Fig. 30.1
1a, 2a represents the normal morphology of the RV and LV in systole and diastole. 1b, 2b represents ventricular interdependence in RV dysfunction. There is dilation of the RV, flattening of the interventricular septum, and compression of the LV that resembles a D shape (D-shaped LV). This leads to a decrease in LV compliance leading to further increase in afterload
The right ventricular wall is made out of a superficial layer of oblique fibers that continue with the superficial myofibers of the LV and a deep layer of muscular fibers longitudinally aligned (Haddad et al. 2008b).
The normal contraction of the RV resembles a peristaltic movement that begins at the inflow tract, through the apical trabeculated portion and through the infundibulum. The normal ejection from the RV is due to the longitudinal shortening of the free wall as well as a reduction in the distance between the septum and the free wall causing a bellow effect. Under normal conditions, the LV contributes to 20–40 % of the RV contractile function.
RV perfusion happens in both systole and diastole, making it less susceptible to ischemia than the LV.
With this anatomical bases, we can see the relationship between the two ventricles and deduce that RV pathology can affect the LV and vice versa through a phenomenon called ventricular interdependence.
Furthermore the relationship volume over ventricular mass gives the RV a high compliance which allows it to manage greater volumes with minimal increase of the intracavitary pressure (Greyson 2008; Haddad et al. 2008b).
There are two fundamental aspects of the RV physiology. First is that it is characterized by a high compliance that can accommodate to large variations in venous return without a high impact in the end-diastolic pressure (EDP). We can make this assumption by observing a pressure–volume curve comparing the two ventricles, where we will see that the triangular shape of the RV is less steep during its diastolic phase than the LV’s (Haddad et al. 2008a; Denault et al. 2013; Vandenheuvel et al. 2013).
Second is that the RV physiology is highly dependent on the afterload and slight elevations of the PVR lead to a marked reduction in its systolic function. In Fig. 30.2, we can observe the effect of afterload on stroke volume (SV) compared on both RV and LV. For every increase in the afterload, the decrease in the SV is greater in the RV than in the LV (Haddad et al. 2008b).
Fig. 30.2
Effect of afterload on stroke volume (SV) compared to both RV and LV
The RV is attached to the pulmonary vascular bed that is a high-flow and low-resistance system; it is low resistance because the pulmonary arterioles have a thin media layer and few smooth muscle cells, making them very elastic, with a greater capacitance and capable of handling volume when recruited (Haddad et al. 2008a; Greyson 2012).
Even though the RV afterload is determined by many factors (pulmonary vascular resistance (PVR), distensibility of the pulmonary arterial system, and a dynamic component called inductance), PVR remains the most commonly used index to determine RV afterload (Price et al. 2010).
Pulmonary vascular tone is predominantly controlled by the vascular endothelium and by a balanced production of vasodilators (prostacyclin, nitric oxide) and vasoconstrictors (endothelin 1, thromboxane A2, and serotonin). PVR is defined as the mean pulmonary arterial pressure (mPAP) minus pulmonary artery occlusion pressure (PAOP that provides an indirect measure of the left atrial pressure) divided by the cardiac output (CO). The normal range is 155–255 dyn/s/cm5:
This shows us very important details about the cardiac physiology:
- 1.
PVR can be affected by an increase in the left atrial (LA) pressure; this can be due to diastolic, systolic, or mixed dysfunction of the LV and/or mitral disease (stenosis or regurgitation).
- 2.
CO disorders can increase PVR; this is the case of congenital heart disease (CHD) with left to right shunt, fluid overload, or hyperdynamic states.
- 3.
The lungs and the heart are linked together very closely, and their interaction is very important for the normal physiology. A disruption in the lungs can lead to an increase in PVR (e.g., interstitial lung disease, pulmonary embolism) (Zochios and Jones 2014).
Definition
RV failure is defined as a clinical syndrome resulting from the inability of the RV to maintain an adequate blood flow to the pulmonary circulation with a normal CVP and which progressively will lead to systemic hypoperfusion (Zarbock et al. 2014).
Etiology
It can be divided based on the pathophysiology (Vandenheuvel et al. 2013):
- 1.
Volume overload
- 2.
Altered contractility
- 3.
Pressure overload
There are several perioperative factors that can alter these three elements of the cardiac output.
Volume Overload
The volume overload is caused by conditions such as tricuspid regurgitation (TR), atrial septal defects, and ventricular septal defects. A very important cause of volume overload in the perioperative setting is excessive administration of IV fluids. Based on what was discussed in reference to the anatomical and physiologic characteristics, the RV can accommodate more easily to volume overload with a relatively low increase in the wall tension. Therefore chronic volume overload is well tolerated but puts the patient at risk of acute decompensation, because a chronically overloaded RV has a limited capacity of increasing its contractility in the event of an acute increase of PVR.
