P<0.0012) and LV systolic function progressively deteriorated (P<0.0001) post-MI. CO and RCCA FL showed a moderate but significant decrease over the course of MI with similar fluctuation pattern such that both variables were decreased at day 1, increased at day 7, and decreased at 30 days post-MI. Correlation and regression analyses between CO and RCCA FL showed a strong correlation with significance at baseline and day 30 post-MI . Days 1 and 7 analyses between CO and RCCA FL showed moderate correlation with non-significance post-MI . In summary, CBF significantly decreased following AMI and remained significantly decreased for up to 30 days, suggesting a potential risk for brain damage that could contribute to cognitive dysfunction later in life.Heart failure is associated with low cardiac output (CO) and low brain perfusion that imposes a significant risk for accelerated brain ageing and Alzheimer’s disease (AD) development. Although clinical heart failure can emerge several years following acute myocardial infarction (AMI), the impact of AMI on cerebral blood flow (CBF) at early stages and up to 30 days following MI is unknown. Sixteen months old male mice underwent left anterior descending (LAD) coronary artery ligation. Hemodynamics analyses were performed at baseline and at days 1, 7, and 30 post-MI. Left ventricular (LV) ejection fraction (EF), LV volumes, CO, and right common carotid artery (RCCA) diameter were recorded by echocardiography. RCCA flow (RCCA FL) was measured by Doppler echocardiography. LV volumes consistently increased ( Appropriate tissue blood perfusion is necessary for normal organ functions and is dependent on several factors including cardiac output (CO), blood volume, systemic blood pressure (BP), and local vasculature autoregulation, all of which positively depend on metabolic demand ,2. DistiCerebral perfusion is supplied by two carotid arteries and two vertebral arteries. Each carotid artery supplies approximately 40% to the total cerebral perfusion, while the two vertebral arteries supply the remaining 20% . CerebraRecent studies suggest that impaired CBF as a result of CO reduction in heart failure patients may be a critical risk factor for Alzheimer’s disease (AD) development and accelerated brain ageing processes . To dateAt the onset of MI, cardiac function, measured by CO and other hemodynamic parameters, rapidly deteriorates and persists until progressive restoration through medical intervention ,16,17. DIn addition to direct alteration of CO through myocardial mechanical injury and LV remodeling ,21,22, Mn=9) and sham operated group (n=6). Sixteen months old C57BL/6J male mice weighing 30–35 g underwent left anterior descending (LAD) coronary artery ligation surgery as previously described [All animal experiments and procedures were performed according to an experimental protocol approved by AUB Institutional Animal Care and Use Committee in compliance with the Guide for Care and Use of Laboratory Animals of the Institute for Laboratory Animal Research of the National Academy of Sciences, U.S.A. Mice were allocated into two groups: study group . Measurements were performed at day 30 post-MI in restrained and conscious experimental animals. Real-time measurements of systolic, diastolic, and MAP were recorded. Any irregular recording noted as false recording by the system were excluded.Transthoracic echocardiography was performed using Vevo 2100™ High-Resolution Imaging System . Mice were anesthetized with 1–2% isoflurane in an oxygen mix and placed on an electrical heated platform. B-mode (2D) images of left ventricle were acquired from the parasternal long axis view in supine position. Right common carotid artery (RCCA) was acquired from B-mode imaging in supine position A. Body tLV volumes were calculated based on modified ellipsoid (Teichholz) formula :LVEDV (LV stroke volume (SV) and ejection fraction (EF) were derived from the LV end diastolic volume (LVEDV) and LV end systolic volume (LVESV).CO was derived from multiplication of SV and heart rate.RCCA was assumed to be a cylinder, and its cross-sectional area was calculated based on the following formula:  = π × R2, where CRCCA FL was calculated based on the following equation: VTI × HR,34, wherFractional RCCA FL was calculated according to following equation:Following the removal of the right ventricle, the left ventricle was sliced along its longitudinal axis and immersed for 5 min at 37°C in 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) (5 mg/ml) for demarcation of infarcted region. The infarcted region was defined as the unstained section following incubation with TTC. ImageJ software  was used for infarct size measurement. The whole LV area along with the unstained region was traced and the measurement was done automatically by the program in pixels. The infarct area was expressed as a percentage of the left ventricle.2) coefficients <0.3 were considered weak, >0.3 and <0.6 were considered moderate, and >0.6 were considered strong. The R2 and P-values in corresponding regression analysis represent goodness-of-fit and significance of the regression model. For multiple groups comparison, we used one-way ANOVA followed by Tukey’s post-hoc. Data are expressed as mean ± S.D. Analyses were done using GraphPad Prism version 7.03 for Windows ; a P-value of <0.05 was considered statistically significant in all analyses.When appropriate, correlation and regression analyses were performed. The correlation (R) and regression  and progressively deteriorating systolic function measured by EF  and CO (Data presented in this section are summarized in ) and CO . Unlike ) and CO .2 = 0.37, P<0.0001, R = −0.44, R2 = 0.19, P<0.0082, respectively). In sham operated mice however, both RCCA FL and CO fluctuated during 7 days post-op while remaining within the baseline level .We then investigated the impact of impaired LV systolic function on brain perfusion and measured the RCCA FL via Doppler echocardiography. Similar to CO, the RCCA FL showed a moderate but significant decrease over the course of MI with similar fluctuation pattern observed on days 1, 7, and 30 post-MI when compared with baseline . However, the relationship of these changes was only significant for the CO .Both CO and RCCA FL were inversely correlated with the infarct size ; granulation phase (1–7 days); and maturation/wound healing phase (weeks) ,27. AlthThe major finding of the present study is that CBF decreases at the onset of MI and remains lower than baseline for 30 days /Figure 3Systemic regulatory mechanisms following both cardiac dysfunction and decrease in major organ blood perfusion are well documented ,38. DecrWith respect to BP variation and its impact on CBF, patients with uncomplicated MI and intact autonomic nervous system are usually normotensive . Our finIn summary, intact compensatory and regulatory mechanisms were not able to restore normal CBF in mouse model of 30 days of MI. These findings emphasize the importance of an appropriate intervention at cerebral, cardiac, and/or systemic level including inflammatory resolution to immediately restore CBF post-MI and prevent cerebral hypoperfusion ramifications on potential acute or time-dependent cerebral injury.133Xe clearance technique [Although several imaging techniques are currently available to assess CBF , Dopplerechnique ,43. Commechnique . Previouechnique ,47. In fechnique ,47. HoweIn the present study, common carotid artery but not internal carotid artery was used for flow measurement given the easier access due to the size of the animal studied and as previously reported ,42. InteWith regard to anesthesia, CO and RCCA FL were measured under isoflurane inhalation. Isoflurane is known to reduce systemic vascular resistance and produce minimal cardiac depression ,53. AlthWith respect to CO and CBF relationship, previous report showed that CO and CBF relationship was different at rest and during exercise in healthy individuals . The autAlthough CO and CBF are directly connected, one cannot rule out the effect of aortic compliance on the heart–CBF transition. Under physiological conditions, the blood volume is ejected from the left ventricle into the central arteries such as aorta and carotid arteries and transmitted to the brain with minimal pulsatile fluctuation. In fact, attenuated hemodynamics fluctuation at the cerebrovascular level is an important determinant of cerebrovascular health . Tomoto Last but not the least, in order to eliminate the impact of surgical stress on the relationship between CO and RCCA FL, a sham group was included in the present study. Both CO and RCCA FL fluctuated within the baseline levels till day 7 post-op . We alsoOur novel findings report the association between CBF and CO in early stages of cardiac remodeling and up to 30 days following acute MI. We showed that CBF significantly decreased along with CO following acute MI; however, regulatory systems could not restore CBF completely following reduced CO. The present study highlights the importance of impaired CBF at early and advanced stages of acute MI and its potential impact on cerebrovascular prognosis. Early intervention to fully restore normal CBF following acute MI is critical and warrant future investigation.


