What role does the right side of the heart play in circulation?
Critical Care volume 10, Article number: S5 (2006)
Right ventricular failure (RVF) is an underestimated problem in intensive care. This review explores the physiology and pathophysiology of right ventricular function and the pulmonary circulation. When RVF is secondary to an acute increase in afterload, the picture is one of acute cor pulmonale, as occurs in the context of acute respiratory distress syndrome, pulmonary embolism and sepsis. RVF can also be caused by right myocardial dysfunction. Pulmonary arterial catheterization and echocardiography are discussed in terms of their roles in diagnosis and treatment. Treatments include options to reduce right ventricular afterload, specific pulmonary vasodilators and inotropes.
The lungs are the only organs to receive the entire cardiac output. The role of the 'right side of the heart' is to accept the blood from systemic circulation and pump it through the pulmonary circulation. Even if the cardiac output from the right and left sides of the heart are approximately equal (there is a physiological shunt for the bronchial vessels), the way in which these two cardiac outputs are conducted by the ventricles is very different. Differences between the right and left sides of the heart are multiple and numerous. These differences contribute to both normal and abnormal physiology and pathophysiology. Much attention has recently been directed toward the left ventricle (LV), whereas the role played by the right ventricle (RV) has remained comparatively neglected. This is paradoxical when we consider that intensive care units (ICUs) have been using a 'right heart catheter', namely the pulmonary artery catheter (PAC), for more than 20 years. The fundamental duty of an intensivist could be simplified to ensuring that there is adequate cardiac output to systemic circulation. This is clearly a goal that should be achieved in any patient, but we should not discount the role of the pulmonary circulation in cardiac homeostasis because the left and right sides of the heart are interrelated in terms of function.
Important differences between right and left sides of the heart
The right atrium (RA) and the RV form the right side of the heart. The RA receives venous blood from superior and inferior venae cavae, ejecting it through the pulmonary arteries. The tricuspid and pulmonary valves prevent regurgitation into the RA and RV, respectively. The right ventricular myocardium is about one-third the thickness of its left counterpart because it is a comparatively low pressure system. During systole, the LV protrudes into the RV. These chambers are separated by the septum and are surrounded by pericardium. These basic anatomical arrangements explain why compliance of one ventricle can modify that of the other. This interaction is known as diastolic ventricular interaction and is important in understanding the pathophysiology of right heart failure.
In the average person, the systolic pressure of the RV reaches a mere 25 mmHg, which is in contrast to the 120 mmHg systolic pressure of the LV. This difference in pressure is essentially due to the discrepancy in compliance between pulmonary and systemic blood vessels, with pulmonary vessels having a relatively large diameter and thin walls (conditions that allow for the high compliance of the pulmonary system). Like any vessel in the body, the pressure in the pulmonary system depends on cardiac ouput, resistance and compliance. An increase in pulmonary arterial pressure could be due to any combination of increases in the first two factors or a decrease in the third. The pulmonary vascular resistance has a particular dependency on alveolar oxygen tension, whereby alveolar hypoxia leads to pulmonary arterial vasoconstriction.
Pulmonary compliance has a value of about 2 ml/mmHg. This allows the right heart to pump the blood with a blood pressure lower than the systemic arterial pressure, ensuring that the pulmonary circulation is a 'low pressure system' . Being a pump that works under low pressure conditions, the RV is affected by an increase in afterload [2, 3], even when the oxygen consumption in the right heart is accounted for. The RV is mainly perfused by the right coronary artery (RCA) and partially by the left coronary arteries. The RCA is perfused in both systolic and diastolic phases in the healthy human as a result of the low systolic pressure (25 mmHg), which does not occlude the vessel that has a systemic pressure. When afterload is high, and therefore the pressure necessary to contract the RV successfully is also high, partial occlusion of the RCA may occur, leading to ischaemia.
Pathophysiology of right ventricular failure
In ICUs there are many conditions that can lead to an increase in right ventricular afterload. These include pulmonary embolism (PE), positive pressure ventilation, acute respiratory distress syndrome (ARDS) and increased pulmonary vascular resistance (especially after cardiac surgery or in hypoventilatory states).
When there is an increase in right ventricular afterload, right ventricular systole takes longer, even if the ejection time is reduced. This elongated systole can last longer than left ventricular systole. Because the RV is still contracting as the left begins to relax, the septum displaces to the left while the LV starts diastole and is moved back rightward when left systole begins again. In summary, the net result is an abnormal reversal of the left-to-right pressure gradient at end-systole/onset of diastole and an altered cardiac performance (Figure 1) . Septal dyskinesia seen at echocardiography is considered a sign of increased right ventricular afterload. This mechanism involves the diastolic ventricular interaction.
