acute right heart syndrome ( arhs ) may be defined as sudden deterioration in the right ventricular ( rv ) function and failure of the rv of the heart to deliver adequate blood flow to the pulmonary circulation , resulting in systemic hypoperfusion . in the context of critical illness
evidence of central venous pressure ( cvp ) overload in conjunction with rv contractile dysfunction , is usually present in arhs .
we searched pubmed , embase , cochrane library and google scholar , for articles reporting on rv dysfunction and failure .
the relevant papers were extracted in full and references from extracted papers were checked for any additional relevant articles .
an overview of the arhs pathophysiology , diagnostic tools for the assessment of the acutely failing rv in critical illness and measures including vasoactive agents , ventilatory strategies and mechanical support is provided in the current paper .
the main functions of the rv are : a )   maintenance of adequate pulmonary perfusion pressure in order to deliver desaturated mixed venous blood to the respiratory membrane ; b )  maintenance of low systemic venous pressure in order to prevent organ congestion .
the rv is anatomically adapted for the generation of low - pressure perfusion and it is very sensitive to changes in afterload . .
the differences between the structure and function of the rv compared to the left ventricle ( lv ) are outlined in table 1 and figure 1 compares the pressure - volume ( p - v ) loop of the rv with that of the lv .
little time is spent in isovolumetric contraction , giving a triangular - shaped rv p - v loop , in contrast to the almost square loop of the lv ( 25 ) .
the rv in critical illness arhs is not necessarily associated with an increase in pulmonary vascular resistance ( pvr ) and pulmonary arterial hypertension ( pah ) .
the syndrome can be due to rv pressure / volume overload or rv contractile dysfunction .
consequence is low cardiac output ( co ) with low mean arterial pressure ( map ) , exacerbating rv dysfunction .
rv failure begets rv failure  leading to a progressive downward spiral of worsening ischemia , myocardial dysfunction and shock . in mechanically ventilated patients with arhs ,
low co is multifactorial and could be due to rv systolic dysfunction , tricuspid regurgitation , ventricular interdependence ( dilatation of the rv shifting the interventricular septum toward the left and decreasing the lv distensibility and preload ) , arrhythmias or suboptimal preload .
rv diastolic dysfunction causes impaired rv filling and high diastolic rv and right atrial ( ra ) pressures leading to organ congestion .
the causes and precipitating events of arhs are summarized in table 2 . precipitating events / causes of arhs in the icu ( 7 - 15 ) .
arhs = acute right heart syndrome ; icu = intensive care unit ; rv = right ventricular ; lv = left ventricular .
arhs in acute respiratory distress syndrome ( ards ) ards is one of the most common causes of arhs secondary to rv pressure overload ( acute cor pulmonale ) . in critically ill ventilated patients with ards
, arhs occurs in 61% of patients submitted to conventional tidal volume mechanical ventilation ( mv ) and 25% of those receiving lung protective mv using low tidal volumes [ 15 , 16 ] .
apart from mv , the pathologic features of the syndrome per se , contribute to increased pulmonary vascular tone , acute pulmonary arterial hypertension ( pah ) and cor pulmonale .
contributors to elevated pulmonary vascular resistance ( pvr ) in ards include : vasoconstrictor : vasodilator imbalance ( excess et-1 , 5ht , pde , reduced no and prostanoids ) , endothelial injury , hypoxic pulmonary vasoconstriction ( 80% arteriolar ) , hypercapnia ( including permissive hypercapnia ) , acidemia , in situ thrombosis and pulmonary vascular remodelling ( muscularization of non - muscularized arteries ) [ 8 , 16 , 17 ] .
arhs in the setting of massive pulmonary embolism ( pe )   critically ill patients are at risk of pe despite thromboprophylaxis [ 3 , 18 ] . in a ten - year retrospective study , vieillard - baron et al
.   showed that arhs was present in 61% of medical intensive care unit ( icu ) patients with massive pe and carried a 23% mortality .
the normal rv can generate a mean pulmonary artery pressure up to 40 mmhg , requiring 50 - 75% of the pulmonary vasculature to be occluded by emboli before acute rv failure occurs .
