Acute Right Ventricular Failure Postintubation in a Mitral Stenosis Patient.

Mitral stenosis (MS) is prevalent in 0.02-0.2% of the population in developed countries. The pathophysiology of MS results in elevated left atrial pressures and over-time results in pulmonary hypertension (HTN) which ultimately affects the right ventricle. In addition, MS restricts the diastolic filling of the left ventricle. Therefore, during induction patients with MS are limited by their ability to increase cardiac output by increasing stroke volume. Anesthesia goals in severe MS are to avoid sudden changes in heart rate, as well as systemic and pulmonary artery pressures. We report a patient who sustained severe hypotension upon induction and intubation which was resistant to conventional medications. Intraoperative transesophageal echocardiography displayed unique right atrial and right ventricular dilatation. In addition, the leftward inter-ventricular, inter-atrial septal shift and septal bounce were noted as the characteristic findings. Intravenous epinephrine bolus was administered to achieve normo-tension and normal chamber dimensions and interventricular septal position.

CASE

This is a patient-consented and approved submission. A 70-year-old male (Height = 180 cm and weight = 104 kg) was scheduled to undergo a mitral valve (MV) replacement and coronary artery bypass grafting. His past medical history included rheumatic fever, coronary artery disease with a single stent in the left anterior descending artery (LAD), hypertension (HTN), diabetes mellitus, insertion of a pacemaker and defibrillator. Preoperative transthoracic echocardiography (TTE) revealed normal biventricular function, severe mitral stenosis (MS) with an area of 0.6 cm2, moderate mitral regurgitation, and mild tricuspid regurgitation (TR). Cardiac catheterization revealed a right dominant circulation, patent LAD stent, and 100% right coronary artery (RCA) stenosis. Pulmonary artery (PA) pressures were 75/27 (46) mmHg and the mean MV gradient was 23 mmHg.

A preinduction arterial line, triple lumen central venous access, and a PA catheter were secured under local anesthesia, conscious sedation, and oxygen. Blood pressure preinduction was 114/69 mmHg. Baseline PA pressures were 68/29 mmHg. Norepinephrine and vasopressin infusions were infused to avoid hypotension, and epinephrine was on standby. Induction was accomplished with sufentanil, etomidate, and rocuronium. The patient was mask ventilated, and endotracheal intubation was performed followed by insertion of a transesophageal echocardiography (TEE) probe. Hypotension was observed along with increase in central venous pressures (CVP) and PA pressures. Intermittent epinephrine boluses (10 mcg) were given to restore the mean arterial blood pressure (MAP). The TEE findings postinductions were as follows.

ECHOCARDIOGRAPHIC FINDINGS

A midesophageal (ME) two-dimensional (2D) 4-chamber view revealed a dilated right atrium and right ventricle (RV), a “bi-septal shift,” i.e., left shift of interatrial septum (IAS), and interventricular septum (IVS) [Video 1]. The septal leaflet of the tricuspid valve (TV) was not visualized [Video 1] and a live 3D view also showed a bi-septal shift [Video 1]. An ME 4-chamber color flow Doppler (CFD) view displayed a moderate TR [Video 1]. An ME long-axis view displayed a narrowed left ventricular outflow tract and dilated RV [Video 1]. After administering epinephrine bolus, ME 4-chamber view revealed a midline IAS and IVS, and septal leaflet of the TV was visualized [Video 2]. Application of CFD displayed a reduced TR [Video 2]. An abnormal IVS motion (bounce) was also a characteristic finding during the TEE examination [Video 2]. The ME aortic valve short-axis CFD view also revealed no TR [Video 2]. In the ME 4-chamber, 2D view RV function appeared normal after MV replacement [Video 2]. Application of CFD in the same view revealed no TR [Video 2]. A 3D MV en face (surgeon’s) view before the MV replacement and after restoring the MAP revealed a stenotic MV [Video 3]. Medial and lateral commissures appeared fused with deposits of calcium at anterolateral commissure area [Video 3]. A continuous wave Doppler across the MV in the ME 4-chamber view revealed a mean gradient of 23 mmHg. The MV was replaced using a 29 mm St Jude valve, and RCA was bypassed using a venous graft. The prosthetic MV was normal after cardiopulmonary bypass (CPB) on 2D and 3D examination [Video 2 and 3]. Total CPB and aortic cross-clamp time was 157 and 102 min, respectively.