Dilatation of right heart is a compensatory mechanism that allows the RV to maintain stroke volume despite a decreased ejection fraction [5, 6]. When this enlargement is acute and due to a sudden increase in afterload, it is termed acute cor pulmonale. The two main causes are massive PE and ARDS [7–9]. More importantly, when the underlying cause of acute cor pulmonale is treated, the situation reverses . If intervention does not occur, enlargement of the RV can lead to tricuspid annular dilatation with regurgitation, an increase in right ventricular end-diastolic volume and leftward movement of the septum, with final impairment of the LV . This progression can be rapid because the RV has a peculiar auto-aggravation cycle. Tricuspid insufficiency can aggravate splanchnic congestion, resulting in decreased venous return and therefore preload. The cardiac output, already compromised because of the low preload state of the LV induced by the right ventricular failure (RVF), decreases further. Consequential systemic hypotension exacerbates the impairment in organ perfusion and coronary artery perfusion. Cardiac ischaemia (commonly the next pathophysiological observation) is characterized by further aggravation of cardiac performance and its cycle.
Acute PE represents an example of the aetiology of increased right ventricular afterload. In massive embolism blood flow is obstructed, resulting in a low cardiac output with systemic hypotension. Jardin and coworkers  reported a study conducted in 14 patients with massive PE. In these patients, during the acute phase both the RA and the RV showed signs of hypertrophy and elevated right atrial pressure, with reversal of trans-septal diastolic pressure gradient. More importantly, the LV was impeded by the leftward movement of the septum and had a reduction in left ventricular diastolic area. As described by Morris-Thurgood and Frenneaux , further volume loading in this case can have detrimental effects enhancing diastolic ventricular interaction. Belenkie and colleagues  studied volume loading in a canine model, before and after pulmonary embolization. After embolization, volume loading moved the septum leftward and led to reduced left ventricular area index and left ventricular stroke work. Different findings were reported by Mercat and coworkers ; they evaluated 30 patients with acute massive PE and found that fluid loading (500 ml dextran 40) improved cardiac output. The latter study highlighted the patients who improved the most after the fluid loading, namely those who had a lower right atrial pressure at baseline, which suggests that when an interventricular dependency phenomenon was present there was a lesser response to fluid loading. It is possibly untrue that fluid loading should be avoided in the case of right ventricular failure, but the fluid management should only correct hypovolaemia. Clinicians must be aware of the consequences of excessive fluid loading, namely impairment in left ventricular (LV) performance and worsening of the 'auto-aggravation cycle'.
Intermittent positive pressure ventilation is often used alongside treatments to optimize left ventricular function, with benefits in terms of reductions in both preload and afterload. The RV has a different response to intermittent positive pressure ventilation; the preload decreases but pulmonary vascular resistance and consequently afterload increase. This is further accentuated with positive end-expiratory pressure. If intermittent positive pressure ventilation is necessary in the setting of RVF, then high levels of plateau pressure and positive end-expiratory pressure should be avoided to minimize the right heart–lung interaction. For the same reason, high respiratory rates, which can lead to air trapping and intrinsic positive end-expiratory pressure, should be avoided. The minimal level of plateau pressure, mean airway pressure and positive end-expiratory pressure necessary for pulmonary recruitment should be maintained.
Acute respiratory distress syndrome
In ARDS two factors contribute to right heart failure. First, increased pulmonary vascular resistance occurs as a result of the distal occlusion of the pulmonary arterial bed. Second, most patients require mechanical ventilation to maintain adequate oxygenation and, as described above, intermittent positive pressure ventilation can worsen RVF. The incidence of acute cor pulmonale in ARDS is about 25%  if a protective ventilation strategy (low tidal volume/low plateau pressure) is used. A study conducted in 1985, when high tidal volume was used (≥13 ml/kg), identified an incidence of acute cor pulmonale in ARDS of 65% [4, 15].
With respiratory failure, as occurs in patients with chronic obstructive pulmonary disease, some areas of the lungs are hypoventilated. This stimulates the pulmonary vasoconstrictor reflex, thereby increasing pulmonary vascular resistance. Concomitant hypercapnia and acidosis are often present, and this worsens both vascular resistance and ventricular contractility. In these situations, acidosis should be corrected as well as hypercapnia.
Right ventricular dysfunction, as demonstrated with radionuclide angiography and echocardiography, is common in sepsis (up to 32%) [4, 16, 17]. RVF should be kept in mind in all septic patients who do not respond to volume expansion.
Reduced right ventricular contractility
Chronic heart failure
The response to chronic increased afterload of the RV is characterized by an initial dilatation and then by tricuspid regurgitation and low cardiac output. In recent years a number of studies have supported right ventricular performance being an important prognostic determinant in chronic heart failure  and, most importantly, right ventricular ejection fraction (RVEF) and pulmonary arterial pressure are independent predictors of survival .
