RIGHT VENTRICULAR FAILURE

Physiology

RV function determined by 3 P’s: preload, pump (RV contractility), and pipes (afterload)

RV is different than LV

• Thin walled, less muscular, more compliant, working against less afterload (PVR 1/10 of SVR)
• More dependent on volume loading than pressure to accomplish work of ventricle
• LV contracts in a wringing motion, RV contracts in a longitudinal up-and-down motion and compresses medially against septum
• RV doesn’t adapt well to acute changes in pressure/volume à dilates and becomes stiffer (takes 96 hrs to adapt)

Ventricular interdependence = LV and RV function are dependent on one another.

• LV preload = RV stroke volume, failing RV = decreased LV preload
• LV and RV share a muscular septum – contributes 20-40% of the work of RV contraction when LV contracts
• Dilated failing RV pushes IV septum into LV impairing LV filling/contractility and also impairing role of RV septum on RV contractility

ECHO: How to evaluate for RV failure at bedside

• Apical 4 chamber to evaluate relative size of RV to LV and to evaluate how RV “looks”
• If you are skilled, focus on lateral tricuspid annulus movement (TAPSE) 1.6
• McConnell’s sign may be indicative of acute RV failure with RV ischemia, not just seen in acute PE
• Parasternal short at level of mid-papillary to eval relationship between volumes and size of LV and RV and intraventricular septum – look for septal shift and the “D” Sign
• Plethoric IVC regardless of volume status--can't use IVC variation to try to decipher fluid volume status . . .
• As RV dilates in chronic failure, there will be disruption of the tricuspid annulus leading to tricuspid regurgitation

Six step approach to management of acute RV failure

Step 1: Optimize volume status

• Lasix vs. fluids, use PSAX echo view to decide
• Err on the side of volume constriction, they are often overloaded unless the patient has a known source of volume loss--might not want to give volume bolus[unless they are hemorrhaging, vomiting, diarrhea, etc.] . . . using U/S to assess volume status will be near impossible. . . IVC will be bulging from RV failure regardless if they're hypovolemic or hypervolemic. . .
• Passive Leg Raising is probably a clever move before each small fluid bolus
• See: Diuretics in Normotensive Patients With Acute Pulmonary Embolism and Right Ventricular Dilatation (Circ J, 2013; 77: 2612–2618)

Step 2: Maintain coronary perfusion to limit RV ischemia (Keep MAP up)

• Common final pathway in acute RV failure associated with pulm HTN is RV ischemia
• Also dilated RV = increased wall tension = decreased coronary perfusion
• Important to maintain SVR >> PVR to maintain R coronary perfusion pressure à Use pressors (norepi, vasopressin--no pulm vasoconstriction) not volume or chronotropes (norepinephrine, then dobutamine); dobutamine may drop BP as it augments cardiac output;  avoid pure alpha-agonist like phenylephrine which will worsen pulm vasoconstriction.
• The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations. (Circulation. 1981 Jan;63(1):87-95)
• Treatment of shock in a canine model of pulmonary embolism. (Am Rev Respir Dis 1984, 130:870-874)
• Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs. (Anesthesiology 1984, 60:132-13)

need to have high pressure at the aortic root . . .

Step 3: Enhance RV inotropy

• Dobutamine
• Milrinone
  • Dobutamine and milrinone may need to be combined with vasoconstrictor (norepi or vasopressin) to counteract systemic hypotension
• Epinephrine: beware tachycardia--lose all of that filling . . .
• (Levosimendan)

Step 4: Reduce RV afterload

• Inhaled pulmonary vasodilators (iNO, epoprostenol, iloprost)
  • Dilates pulmonary vasculature in only ventilated areas – improves V/Q mismatch and oxygenation, decreases PVR
• Systemic pulmonary vasodilators (IV and po) – avoid in critically ill unless Group I already on the med, causes systemic hypotension and worsens oxygenation
• Oral PAH therapy – no role in critically ill

Step 5: Support Oxygenation and Ventilation

• Hypoxic vasoconstriction – normal physiologic response to unventilated lung segments, causes increased PVR
• Positive pressure ventilation – increased RV afterload and decreased RV preload may worsen RV failure
• Improved oxygenation with PPV may improve hypoxic vasoconstriction and decrease PVR, sum of effect of PPV in RV failure unpredictable
• Hypercapnea causes pulmonary vasoconstriction and increased PVR
• Low-tidal volume ventilation to keep plateau pressures low
• Intensive care med 2009 11 pts, PPV with plateau maintained
• acidosis and hypercapnea induced
• these pts may code upon induction agents as you prepare to intubate . .  the sedatives will cause vasodilation, dropping SVR . . . worsening MAP . . . RV ischemia

Step 6: Treat the underlying cause

Rescue therapies

RVAD, VA ECMO

If you’re really worried the patient will die on the ventilator, might be worth preparing and/or starting inhaled epoprostenol or nitric acid via the ventilator immediately after intubation. This takes a bit of time to set up, so ideally should be ready to go prior to intubation. Inhaled pulmonary vasodilator can be a powerful force of goodness in these patients by simultaneously improving oxygen saturation and reducing pulmonary pressures.