hypoxemia induced by the emboli results in pulmonary vasoconstriction and the physiological response to platelet activation leading to release of vasoactive agents such as serotonin , thromboxane and histamine , causes further increase in pvr and rv pressure overload [ 19 , 20 ] . in severe sepsis and septic shock
rv systolic dysfunction in sepsis is directly associated with markers of endothelial dysfunction ( endothelin 1 , vascular cellular adhesion molecule 1 ) and directly related to the severity of sepsis . a proposed mechanism for arhs in sepsis is increased pvr secondary to sepsis - induced endothelial cell injury and altered vaso - reactivity , despite concomitant decrease in systemic vascular resistance ( svr ) .
substantial increases in pvr also occur when the left ventricle needs to considerably increase the cardiac output in order to compensate for the fall in the svr , causing further increase in rv afterload [ 21 , 22 ] .
diagnosis of arhs   in the critically ill clinical features    the clinical features of arhs , including acute onset shortness of breath , orthopnea and bilateral lower extremity edema , are non - specific and difficult to identify in the sedated critically ill patient . increased oxygen requirements or sudden cardiovascular collapse might be the chief clinical manifestations of arhs in a mechanically ventilated patient .
other prominent clinical signs include atrial or ventricular arrhythmias , raised jugular venous pressure and gallop rhythm at the left sternal edge , systolic murmur of tricuspid regurgitation , organomegaly , signs of deep venous thrombosis ( in the context of venous thromboembolism ) .
it is important to consider arhs in persistent respiratory weaning failure ( rv dysfunction leads to an imbalance between ventilator needs and cardiorespiratory capacity ) , especially in patients with lv systolic dysfunction [ 6 , 9 , 24 , 25 ] .
a high index of suspicion is needed in high risk patients such as those with pre - existing pah and recent deep venous thrombosis .
available bedside studies include : chest x - ray ( cxr ) , electrocardiography ( ekg ) , arterial blood gas ( abg ) analysis , hemodynamic and echocardiographic diagnostic tools .
however , cxr can not be utilized to confirm the diagnosis of arhs and should only contribute to the diagnostic approach by ruling out conditions that mimic arhs in the icu , such as atelectasis , pleural effusions , pulmonary edema and pneumothorax .
showed that qr in v1 is a strong predictor of rv dysfunction , and it is highly associated with troponin leakage and myocardial shear stress .
it has also been demonstrated that in patients with right bundle branch block , r duration in lead v1>100 ms is predictive of rv systolic dysfunction .
other ekg findings suggestive of rv strain include inversion of t waves in leads v1-v4 and the classic s1q3t3 pattern . acute anterior q - wave pattern in leads v1-v3 , as well as a right - sided q pattern in leads v3r - v6r , might suggest rv infarction .
arterial blood gas analysis abg analysis may reveal grossly impaired gas exchange and low cardiac output might result in acidemia with lactic acidosis due to tissue hypoperfusion .
hemodynamic bedside diagnostic modalities central venous catheters and central venous pressure an accurately placed central venous catheter ( in the superior vena cava ) , can provide information on cvp and used as a surrogate for rv end - diastolic volume ( rvedv ) and rv end - diastolic pressure ( rvedp ) [ 25 , 28 ] . in severe tricuspid regurgitation causing arhs , a broad , tall systolic c - v wave
is seen due to abnormal systolic filling of the right atrium ( ra ) and the cvp trace is said to be ventricularized because it resembles right ventricular pressure [ 25 , 28 ] .
rvedp reflects rvedv ( which is proportional to preload ) only when ventricular compliance is normal
. therefore , in conditions such as pah , tamponade and myocardial ischemia , where rv compliance is decreased , cvp is likely to be raised and can not be accurately assessed [ 28 , 29 ] .
right heart catheterization right heart catheterization using a pulmonary artery catheter ( pac ) is frequently required when arhs is clinically suspected and interpretation of imaging studies is difficult or inconclusive .
hemodynamic data obtained from an accurately placed pac , by thermodilution , may provide diagnostic clues and guide therapy .
pac allows direct simultaneous measurement of ra , rv , pa and pulmonary artery wedge pressures and indirect measurement of cardiac output , cardiac index ( ci ) , rv stroke work index , mixed venous oxygen saturation , pvr and svr [ 29 , 30 ] .
hemodynamically , arhs is suspected if ra pressure > 8 - 10 mmhg , or ra pressure to pulmonary capillary wedge pressure 0.8 ( isolated rv failure ) and ci is low . in the presence of rv - pa gradient
> 25 mmhg , rv outflow tract obstruction should be excluded by echocardiography . in the context of pah and suspected arhs ,
right heart catheterization allows assessment of left - sided heart disease and its contribution to pah . besides ,
calculation of pvr and svr help decide whether pulmonary or systemic vasodilators / pressors are needed and monitor response to therapy . in patients with pre - existing pah , a decrease in pa pressure might reflect low rv ejection fraction and worsening rv dysfunction .