Right ventricular myocardial infarction
There is a high prevalence of single vessel coronary disease in myocardial infarction (MI) of the RV compared with MI of the LV. When shock is present in patients with MI of the RV, the mortality is high and similar to that in patients with cardiogenic shock from infarction of the LV . The aetiology of such MIs can be related back to an occlusion of the proximal part of the RCA. This leads to depressed right ventricular function and decreased left ventricular preload. Cardiac output is low and systemic hypotension appears as a consequence, even if left ventricular function is normal . Right heart failure can be exacerbated if the posterior portions of the interventricular septum are also involved, because the septum plays an important role in right ventricular contraction [4, 21, 22].
Pulmonary arterial hypertension is usually absent but MIs have been reported to occur more frequently when right ventricular hypertrophy (which can be consequent to sustained increased afterload) is present. Indeed, many RCA occlusions do not lead to MI. The simple explanation for this is that myocardial hypertrophy increases oxygen demand and thereby leads to more ischaemic damage .
Because the clinical presentation of right heart failure is very nonspecific, it is difficult to make a diagnosis of RVF by clinical examination alone. In the ICU scenario there are essentially two ways to assess right-sided function: pulmonary artery catheterization and echocardiography. The latter can be divided into transthoracic and transoesophageal methods. Magnetic resonance and radionuclide ventriculography are two other valid methods of assessment, but because their use at the bedside is difficult we do not consider them here. Electrocardiography and troponin assessment are also useful when MI is suspected.
Pulmonary artery catheter
Pulmonary arterial catheterization is the most invasive and oldest method of assessing right-sided cardiac function. It is the only available continuous monitoring device that permits evaluation of the efficacy of treatment. In fact, it permits continuous monitoring of right atrial pressure, right ventricular pressure, pulmonary arterial pressure, pulmonary artery wedge pressure (PAWP), continuous cardiac output and mixed venous oxygen saturation. Modern PACs can also be used to measure RVEF and right ventricular end-diastolic volume [23–25]. The diagnosis of RVF is made in situations of systemic hypotension, decreased cardiac output and low mixed venous saturation, and when there is a high right atrial pressure that is higher than a usually normal PAWP. Diagnosis of pulmonary artery hypertension (PAH) is easily made by assessing pulmonary pressure. Fluid loading in RVF can be dangerous.
New catheters permit continuous measurement of right ventricular end-diastolic volume index (RVEDVI) and RVEF. RVEDVI is a novel preload index. Interestingly, it seems that better understanding and use of RVEDVI result from its consideration together with RVEF, a parameter that can define the contractility status of the RV. Indeed, as Sarnoff and Berglund  reported, contractility is derived from a series of ventricular function curves, with each curve having a particular ejection fraction and optimal preload (end-diastolic volume). Thus, it appears that correct interpretation of RVEDVI is strongly dependent on RVEF . Currently, there is little evidence to support routine use of RVEDVI and RVEF in RVF.
Table 1 shows how RVEDVI and RVEF can be used to guide fluid and drug management. In this clinical example, a patient monitored with a PAC was given fluids and dobutamine. After the volume challenge the CI did not improve and the RVEDV increased. The RVEF decreased and the mean pulmonary artery pressure increased from 18 to 28 mmHg, indicating that the patient was not responding to volume expansion. The mixed venous oxygen saturation did not change and lactate level increased. Consequent administration of dobutamine without further volume expansion increased RVEF from 25% to 38%. At the same time, mean pulmonary artery pressure decreased from 28 to 16 mmHg. Although the CI does not improve, the improvement in cardiac performance is reflected by decreases in mean pulmonary artery pressure and lactate levels, and increases in RVEF and mixed venous oxygen saturation.
One of the primary aims in the setting of acute RVF is to achieve a reduction in right ventricular afterload. The best way to gauge the effectiveness of this treatment strategy is to monitor the patient continuously. This can only be done using the PAC.
The role of echocardiography has expanded in recent years. The most powerful characteristic of this technique is that it permits immediate qualitative diagnosis of heart disease, simultaneously allowing for estimation of flows and pressures. In order to explore the right side of the heart, transthoracic echocardiography can be used as long as the patient remains unventilated. When mechanical ventilation is being used, a transoesophageal approach should be used, resulting in better imaging. Diagnosis of RVF is made qualitatively and, as emphasized by Jardin and Viellard-Baron , septal dyskinesia is the hallmark of RVF. Transoesophageal echocardiography may confirm an initial suspicion of RVF (high central venous pressure) if absence of the respiratory variation in vena cava diameter is detected. Both transthoracic and transoesophageal echocardiography can be used to estimate pulmonary pressures. The qualitative aspect of echocardiography allows a diagnosis of RVF to be made along with recognition of its cause. It is possible to recognize RVF secondary to a PE, ARDS, or coronary obstruction simply by analyzing the different recorded images . Furthermore, echocardiography can assess both the right and left sides of the heart, and can allow measurements to be taken in systolic and diastolic phases that can be repeated, allowing intermittent monitoring of the efficacy of treatment.
