Dr Chris Harrington (FACEM)  presents 2 cases for this month.  Both demonstrate the importance of ECHO in the context of the deteriorating patient with heart failure.

A 48F is referred to the Emergency department by her cardiologist with exacerbation of right heart failure and rapid AF

PHx

  • aortic valve repair (for congenital aortic stenosis)
  • severe RV dilatation /HF
  • rapid AF
  • Severe TR (failed annulosplasty)
  • Hypothyroidism

Standard heart failure treatment was commenced.

Shortly afterwards her BP fell to 44 mmHg systolic with associated dizziness. She was transferred  to resus.  Bloods were retaken . Lactate was found to have increased from 3 to 12 . Creatinine and liver function tests confirmed DIC . An ECHO was performed.

This is her PLAX view. Describe what you see

  • The RV is grossly dilated . It is much larger than the LV
  • The RV is contracting very poorly. Watch the free wall of the RV – there is almost no longitudinal contraction of the wall
  • The LV cavity is small and the LV is very poorly contracting.
  • The IVS is flattened towards the LV because of the high RV pressures.

This is her PSAX view. Describe what you see

  • The RV is large. It should be smaller than the LV. It is much larger.
  • The RV is poorly contracting
  • The pressures in the RV are so high that the IVS is flattened and the LV has a D shape
  • The LV is poorly contracting

This is an atypical 4 chamber view. Describe what you see

The RV is larger than the LV, the RV is poorly contracting and is squashing the LV. Note that it is squashing the LV throughout the cardiac cycle but even more on inspiration due to increased venous return on inspiration. The movement of the IVS is due to interventricular dependence.
 

This is her IVC. Can you comment on it’s size?

The IVC is severely dilated at 2.33 cm.

The IVC can be used to estimate RA pressures. The estimated RA pressure with an IVC which is less than 2.1cm and collapsing more than 50% is 3 -5 mmHg, if collapsing less than 50% then it is estimated at 8mmHg. If it is more than 2.1 cm and collapsing less than 50% then the estimated RA pressure is 15mmHg, if collapsing more than 50% it is estimated as 8mmHg.

In this case the IVC is fixed and dilated . The RA pressures can be estimated as 15mmHg – 20mmHg

An abdominal scan showed cardiac ascites.

Sepsis in the setting of severe RHF was the working diagnosis. Antibiotics,  ionotropes (noradrenaline) and vasopressors (doputamine)  were commenced. She was transferred to ICU and made a slow but good recovery.

Case 2

A 67F  with influenza A  is admitted for syncope and cough

PMhx

  • severe pulmonary hypertension on the background of emphysema, COPD and HFrEF (45%)

Episode of hypotension (82mmHg) and worsening abdominal pain whilst in ED.

An abdominal scan  showed cardiac ascites.

This  is her ECHO.

PLAX view

PSAX view

4CV

IVC

This ECHO again shows all the hallmarks of severe pulmonary hypertension and RV failure.

  • A large RV in the PLAX squashing the LV. The RV here is contracting better that in case one but it is still reduced. There is flattening of the IVS
  • A large RV in the PSAX view and a D shaped LV due to high RV pressures causing flattening of the IVS
  • A large RV in the 4CV again with flattening of the IVS. Note that the apex of the RV is “taking over the LV” indicating it is very dilated. In a normal heart, the LV apex should be more prominent than the apex of the LV
  • Fixed and dilated IVC

On the basis of the scan she was started on vasopressors (Noradrenaline) and referred to ICU. A formal ECHO 7 days later showed a dilated RV, mod-severe RV dysfunction,a severely dilated RA, severe pulmonary HTN (85mmHg) and ascites. She was treated with inotropes, oseltamivir and discharged on augmentin duo forte, oseltamivir and frusemide for pulmonary hypertension clinic follow up.

Take home points:

  • Cardiac ascites (and/or abdominal pain ) is a sign of deteriorating right heart function.
  • Hypotension is a late finding  and should be treated with ionotropes
  • The treatment of a patient with severe right HF is not the same as that of a patient with left HF with pulmonary oedema. In left HF  nitrates cause venodilation, increasing venous capacitance and lowering preload and at high doses can cause coronary artery dilation allowing better cardiac oxygenation. In right HF there is poor right ventricular contraction and patients are very preload sensitive . Nitrates may in fact cause severe hypotension exacerbating  right HF and causing the patient to deteriorate.
  • Whilst frusemide is used in the treatment of congestive heart failure, in the context of pulmonary hypertension and severe right HF, it may  exacerbate hypotension. Use judiciously. Start with 40mg

Treatment is  based on

  •  Careful and judicial fluid administration to increase preload in the early stages of the disease.
  •  Reducing afterload, which in most cases , if associated with chronic lung disease and chronic heart disease is difficult to reverse,  but possible in acute RHF from a submassive PE for example
  • Optimising factors which will not increase pulmonary vascular resistance such as improving oxygenation (SaO2 > 92%) , aiming for normocapnia and reducing acidaemia 
  • Improving RV contractility using vasopressors or ionotropes such as noradrenaline and /or using low dose Dopamine (<5 μg kg−1 min−1) which increases cardiac contractility without compromising pulmonary vascular resistance
  • Expedite transfer to ICU
  • Avoid intubation at all costs

Any questions about this case please email Chris at Christopher.Harrington@health.nsw.gov.au

For any questions about the RPA ED COM or if you have any suitable cases please email Jay at jayashanki.perera@health.nsw.gov.au or Genevieve at genevieve.carbonatto@health.nsw.gov.au

 

References

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4225807/

2.

Right Ventricular failure