The precise nature of packing together of the cardiomyocytes within the ventricular walls has still to be determined. The spiraling nature of the chains of interconnected cardiomyocytes has long been recognized. As long ago as the end of the nineteenth century, Pettigrew had emphasized that the ventricular cone was not arranged on the basis of skeletal muscle. Despite this guidance, subsequent anatomists described entities such as “bulbo-spiral muscles”, with this notion of subunits culminating in the suggestion that the ventricular cone could be unwrapped so as to produce a “ventricular myocardial band”. Others, in contrast, had suggested that the ventricular walls were arranged on the basis of “sheets”, or more recently “sheetlets”, with investigators seeking to establishing the angulation of these entities using techniques such as magnetic resonance imaging. Our own investigations, in contrast, have shown that the cardiomyocytes are aggregated together within the supporting fibrous matrix so as to produce a three-dimensional myocardial mesh. In this review, we summarize the previous accounts, and provide the anatomical evidence we have thus far accumulated to support the model of the myocardial mesh. We show how these anatomic findings underscore the concept of the myocardial mesh functioning in antagonistic fashion. They lend evidence to support the notion that the ventricular myocardium works as a muscular hydrostat. Any review of the “functional morphology” of the heart must provide an accurate account of the way in which the individual cardiomyocytes are aggregated together within the ventricular walls. It is the cardiomyocytes that are the working units of the myocardium. By their contraction, they provide the force for the ejection of the blood. Their precise arrangement within the walls, however, remains remarkably contentious. Advances in imaging techniques, nonetheless, are now permitting visualization of the transmural architecture in three-dimensions at ever increasing spatial resolution. This new level of morphological information suggests the myocardium is best described on the basis of a model which can be considered a three-dimensional myocardial mesh ,2,3. In In this regard, it was established quite some time ago that each cardiomyocyte is supported by the endomysial weave of the mural fibrous matrix . PerimysIn this review, we summarize again this anatomical evidence as collected by ourselves. More importantly, we present it in the context of historical evidence, some of which has been available for centuries. The pre-existing evidence itself has long served to challenge the notion that the ventricular myocardium can be analyzed in the fashion of skeletal musculature. These earlier findings negate the notion that the ventricular mass can be unwrapped as an anatomically traceable longitudinal band of muscle with both an origin and insertion ,5. The aThe interest in myocardial architecture dates back hundreds of years. In Leonardo da Vinci’s drawings from the fifteenth century, we find notions on the varying alignment of the cardiomyocytes within the myocardium . This waIt was such studies using gross dissection that formed the basis of the monumental studies of Pettigrew. Based on his dissections, Pettigrew had already determined that it was inappropriate to compare the arrangement of the cardiomyocytes within the heart with those of skeletal muscles ,27. As hIt is perhaps surprising that, neither in his own detailed account , nor in Streeter  also disWe can clarify the controversy as to whether all cardiomyocytes are aggregated together in tangential fashion. In this regard, Streeter had recognized the difficulty of measuring the true transmural orientation of the cardiomyocytes, which he named as the angle of imbrication, when using histological sections cut in the orthogonal planes of the ventricular wall . He had These studies using circular knives have revealed the presence of chains of cardiomyocytes that deviate significantly from the tangential plane. The results parallel the conclusions of Streeter ,35,36, aAdvances in the techniques now available for imaging autopsied specimens, such as micro-computed tomography and diffusion tensor magnetic resonance imaging, have changed the way we investigate cardiac architecture. We are no longer required to make assumptions based on quasi-three-dimensional techniques, such as dissection, peeling, or histology. Using so-called “eigen analysis” of the three-dimensional structural tensor , we can Those who continue to support the notion of the “myocardial band” had postulated that the ‘bright line’ represented a mid-septal space, allegedly interposed between the ‘limbs’ of the alleged band . AnalysiControversy has also continued regarding the presence of chains of cardiomyocytes with an orientation that deviates from the epicardial tangential plane, in other words those with a transmural orientation. Those denying the existence of such transmural aggregations seemingly ignore the evidence now provided by detailed three-dimensional imaging of autopsied hearts , which cBrachet’s concept , howeverRecent studies using diffusion tensor magnetic resonance imaging have shown that re-orientation of the myocytes is not only crucial for normal contraction, but that the mobility of this process is altered in disease . Thus, tWhen assessing the ventricular mural architecture in the setting of ventricular function, it is pertinent to consider the concept of the muscular hydrostat. The basis of this notion is that distinct muscle bundles reduce one dimension of an enclosed fixed volume by their active contraction, thereby causing an increase in another dimension . Such anAs we explore ventricular architecture with ever increasing elegance and resolution, it becomes increasingly apparent, at least in our opinion, that the most suitable description of ventricular architecture, and its correlation with ventricular function, is provided by the model of the myocardial mesh. The findings described in our review are not themselves new, although we are currently expanding them using micro-computed tomography. We consider it necessary to bring our findings to the forefront once more. This is because, despite the existence of much evidence already negating the concept, some continue to argue in favor of the ventricular cone being arranged on the basis of a “ventricular myocardial band” . As emph


Several new innovative cardiac devices have been created over the last few decades. Chest radiographs (CXRs) are the most common imaging investigations undertaken because of their value in evaluating the cardiorespiratory system. It is important for the interpreting radiologist to not only identify these iatrogenic objects but also to assess for their accurate placement, as well as for any complications related to their placement, which may be seen either on the immediate post-procedural CXR or on a follow-up CXR. Almost all of the patients with implanted cardiac devices such as pacemakers, implantable cardioverter defibrillators (ICDs), cardiac resynchronisation therapy (CRT) devices, implantable loop recorders (ILR) and cardiac prosthetic valves undergo chest radiographs (CXRs) on a regular basis. Therefore, it is not uncommon for the resident, radiologist, intensivist or physician to be presented with a conundrum of CXRs having a variety of these devices on a day-to-day basis. Chest radiographs are the initial modality for evaluating the device location and its integrity after implantation and for diagnosis of complications and malfunction.2 In the United States, approximately 100 000 ICDs and 300 000 pacemakers are implanted annually,3 while in the UK, the 10-year average growth rate for pacemakers and ICDs is 4.7% and 15%, respectively.4 It is important to understand the basic functions and differences between various CIEDs, as well as to recognise them on a radiograph.Cardiovascular implantable electronic devices (CIEDs) include implantable cardiac pacemakers, ICDs, CRT devices  and implantable cardiac monitors. In 2012 alone, at least 3 million patients were implanted with CIEDs.5 Lead tips can be fixed actively or passively. Leads placed passively have radiolucent ‘tines’ at their end that anchor the lead tips in position. With time, the myocardium surrounding the lead tip undergoes fibrosis, further securing the lead tip in place. Active fixation leads have a retractable screw at its end which is deployed when the lead is placed in position. Specific situations where active fixation is used include right ventricular (RV) leads in the outflow tract and in situations where the right atrial (RA) leads must be secured to the tissue for stability. Active fixation leads are more commonly used in younger patients as it can be extracted much easier than passive fixation leads.6The CIED is composed of two main components: the pulse generator encased in titanium and the pacemaker or ICD lead(s). The pulse generator  comprise5 Pacemakers can be temporary or permanent.A pacemaker is a medical device that regulates the heart rate by electrical impulses delivered through electrodes to the heart muscles. The primary aim of this device is to maintain an adequate heart rate so as to not fall below a certain limit (mostly 60 beats/min), either because of a dysfunction of the heart’s natural pacemaker or because of a block in the electrical conduction system of the heart.6 The method of choice for temporary pacing in the intensive care unit (ICU) is transvenous pacing. Temporary epicardial pacing is the most common choice following cardiac surgery and for permanent pacing in children. Other alternatives include transthoracic, transesophageal or transcutaneous pacing routes.8These pacemakers are meant for short-term use during hospitalisation such as for bradydysrhythmia following a heart attack, cardiac surgery or drug overdose. The main equipment of the temporary pacemaker  is located outside the body and may be attached to the patient’s skin by a tape or body by a belt.9 The leads of the permanent pacemakers are inserted using a transvenous route usually through the left or right subclavian vein or rarely through the internal jugular, axillary or femoral vein. The pulse generator is implanted into the subcutaneous layer of chest below the clavicle and above the pectoral muscle . Rarely, the pulse generator may be placed under the skin of the abdomen, inframammary site in women for cosmetic reasons and right infraclavicular site for the left handed.10 During the insertion of a pacemaker, the standard procedure is a fluoroscopic evaluation of the positioning of the pacemaker electrodes, followed up by a CXR post insertion. Chest radiographs are also useful for identifying abandoned pacemaker leads  lead in the right atrium and a pacing (and/or sensing) lead in the right ventricle. Permanent pacemakers can be single-chamber pacemakers , dual-chamber pacemakers   and b orer leads  and comper leads  and b wh11Recently, leadless pacemaker systems have been developed as a minimally invasive option for patients requiring single-chamber pacemaker placement. The two RV leadless pacemaker systems currently available for clinical use are the Nanostim™ Leadless Pacemaker System (LPS)  and the Micra™ Transcatheter Pacing System (TPS) (Medtronic), both of which are inserted via femoral venous access and implanted directly into the RV wall. On CXRs, these devices appear as a linear radiopaque material implanted into the RV wall. Potential complications that can be identified on CXRs include device dislodgment and cardiac perforation.12 A newer approach is to place a subcutaneous ICD lead to the left of the sternum  and for preventing cardiac arrest. An ICD usually comprises of a single lead with one or two shock coils. A shock coil has a relatively thick electrode to reduce the risk of damage to the myocardium from the defibrillating shock. When a two-shock-coil device is placed accurately, one shock coil will be terminating at the brachiocephalic vein–SVC junction and the second coil in the RV  and b. A sternum .9During surgery in the operating room, a CIED can sense an external magnetic interference (EMI) that can affect its pacing function. The source of the EMI may include electrocautery, external defibrillation, radio frequency ablation (RFA) and dental instruments. A cardiac device magnet  may be uA detailed stepwise approach to the assessment of an ICD including its associated complications  and 10 o12 The assessment of a CRT device on a CXR is no different from the other CIEDs.ICD and pacemaker leads can be used in various combinations to produce a CRT device. The most common combination is a biventricular pacemaker with an ICD  and b, w13 although some of these contraindications remain slightly disputed.14By closely evaluating the CIED generator, a radiologist can determine if the device is MR conditional, as there are several ‘absolute’ contraindications to performing magnetic resonance imaging (MRI) in patients implanted with non-MR conditional CIEDs  or ILR  is a min16 on a PA CXR and a line extending from the carina to the apex on the lateral view, positions of the valves can be roughly estimated. The pulmonic valve is the most superiorly positioned valve in both views, appearing in partial profile on both projections. On both views, the aortic valve is located superior to the axis line, appearing in profile and in front on the frontal and lateral views, respectively. In contrast, the mitral valve is located inferior to the axis lines on both views, appearing en face on the frontal projection and in profile on the lateral view. The tricuspid valve is located the most inferiorly on both projections, appearing anteriorly and en face on the lateral view. Nevertheless, because of anatomical and physiological variations and differences in radiographic projections, valve identification based solely on CXR can be unreliable, necessitating the need for additional details such as clinical history.16Landmarks of the cardiac silhouette and of the thorax can enable the identification of heart valves on a CXR. By drawing an imaginary line extending from the left atrial appendage to the right cardiophrenic angle 16 on a P17 The various types of biological and mechanical prosthetic valves have been highlighted in 19Valvular heart disease is associated with significant morbidity and mortality and affects roughly more than 100 million people worldwide, and the current standard of management is surgical valve replacement –20. Alte20 providing detailed algorithms guiding in the identification of prosthetic heart valves on CXRs which is beyond the scope of this article.Identification of the prosthetic heart valve on a CXR is made possible by detecting any or all its radiopaque parts which may include the base ring, stent, struts, cage, ball or disc. In some cases, a prosthesis may have no radiopaque component and hence cannot be identified radiographically. In most cases, the base ring is radiopaque. Several prosthetic valves have radiopaque struts or stents above or below the base ring. If the projections are long, the prosthetic heart valve is either a ball-in-cage or bioprosthesis. Literature sources are available,21A stepwise approach to the evaluation of CXRs following cardiac valve replacement is elaborated in 22 ASO migration or embolisation is a recognised complication with an incidence of 0.4% – 1.1%, which can be identified on a CXR. Common sites of migration are the right cardiac chambers and pulmonary artery, while left-sided migration is rare.23The Amplatzer septal occluder (ASO)  is the most commonly used device for transcatheter closure of secundum atrial septal defects. The location of the ASO on a CXR is based on the position of the secundum atrial septal defect (ASD). On frontal CXRs , the ASO24The Amplatzer ductal occluder (ADO) is a mushroom-shaped self-expandable nitinol wire mesh used for occluding large patent ductus arteriosus (PDA), while smaller PDAs are occluded by the transcatheter method using Gianturco coils. A recognised complication with the ADO, like the ASO, is device embolisation or migration  and b.24All ethical considerations have been taken into account. No patient identity or patient information has been revealed.As more and more patients are living with CIEDs and prosthetic valves, it is important that residents, radiologists and physicians are aware of these devices and recognise them on a CXR. Radiologists in particular have a specific and important role in the evaluation of these devices. An early and accurate identification of device malfunction, fracture or migration can help prompt the physician or surgeon to intervene in a timely manner and help avoid preventable life-threatening catastrophes.