Treatment strategies (with an emphasis on monitoring techniques)
The aim of treatment for right heart failure is to achieve optimal 'contraction status' by breaking the auto-aggravation cycle. A decrease in afterload should always be sought and an adequate preload should be maintained with appropriate fluid administration. Although overload should be avoided, hypovolaemia is unacceptable. Inotropes can be used to optimize ventricular contraction. Afterload can be decreased with the use of drugs and by minimizing the effects of ventilation on the heart. While providing these supportive therapies, definitive therapies such as coronary reperfusion should be delivered.
Management of myocardial infarction
Reperfusion of the occluded coronary is beneficial and should be a primary goal in proven right-sided infarction [28, 29]. The goals suggested by Pfisterer  for right ventricular infarction are as follows: early recognition, early reperfusion, maintenance of adequate preload, reduction in right ventricular afterload (inotropes, balloon counter-pulsation), preservation of right ventricular synchrony and avoidance of vasodilators, nitrates, morphine and β-blockers. It is very important that the left ventricular pressure be kept as close to normal as possible; this can help to restore the normal position of the interventricular septum and thereby improve contraction of the RV .
Because of the interventricular dependence phenomenon, volume overload can dilate the RV so much that it may impair left ventricular function and the entire circulation. Conversely, adequate fluid loading is necessary to achieve optimal contraction. So what should happen at the bedside in a patient with RVF? In the ICU fluid therapy is often guided by fluid challenges. Mercat and coworkers  discovered that, in acute PE, fluid challenges improve cardiac output, especially in patients with low baseline atrial pressure, who probably represent those in whom interventricular dependence is not yet playing a substantial role. Using mean pulmonary arterial pressure as a guide to fluid challenge, it seemed reasonable to stop filling beyond a mean pulmonary artery pressure of 30 mmHg [5, 30]. This is supported by findings reported by Atherton and coworkers , even though their population included patients with chronic heart failure. In that study the investigators used a device that results in acute volume unloading by generating lower body suction of 30 mmHg, and they measured how right and left volumes changed. Interestingly, among the patients with heart failure, those with an increased left ventricular end-diastolic volume after the volume unloading were also those with higher right resting atrial pressures, mean pulmonary arterial pressure, and PAWP.
During the past few years a new way to assess fluid responsiveness in ventilated patients has become popular. Pulse pressure variation, evaluated by a simple analysis of the arterial pressure wave, has been proven to identify patients who may benefit from fluid challenge. In the setting of the patient with RVF undergoing mechanical ventilation, pulse pressure variation can be high not because of hypovolaemia alone but also because of ventricular impairment exacerbated by the mechanical ventilation [27, 32].
Therefore, if a fluid challenge is followed by an increase in filling pressure without change in cardiac output, then fluid loading should be stopped. PAC is a valuable tool in this context because it allows the clinician to assess pulmonary pressure and CI on a continuous basis. The efficacy of fluid challenge can be monitored by watching changes in CI, SVI, RVEDVI and RVEF. Fluid removal with diuretics or haemofiltration may then be beneficial . However, fluid withdrawal is effected, it is important that cardiac output monitoring be used to assess the efficacy and safety of treatment.
Drugs are employed either to decrease pulmonary vascular resistance or to increase cardiac contractility.
Inhaled nitric oxide (iNO) is a vasodilator that can be given to ventilated patients. It causes vasodilatation by increasing levels of cGMP in vascular smooth muscle cells. cGMP has a short half-life because it is degraded by endogenous phosphodiesterases. On entering the pulmonary circulation, iNO binds with plasma proteins and is immediately inactivated by haemoglobin. In this way its effects are localized solely to the pulmonary vasculature . Moreover, its effect is to vasodilate only ventilated areas of the lungs, maintaining an efficient ventilation/perfusion ratio. Indeed, systemic administration of vasodilators such as nitroglycerine or prostaglandin E1 can improve RVF, but by being unselective for ventilated areas these agents can worsen the ventilation/perfusion ratio [34, 35]. iNO is considered the 'gold standard' in the management of PAH. Its role has been studied in primary PAH, and in this way it has been used to identify patients who would benefit from long-term treatment with nifedipine . In acute RVF its ability to lower pulmonary artery resistance and pressure has been proved, even though it has not been demonstrated to decrease mortality in those patients who respond to the therapy . iNO can be associated with a rebound increase in pulmonary arterial pressure, especially when its use is prolonged and its withdrawal sudden . Its role is more controversial when we consider its effect on the LV. Indeed, some reports indicate that a decrease in cardiac output and an increase in PAWP may occur during iNO therapy for left ventricular impairment [39, 40]. On the other hand, in a small study in patients with severe isolated right ventricular dysfunction  it was found that high concentrations of iNO (35–40 parts/million) not only decrease afterload but also increase cardiac output. Considering all the published studies, iNO appears to be a rapid acting and effective treatment in acute RVF.