arterial pulse contour analysis arterial pulse contour analysis enables calculation of co , pulse pressure variation ( ppv ) , stroke volume variation ( svv ) and svr , from the arterial pulse pressure waveform , in mechanically ventilated patients .
dynamic indices ( svv , ppv ) have been used to predict preload responsiveness and monitor the hemodynamic effect of volume expansion in critically ill patients .
wyler von ballmoos et al . reported that ppv is not accurate predictor of fluid responsiveness in mechanically ventilated patients with acute pah ( at risk of arhs ) , early after cardiac surgery and in septic shock .
in the context of a pressure overloaded rv , increased ppv values are related to an increase in the rv afterload and not to a decrease in rv preload and therefore , further volume expansion could potentially be harmful [ 33 , 34 ] .
however , it could be reasonably contended that lack of response to a fluid challenge , while ppv or svv is high , could be seen as an indicator of rv dysfunction necessitating further investigations .
bedside imaging modalities transthoracic ( tte ) and transesophageal echocardiography ( tee ) are bedside diagnostic tools which also provide rapid risk stratification and could potentially direct therapeutic strategies . in experienced hands , echocardiography allows assessment of the rv performance and loading conditions .
useful echocardiography - derived measures of rv function , when arhs is clinically suspected are outlined in table 3 .
echocardiographic quantitative parameters pointing towards arhs ( 36 - 38 ) rv = right ventricular ; tapse = tricuspid annular plane systolic excursion ; 2drvfac = two - dimensional right ventricular fractional area change ; rimp = right ventricular index of myocardial performance ; e / a = early ( e ) to late ( a ) ventricular filling velocities ratio ; rvot = right ventricular outflow tract .
tte is an easy and non - invasive way to assess the size and kinetics of the rv .
the diagnosis of arhs due to rv pressure overload , with tte , has good positive predictive value for indirect diagnosis of massive pe .
main limitations of tte in critically ill patients ventilated with high level of positive end - expiratory pressure ( peep ) include : inadequate imaging due to interposition of the inflated lung between the heart and the chest wall , low diagnostic accuracy in the patients with pre - existing cardiopulmonary disease , the operator dependent nature of tte .
it has been suggested that in the presence of significant and otherwise unexplained rv strain without clots present on tte , tee should rapidly follow at the bedside , providing there is local availability and expertise .
tee is a semi - invasive procedure and commonly reported complications associated with tee in critically ill patients receiving mv , include : hypo- or hypertension , dysrrhythmias , trauma to the gastrointestinal tract , hypoxemia and dislodgment of endotracheal or nasogastric tubes .
the over - all complication rate associated with tee use is low and it is estimated to be approximately 2.6% .
additional imaging modalities computed tomography ( ct ) ct pulmonary angiography ( ctpa ) is being used increasingly as a diagnostic tool in pe , with documented sensitivities of 50 - 100% and specificities of 81 - 100% .
ctpa has become the preferred diagnostic modality for suspected arhs due to pe , in hemodynamically stable icu patients .
chest ct signs suggestive of arhs include : flattening or displacement of the intraventricular septum toward the lv , reflux of contrast into the inferior vena cava , rv diameter ( rvd ) to lv diameter ( lvd ) ratio on axial sections greater than 1.0 ( rvdaxial / lvdaxial > 1 ) .
cardiovascular magnetic resonance ( cmr ) cmr is the most sensitive method to assess the rv size and function .
however , cmr is rarely used for icu patients receiving mv , as the mr environment carries significant risks to patients during transportation and prolonged periods in the mr scanner .
the usefulness of laboratory tests such as d - dimmer , troponins and b - type natriuretic peptide levels , as diagnostic tests in icu patients with suspected rv failure , is limited , as they are non - specific and confounded in the context of critical illness [ 41 , 42 ] . in summary , in critically ill patients with clinically suspected arhs , echocardiography ( tte and/or tee ) and right heart catheterization are the preferred diagnostic modalities .