Systolic anterior motion (SAM) after mitral valve repair (MVR) can adversely affect hemodynamics due to exacerbation of left ventricular outflow tract obstruction and mitral regurgitation. Intraoperative transient SAM after MVR can usually be managed with hemodynamic maneuvers under continuous monitoring by transesophageal echocardiography (TEE). However, during postoperative intensive care management, transient SAM is seldom diagnosed and the start of treatment may be delayed. We present a case of transient SAM after MVR with abrupt deterioration due to junctional rhythm in the intensive care unit (ICU). TEE revealed that conversion from normal sinus rhythm into junctional rhythm induced the exacerbation of SAM. TEE was useful for identifying the etiology of unstable hemodynamics after cardiac surgery in the ICU, similar to its use in the operating room.The online version of this article (10.1186/s13089-018-0111-6) contains supplementary material, which is available to authorized users. Systolic anterior motion (SAM) after mitral valve repair (MVR) can adversely affect hemodynamics due to exacerbation of left ventricular outflow tract obstruction (LVOTO) and mitral regurgitation (MR) . AlthougA 55-year-old man with severe MR and middle scallop prolapse due to torn chordae underwent MVR. Preoperative LV ejection fraction, tricuspid annular plane systolic excursion and right ventricular fractional area change were 62%, 26 mm and 44%, respectively. MVR was performed with folding middle scallop and annuloplasty with a 30-mm Physio II annuloplasty ring . MR was well controlled. Despite difficulty weaning from cardiopulmonary bypass and some persistent surgical bleeding, he was hemodynamically stabilized on admission to the ICU without evidence of SAM and LVOTO.2, right ventricular stroke work index (RVSWI) 1.6 g/m2/beat, and mixed venous oxygen saturation (SvO2) 54%.He became hemodynamically unstable on the first postoperative day, with parameters as follows: heart rate 87 beats/min (bpm), sinus rhythm, arterial pressure 80/48 mmHg, pulmonary artery pressure 28/20 mmHg, central venous pressure 17 mmHg, cardiac index 1.7 L/min/mTransthoracic echocardiography (TTE) was performed to investigate the cause of hemodynamic deterioration; however, adequate images could not be obtained. TEE was then performed and showed right ventricular (RV) dysfunction without SAM and LVOTO. We decided to increase the dose of inotrope  to improve RV function and the hemodynamics stabilized.2, RVSWI 2.4 g/m2/beat, and SvO2 48%. The ventilator settings were as follows: pressure assist-control ventilation, respiratory rate 14 breaths/min, peak inspiratory pressure 16 cmH2O, inspiration time 1.6 s, positive end-expiratory pressure 10 cmH2O, and fraction of inspiratory oxygen 0.6.Severe hypotension developed on the second postoperative day. Hemodynamic parameters were as follows: heart rate 90 bpm, arterial pressure 50/42 mmHg, pulmonary artery pressure 28/20 mmHg, central venous pressure 13 mmHg, cardiac index 1.6 L/min/mAlthough the dose of dopamine, dobutamine and adrenaline was greatly increased to 5.4 µg/kg/min, 5.4 µg/kg/min and 0.05 µg/kg/min, respectively, and intra-aortic balloon pumping was started, hemodynamic parameters did not show improvement. No pulmonary vasodilator was used because of avoiding hypotension.Repeat TEE revealed the hyperdynamic left ventricle (LV) without any regional wall motion abnormality, as well as LVOTO and severe MR (vena contracta 8 mm) due to SAM Fig. . In addiWe identified two important clinical issues. Junctional rhythm can cause deterioration of SAM, LVOTO, and MR, and atrial pacing can improve hemodynamics in unstable normal sinus rhythm. TEE is useful for the identification of causes of unstable hemodynamics after cardiac surgery in the ICU as well as in the operating room.First, junctional rhythm can cause deterioration of SAM, LVOTO, and MR and atrial pacing can improve hemodynamics. Some mechanisms of SAM are related to geometric factors, kinetic factors, and structural abnormalities . GeometrThe management of SAM depends on the underlying mechanism and severity. In most cases, volume loading, discontinuation or reduction of inotropic drugs, and administration of beta blockers and vasopressors can resolve SAM –12. It hSecond, TEE in the ICU is useful for the identification of causes of unstable hemodynamics after cardiac surgery. The usefulness of echocardiography for diagnosis and decision-making has been shown in the ICU, and basic echocardiography skills have become mandatory for all intensivists in some guidelines –17. On tAfter cardiac surgery, obtaining useful images is sometimes difficult due to the narrowing of acoustic windows caused by the surgical incision, drapes, and drains. In addition, unclear images are insufficient for clinical decision-making in critical situations. Strengths of TEE include less dependence on operator skills and better spatial resolution compared to that of TTE . In the This case report shows that junctional rhythm can cause deterioration of SAM, LVOTO, and MR, and can lead to unstable hemodynamics in a patient with right ventricular failure after MVR. Atrial pacing can resolve SAM, LVOTO, and MR and can improve hemodynamics in a patient with unstable normal sinus rhythm. TEE in the ICU can play a pivotal role in clinical decision-making. Given that there are various causes of hemodynamic deterioration after cardiac surgery and some cannot be diagnosed without TEE, both TTE and basic TEE skills are required for intensivists.Additional file 1. Mid-esophageal long axis view on the second postoperative day. Massive mitral regurgitation and turbulent flow is seen in the left ventricular outflow tract.Additional file 2. Mid-esophageal long axis view in normal sinus rhythm.Additional file 3. Mid-esophageal long axis view in junctional rhythm.Additional file 4. Mid-esophageal long axis view in junctional rhythm .