Gregg Chesney's algorithm for intubating patients with RV failure – Laryngoscope as a murder weapon

Intubating patients with Acute RV failure: Very high risk

• Intubation with RSI = Loss of native catecholamines leading to vasodilation and decreased venous return/preload leading to RV cardiac output to worsening RV ischemia to worsening RV failure
• Intubation with inadequate sedation leads to pain and agitation with airway manipulation leading to increased intrathoracic pressure and increased PVR to decreased venous return/preload leading to in RV cardiac output leading to worsening RV ischemia leading to worsening RV failure
• Strongly consider fentanyl, ketamine awake intubation

How to Do it

• PREPARE and GET HELP
• If urgent/semi-emergent intubation
  • Place arterial line, obtain good vascular access
  • Optimize volume status
  • Consider awake intubation or awake fiberoptic intubation
    • May help minimize hemodynamic perturbation
    • Use topical lido + small dose of safe sedative
  • Utilize video laryngoscopy
  • Most experienced intubator
• If emergent intubation
  • RSI with etomidate
  • Anticipate hemodynamic collapse – use push-dose epinephrine, have norepinephrine or epinephrine drip already hanging
  • I will “premedicate” pts with RV failure with push dose of 10-20mcg of epinephrine and 1-2U of vasopressin just prior to induction even if they aren’t hypotensive
• Re-evaluate volume status following intubation
• lowest PEEP; low TV ventilation to avoid increasing intrathroacic pressure; check ABGs

CPR and Goals of Care

Pts unlikely to survive cardiac arrest when have RV failure, have ineffective CPR d/t poor pulmonary blood flow, (Hoeper, et al. (2002))

Pinsky's Thoughts on the RV

Unmasking right ventricular physiology The determinants of RV function are uniquely different from those determining LV function even though both ventricles have anatomically and functionally similar cardiac myocytes and the same beat frequency. First, RV filling occurs without any measurable change in RV distending pressure [1, 4]. Thus, preload is independent of RV EDV unless the RV is hypertrophied. At which point, central venous pressure increases in proportion to the increase in RV EDV [26]. Since venous return is the primary determinant of steady state cardiac output and since central venous pressure is the backpressure to venous return [27] acute RV overload must be associated with both increases in central venous pressure and cardiovascular compromise (acute cor pulmonale). Thus giving more intravenous volume challenges to patients with acute cor pulmonale (acute right heart failure) will only decrease cardiac output further. Second, that RV filling occurs below its unstressed volume has fundamental survival advantages for the host. Since spontaneous inspiration usually decreases intrathoracic pressure, central venous pressure will also decrease increasing the pressure gradient for venous return [27]. Thus, both RV filling and subsequently RV stroke volume will increase pulmonary blood flow at the same time alveolar gas is being refreshed by the tidal breath [28]. For this to provide maximal venous return, central venous pressure must not increase as RV EDV increases. Accordingly, the natural high RV diastolic compliance allows the increased venous return to be maximal. Furthermore, for this process to be effective, pulmonary vascular resistance must remain low. Under normal circumstances, with normal pulmonary vasculature and tidal volumes, pulmonary artery pressure does not increase more than a few millimeters of mercury as flow increases greatly [28]. Thus, the cardiopulmonary system is ideally adapted to maximize blood flow and gas exchange during spontaneous breathing and to increase them rapidly with exercise. Third, positive-pressure breathing by dissociating tidal air inflow from pulmonary blood flow [26] will result in poorer ventilation/perfusion matching and worse gas exchange than spontaneous ventilation. Furthermore, if the tidal breaths are too large, they will also impede venous return causing acute cor pulmonale and a decrease in cardiac output [19].

Right ventriculo-centric cardiovascular rules

1. Central venous pressure is only elevated in disease Normally central venous pressure is zero or slightly higher than intrathoracic pressure
2. If central venous pressure rises and remains elevated following a fluid challenge: STOP Make sure the patient is not slipping into acute cor pulmonale before proceeding
3. For cardiac output to increase the RV must dilate There is a physical limit to which fluid resuscitation alone can increase cardiac output
4. Right ventricular hypertrophy is essentially a deal with the devil: it is a losing proposition Increased filling must be associated with increased filling pressure limiting venous return and impairing LV diastolic compliance

Source:  

https://emcrit.org/emcrit/pulmonary-hypertension-right-ventricular-failure/