Altered Contractility
The contractility can be affected by myocardial ischemia due to coronary artery disease or decrease in the perfusion pressure due to hypotension, arrhythmias, and intrinsic myocardial disease such as cardiomyopathies or cytokine-induced myocardial depression like sepsis. In observational studies, up to 40 % of patients with sepsis have evidence of RV failure due predominantly to primary RV dysfunction (Itagaki et al. 2012).
Pressure Overload
The pressure overload is the most common cause of systolic dysfunction of the RV (Greyson 2012; Vandenheuvel et al. 2013).
PVR increases by perioperative factors like:
Pulmonary vasoconstriction secondary to hypoxia, hypercapnia, and acidosis and cytokine release due to blood transfusion and protamine
Reduction or compression of the pulmonary vascular bed induced by acute respiratory distress syndrome (ARDS), pulmonary embolism (PE), pneumothorax, and ventilation with large tidal volumes, high plateau pressures, and high positive end expiratory pressures (PEEP)
Congestion of the pulmonary vascular bed in case of pulmonary hypertension secondary to valvular disease or chronic obstructive pulmonary disease (COPD) and LV failure that results in retrograde increase of pulmonary artery pressure (PAP)
Mechanical obstruction like the one we see in pulmonary stenosis
RV dysfunction is present in many critically ill patients. ARDS is one of the most common conditions that challenges the right ventricle. The incidence of acute cor pulmonale in patients with ARDS is around 60 % without protective mechanical ventilation and 25 % with protective mechanical ventilation.
Postoperative RV failure is around 0.1 % in patients postcardiotomy, 2–3 % after a cardiac transplant, 25 % in CHD repair patients, and 30 % after the implantation of a ventricular assist device (VAD) (Greyson 2010; Krishnan and Schmidt 2015).
In patients with PE, the echocardiographic findings of RV dysfunction can be present in 29–56 % of the cases (Krishnan and Schmidt 2015).
The presence of RV failure is an independent predictor of mortality in any of the cases. Table 30.1 summarizes the causes of RV failure.
Table 30.1
RV dysfunction etiologies
Preload | Low | Hypovolemia (e.g., third spacing, copious urine output) |
Tamponade | ||
High | Fluid overload | |
Left to right shunting (e.g., PFO, ASD, VSD, PDA) | ||
Valvular disease: tricuspid regurgitation, pulmonary regurgitation | ||
Contractility | Decreased inotropism | Preexisting RV dysfunction due to CAD or valvular disease |
Myocardial stunning after cardiopulmonary bypass (CPB) | ||
Poorly protected myocardium | ||
Arrythmias | Atrial fibrilation, SVT, and VT | |
Hypoperfusion | RCA occlusion | |
RCA thromboembolism | ||
RCA air embolism | ||
Hypoperfusion secondary to LV dysfunction | ||
Mechanical obstruction or kinking of RCA or graft | ||
Afterload | Mechanical obstruction | RVOT obstruction |
Pulmonary stenosis: | ||
Valvar | ||
Subvalvar | ||
Supravalvar | ||
Anastomotic stenosis | ||
Pulmonary veno-occlusive disease (PVOD) | ||
Pulmonary vasoconstriction | Hypoxia | |
Hypercarbia | ||
Acidosis | ||
Blood transfusions | ||
Drugs: protamine | ||
Congestion of the pulmonary vascular bed | Preexisting PHTN due to valvular disease and COPD | |
Postoperative LV dysfunction | ||
Compression and/or reduction of the pulmonary vascular bed | Pulmonary embolism | |
Pneumothorax | ||
Acute lung injury or ARDS | ||
Positive pressure mechanical ventilation with high PEEP |
Pathophysiology
The initial response to acute RV overload is the increase in ventricular contractility. The rapid increase in contractile function in response to an increase in demand, called homeometric autoregulation or the Anrep effect, appears to be mediated through rapid alterations in calcium dynamics (Greyson 2008, 2010). As the pulmonary impedance increases, the sympathetic nervous system is activated releasing catecholamines which allow an increase in the pressures of the RV by increasing inotropy. If the PVR continues to increase, the RV dilates and the systolic volume is maintained by the Frank–Starling mechanism, since an increase of the end-diastolic volume (EDV) of the RV increases contractility (Simon 2010).
Once the ventricle reaches its limit of compensatory reserve, a greater increase in the afterload can induce a sudden hemodynamic collapse.
We must highlight three points in regard to a sudden hemodynamic collapse due to RV failure:
- 1.
The decrease in cardiac output is a consequence of the ventricular interdependence; the dilation of the RV deviates the interventricular septum to the left decreasing LV compliance which in a retrograde fashion increases the RV’s afterload furthermore (Fig. 30.1b).
- 2.
The second element is the sustained increase in the PVR.
- 3.
The third element of the hemodynamic collapse is the RV ischemia secondary to a decrease in the blood pressure (BP) which affects the contractility even more.
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