Arrhythmias are increasingly recognized as serious, end-stage complications of pre-capillary pulmonary hypertension, including pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Although arrhythmias contribute to symptoms, morbidity, in-hospital mortality, and possibly sudden death in PAH/CTEPH, there remains a paucity of epidemiologic, pathophysiologic, and outcome data to guide management of these patients. This review summarizes the most current evidence on the topic: from the molecular mechanisms driving arrhythmia in the hypertrophied or failing right heart, to the clinical aspects of epidemiology, diagnosis, and management. As outlined in the most recent European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines, PH is subdivided into groups 1–5: group 1 ; group 2 (PH due to left heart disease); group 3 (PH due to lung diseases and/or hypoxia); group 4 (chronic thromboembolic PH [CTEPH]); and, lastly, group 5 .57 Arrhythmias, such as sinus tachycardia, atrial tachycardia, atrial fibrillation (AF), atrial flutter (Afl), sinus bradycardia, ventricular tachycardia (VT), and ventricular fibrillation (VF), have been recognized as serious, end-stage complications of PAH and CTEPH.8 Despite evidence that these arrhythmias contribute to symptom burden, morbidity, in-hospital mortality, and possibly sudden death,812 there remains scant data regarding the epidemiology, pathophysiology, and outcome of PAH patients with arrhythmia.The primary cause of death in PAH is thought to be right heart failure, occurring as a direct consequence of elevated PAP, although in some studies approximately 50% of patients died from another cause, with PH as a contributing factor.In this review, we explore the maladaptive and arrhythmogenic response of the right heart to group 1 and group 4 PH. We discuss the current patterns of clinical management, noting where these are evidence-based, and consider options for management of arrhythmia in PH. We also identify knowledge gaps and propose future directions.While arrhythmia has been identified to coexist in all subgroups of PH, we will focus mainly on group 1 PH (PAH) and CTEPH in this review for two reasons. First, the majority of basic science studies pertaining to this topic have been conducted in PAH animal models and most clinical studies have predominantly included patients with PAH (group 1) and/or CTEPH (group 4). Second, the other subgroups (notably groups 2 and 3) have distinct etiology and pathophysiology, and therefore likely have differences in the mechanism of arrhythmogenesis, types of arrhythmia, and in the incidence and outcomes of these arrhythmias. For clarity and simplicity of text, we will refer to the group 1 (PAH) and group 4 (CTEPH) patients collectively as PAH/CTEPH, unless otherwise noted.12 In subsequent decades, a more granular mechanistic exploration has unfolded, revealing complex alterations in structure, electrophysiology, metabolism, and signaling pathways in the right heart.A number of potential mechanisms have been identified as contributing to arrhythmia susceptibility in patients with elevated PAPs and pressure- and volume-overloaded right atrium and ventricle. One of the earliest studies noted vascular degeneration and infarction in the sinus and AV node and sudden death in patients with what was then called primary PH (now referred to as idiopathic PAH [IPAH]).13 and has been implicated in pathogenesis of arrhythmia and sudden cardiac death (SCD).14 Sympathetic overdrive in PAH is manifested by decreased heart rate variability, a blunted baroreflex, and poor exercise capacity, and is associated with associated with worse clinical status and prognosis.1517 Increased sympathetic activity has also been correlated with premature ventricular contractions and ventricular arrhythmia in PAH patients.18 Iodine-123-metaiodobenzylguanidine (mIBG) myocardial imaging, a technique used to evaluate cardiac sympathetic nervous activity using single-photon emission computed tomography (SPECT), supports the aforementioned findings. Uptake of 123I-mIBG, a stable, modified form of guanethidine, occurs via the uptake-1 mechanism that normally uptakes norepinephrine.19 By comparing activity at 3-h scans to those at 30 min, one can assess washout of the mIBG, which is a measure of the retained NE within sympathetic neurons. When the sympathetic system is activated there is a reduction of pre-synaptic norepinephrine uptake, manifest as lower retention of mIBG. A low heart to mediastinal (HMR) ratio of mIBG (≤ 1.2) in late images predicts event-free survival in left heart failure.20 Increasing mPAP correlates with decreased mIBG activity in the right ventricle (RV), indicative of increased RV sympathetic activity. This decreased mIBG activity is associated with worse cumulative survival in PAH patients.2123 Additionally, there is evidence of adrenergic remodeling in the RV, including downregulation and desensitization of β1-adrenergic receptors, as well as downregulation of α–adrenergic and dopaminergic receptors.25 In PAH patients with RV failure, there is also decreased adenylyl cyclase responsiveness to β-agonists and depletion of norepinephrine,27 with a loss of the ability to augment catecholamine levels with exercise.28The autonomic nervous system plays a key role in the development and progression of PAH and right heart failure29 The dogs with PAH were more vulnerable than controls to induced AF/AFl. Histopathology demonstrated increased densities of sympathetic nerves and β-1 autonomic receptors in the right atrium, in contrast to the downregulation of β-adrenergic receptors in the failing RV.27 By systematically ablating the ganglionic plexi, which contain cholinergic and adrenergic neurons affecting the atrial myocardium, this reduced susceptibility to atrial arrhythmia, thereby demonstrating a pivotal role for the adrenergic component of the autonomic nervous system in regulating vulnerability to atrial arrhythmia in PAH.The intrinsic and extrinsic cardiac nervous systems have been implicated in the susceptibility to supraventricular arrhythmia (SVA) in PAH. In a recent study, Huang et al. studied atrial arrhythmia using a canine model in which PAH is induced in beagles using a single injection of 2 mg/kg of dehydromonocrotaline followed by an eight-week interval of observation while PAH develops.3033 An electrophysiology study comparing the right atrium of eight patients with longstanding IPAH versus 16 matched controls demonstrated prolongation of sinus node recovery time and reduction in tissue voltage with electrically silent areas in the atrium. There was also slowing of atrial conduction and activation times and an increase in areas of complex fractionated activity .35 These factors are associated with increased susceptibility to induction AF, as stimulated by either increased automaticity (ectopy) or single and multiple re-entrant pathways.36Stretch and fibrosis of the right atrium constitute an arrhythmogenic substrate, which combined with electrical remodeling due to changes in expression and function of ion channels in cardiomyocytes, increases susceptibility to and propagation of arrhythmia.37 Downregulation of inward rectifying potassium channels and slowed ventricular conduction  impairs depolarization and repolarization in RVH.38 Similar changes also cause arrhythmogenic early and late after- depolarizations and increase susceptibility to spontaneous or induced ventricular arrhythmia in models of RVH and left ventricular hypertrophy (LVH).3941 Changes in Ca2+ handling has also been implicated in the prolongation and dispersion of action potential duration in rat models of PH.43 In aggregate, these active and passive changes in the electrical system in the RV predispose to creation of reentrant circuits and arrhythmia.45 Structural remodeling, for instance myocyte fiber angle disarray, can also change electrical conduction leading to prolonged action potential duration and arrhythmia vulnerability, as seen in the monocrotaline-PAH rat model.46Right ventricular hypertrophy (RVH) and fibrosis are seen in patients with PAH/CTEPH and are associated with increased all-cause mortality.48 likewise, RV ischemia is thought to contribute to arrhythmia vulnerability in PAH/CTEPH. Elevated troponin levels in PAH patients reflect this ischemia and are associated with increased mortality, although not specifically with arrhythmia.49 The genesis of ischemia in RVH is multifactorial, reflecting some combination of changes in epicardial coronary artery perfusion pressure  and microvascular abnormalities (impaired angiogenesis manifest as capillary rarefaction related to decreased angiogenic gene expression).5254 Secondary ischemia-related metabolic changes in the maladaptive RV, such as induction of increased rates of uncoupled glycolysis, are thought to perpetuate the vicious cycle of ischemia.54Ischemia is a known pro-arrhythmic factor in the left ventricle;11 reviewed 171 ECGs of 101 patients with PAH and found “arrhythmia” in 17.8% of all cases, with a higher prevalence (33.9%) among the deceased cohort. Three abnormalities accounted for 70% of all observed arrhythmias: sinus tachycardia (38%); sinus bradycardia (18%); and first-degree A-V block (15%); with sinus tachycardia being significantly associated with mortality. A more contemporary investigation examined the progression of ECG changes in 50 PAH patients and found a significant increase in median heart rate, PR interval, QRS duration, R/S ratio in lead V1, and QTc duration in the ECG recorded closest to death, compared to the ECG recorded at the time of initial diagnosis. No PAH patient retained a normal ECG close to death.55Changes in the ECG are common in patients with PAH/CTEPH; however, there is controversy regarding the clinical significance of these abnormalities, and therefore uncertainty regarding the utility of screening electrocardiography. Kanemoto et al.15 In addition, in patients with RV failure and PH, stroke volume may be fixed (and low) and sinus tachycardia is likely a reactive mechanism to maintain cardiac output. Loss of heart rate variability is a marker of autonomic dysfunction that reflects tonic activation of the autonomic nervous system and may also be a homeostatic attempt to maintain cardiac output. Heart rate variability is blunted during exercise testing of PAH patients; a decrease in heart rate variability at rest parallels the severity of PH in PAH, as measured by mPAP.56 Sinus tachycardia and decreased heart rate variability may be useful predictors of susceptibility to SVA.As previously discussed, sinus tachycardia likely reflects autonomic dysregulation.5764 In PAH, longer QTc and QTc dispersion are correlated with increasing mPAP.65 In an age- and sex-matched cohort study of patients receiving PAH-specific therapy, both QRS duration and QTc interval were prolonged in 202 PAH patients versus 100 controls. A QTc duration ≥480 ms was an independent predictor of mortality, even in the subgroup of PAH and CTEPH.66 There was no difference in serum potassium to explain the prolongation of QTc, as might be expected with aggressive diuretic use. QTc prolongation correlated with impaired RV function, increased RV mass (measured by cardiac MRI), and poor prognosis.In left heart disease and other non-cardiac conditions, prolongation of the QT interval on ECG is described as a precursor to ventricular arrhythmia and is associated with increased mortality and sudden death.43 In the monocrotaline-rodent PAH model, QT prolongation is associated with decreased expression of repolarizing, voltage-gated (Kv) potassium channels  in the RV myocytes and is reversed with metabolic therapies, such as the pyruvate dehydrogenase kinase inhibitor, dichloroacetate.38 The etiology of prolonged QTc in patients with PH has not been clearly defined but may be a result of chronic ischemia in RVH and/or changes in the sympathetic nervous system, as discussed previously.67 Extrapolation from other disease processes would suggest an that such ionic remodeling and QTc prolongation would increase susceptibility to ventricular arrhythmia; however, this has not been directly studied in PAH/CTEPH patients and presents an opportunity for future investigation.In animal models of PAH, QT prolongation is associated with longer action potential duration and a proarrhythmic state.66 More specifically, prolonged QRS duration can contribute to RV dysynchrony, which is frequent in PAH and is an independent predictor of clinical worsening.69QRS