Prostacyclin (prostaglandin I2) is both a vasodilator and a potent inhibitor of platelet aggregation. It can be administered systemically or locally as inhaled prostacyclin as an alternative to iNO . The preferred method of administration is inhalation for two reasons: first, it vasodilates ventilated areas of lung; and second, no PAH rebound on finishing treatment has been described. Systemic prostacyclin is available for administration by intravenous , subcutaneous , and oral  routes. Iloprost is a prostacyclin derivate molecule (carbacyclin). In comparison with prostacyclin and iNO, it has a longer half-life and its effects persist for 1 hour after administration .
Sildenafil is an inhibitor of phosphodiesterases that was initially used in the management of erectile dysfunction. Its effect is greater on pulmonary than on the systemic circulation because it inhibits phosphodiesterase-5 more than its analogous isoforms. This particular enzyme is expressed mainly in pulmonary vessels and in the corpora cavernosa. Oral administration has proven to reduce hypoxia-induced PAH. In cardiac surgery sildenafil has been used to wean patients from inhaled iNO . Its synergistic effects both with iNO and iloprost have been demonstrated.
Interestingly, Ghofrani and coworkers  found that oral sildenafil but not intravenous prostacyclin induced pulmonary vasodilatation in patients with pulmonary fibrosis, thereby maintaining an optimal ventilation/perfusion ratio. Combinations of sildenafil and iNO can be used to achieve effects on PAH better than those with administration of a single drug .
Selective right heart inotropes do not exist. Contractility can be manipulated with the use of inotropes that are usually used in the management of left ventricular failure. These drugs act on the entire myocardium, improving both right and left ventricular contractility. In fact, increased left ventricular contraction can, in turn, facilitate right ventricular contraction. In the ICU β-mimetics such as dobutamine can be used to promote myocardial contraction and to improve cardiac output. Indeed, phosphodiesterase inhibitors and a new class of drugs, namely the calcium sensitizers, can also be used. Levosimendan is the first calcium sensitizer to be employed in clinical practice. In animal models, in comparison with milrinone, levosimendan was reported to increase cardiac output without increasing intracellular calcium levels, and so without increasing oxygen demand . Moreover, the LIDO trial reported lower mortality at 6 months for levosimendan in comparison with dobutamine in low output cardiac failure . More important in the context of right heart failure is that it acts as a vasodilator by opening ATP-sensitive potassium channels. It decreases pulmonary capillary wedge pressure, pulmonary artery pressure and mean right atrial pressure. Compared with dobutamine, levosimendan produces a similar increase in cardiac output but profoundly greater decreases in PAWP . However, it is not a selective pulmonary vasodilator, and can lead to systemic hypotension. Whatever inotrope is used, cardiac output monitoring is essential for guiding therapy. The PAC can provide the clinician with information on both cardiac output and pulmonary pressure changes during inotrope use.
It is not easy to arrive at a clinical diagnosis of RVF. The first clinical sign is commonly systemic hypotension. In the ICU this is usually treated with fluid administration and infusion of a vasoconstrictor. However, caution is needed because vasoconstrictors can also have a detrimental effect on the pulmonary vasculature by increasing pulmonary vascular resistance. In clinical practice, norepinephrine (noradrenaline) increases mean arterial pressure and this in turn improves coronary perfusion, as well as left and right ventricular contraction. Animal studies demonstrated the effect of norepinephrine on pulmonary resistance during heart failure [50, 51] and revealed that norepinephrine restores mean arterial pressure and improves cardiac output. Right ventricular impairment can persist for some time after resolution of PAH . In one model of RVF, after elimination of PAH, dobutamine was shown to be better than noradrenaline in restoring both cardiac output and mean arterial pressure .