if pe is the most likely cause of arhs , then ctpa is necessary to confirm the diagnosis , provided the patient is suitable for transfer to radiology . in any given scenario ,
the diagnostic approach will depend upon the expertise and availability of the different diagnostic modalities .
the principles and key components of arhs management include reversal of precipitating events and control of contributing factors ( hypoxemia , hypercapnia , anemia , acidemia , sepsis , dysrrhythmias ) , fluid volume optimization , maintenance of perfusion pressure , positive inotropy , use of pulmonary vasodilators and protective mv [ 12 , 43 ] .
control of contributing factors , general icu care and reversible causes of arhs   infection prevention , treatment of sepsis in accordance with the surviving sepsis campaign bundles , normoxia , normocapnia , thromboprophylaxis , peptic ulcer prophylaxis , correction of acid - base imbalance and electrolytes and glycemic control are mandatory and applied to most icu patients . pulmonary vasodilators and/or inodilators ( in acutely decompensated pah ) , thrombolysis ( in massive pe ) , revascularization ( in rv infarction ) and sequential av pacing and/or cardioversion ( in significant dysrrhythmias ) , could potentially correct the abnormal rv physiology .
rv ejection fraction is dependent on rv pre - load , in the abscence of pah and it is likely that rv output will be inadequate in hypovolemia .
the rv can increase the stroke work through an increase in rv free wall stretch ( via the frank - starling mechanism ) .
a systematic review of 24 studies demonstrated a poor relationship between cvp and intravascular fluid status and the inability of cvp / delta - cvp to predict the hemodynamic response to a fluid challenge [ 32 , 45 ] .
depending on where the patient is on the frank - starling curve , some may be adequately resuscitated with a cvp of 6 - 7 mm hg , while others may still be intravascularly volume depleted at a cvp of 10 mm hg . in a recent meta - analysis ,
marik et al . showed that there is paucity of data to support the widespread practice of using cvp to assess intravascular fluid status and guide fluid therapy .
more reliable hemodynamic assessment tools , such as pac , pulse contour analysis , tte and/or tee when available , may be utilized to guide fluid therapy in arhs .
showed that in critically ill medical patients with circulatory failure ( defined by ci 2 ) , due to massive pe , fluid loading with 500 ml of colloid increased the cardiac index significantly and improved hemodynamic status .
if the hemodynamic response to initial fluid challenge is poor , in the context of arhs , further volume loading may cause rv overdistension , increased ventricular interdependence , decreased lv filling and rv ischemia , leading to worsening shock . in rv volume overload , acute kidney injury due to venous congestion ( cardiorenal syndrome ) , continuous veno - venous hemofiltration ( cvvh ) facilitates greater clinical improvement compared with aggressive diuretic therapy , in heart failure patients , who are diuretic resistant .
the role of vasopressors in arhs in order to preserve adequate right coronary blood flow , systemic pressure should be maintained above the pa pressures .
it has been shown that in patients with sepsis , pah and rv dysfunction , norepinephrine increases systemic pressure through alpha-1 receptor agonism and may improve the rv oxygen supply / demand ratio , but this potentially beneficial effect on rv ejection fraction may be offset by a concomitant increase in pvr and rv afterload , at high doses ( > 0.5 mcg / kg / min ) [ 43 , 49 ] . besides , norepinephrine , through beta-1 receptor agonism could potentially improve rv - pa coupling and co .
low dose vasopressin ( 0.033 - 0.067 u / min ) mediates pulmonary arterial vasodilation and may be useful in vasodilatory shock and pulmonary vascular dysfunction , especially in norepinephrine resistant patients [ 43 , 49 , 50 ] .
inotropes and inodilators in arhs   dobutamine ( beta-1 receptor agonist ) can be used as the first - line inotropic agent in arhs due to rv contractile dysfunction .
low dose dobutamine ( 2 - 5 mcg / kg / min ) increases ci , sv and decreases pvr and svr [ 12 , 43 , 51 ] . at higher doses ( > 10 mcg / kg / min ) dobutamine causes tachycardia , increased oxygen consumption ,
increased pvr and leads to systemic hypotension and addition of a vasopressor might be required [ 12 , 51 ] .
high quality evidence suggests that dopamine is associated with increased tachyarrhythmias and is not recommended in cardiogenic shock .
it has been demonstrated that in patients with septic shock and arhs , who are unresponsive to fluid loading , dopamine or dobutamine , epinephrine improves rv contractility in spite of a rise in mean pap by 11% ( p<0.05 ) .
