RV dysfunction


See TTE exam RV for all measurements.

Assessment of the RV is essential knowledge for the critical care echocardiographer. As the cardiac output of 1 side of the heart has to equal the cardiac output of the other side it is just as important as the LV. In fact assessment of the RV is arguably more important than the LV as the RV is very sensitive to fluid balance, positive pressure variation and many critical illness pathologies.

The RV is made up of inflow and outflow regions. Contraction is longitudinally, radially (free wall towards septum) and rotation pulled by the LV. It empties into a low pressure system (pulmonary vasculature) so is less muscular than the LV. Ejection of its SV continues into its relaxation so its outflow is semi continuous. It will dilate acutely in response to increased afterload and is able to become hypertrophied in 48h. The RV is perfused in both systole and diastole so its function is dependent on an adequate mean blood pressure.

Cor Pulmonale

This is RV dysfunction caused by increased RV afterload. This overloads the RV in diastole and systole.

RV overload will typically be associated with high PA pressures but if the RV is failing these may pseudonormalise.

Diastolic overload
RV dilatation.
RVEDA:LVEDA <0.6 is normal. 0.7-0.9 moderate. >1 severe.
The RV is very compliant so volume can increase with little change in pressure initially.
TR will also develop and worsen as the leaflet tips are pulled further away from one another (functional TR).
If severe, the RV will move over top of its Starling curve and start to fail.
RV dilatation results in reduced LV filling as the RV takes up space at the expense of the LV in the fixed size pericardium.
The RA will be dilated.

Systolic overload
Septal dyskinesia (D-shaped septum at end systole).
Increased RV afterload prolongs ejection time so the RV is still contracting as the LV begins to relax at the end of systole. RV pressure is transiently higher than LV pressure pushing the IVS into the LV.
This can either be eyeballed or measured at end systole.
The RV dilates very quickly in response to increased afterload so will also demonstrate diastolic overload (dilatation) too.
May open up a PFO and cause R to L shunt and worsen hypoxaemia. In this case, recruitment in ARDS will worsen hypoxaemia. Contrast echo will reveal a PFO.

Acute vs chronic cor pulmonale

Acute

  • PE, ARDS, fluid overload.
Chronic
  • ASD, VSD, severe TR or PR, PS, pulmonary hypertension (recurrent PE, L sided regurg, L heart failure, COPD, interstitial lung disease).
The RV wall becomes thickened relatively quickly in response to increased afterload. It is normally <5mm but can double within 48h.
RV hypertrophy means the RV can develop high pressures >50 mmHg.
If acute then pressures will typically be <50-60.
If acute then normality will return after recovery whereas an abnormality will remain if chronic.
RV very sensitive to increase in afterload and will quickly result in dilatation and failure if acute.
A hypertrophied RV (chronic/sub-acute) will tolerate increased afterload better than a non-hypertophied acutely overloaded RV.

RV failure

Cor pulmonale causes RV dysfunction. Causes of intrinsic dysfunction include:

Sepsis
Myocardial ischaemia (R coronary which also supplies inferior LV)
Myocarditis
Myocardial contusion (most anterior cardiac chamber).
RCA air embolus post cardiac surgery.

Intrinsic dysfunction will show RV failure without elevated PAP (remember can have pseudonormal PAP with cor pulmonale and failing RV).

Assessment of contractility
Movement of RV free wall.
Annular longitudinal motion (TAPSE or TDI)
Fractional area change
Tei
Dp/dt

In practice RV contractility is assessed by eye-balling and tricuspid annular motion.

Management

Any RV dilatation reflects dysfunction.
A dilated RV should prompt extreme caution in fluid administration.
Some patients with mild to moderate RV dilatation and failure may tolerate fluid loading. The more severe it is the less likely they are to tolerate fluid. Paradoxical septal motion means no fluid should be given.
Failure to increase aortic VTI or SV with fluid or PLR with RV dilatation means no more fluid should be given.
Fluid removal (diuresis/RRT) will improve SV if the RV is volume overloaded.
Predominant RV failure can be improved with increasing coronary perfusion with vasopressors. What about an increase in PVR with noradrenaline?...‘most of the convincing literature comes from pulmonary embolism data. In these conditions, most of the raise in PAP is somewhat fixed, as it is due to clots, and thus not very sensitive to constriction/dilation. In other conditions, the small beta effect is responsible for a slight dilation in patients still responsive while alpha effect may increase pulmonary artery capillary pressure (and hence PAP) by an increase in pulmonary vein resistances. Nevertheless this effect is quite limited, and negligible compared to the benefit provided by increasing RV perfusion’. Daniel De Backer by email.
Vasopressin increases vascular smooth muscle tone and BP but causes pulmonary vasodilatation. It should therefore be used as 1st line if there is pulmonary hypertension +/- R heart failure. (Price et al. Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review. Critical Care 2010;14:R169.)
Minimise ventilation pressures with IPPV. If high PEEP is needed, TV reduction is the best way to do this. PEEP reduction may however be needed. The patient with ARDS with very high O2 requirements and a failing RV presents a particularly difficult challenge - one which we don’t always win.
Prone positioning can unload the RV.
Aim to keep PVR minimised - basic measures and consider drugs (sildenafil, prostacyclin, inhaled nitric oxide).
Improve RV function with inotropes.

PVR
Increased by:
Extremes of lung volume (lowest around FRC)
Decreased pulmonary blood flow (increased flow and pressure will recruit closed vessels)
Haematocrit and blood viscosity.
Hypoxia
Hypercapnoea
Acidosis
Vasoconstrictors, 5HT, histamine
Alpha stimulation
Local/regional PVR increased by PE, compression (pleural effusion, atelectasis).

Decreased by:
Low TV and pressures.
Improving cardiac output.
Reducing blood viscosity.
Oxygenation
Normocapnoea
Avoidance of acidosis
Vasodilators - sildenafil, prostacyclin, inhaled nitric oxide

Practical guideline for RV failure:
  • Fluid removal (diuresis, RRT).
  • Minimise mean airway pressures (TV then PEEP).
  • Maintain MAP >70 with noradrenaline.
  • Sildenafil or prostacyclin or both.
  • Dobutamine
PE

Thrombus may be visualised in the R heart or proximal pulmonary arteries.
Acute Cor Pulmonale (ACP) will result if the PE is big enough. The easiest way to assess this is the RV:LV ratio.
In acute PE, PA pressures will not usually exceed 50 mmHg.
2 other signs (which have a low sensitivity):
  • McConnell sign hypokinesis of the RV free wall with apical sparing.
  • 60/60 sign: RVOT acceleration time <60 ms with a PASP <60
Whether ACP has prognostic implications or means thrombolysis should be used is unclear.

TTE features plus metabolic acidosis (60% mortality) may be an indication for thrombolysis. (ICM 2001). 3% risk of significant haemorrhage with thrombolysis.
RVEDA:LVEDA >0.9 is associated with higher mortality in PE.

ARDS

ACP is present in 25% with ARDS and lung protective ventilation.

Sepsis

⅓ of patients have RV dysfunction.
This may explain fluid unresponsiveness.
It may only be unmasked when IPPV is applied.
See sepsis for more info.