prolongation has also been an area of active study in PAH. QRS duration has been found to be longer in patients with PH compared to controls and is associated with indices of decreased RV function.7072 In this discussion of SVA, we are referring specifically to AF, AFl, atrioventricular nodal reentrant tachycardia (AVNRT), or atrial tachycardia, and not to sinus tachycardia. The onset of SVA often signals progressive right-sided cardiac dysfunction and frequently precipitates clinical decompensation by eliminating the atrial kick which is important to diastolic RV filling in the hypertrophied RV.74 Four retrospective and three prospective studies have examined the incidence and clinical relevance of SVA in PAH, in some cases including patients with CTEPH and in one study including patients with group 3 PH.7579 The details of these studies are outlined in SVAs are the most prevalent rhythm disturbance observed in patients with PAH/CTEPH and they occur with greater incidence than in the general population.80 and markers of overall cardiac dysfunction, such as decreased cardiac index/output, increased RV diameter, and elevated NT-proBNP.80 Only in a minority of studies were pulmonary vascular resistance (PVR) and mPAP associated with incident SVA,78 perhaps suggesting it is the adaptation of the heart to increased afterload, rather than the afterload itself, that predicts development of SVA. There is biologic plausibility to this finding, given that the maladaptive response of the right heart is thought to predispose to atrial arrhythmias.30Baseline characteristics do not reliably predict which patients will develop SVA  and 2. HDifferences in non-invasive measures of disease severity, such as 6-minute walk distance (6MWD) and World Health Organization (WHO) functional class (FC), did not predict development of SVA in any of the studies. This is unexpected but may be a consequence of the overall homogeneity of the included cohorts, which largely included patients with poor functional state, or the relatively small sample size with less sensitive and more subjective measures.80 The clinical significance of thyroid disease, which is prevalent in PAH, was not explored in the other studies and may be an underrecognized contributing factor to development of arrhythmia.81Likewise, in most studies, the baseline PAH therapy and co-morbidities were no different between PAH/CTEPH patients with SVA versus those without. An exception is the study by Mercurio et al., who found a significantly increased frequency of thyroid disease  in the SVA group compared to those without SVA (69% vs. 43%).82 while another noted that arrhythmia led to admission to the intensive care unit and vasopressor use in approximately 30% of SVA episodes.80Onset of SVA often correlates with a clinically relevant decompensation. Whether the SVA triggers the clinical decompensation or is the result of right heart failure is not always clear; however, in many cases, clinical decompensation onsets abruptly with an episode of SVA and conversely resolves with restoration of sinus rhythm. The majority of patients reported symptoms at time of SVA onset (59–98%). Across all studies, objective and standardized measures of disease severity consistently worsened after development of SVA. The reported measures included worsening of New York Heart Association (NYHA) FC and a decrease in 6MWD. One study reported an increase in PAH-specific therapy in 46% of patients with SVA,While the majority of patients do have symptoms at SVA onset (mean ∼80%), up to 41% of episodes are asymptomatic, with their arrhythmia identified only via screening ECG or ambulatory monitor. With the finding that SVA is associated with increased mortality in patients with PAH/CTEPH, the role for surveillance of PAH/CTEPH patients by means of routine ECG, Holter monitors, or loop recorders warrants further study.76Restoration of sinus rhythm coincides with the reversal of adverse effects of an episode of SVA. Atrioventricular synchrony in sinus rhythm increases cardiac output and is particularly important when there is diastolic dysfunction. Thus, it is likely the active, synchronous atrial loading of the ventricles that results from sinus rhythm increases cardiac output in PAH patients. Restoring sinus rhythm should therefore be strongly considered in patients with PH. However, as will be discussed in the management section, there is a lack of randomized clinical trial data comparing rate versus rhythm control in PAH/CTEPH patients. When reported, restoration of sinus rhythm was associated with objectively confirmed clinical improvement. For example, in one study, at the time of SVA onset, 6MWD decreased from 362 ± 114 m to 258 ± 147 m, returning to a value near baseline (345 ± 137 m) 6–12 weeks after restoration of sinus rhythm. Over the same time period, NT-proBNP decreased from 5926 ± 4648 ng/L at the time of SVA onset to 3360 ± 2804 ng/L after correction.82 Similarly, two of the prospective studies report elevated hazard ratios (HR) for mortality in those who develop SVA (HR = 1.75–2.15).78 A third study describes an increased mortality of 69% in the SVA group compared to 51% in those without SVA, although this was not statistically significant on survival analysis.80 The effect of permanent SVA on mortality is quite striking, as depicted in the survival curves in 78SVA is associated with increased mortality, driven primarily by permanent (as compared to transient) SVA. In the four retrospective studies, mortality was in the range of 22–53% in the SVA cohort compared to 0–13% in those patients without SVA.8386The most common cause of permanent SVA is AF . However, Afl is also prevalent, occurring in 12–50% of the series reviewed . Less co88Additional large-scale investigations are needed to prospectively characterize the incidence of SVA in PH. While onset of SVA appears to be associated with increased mortality, it is not clear if the SVA is causal of deterioration or simply a result of worsening clinical condition. Unfortunately, given the nature of the disease process and the invasiveness required to obtain hemodynamic data, the frequent monitoring required to address this question may require these data be obtained as a part of large clinical trials or international registries. To date, the incidence/prevalence of SVA have not been reported in prospective or large-scale studies.82 the ESC/ERS guidelines state that “although prospective and controlled data are lacking, [these] findings suggest that maintenance of a stable sinus rhythm after cardioversion should be considered an important treatment goal in patients with PAH.”1 The ESC/ERS guidelines also state that SVAs “represent an indication for oral anticoagulation” for stroke prevention, although the risk of stroke in PAH patients with Afl is unclear.1 In the absence of prospective and controlled data, no level of recommendation or strength of evidence for maintaining sinus rhythm or anticoagulation is provided. Furthermore, the 2009 American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) expert consensus document on PH does explicitly address SVA management.89There is currently no standardized guidance regarding management of SVA in PAH/CTEPH, although the options include both pharmacologic and non-pharmacologic interventions . Given t82 In three of the seven studies, 100% of patients with SVA had initial attempts at rhythm control with direct current cardioversion, radiofrequency ablation, or antiarrhythmic drug therapy.78 A rate control strategy was utilized in a minority of patients, typically in those with permanent AF.79 Rhythm control strategies were more successful in atrial flutter (46.2–100%) versus atrial fibrillation (16.7–67.0%). The treatment tactics used and their efficacy are outlined in 82 However, Ruiz-Cano did report that patients with AVNRT  underwent catheter ablation of the slow pathway while those with typical Afl had cavotricuspid isthmus ablation. The management of AF was not discussed and outcomes were simply noted to be “similar to that of the general population.”82Several studies have reported treatment practice patterns, highlighting the heterogeneity in real-world approach and outcomes.91 Many antiarrhythmic drugs have antihypertensive effects based on mechanism of action and may cause systemic hypotension when used concomitantly with phosphodiesterase inhibitors  or prostacyclins (epoprostenol).90 The use of beta-adrenergic blockers in PH is also controversial. There is risk of provoking heart failure or circulatory collapse, based on their well-established negative inotropic and chronotropic effects.93 More contemporary data have started to study the safety and efficacy of beta-blockers in patients with PAH who are free from congestion/heart failure,9496 but the use of beta-blockers for improvement of RV function and/or survival remains a research question and is not standard of care. In contrast, the use of short acting beta-blockers may be helpful in restoring sinus rhythm or regulating heart rate in patients with acute SVA.A variety of pharmacologic strategies were used for SVA  includin97 In the studies of SVA in PAH/CTEPH, AFl and other atrial arrhythmias, such as AVNRT, were more readily converted to and maintained in sinus rhythm with amiodarone in short- and intermediate-term follow-up compared to AF.82Amiodarone  was the most frequently reported antiarrhythmic agent for medical cardioversion and/or maintenance of sinus rhythm. While amiodarone is typically well-tolerated in the short term, the long-term effects may compound morbidity in patients with PAH/CTEPH.98102 In a retrospective analysis of 22 patients with AFl and PAH/CTEPH, Showkathali et al. showed that AFl ablation at the cavotricuspid isthmus was successfully performed without complications in all patients and was associated with a statistically significant improvement in FC.98 The relative success of this interventional strategy can be attributed to the right-sided location of typical flutter or re-entrant pathways, allowing avoidance of trans-septal puncture thereby reducing procedural risks of stroke and bleeding.Electrophysiology studies with catheter ablation are safe, feasible, and successful in patients with PH.79 Pulmonary vein isolation is more invasive compared to catheter-based interventions in the right heart and concerns exist regarding the risk of anesthesia and intubation in patients with PAH/CTEPH. In general, intubation should be avoided in PAH patients due to the problematic effect of sedation on cardiac function and vasodilation leading to hemodynamic collapse.103 In-hospital mortality in PAH patients requiring vasopressor and mechanical ventilation for RV failure approaches 100%,104 justifiably increasing hesitancy to perform more invasive  ablation procedures.Little is known about left heart interventions in PAH/CTEPH patients and it is unclear whether, or to what degree, left-sided pathways contribute to arrhythmia in this cohort. Were pulmonary veins and left atrial pathways to prove important in PAH/CTEPH-related SVA, caution would be required in terms of catheter-based therapeutics. There is uncertainty regarding the effect of pulmonary vein manipulation on pre-capillary pulmonary pressure.106 This highlights the value of more carefully establishing the risks and benefits of anticoagulation for arrhythmia in PAH patients.Since the use of anticoagulation in CTEPH is routine management, anticoagulation for SVA would not alter therapy; however, there is increasing recognition of the absence of benefit and potential for harm with anticoagulation in some forms of PAH.89/Grade IIb1). It is uncertain whether these recommendations should change in the event of permanent atrial fibrillation and it is unknown if the current risk stratification models (such as CHA2DS2-VASc) are valid in PAH/CTEPH.107 Only the prospective studies by Olsson et al., Wen et al., and Mercurio et al. specifically comment on the frequency of anticoagulation therapy in the examined PAH/CTEPH patients: Olsson et al., 92% overall on oral anticoagulants;76 Wen et al., 73% in SVA cohort, overall use not reported;78 and Mercurio et al., 36% of SVA cohort, overall use not reported.80 These differences likely reflect international practice pattern variation and inclusion criteria, e.g. the Olsson study included CTEPH while the others did not. There is no apparent difference in risk of developing SVA or subsequent morbidity or mortality after onset of arrhythmia based on