RVF is a commonly under-diagnosed condition in the ICU. The diagnosis can be made using either pulmonary arterial catheterization or echocardiography. Treating the cause, decreasing afterload and restoring good contractility are paramount; the aims of therapy should be to reduce excessive pulmonary artery pressures and to improve cardiac output and systemic arterial pressure. Fluids should be given only to counteract hypovolaemia (because the risk for worsening both right and left contraction is high), with fluid loading guided by cardiac output monitoring. Pulmonary vasodilators and inotropes may be indicated. Monitoring the results of treatment can be achieved continuously with an in situ PAC and repeated echocardiographic measurements. RVEF and RVEDVI are two new variables that may be useful in monitoring right heart performance in the setting of RVF. Studies evaluating the efficacy of therapy guided by such variables are awaited.
ARDS = acute respiratory distress syndrome
ICU = intensive care unit
iNO = inhaled nitric oxide
LV = left ventricle
MI = myocardial infarction
PAC = pulmonary artery catheter
PAH = pulmonary artery hypertension
PAWP = pulmonary artery wedge pressure
PE = pulmonary embolism
RA = right atrium
RCA = right coronary artery
RV = right ventricle
RVEF = right ventricular ejection fraction
RVEDVI = right ventricular end-diastolic volume index
RVF = right ventricular failure.
Matthews LR, (editor): Cardiopulmonary Anatomy and Physiology. Philadelphia: Lippincott-Raven Publishers; 1996.
Brieke A, DeNofrio D: Right ventricular dysfunction in chronic dilated cardiomyopathy and heart failure. Coron Artery Dis 2005, 16: 5-11. 10.1097/00019501-200502000-00002
Sarnoff SJ, Berglund E: Ventricular function. I. Starling's law of the heart studied by means of simultaneous right and left ventricular function curves in the dog. Circulation 1954, 9: 706-718.
Jardin F, Viellard-Baron A: Monitoring of right sided heart function. Curr Opin Crit Care 2005, 11: 271-279. 10.1097/01.ccx.0000158847.56107.55
Mebazaa A, Karpati P, Renaud E, Algotsson L: Acute right ventricular failure – from pathophysiology to new treatments. Intensive Care Med 2004, 30: 185-196. 10.1007/s00134-003-2025-3
Matthay RA, Arroliga AC, Wiedemann HP, Schulman DS, Mahler DA: Right ventricular function at rest and during exercise in chronic obstructive pulmonary disease. Chest 1992, (Suppl):255S-262S.
Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F: Echo-Doppler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med 2002, 166: 1310-1319. 10.1164/rccm.200202-146CC
Vieillard-Baron A, Schimtt JM, Augarde R, Fellahi JL, Prin S, Page B, Beauchet A, Jardin F: Acute core pulmonale in acute distress syndrome submitted to protective ventilation: incidence, clinical implications and prognosis. Crit Care Med 2001, 29: 1551-1555. 10.1097/00003246-200108000-00009
Jardin F: Ventricular interdependence: how does it impact on hemodynamic evaluation in clinical practice? Intensive Care Med 2003, 29: 361-363. 10.1007/s00134-003-1873-1
Guarracino F, Carriello C, Danella A, Doroni L, Lapolla F, Vullo C, Pasquini C, Stefani M: Right Ventricular failure: physiology and assessment. Min Anest 2005, 71: 307-312.
Jardin F, Dubourg O, Gueret P, Delorme G, Bourdarias JP: Quantitative two dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement. J Am Coll Cardiol 1987, 10: 1201-1206.
Morris-Thurgood JA, Frenneaux MP: Diastolic ventricular interaction and ventricular diastolic filling. Heart Fail Rev 2000, 5: 307-323. 10.1023/A:1026555012135
Belenkie I, Dani R, Smith ER, Tyberg JV: The importance of pericardial constraint in experimental pulmonary embolism and volume loading. Am Heart J 1992, 123: 733-742. 10.1016/0002-8703(92)90514-V
Mercat A, Diehl JL, Meyer G, Teboul JL, Sors H: Hemodynamic effects of fluid loading in acute massive pulmonary embolism. Crit Care Med 1999, 27: 540-544. 10.1097/00003246-199903000-00032
Jardin F, Gueret P, Dubourg O, Farcot JC, Margairaz A, Bourdarias JP: Two dimensional echocardiographic evaluation of right ventricular size and contractility in acute respiratory failure. Crit Care Med 1985, 13: 952-956.
