pulseoxymetry. There was bilateral pitting oedema below the knees. Notably, no significant crackles were heard in the lung bases and CXR was not consistent with significant lung congestion. The patient was put on oxygen supplementation and intravenous furosemide. His BP was stable throughout the hospital stay.

Clinical investigations and diagnostic process. Labs were unremarkable except creatinine of 94 umol/L consistent with CrCl of 50ml/min and PaO2 of 50mmHg from arterial blood gases. Despite the intravenous furosemide the patient was not improving even after further dosage escalations. EKG showed LAHB and AV-block grade 1. We performed transthoracic echocardiography, which revealed a large LV with EDV of 300ml, LV EF of 30% and moderate AR and MR. There was biatrial dilation, moderate TR, dilated RV and estimated systolic PAP was nearly 100mmHg. Notably, the interatrial septum was bulging from right to left and there was a small eccentric RtoL shunt through it, which was evident on colour doppler. We performed compression ultrasound on lower limbs, which revealed bilateral femoropopliteal DVTs and confirmed our suspicion of VTE. CTPA revealed bilateral pulmonary embolism. Patient was classed as high intermediate risk by PESI score. He was put on therapeutic dosage of LMWH and remained stable and gradually improving. However, he insisted of leaving the hospital against our medical advice on day 3 from the diagnosis of PE. We decided to commence NOAC (rivaroxaban 2x15mg for 3 weeks than 20mg) and to discharge him. Several weeks later there was marked improvement in his clinical status. He was no longer limitied by shortness of breath, there was no longer evidence of pulmonary hypertension on transthoracic echocardiography and the interatrial septum was no longer bulging into left atrium.

Conclusions and implications for clinical practice. Patients with chronic heart failure are prone to thrombotic events. This is especially true during periods of prolonged bed rest and decompensations. When unexplained breathlesness, desaturation or out of proportion pulmonary hypertension are present VTE should be excluded.  Presence of DVT on compression ultrasound in patients with suspected pulmonary embolism confirms the diagnosis at bedside. We believe that the main cause of desaturation in this case was the pulmonary embolism. The right-to-left shunt was caused by stretched PFO opened by the high right atrial pressure and had only partial contribution to the desaturation. Notably, this patient had bilateral DVT, which is rare. In such cases the usual signs of DVT can be masked or may affect both legs making the clinical diagnosis of DVT impossible.

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