the use of anticoagulation;78 however, vascular outcomes such as stroke were not specifically addressed. Unfortunately, neither of the recent publications that examined the utility of anticoagulation in PAH (COMPERA and REVEAL) comment on atrial arrhythmias,108 the presence of which might alter the benefits of anticoagulation. With up to 41% of patients experiencing asymptomatic atrial arrhythmias  and QTc prolongation. VF has been demonstrated in a monocrotaline-induced PAH rat model,41 but clinical investigations have only identified VT/VF in a minority of PAH patients with SCD (8%).641Ventricular tachyarrhythmias (VT or VF) are thought to cause the majority of SCDs in adult patients.112 Nonetheless, in a follow-up study, NSVT was not correlated with increased mortality in PAH/CTEPH.113 Since routine and sustained rhythm monitoring in PAH/CTEPH is not a standard clinical practice, the possibility that VT/VF contributes to a higher proportion of SCD cannot be excluded.Non-sustained ventricular tachycardia (NSVT) was recently identified to be more prevalent than previously thought in a cohort of non-group 2 PH patients.111 ICD implantation is often offered to non-PH patients who have a cardiac arrest secondary to documented VT or VF,114 but clinical judgment must be employed regarding use of ICDs or prophylactic antiarrhythmic agents in PAH/CTEPH, given the absence of any clinical trials demonstrating benefit in this cohort.There are currently no data to show that patients with PAH/CTEPH and RV dysfunction benefit from defibrillator implantation to prevent SCD. The guidelines and management for arrhythmia in left heart failure may not apply to RV failure, due to differences in the underlying disease processes. Just as medications that are beneficial for group 1 PAH have been shown to be harmful or ineffective in group 2 PH (and vice versa), strategies to prevent and treat SCD may also differ. Practice guidelines for prevention of SCD in PAH state that “antiarrhythmic therapy is not indicated for prevention of SCD in patients with PAH,” and, further, that patients may be at “high risk during surgical procedures, such as ICD implantation.”116 Ventricular dyssynchrony is observed in progressive RV failure associated with PAH, often visualized as paradoxical septal movement caused by RV pressure/volume overload that compresses the left ventricle.118 This dyssynchrony is thought to hinder LV diastolic filling resulting in decreased LV stroke volume.119 RV free wall pacing with resynchronization improves RV function in a computer simulation model of PAH, an animal model of PAH, and clinically in a small cohort of patients with CTEPH.120122 However, further investigation is needed to confirm whether CRT is a valid therapeutic strategy in PAH/CTEPH patients with RV failure. Of note, in left heart failure, CRT has not been shown to be beneficial in patients with right bundle branch block or with QRS intervals of <160 ms, two features that are common in patients with RV failure from PH. This raises some skepticism about the potential role CRT in PAH/CTEPH.Likewise, the role of cardiac resynchronization therapy (CRT) in right heart failure due to PAH/CTEPH remains undefined.123 Despite ongoing research, there remain numerous gaps in knowledge, which limit a clinician's ability to optimally identify and manage arrhythmia in PAH/CTEPH (In summary, arrhythmias are an increasingly recognized cause of morbidity and mortality in patients with PAH/CTEPH.AH/CTEPH . SVAs, iAH/CTEPH . Improve


Pulmonary hypertension (PH) is a known complication of HCM and is a strong predictor of mortality. We aim to investigate the relationship between microvascular dysfunction measured by quantitative PET and PH in HCM patients.13N-NH3 dynamic PET scans for rest and stress conditions, respectively. A 2-tissue irreversible compartmental model was used to fit the segments time activity curves for estimating segmental and global myocardial blood flow (MBF) and myocardial flow reserve (MFR). Echocardiographic derived PASP was utilized to estimate PH.Eighty-nine symptomatic HCM patients were included in the study. Each patient underwent two 20-min p = 0.024) and MFR , while the MBFs at rest between the two groups were similar. There were significant negative correlations between global stress MBF/MFR and PASP ; for regional MBF and MFR measurements, the highest linear correlation coefficients were observed in the septal wall . Global MFR was identified to be independent predictor for PH in multivariate regression analysis.Patients were categorized into two groups across PASP: PH (PASP > 36 mmHg) and no-PH (PASP ≤ 36 mmHg). patients with PH had larger left atrium, ratio of higher inflow early diastole (E) and atrial contraction (A) waves, E/A, and ratio of inflow and peak early diastolic waves, E/e', significantly reduced global stress MBF (1.85 ± 0.52 vs. 2.13 ± 0.56 ml/min/g; 13N-NH3 dynamic PET. Global MFR is suggested to be an index of PH in HCM patients.Echocardiography-derived PASP is negatively correlated with global MFR measured by  Hypertrophic cardiomyopathy (HCM) is the most common heritable cardiomyopathy, characterized by cardiac hypertrophy and phenotypic heterogeneity , 2. Alth13N-NH3 dynamic PET imaging to explore the possible quantitative relationship between MBF/MFR and pulmonary artery systolic pressures (PASP) measured by Doppler echocardiography.Coronary microvascular dysfunction is an central physiopathology in HCM, and has major prognostic implications as well . Growing13N-NH3 dynamic PET imaging within a 1-month period. 29 patients were excluded from this analysis because of moderate or severe valval heart disease, severe lung disease and unavailable measurement of peak tricuspid regurgitation gradients, as well as patients whose PET images were missing or uninterpretable owing to poor image quality.This project was reviewed and approved by the John Hopkins Institutional Review Board No. 00029377), All procedures and methods were performed in accordance with the updated guidelines and regulations. All patients provided consent to use clinical data for research purposes, and written informed consents were obtained from all participants. The retrospective study enrolled 118 patients with HCM at Johns Hopkins Hospital, Baltimore, USA, from June 2011 to December 2015 referred to cardiac PET/CT. The clinical diagnosis of HCM was based on 2-dimesional echocardiographic evidence of LV hypertrophy  in the absence of other cardiac or systemic disease such as obstructive coronary artery disease (> 50% diameter stenosis) by invasive coronary angiography or computed tomography angiography, hypertension, sarcoidosis capable of producing hypertrophy [9377, AllTwo-dimensional Doppler echocardiographic studies were performed using a GE Vivid 7 or Ezuochuang-9 ultrasound machine  on each patient. Echocardiographic assessments were based on the current guideline . Pulmona13N-NH3 was injected intravenously as a bolus (using a power injector as constant rate of 1200 ml/h), and a list-mode dynamic PET scan was obtained over 20 minutes. Approximately 60 minutes after injection of the rest dose, Regadenoson  (0.4 mg/5 ml) was administered for vasodilator stress, and the stress PET scan was started about 30 sec after Regadenoson administration. Heart rate, blood pressure, and a 12-lead electrocardiogram were recorded before, during, and after completion of the stress protocol.All patients underwent cardiac PET/CT scanning using a GE 64-slice Discovery Rx VCT PET/CT system . Patients were positioned with the assistance of a computed tomographic (CT) scout, a low-dose CT scan  was performed for attenuation correction of PET emission data. Subsequently, 20-min dynamic PET images were acquired using a same-day rest/stress protocol  as folloThe attenuation- and decay-corrected 36-frame  dynamic PET images  and gated PET images  were reconstructed using an iterative ordered-subset expectation-maximization (OS-EM) algorithm  with post-processing filtering .2, k3, Vb) (15) was employed for fitting the 17-segments tracer time-activity curve (TAC). Volume of interests (VOIs) were manually drawn in the mitral of LV and in the right ventricle on PET images. The LV TACs and the average of LV and RV TACs were used as input function and blood volume correction, respectively. Our in-house software were used for model fitting [All reconstructed dynamic PET images were transferred to a workstation for image processing and quantification using the PCARDP tool . The images were reoriented along the heart axis, and segmented into the AHA 17-segments within the detected endo- and epicardial borders . A 2-tis k3, Vb)  was emplStress and rest LV ejection fraction (LVEF), LV end-diastolic volumes (LVEDV) and LV end-systolic volumes (ESV) were automatically calculated from gated datasets by using QGS package . The LVEF reserve was computed as stress LVEF minus rest LVEF. A drop larger than– 5 LVEF units was considered abnormal LVEF reserve as previously reported .2 test. Spearman’ correlation coefficients were calculated for potential correlation between MBF/MFR and other variables. Univariable and multivariable linear regression analyses were performed to study the independent contributions of various parameters on PASP. A p < 0.05 was required for statistical significance. The IBM SPSS 23.0 software  was used for all statistical analysis.Simple statistics including mean, standard deviation (SD), and proportions were calculated for continuous variables and categorical variables, respectively. The comparison between groups of continuous samples was performed with a Student’s t test, Mann–Whitney U test and one-way ANOVA depending on the nature of data. Categorical variables between groups were compared using the χp < 0.01; p < 0.05, respectively). In addition, PH group had more increased left atrial size  than no-PH group.Overall, the PH (PASP > 36 mmHg) was observed in 31 (35%) patients. Moderate or severe PH (PASP > 50 mmHg) was presented in 5 (6%) patients. Clinical and echocardiographic features of the patients with PH versus patients without PH are summarized in 2, k3 and Vb estimated from 17-segmental TACs based kinetic modeling for all patients are summarized in the p < 0.05 and p < 0.01 for MBF ≤ 1.8 ml/min/g and MFR ≤ 2.5, respectively. The last 18-min mean stress/rest PET images with representative global MBF and MFRs for HCM patients with and without PH are demonstrated by p > 0.05). During vasodilator stress, patients with PH exhibited impaired LVEF compared to the patients without PH . As a consequence, group of PH yielded lower LVEF reserve values  and high prevalence of abnormal LVEF reserve  as above defined  patients were classified as no-obstructive HCM, 32 (36%) had latent obstruction and 25 (28%) had rest obstruction. Obstructive HCM patients were more likely to have higher E/e’ ratio; Otherwise, there was no significant difference in stress MBF, MFR, minimal CVR and PASP among the 3 groups, as depicted in p < 0.05) and E/A ratio  but not LAD and E/e’ ratio; Similarly, global MFR was only negatively related to PASP values . On the other hand, the global MBFs at rest did not correlate with PASP (p > 0.05). Furthermore, the correlation between regional stress MBF/ MFR and PASP showed that the coefficients in septal wall were the highest  among all regional walls , E/A ratio and systolic blood pressure were the independent predictors for PH as showed in Univariate and multivariate regression analysis were further performed to identify the predictive factors for PH . In univariable analysis, a significant correlation was found between PASP and global stress MBF, MFR, minimal CVR, LAD, E/A ratio and E/e′ ratio. On separate step-wise forward multiple linear regression, only global MFR: the transport rate constant from vascular space to myocardial tissue; k2 (min-1): the efflux rate constant from tissue to vascular space; k3 (min-1): the tracer metabolite rate constant trapped in tissue; Vb (ml/min/g): the fraction of blood volume in tissue.Data are expressed as mean ± standard deviation.*(DOCX)Click here for additional data file.S2 TableData are expressed as number of the patients(percentage). PH:pulmonary hypertension; MBF: myocardial blood flow; MFR: myocardial flow reserve.(DOCX)Click here for additional data file.S3 TableData are expressed as number of the patients(percentage). PH: pulmonary hypertension; LVEF: left ventricular ejection fraction.(DOCX)Click here for additional data file.