The patient was weaned from CPB using milrinone, epinephrine, norepinephrine, and vasopressin. Systemic blood pressure was maintained, mean PA pressure reduced to 24 mmHg, and CVP was reduced to 12–13 mmHg. The patient was transferred to Intensive Care Unit in stable condition and transferred to the floor on day 3. The patient is doing well till date.

DISCUSSION

MS is prevalent in 0.02%–0.2% of the population in developed countries.[1] The pathophysiology of MS results in elevated left atrial pressures and overtime results in pulmonary HTN which ultimately affects the RV. MS restricts the diastolic filling of the left ventricle (LV). Therefore, during induction, patients with MS are limited by their ability to increase cardiac output by increasing stroke volume. Anesthesia goals in severe MS are to avoid sudden changes in heart rate, as well as systemic and PA pressures.[2] Etomidate and opioids such as sufentanil and fentanyl are the recommended agents for induction as long as the above goals are met.

The RV is a low-pressure chamber divided into conus and infundibulum. It provides preload to the LV, and contraction is a bellows-like inward movement of the free wall. In contrast, the LV has a rotational and twisting contractile pattern. RV contraction is sequential which starts at the apex (trabeculated portion) and ends with infundibular contraction.[3] It has a prolonged low pressure emptying by a sustained ejection during both pressure development and decline. Physiologically, RV pressure-volume (PV) loop is triangular and different from the PV loop of LV. It has brief periods of isovolemic contraction and relaxation. The above discussion implies that RV is sensitive to acute alteration in preload and afterload.[4] In chronic pulmonary HTN, the RV dilates overtime in response to an increased afterload. The PV loop subsequently becomes nontriangular and resembles that of the LV.[4]

The IVS significantly contributes to biventricular function particularly the RV. IVS normally augments RV stroke volume by bulging like a piston into the RV during systole. In this patient, with pulmonary HTN, further augmentation of afterload evidently caused the IVS shift after induction. Compromised RV function was a result of the pressurized pulmonary circulation. RV was at risk of ischemic injury due to stenosed RCA at baseline and intraoperative pressure overload during induction. However, perioperative clinical course of the patient revealed no ischemic injury or dysfunction post-CPB.

Acute RV failure during induction may occur due to airway-related (hypoxia, hypercapnia, high airway pressure), perfusion, or afterload changes. A sudden increase in pulmonary vascular resistance or hypoperfusion of the RV due to systemic hypotension may lead to circulatory collapse. Hypotension after intubation suggests that airway pressure changes may have also contributed to the elevated PVR. Norepinephrine has shown to increase the coronary perfusion and also improve MAP in patients with pulmonary HTN.[4] Vasopressin may also be considered as per literature.[56] Data are limited with regard to inotropes but generally support the use of epinephrine, norepinephrine, dobutamine, and milrinone in RV failure.[56] Even with appropriate pharmacologic choices preinduction, this patient sustained severe hypotension and RV failure.

An acute increase in CVP and echo findings (dilated RA, RV, IVS shift, and acute TR) were indicative of an acute RV failure. However, sharp elevation of CVP alone after induction may be seen in other conditions such as pericardial tamponade or tension pneumothorax.[6] These were not the clinically relevant in this situation. Acute TR which reduced after epinephrine was not addressed because of the preoperative TTE findings. In addition, coaptation of the septal leaflet was evident after epinephrine, once the IVS regained its normal position.

Figure 1 is a graphical and schematic representation of CVP, mean PA pressure, MAP, and interventricular septal position.

Figure 1

Graphical and schematic representation of the relation between the interventricular septum on the X-axis (schematics) and mean arterial blood pressure, mean pulmonary artery pressure, and central venous pressure. As the septum shifts from normal position to the left (red arrows), mean arterial blood pressure decreases and mean pulmonary artery pressure and central venous pressure are elevated

CONCLUSION

TEE was diagnostic of acute right ventricular failure after intubation. The IVS shift and bouncing motion were characteristic finding. In addition, we learned the effects of epinephrine on reversing the position of IVS and also the acute TR.

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Conflicts of interest

There are no conflicts of interest.