Schneider AJ, Teule GJ, Groeneveld AB, Nauta J, Heidendal GA, Thijs LG: Biventricular performance during volume loading in patients with early septic shock, with emphasis on the right ventricle: a combined hemodynaic and radionuclide study. Am Heart J 1988, 116: 103-112. 10.1016/0002-8703(88)90256-6
Jardin F, Brun-Ney D, Auvert B, Beauchet A, Bourdarias JP: Sepsis related cardiogenic shock. Crit Care Med 1990, 18: 1055-1060. 10.1097/00003246-199010000-00001
Ghio S, Gavazzi A, Campana C, Inserra C, Klersky C, Sebastiani R, Arbustini E, Recusani F, Tavazzi L: Independent and additive prognostic value of right systolic function and pulmonary artery pressure in patients with chronic heart failure. J Am Coll Cardiol 2001, 37: 183-188. 10.1016/S0735-1097(00)01102-5
Jacobs AK, Leopold JA, Bates E, Mendes LA, Sleeper LA, White H, Davidoff R, Boland J, Modur S, Forman R, et al.: Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry. J Am Coll Cardiol 2003, 41: 1273-1279. 10.1016/S0735-1097(03)00120-7
Pfisterer M: Right ventricular involvement in myocardial infarction and cardiogenic shock. Lancet 2003, 362: 392-394. 10.1016/S0140-6736(03)14028-7
Santamore WP, Gray L Jr: Significant left ventricular contribution to right ventricular systolic function. Mechanism and clinical implications. Chest 1995, 107: 1134-1145.
Klima U, Guerrero JL, Vlahakes GJ: Contribution of the interventricular septum to maximal right ventricular function. Eur J Cardiothorac Surg 1998, 14: 250-255. 10.1016/S1010-7940(98)00179-1
Ganz W, Donoso R, Marcus HS, Forrester JS, Swan HJ: A new technique for measurement of cardiac output by thermodilution in man. Am J Cardiol 1971, 27: 392-396. 10.1016/0002-9149(71)90436-X
Boldt J, Menges T, Wollbruck M, Hammermann H, Hempelmann G: Is continuous cardiac output measurement using thermodilution reliable in the critically ill patient? Crit Care Med 1994, 22: 1913-1918.
Munro HM, Wood CE, Taylor BL, Smith GB: Continuous invasive cardiac output monitoring – the Baxter/Edwards Critical-Care Swan Ganz®Intellicath™ and Vigilance™ system. Clin Intensive Care 1994, 5: 52-55.
Cheatham ML: Right ventricular end-diastolic volume measurements in the resuscitation of trauma victims. Int J Crit Care 2000, 7: 165-176.
Vignon P: Hemodynamic assessment of critically ill patients using echocardiography Doppler. Curr Opin Crit Care 2005, 11: 227-234. 10.1097/01.ccx.0000159946.89658.51
Bowers TR, O'Neill WW, Grines C, Pica MC, Safian RD, Goldstein JA: Effect of reperfusion on biventricular function and survival after right ventricular infarction. N Engl J Med 1998, 338: 933-940. 10.1056/NEJM199804023381401
Kinn JW, Ajluni SC, Samyn JG, Bates ER, Grines CL, O'Neil W: Rapid hemodynamic improvement after reperfusion during right ventricular infarction. J Am Coll Cardiol 1995, 26: 1230-1234. 10.1016/0735-1097(95)00311-8
Sibbald WJ, Driedger AA: Right ventricular function in acute disease states: pathophysiologic considerations. Crit Care Med 1983, 11: 339-345.
Atherton JJ, Moore TD, Lele SS, Thomson HL, Galbraith AJ, Belenkie I, Tyberg JV, Frenneaux MP: Diastolic ventricular interaction in chronic heart failure. Lancet 1997, 349: 1720-1724. 10.1016/S0140-6736(96)05109-4
Michard F, Boussat S, Chemla D, Anguel N, mercat A, Lecarpentier Y, Richard C, Pinsky MR, Teboul JL: Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med 2000, 162: 134-138.
Pepke-Zaba J, Higenbottam TW, Dinh-Xuan AT, Stone D, Wallwork J: Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. Lancet 1991, 338: 1173-1174. 10.1016/0140-6736(91)92033-X
Bundgaard H, Boesgaard S, Mortensen SA, Arendrup H, Aldershvile J: Effect of nitroglycerin in patients with increased pulmonary vascular resistance undergoing cardiac transplantation. Scand Cardiovasc J 1997, 31: 339-342.
Vincent JL, Carlier E, Pinsky MR, Goldstein J, Naeije R, Lejeune P, Brimioulle S, Leclerc JL, Kahn RJ, Primo G: Prostaglandin E 1 infusion for right ventricular failure after cardiac transplantation. J Thorac Cardiovasc Surg 1992, 103: 33-39.
Ricciardi MJ, Knight BP, Martinez FJ, Rubenfire M: Inhaled nitric oxide in primary pulmonary hypertension: a safe and effective agent for predicting response to nifedipine. J Am Coll Cardiol 1998, 32: 1068-1073. 10.1016/S0735-1097(98)00361-1
Bhorade S, Christenson J, O'Connor M, Lavoie A, Pohlman A, Hall JB: Response to inhaled nitric oxide in patients with acute right heart syndrome. Am J Respir Crit Care Med 1999, 159: 571-579.