The approach for treating a hemodynamically unstable patient remains a diagnosticand therapeutic challenge. Stabilization of the patient should be rapid andeffective, but there is not much room for error. This narrow window ofintervention makes it necessary to use rapid and accurate hemodynamic evaluationmethods. Echocardiography is the method of choice for the bedside evaluation ofpatients in circulatory shock. In fact, it was intensive care physicians whorecognized the potential of Doppler echocardiography for the initial approach topatients in circulatory failure. An echocardiogram allows rapid anatomical andfunctional cardiac evaluation, which may include non-invasive hemodynamicevaluation using a Doppler study. Such an integrated study may provide data ofextreme importance for understanding the mechanisms underlying the hemodynamicinstability of the patient to allow the rapid institution of appropriatetherapeutic measures. In the present article, we describe the most relevantechocardiographic findings using a practical approach for critical patients withhemodynamic instability. A hemodynamically unstable patient is a critically ill patient with the potential toprogress to circulatory shock and death within hours. Thus, rapid, accurate andreproducible diagnostic methods should be used to institute appropriate therapeuticmeasures.,2Through anatomic and functional cardiac evaluation, an echocardiogram can providedata of extreme importance for understanding the mechanisms underlying thehemodynamic instability of a patient or even in the context of cardiorespiratoryarrest, allowing appropriate therapeutic measures to be rapidlyestablished. Hemodynamicevaluation with Doppler study was added to the classically performed anatomical andfunctional evaluation, which included cardiac output (CO), central venous pressure(CVP) estimation, peripheral vascular resistance (PVR) calculation, and leftventricle (LV) filling pressure estimation. Over the last few decades, Dopplerechocardiography has become an increasingly widespread tool to the intensive care ofpatients in circulatory shock.-5It was intensive care physicians who recognized the potential of Dopplerechocardiography (echo-Doppler) for the initial approach to patients in circulatoryfailure.The latter refers us to the visual identification of specific findings, allowing forspecific diagnoses, such as cardiac tamponade or pulmonary embolism. Emergencyechocardiography can be considered a basic competency of an emergency physician thatis integrated into the initial assessment protocols necessary for severe patients,especially in the context of advanced life support. However, more thoroughexaminations require higher levels of competence. The competencies required to perform an echocardiogram are usually separated intothree levels of experience, and a prior, more basic level of emergencyechocardiography is recognized.This review is primarily intended for physicians performing emergency and level Iechocardiography. It is classically characterized by persistent hypotension(systolic blood pressure < 90mmHg) and peripheral hypoperfusion .,8 In thiscontext, hyperlactacidemia is a typical analytical finding resulting fromabnormal cellular oxygen metabolism.Circulatory shock is the clinical expression of a state of circulatory failureresulting in inadequate tissue perfusion and poor cellular oxygen supply, whichcan lead to injury and cell death.There are several causes of shock with different hemodynamic profiles and,consequently, different therapeutic needs. Some hemodynamic profiles areclassically associated with some etiologies, such as cardiogenic shock (low COand increased PVR in the presence of elevated ventricular filling pressures) andseptic shock (increased CO and decreased PVR). However, the hemodynamic profilesof each type of shock are not always linear .-10 It should be noted that, inthe SHOCK study, sepsis was suspected in 18% of patients, 74% of which developedpositive blood cultures. These patients had a lower PVR days before thediagnosis of infection.Cardiogenic shock has a component of systemic inflammation that can lead to adecrease in PVR, and patients with cardiogenic shock are more susceptible toseptic complications.,11,12 Thus, besides the etiology ofshock, it is necessary to determine the precise hemodynamic profile of eachpatient, which is not limited to the observed hypotension.However, septic shock may present as a hypodynamic state, as characterized by atransient decrease of the ejection fraction (EF) and lower-than-expected valuesfor CO and PVR, in approximately a third of cases.However, it is also true that exaggerated or misguided resuscitation, forexample through excessive fluid therapy, can lead to deleteriouseffects.Adequate and early support of patients who are in shock is essential to preventmultiorgan dysfunction.Diagnostic evaluation should be as accurate and objective as possible to quicklydetermine the supportive measures most appropriate to the etiology of the shockand its hemodynamic profile. Doppler ultrasound has been used as the diagnosticmethod of choice in this context.The clinical context and the physical examination often make it possible to inferthe most probable etiology of hemodynamic instability for a patient. In thesepatients, echo-Doppler is an important tool for the stratification of shock andthe definition of the most adequate supportive therapy. In other patients,initially, circulatory failure has an unexplained cause. In the latter context,echo-Doppler is a very attractive diagnostic method for the initial study of thepatient.In the present article, we describe the most relevant echocardiographic findingsusing a practical approach directed at patients with hemodynamicinstability.The evaluation of the morphology of the cardiac chambers allows us to infer thetime of evolution of an eventual cardiopathy. The presence of the dilatation ofthese chambers favors a chronic pathology, while cardiac chambers of normal sizepoint to an acute or subacute pathology .-16Moreover, the anatomical and functional evaluation of valves can reveal aregurgitant or stenotic lesion significant enough to justify or at leastcontribute to the hemodynamic instability of the patient. A description of thequalitative and quantitative methods for this evaluation can be found in variousrecommendations of the European Association of Echocardiography.It is important to remember that acute and subacute valvular pathologies are themost frequent causes of significant hemodynamic instability due to the lack oftime for the physiological mechanisms of adaptation to act. Typically, importantvalvular dysfunction is observed with non-dilated cardiac chambers.When hemodynamic instability occurs under acute myocardial infarction (AMI),particular emphasis should be given to the observation of mechanicalcomplications, namely the rupture of the free wall, interventricular septum orpapillary muscle .,18Evaluation of the systolic function of both ventricles is usually part of theassessment of any hemodynamically unstable patient. In urgent cases, there areseveral methods available for assessment of LV systolic function, includingejection fraction (EF) by Simpson's method, mitral annular plane systolicexcursion (MAPSE), and fractional shortening and velocity of the S wave in themitral annular plane by tissue Doppler (TDI: tissue Doppler imaging).The systolic function of the right ventricle (VD) can be assessed by systolicexcursion of the tricuspid annular plane (TAPSE: tricuspid annular planesystolic excursion), fraction of the shortening area  and velocity of the S wave in the tricuspid annular plane byTDI.The evaluation of systolic function also includes the study of segmentalkinetics. Changes in LV regional motility often show the presence of coronarydisease, which may or may not be the cause of the instability under study.Hypokinesis of the medial-basal segments of the RV free wall, known asMcConnell's signal, is a characteristic finding of acute pulmonarythromboembolism (PTE) and RV infarction. Its presence increases the specificityof other echocardiographic findings for the diagnosis of PTE, namely dilation ofright heart chambers and pulmonary hypertension.Echocardiogram is the method of choice for diagnosing and evaluating pericardialeffusion. According to its thickness at diastole, circumferential effusion may begenerically classified as being very small (< 5mm), small (5 to 10mm),moderate (10 to 20mm) or large (> 20mm) in volume. Sometimes, especiallyafter cardiac surgery, effusion may accumulate preferentially over one or twocardiac chambers.The accumulation of fluid in the pericardial space leads to an increase inintrapericardial pressure, which, in turn, may limit cardiac filling if theintracardiac filling pressure is exceeded, leading to cardiac tamponade. Cardiactamponade is a hemodynamic continuum whose maximum expression is circulatoryfailure .Although cardiac tamponade is a clinical diagnosis, the latter should beconfirmed via echocardiography by demonstrating pericardial effusion withevidence of repercussion in cardiac function, namely, in right ventricularfilling: dilation of the inferior vena cava (IVC) and suprahepatic veins and theabsence of their respiratory variability; exaggerated respiratory variability(> 30%) of the transtricuspid and transmitral flows; and finally, diastoliccollapse of the right chambers . The purposeof fluid therapy is preload optimization, one of the four major determinants ofcardiac function .However, excessive fluid therapy in a patient whose preload is already high canhave deleterious effects, especially for the right heart.,23Classically, fluid therapy is the first therapeutic line in the initial phase ofapproaching a hemodynamically unstable patient in sepsis and septicshock.Several echocardiographic parameters have been used to estimate blood volume.Obliteration in LV systole may be an extreme sign of hypovolemia (kissingpapillary muscles sign). However, if this is not found, other echocardiographicdata should be collected and adjusted to the clinical context of the patient toguide the resuscitation measures. Moreover, the presence of dilated chambersdoes not exclude eventual response to