selective phosphodiresterase ( pde ) iii inhibitors ( enoximone , milrinone , amrinone ) , augment myocardial contractility and cause systemic and pulmonary vasodilaton , by increasing cyclic adenosine monophosphate ( camp ) and thus reducing pa pressures and improving rv function in patients with arhs due to pressure overloaded rv .
it has been demonstrated that levosimendan , a calcium sensitizer with pulmonary vasodilator properties ( inodilator ) , improves rv performance in arhs secondary to sepsis - induced ards and in experimental arhs restores rv - pa coupling better than dobutamine . in arhs
, levosimendan has been shown to reduce the increased rv afterload and ventricular interdependence , improve rv contractility and rv diastolic function , without significant increase in oxygen consumption , mediated by opening of sarcolemmal and mitochondrial potassium - adenosine triphosphate channels [ 54 , 55 ] .
although levosimendan is indicated for the treatment of acute heart failure ( class of recommendation iia , level of evidence b ) , it is has not yet been approved in all countries [ 54 , 55 ] .
pulmonary vasodilation in arhs the goals of pulmonary vasodilation in arhs are : 1 )   decrease pvr and impedance ; 2 )  increase rv stroke volume and output ; 3 )  avoid systemic hypotension and maintain coronary perfusion ; 4 )  avoid hypoxemia from ventilation - perfusion mismatch . it is recommended that inhaled nitric oxide ( no ) , which increases intra - cellular cyclic guanosine monophosphate ( cgmp ) , should be considered as short term therapy to improve pao2/fio2 ratio and co , in ventilated patients with arhs secondary to ards .
it has also been suggested that no may be effective in stabilizing patients with arhs due to massive pe until more definitive treatment is available [ 29 , 56 ] .
prostanoid formulations ( epoprostenol , iloprost ) are potent pulmonary and systemic vasodilators with anti - thrombotic and anti - proliferative actions .
they reduce pvr and improve rv function and they have been used in arhs due to rv pressure overload .
it has been shown that use of intravenous epoprostenol in mechanically ventilated patients with ards reduces pvr and improves rv performance .
sildenafil , a pde 5 inhibitor , increases downstream cgmp signaling and potentiates the beneficial effects of no .
showed that mechanically ventilated patients with arhs from pah , who were dependent on dobutamine , were treated with oral sildenafil and in many cases they were successfully weaned from inotropic and ventilatory support .
mechanical ventilation strategies in arhs   optimal mv ventilation management in arhs consists of : avoidance of hypoxemia , hypercapnia , high levels of peep ( > 10 cmh2o ) and both high and low extremes of lung volumes and use lung protective ventilation strategies if possible [ 43 , 60,61,62 ] .
the rv afterload is governed by pvr which is directly affected by changes in lung volume .
this is due to the elastic recoil forces of the lung parenchyma leading to extra - alveolar vessel collapse and terminal airway collapse leading to alveolar hypoxia and hypoxic pulmonary vasoconstriction ( hpv ) and at high lung volumes due to collapse of the alveolar vessels via stretch of the alveolar wall .
when pvr is plotted against lung volume , a typical u - shaped curve occurs with the lowest pvr occurring at functional residual capacity ( frc ) ( figure 2 ) .
effect of changing lung volume on pulmonary vascular resistance ( pvr ) ( 62 ) .
rv = residual volume ; frc = functional residual capacity ; tlc = total lung capacity .
schmitt et al . assessed the impact of peep on the rv outflow impedance using doppler data obtained by tee , in mechanically ventilated icu patients with ards .
they demonstrated that high peep ( 134 cmh2o ) was associated with increased rv afterload and worsening rv systolic dysfunction . the significant decrease in the incidence of arhs ( from 61% to 25% ) in ards since ardsnet trial was published ,
reflects a change in mv practice and suggests that lung protective strategies ( tidal volume : 6 - 8 ml / kg predicted body weight ( pbw ) , low plateau pressures and peep ) reduce the incidence of arhs . in patients with arhs , during lung protective ventilation , permissive hypercapnia should be avoided as acute hypercapnia could lead to pulmonary vasoconstriction or exacerbate hypoxic pulmonary vasoconstriction and could potentially worsen rv dysfunction . a prospective observational study , which evaluated the relative roles of acute permissive hypercapnia and peep variations on rv function , in severe ards patients , showed that increasing peep at constant pplat induces acute hypercapnia that may impair rv function and decrease ci .