Christenson J, Lavoie A, O'Connor M, Bhorade S, Pohlman A, Hall JB: The incidence and pathogenesis of cardiopulmonary deterioration after abrupt withdrawal of inhaled nitric oxide. Am J Respir Crit Care Med 2000, 161: 1443-1449.
Semigran MJ, Cockrill BA, Kacmarek R, Thompson BT, Zapol WM, Dec GW, Fifer MA: Hemodynamic effects of inhaled nitric oxide in heart failure. J Am Coll Cardiol 1994, 24: 982-988.
Loh E, Stamler JS, Hare JM, Loscalzo J, Colucci WS: Cardiovascular effects of inhaled nitric oxide in patients with left ventricular dysfunction. Circulation 1994, 90: 2780-2755.
McLaughlin VV, Genthner DE, Panella MM, Rich S: Reduction in pulmonary vascular resistance with long-term epoprostenol (prostacyclin) therapy in primary pulmonary hypertension. N Engl J Med 1998, 338: 273-277. 10.1056/NEJM199801293380501
Simonneau G, Barst RJ, Galie N, Naeije R, Rich S, Bourge RC, Keogh A, Oudiz R, Frost A, Blackburn SD, et al.: Continuous subcutaneous infusion of treprostinil, a prostacyclin analogue, in patients with pulmonary arterial hypertension: a double blind, randomized, placebo-controlled trial. Am J Respir Crit Care Med 2002, 165: 800-804.
Channick RN, Simonneau G, Sitbon O, Robbins IM, Frost A, Tapson VF, Badesch DB, Roux S, Rainisio M, Bodin F, et al.: Effects of the dual endothelin-receptor antagonist bosentan in patients with pulmonary hypertension: a randomized placebo-controlled study. Lancet 2001, 358: 1119-1123. 10.1016/S0140-6736(01)06250-X
Mychaskiw G, Sachdev V, Heath BJ: Sildenafil (Viagra) facilitates weaning of inhaled nitric oxide following placement of a biventricular-assist device. J Clin Anesth 2001, 13: 218-220. 10.1016/S0952-8180(01)00252-5
Ghofrani HA, Wiedemann R, Rose F, Schermuly RT, Olschewski H, Weissmann N, Gunther A, Walmrath D, Seeger W, Grimminger F: Sildenafil for treatment of lung fibrosis and pulmonary hypertension: a randomised controlled trial. Lancet 2002, 360: 895-900. 10.1016/S0140-6736(02)11024-5
Preston IR, Klinger JRJ, Houtches J, Nelson D, Farber HW, Hill NS: Acute and chronic effects of sildenafil in patients with pulmonary arterial hypertension. Respir Med 2006, in press.
Kaheinen P, Pollesello P, Levijoki J, Haikala H: Effects of levosimendan and milrinone on oxygen consumption in isolated giunea-pig. J Cardiovasc Pharmacol 2004, 43: 555-561. 10.1097/00005344-200404000-00011
Cleland JG, Takala A, Apajasalo M, Zethraeus N, Kobelt G: Intravenous levosimendan treatment is cost effective compared with dobutamine in severe low-output heart failure: an analysis based on the international LIDO trial. Eur J Heart Fail 2003, 5: 101-108. 10.1016/S1388-9842(02)00246-5
Kivikko M, Lehtonen L: Levosimendan: a new inodilator drug for the treatment of decompensated heart failure. Curr Pharm Des 2005, 11: 435-455. 10.2174/1381612053382043
Ghignone M, Girling L, Prewitt RM: Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs. Anesthesiology 1984, 60: 132-135. 10.1097/00000542-198402000-00009
Kerbaul F, Rondelet B, Motte S, Fesler P, Hubloue I, Ewalenko P, Naeije R, Brimioulle S: Effects of norepinephrine and dobutamine on pressure load-induced right ventricular failure. Crit Care Med 2004, 32: 1035-1040. 10.1097/01.CCM.0000120052.77953.07
Greyson C, Xu Y, Cohen J, Schwartz GG: Right ventricular dysfunction persists following brief right ventricular pressure overload. Cardiovasc Res 1997, 34: 281-288. 10.1016/S0008-6363(97)00038-2
We acknowledge Professor G Della Rocca for his help and expert opinion regarding this subject.
AR has worked as a consultant for Edwards Lifesciences. AR and MC perform research that is partly funded by Edwards Lifesciences. EJ declares that he has no competing interests.
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Cecconi, M., Johnston, E. & Rhodes, A. What role does the right side of the heart play in circulation?. Crit Care 10, S5 (2006). https://doi.org/10.1186/cc4832
- Right Ventricle
- Pulmonary Vascular Resistance
- Right Coronary Artery
- Pulmonary Artery Catheter