fluid therapy. However,estimation of blood volume using this method has several limitations, especiallyin patients with previous respiratory disease or under positive pressureventilation. Generally, dilated IVC without respiratory variability suggestselevated CVP, whereas reduced-diameter IVC with great variability suggestsreduced CVP.The diameter of the IVC and the analysis of its respiratory variability have beenused to infer the pressure of the right auricle and, consequently, theCVP.However, more important than the estimate of blood volume is the determination ofif its increase will bring an increase in CO.Additionally, in patients breathing spontaneously, the increase in CO by 15%with passive raising of the lower limbs above 30º (passive leg raising)was a predictor of response to volume, with 77% sensitivity and 100%specificity. Inpatients under mechanical ventilation, an IVC distensibility index([maximum diameter - minimum diameter]/[maximum diameter +minimum diameter)/2]) > 12% allowed responders to volume expansion tobe identified with positive and negative predictive values of 93% and 92%,respectively.However, this acuity in predicting the response to fluid therapy was notobserved in other studies with more heterogeneous populations, which points tothe limitations of the generalization of these indices.In spontaneously breathing patients, an IVC distensibility index ([maximumdiameter - minimum diameter]/maximum diameter) > 40% was associatedwith fluid therapy response, and a value < 40% did not exclude theresponse. Byconsidering that CO depends on the variations not only of VolEj but also of CF,we advise verifying an increase of CO by > 15% as a criterion of response tofluid challenge. The calculations of VolEj and CO by echocardiography, as wellas ways of streamlining them in successive re-evaluations, are explained indetail in the following section.The evaluation of the response to fluid therapy can also be performed byevaluating the ejection volume (VolEj) via echocardiography before and afterfluid challenge administration. The increase in VolEj by > 15% in response toa fluid challenge probably provides the most evidence of the response to fluidtherapy. The appearance of pattern B on lung ultrasound mayallow the fluid therapy to be stopped before it becomes excessive anddeleterious. Based on this premise, Lichtenstein developed the FluidAdministration Limited by Lung Sonography (FALLS) protocol. While the purpose ofthis review is not to address pulmonary ultrasonography, we recommend readingLichtenstein's recent review of the subject.The role of echocardiography in the orientation of fluid therapy can still becomplemented by pulmonary ultrasonography.,28 Various clinical findings, physical examination andultrasound should be integrated to increase the diagnostic acuity and predictivevalue of various parameters.Many of the parameters used in determining blood volume and fluid therapyorientation are not specific and, as such, have limitations. CO is undoubtedly the most important hemodynamic parameterfor critical patients.Although the evaluation of biventricular systolic function is important for theevaluation of patients in shock, it has some limitations: there is no linearcorrelation between biventricular systolic function and the hemodynamic state,as there may be a severe depression of LV systolic function without circulatoryshock and, conversely, there may be circulatory shock with only moderatedepression of LV systolic function.2 × π, where Dlvot is the diameter of lvotmeasured along the parasternal long axis. The area of lvot is multiplied bythe time-velocity integral of lvot flow (TVIlvot), as measured at apicalincidence 5 chambers at the same location as the lvot measurement, which givesus VolEj. In turn, CO is obtained by multiplying VolEj by HR. The cardiac index(CI) can be derived by dividing CO by body surface area (BodySurf). Thus, wehave:Echo-Doppler allows us to calculate CO relatively easily . The are,31 However, there are some potential sources of error inthe estimation of CO, namely the measurement of lvot and the presence ofarrhythmias causing great variability in TVIlvot. Thus, estimating CO viaecho-Doppler should be seen more as as a semi-quantitative method, categorizingCO as very low, low, normal or high.Cardiac output calculation via echo-Doppler was validated in several studies,where the thermodilution method was used as the gold standard.In turn, the CO estimate allows PVR to be calculated as follows:The estimation of CO and PVR allows the hemodynamic profile of a given patient tobe defined. Because blood pressure is derived from the product of CO and PVR,defining the hemodynamic profile (CO and PVR) allows the origin of hypotensionto be defined, i.e., whether it is dependent on low CO and/or vasoplegia.Echo-Doppler allows us to reassess the patient and assess the efficacy oftherapeutics, mainly in the absence of continuous hemodynamic monitoring. Forthis purpose, it is suggested that the same lvot measurement is maintained,which essentially values the variations in the product TVI × HR asequivalent to CO. In fact, in serial evaluations, the variations in TVI ×HR is what will be important in clinical practice.2), the pressure gradient between RV and the rightauricle is obtained, which, together with right ventricular pressure, allowsPASP to be estimated (in the absence of pulmonary stenosis or other obstructionof the RV outflow tract).Pulmonary artery systolic pressure (PASP) can be determined from tricuspidinsufficiency. Using the modified Bernoulli equation . Inthese cases, a normal RV cannot maintain normal function under abrupt rises inpost-load. There is a 25% decrease in RV VolEj when the pulmonary artery meanpressure reaches approximately 30mmHg (corresponding to a PASP of approximately45mmHg) and a marked and rapid decline in RV VolEj under, even slight,additional elevation of the afterload.,34 Theimmediate compensatory response will be RV dilation, with bulging of theinterventricular septum towards the LV to maintain the CO  is classically inferred by pressuresobtained from the placement of a pulmonary catheter, mainly by means ofpulmonary capillary wedge pressure (PCWP).Echo-Doppler allows semiquantitative estimation of LVFP in normal or elevatedconditions, and this approach was summarized in joint recommendations by theAmerican Society of Echocardiography and European Association of CardiovascularImaging.The first parameter to be evaluated is transmitral flow, which is the ratiobetween the early filling velocity E of the transmitral flow and the latefilling velocity A of the pulsed Doppler (E/A ratio). An E/A ratio < 1 with E< 50cm/s indicates normal LVFP, while an E/A ratio > 2 with an E-wavedeceleration time < 150ms favors high LVFP. For an E/A ratio between 1 and 2or E/A < 1 with a velocity of E > 50cm/s, additional parameters  are necessary to estimate LVFP, and atleast two of three parameters are necessary to define LVFP . In thesecases, it may be necessary to complement the evaluation of the patient withinvasive methods for the validation of the echocardiographic evaluation.There are, however, limitations for the estimation of LVFP, especially inpatients with advanced heart failure and greatly increased ventricularvolumes. Based on these twoparameters, diastolic dysfunction can be assumed when Ea < 8cm/s and E/Ea> 14. Despite some limitations, this simplified assessment has been shown toplay a role in the stratification of critically ill patients, such as patientswith severe sepsis, for whom the presence of diastolic dysfunction hasidentified patients with poor prognosis. Diastolic dysfunction may also allow theidentification of patients with a higher probability of failure at ventilatoryweaning. Finally,evaluation of diastolic function may also play a role in the orientation ofresuscitation with fluid therapy, especially in limiting it in septicpatients.In the context of intensive care, the evaluation of diastolic function and theconsequent estimation of LVFP can be simplified by considering only the earlyrelaxation velocity Ea of tissue Doppler and the E/Ea ratio.In cor pulmonale and severe leftventricular dysfunction, are easy to see and may be suited for emergencyechocardiography. Other elements are more complex and require a higher level oftraining (level I at least), as is the case for CO calculation and LVFPestimation.Some findings of the echocardiographic examination, mainly cardiac tamponade,pulmonary embolism with acute Transthoracic echocardiography (TTE) has good diagnostic accuracy in theevaluation of critically ill patients, even for patients under mechanicalventilation; therefore, it is the first option. However, it is not alwayspossible to acquire adequate TTE images. Frequent causes of poor transthoracicechocardiography include obesity, emphysema, elevated levels of positiveexpiratory pressure or the presence of dressings and surgical drains. In thiscontext, transesophageal echocardiography (TEE) is the ideal alternative.shunts or cardioembolic sources. However, TEErequires a more advanced level of training in echocardiography .Transesophageal echocardiography remains the reference echocardiographicexamination in situations such as valvular prosthesis dysfunction, suspectedinfective endocarditis, and aortic dissection and in the presence ofintracardiac Echo-Doppler is the ideal tool for the initial approach to patients with hemodynamicinstability. In addition to morphological and functional cardiac characterization,it allows a comprehensive evaluation of the hemodynamic status of the critically illpatient.Performing echo-Doppler is often necessary in the evaluation of hemodynamicallyunstable patients. Echo-Doppler used as a hemodynamic tool allows a great deal ofinformation to be obtained, which gives it not only a diagnostic role but also atherapeutic role, by helping define circulatory resuscitation strategies.Finally, echo-Doppler should not be viewed as a substitute for continuous, invasiveor semi-invasive monitoring methods. As complementary methods, echo-Doppler isnaturally preferred in the initial evaluation of unstable patients, while continuousmethods play a role in the continuous monitoring of patients.