Outline the therapeutic options with rationale for the treatment of right ventricular dysfunction in an ICU patient.
By titrating fluid if hypovolaemic or diurese or dialyse off volume if required.
Most conditions that lead to RV dysfunction in the ICU are due to increased afterload & an enlarging RV may worsen coronary perfusion as well as impede LV filling through ventricular interdependence. Hence reducing RV excessive preload can both reduce RV stretch and function as well as improving the performance of the LV.
In those specific circumstances where RV output is impaired due to contractile dysfunction e.g. in the setting of a normal afterload, a higher preload is needed to maintain forward flow. e.g. RV infarction
General measures to improve contractility:
Avoid over stretch of the RV free wall with optimisation of preload and afterload.
Maintenance of Sinus rhythm – correct electrolytes, acidaemia, use of anti-dysrhythmics, and if needed AV sequential pacing.
1. Noradrenaline improves coronary perfusion in the RV but will increase pulmonary vascular resistance (PVR); however, the overall impact is that noradrenaline has been shown be helpful in RV dysfunction
2. Adrenaline improves RV contractility without increasing (PVR)
3. Milrinone (50mcg/kg bolus -> 0.2-0.8mcg/kg/min) a PD3 inhibitor improves inotropy and promotes vasodilatation (systemic and pulmonary). Can be associated with hypotension so paired with noradrenalin.
4. Dobutamine -can be paired with noradrenaline but can cause tachyarrhythmias
5. Levosimendin is a calcium sensitiser and can improve RV function in left heart disease.
Mechanical devices to support the RV: whist we treat the underlying cause. These include: ECMO; RV assist devices/Impella.
Excessive afterload plays some role in nearly all cases of acute RV failure.
Reduction best achieved by a range of general measures and specific pharmaco-therapies including pulmonary vasodilators.
General measures to improve hypoxia hypercarbia and acidosis
1. Oxygen therapy
2. Lung protective mechanical ventilation using the lowest effective plateau pressure tidal volume and PEEP whilst avoiding hypoxia and hypercarbia.
e.g. Vt 4-6ml/kg Ideal BW; minimise PEEP; P plat < 30 mmHg; treat hypercarbia, acidosis. (PVR lowest at FRC)
3. Avoidance of hypothermia
4. Treatment of thromboembolic disease if acute cor pulmonale from PE.
Several classes of drug in this setting and all have the potential to cause systemic hypotension and blunt hypoxic pulmonary vasoconstriction and can worsen VQ mismatch.
a) Inhaled nitric oxide 20-40ppm; rapid onset short offset short half-life is the inhaled vasodilator of choice in the critically ill. Has been shown to improve RV ejection fraction and end-diastolic volume in these patients, improve pulmonary hemodynamics and mixed venous oxygen saturation in patients with acute RV failure.
b) Inhaled prostacyclin analogues have been shown to be effective in post cardiac surgery patients with pulmonary hypertension, refractory hypoxaemia or right heart dysfunction.
The level of detail in template was not required. Discussion of preload optimisation, contractility and pulmonary vasodilation was required for a pass.
This is the second question on right heart failure in the same paper, the other being Question 5 (focusing on the investigations for right heart failure). Management of RV dysfunction is discussed in (much) greater detail elsewhere, and so the nitty-gritty of it are omitted from this discussion section because under the stress of years of (many) RV failure questions that section has hypertrophied to a completely unmanageable thickness, to the point where it no longer functions as a revision resource for the time-poor candidate.
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