it is therefore recommended that in cases of arhs , lung protective ventilation should be gradually adapted to limit hypercapnia and rv overload . in mechanically ventilated icu patients with arhs
, refractory hypoxemia and/or hypercapnia and high peep requirements , extracorporeal membrane oxygenation ( ecmo ) could be used as a bridge to the recovery of respiratory function .
oxygenation and carbon dioxide clearance are provided by the extracorporeal circuit , minimizing pulmonary vasoconstriction due to hypoxemia and/or hypercapnia [ 66 , 67 ] . in patients with arhs due to severe ards , where lung protective ventilation may not be adequate in managing hypercapnic acidosis ,
extracorporeal carbon dioxide ( ecco2 ) removal devices are an option , as they are less invasive than ecmo and may play a role in instituting  ultra - protective  lung ventilation ( tidal volume : 4 ml / kg pbw ) .
it should be noted that the cardiac consequences of weaning from mv may be responsible for weaning failure in patients with arhs . in these patients ,
an increase in weaning - induced rv afterload may occur due to marked increase in work of breathing , hypoxemia or high intrinsic peep , leading to further worsening rv enlargement during weaning .
this may result in leftward shift of the interventricular septum , impeding lv diastolic filling and lv output ( ventricular interdependence ) , causing pulmonary edema and failure to wean from mv .
mechanical circulatory support low cardiac output syndrome caused by arhs after cardiac surgery , particularly coronary artery bypass graft surgery and heart transplant , may be an indication for intra - aortic balloon pump ( iabp ) [ 70 , 71 ] .
it has been demonstrated that iabp improves hemodynamics and rv efficiency in acute ischemic rv failure . however , a recent rct failed to demonstrate any mortality benefit in patients with cardiogenic shock complicating acute myocardial infarction .
veno - arterial ( va ) ecmo has been used as a salvage therapy in cases of arhs due to massive pe and refractory cardiogenic shock , after systemic thrombolysis .
it can be used as a means of unloading the rv and supporting systemic circulation , in medically refractory rv failure with accompanying hypotension and end - organ failure and as a bridge to transplant [ 74 , 75 ] .
right ventricular assist devices ( rvads ) in arhs may be used as a bridge to recovery or transplant , or as a definitive surgical treatment , in primary rv dysfunction . in patients who are successfully weaned from the rvad ,
it has been suggested that rvads should be avoided in patients with arhs secondary to rv afterload resistance ( with severely elevated pvr ) , as pumping blood into the pa could potentially cause worsening pah and lung injury , whereas co and ci remain low . in such cases
the use of mechanical cardiovascular support devices depends largely on local availability of specialized facilities , cardiopulmonary pathophysiology expertise and operator experience .
arhs is difficult to diagnose in the critically ill as those patients have ongoing physiological derangement presenting the intensive care specialists with a diagnostic dilemma .
cardiac echo and right heart catheterization are invaluable diagnostic tools in the assessment of the rv at the bedside , which also provide a rapid risk stratification and could direct treatment strategies . characterizing , identifying and correcting reversible factors
is of paramount importance . minimizing rv afterload ( pulmonary vasodilators , inodilators , rv  protective  mv strategies ) and maximizing rv performance (
preload , inotropy , mechanical circulatory support ) are the major components of arhs management .
need for mechanical circulatory support , merits referral to specialized treatment centres , if there is insufficient local expertise or capacity .
there is lack of definitive data regarding the management of arhs in icu patients , without pre - existing cardiopulmonary disease .
well - designed and adequately powered rcts are required to estimate the prevalence of arhs among critically patients receiving mv , improve the understanding of its mechanisms in the context of critical illness and evaluate the efficacy of therapy guided by invasive and non - invasive hemodynamic monitoring tools .
 acute right heart syndrome is a sudden deterioration in right ventricular performance , resulting in right ventricular failure and confers significant in - hospital morbidity and mortality . in critically ill patients , the syndrome is often undiagnosed and untreated , as these patients do not usually exhibit the common clinical manifestations of the condition , making the diagnosis challenging for the intensivist . in this narrative review 
 we focus on the pathophysiology of acute right heart syndrome , in critical illness , diagnostic modalities used to assess right ventricular function and management of acute right heart syndrome , including mechanical ventilation strategies and circulatory support . 
Introduction
Conclusion