On the right right side of the heart-The challenges in diagnosis and management of acute right heart failure

August 31, 2020, by Shahriar Lahouti



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For many years the right heart has been downplayed to a bystander chamber. It has been accepted that the right heart is a conduit structure (dates back to the 16th century) that is a secondary actor in the interplay of heart failure, with primacy accorded to the left heart. Recent research efforts have uncovered that the right heart is structurally, and physiologically discrete, with a distinct pathobiologic pathway in right heart failure.1

Right ventricular failure is a clinical syndrome caused by multiple causes. It is a formidable clinical challenge in both ED, and Intensive care units. Uniquely, therapy that influences the left ventricle favorably may not impact the dysfunctional right ventricle and vice versa.

Anatomy and Echocardiography of the Right Heart

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The right ventricle (RV) is anatomically composed of 3 distinct portions; inlet, apical myocardium and outlet.

The first portion is the inlet, which includes the tricuspid valve,chordae tendineae and papillary muscles.The second portion is the apical myocardium which is prominently trabeculated; and finally the outlet region (infundibulum or conus) including pulmonary valve (figure1).2 3

Morphologic features of the right ventricle that allow allow differentiation between the right and left ventricle are: 4

  • Separate inflow and outflow tract in the right heart, such that the tricuspid valve is not in continuity with the pulmonary valve, as opposed to the aortomitral continuity seen on the left side (figure 2 below).5
  • A more apically situated hinge point of the septal leaflet of the tricuspid valve relative to the corresponding anterior leaflet of the mitral valve (figure 3 below).5
  • Presence of the moderator band in the RV cavity (figure 4 below):
    • Moderator band (aka septomarginal trabecula) is a muscular band of heart tissue in RV; extending from the base of the anterior papillary muscle to the ventricular septum. It carries part of the RBB to the anterior papillary muscle.This shortcut across the chamber of RV Seems To Facilitate conduction time, allowing coordinated contraction of anterior papillary muscle
  • Highly trabeculated endocardial surface (figure 5).5

There are several discrete muscular ridges or bands in the right heart, which sometimes are mistaken for tumor or thrombi. These may include: 5 6

  • Crista terminalis is a well-defined fibromuscular ridge that extends internally from the superior vena cava to IVC along the lateral RA wall. It separates the RV inflow tract from the RV outflow tract. A prominent crista terminalis may be confused for RA tumor on TTE (figure 6).
  • Eustachian valve is a remnant of the embryonic valve of IVC. It appears as a crescent-like fold of variable size at posterior margin of IVC (figure 7). Occasionally, a prominent Eustachian valve appears to divide RA into two chambers making apparent cor triatriatum dexter (figure 8).
  • Chiari network is a thin, web-like fenestrated membrane that attaches along the ridge connecting vena cavae and interatrial septum. It is found in 2-3% of normal hearts at autopsy. In echocardiography, the Chiari network appears as a free floating curvilinear structure that waves with blood flow in RA. A part of the Chiari network arises from the orifice of IVC like the Eustachian valve, but the Chiari network is much more mobile and thinner. In echocardiography, the Chiari network may be confused for tricuspid vegetation, flail tricuspid valve, free RA thrombus, and pedunculated tumors.Careful tracing to identify its attachment to the orifice of IVC makes a differential diagnosis (figure 9).


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Indeed the LV and RV cannot be analysed as separate entities, although they generally are; there are fibres that course between them at both superficial and deeper layers, and the two ventricles interact functionally. Given the anatomic discussions, it is perhaps spurious to discuss RV physiology as an independent phenomenon. This concept will be further explored in the section below regarding ventriculo–ventricular interactions. Nonetheless, the RV has a unique physiology, largely dependent upon the low hydraulic impedance characteristics of the pulmonary vascular bed.7

Mechanical Aspects of Ventricular Contraction

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There are two layers of RV myocardium. The fibers of the superficial layer are circumferentially arranged, while the fibers of deep muscle layer are longitudinally aligned.6

RV relies on longitudinal fiber for ejection. In comparison, the LV also has an additional middle layer containing circumferential constrictor fibres that provide the main driving force of the LV by reducing ventricular diameter. Shortening of the RV is greater longitudinally than radially. In contrast to the LV, twisting and rotational movements do not contribute significantly to RV contraction. Moreover, because of the higher surface-to-volume ratio of the RV, a smaller inward motion is required to eject the same stroke volume.

Cardiovascular Physiology and RV Cardiodynamic

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Systemic perfusion is defined by cardiac output (CO), which is the amount of blood pumped per minute from each ventricle (In physiologic states, RV cardiac output is equal to the LV cardiac output).8

The product of heart rate (HR) and stroke volume (SV) determines cardiac output (CO= HR x SV); shown below.

It should be evident from this relationship that all influences on cardiac output must act through changes in either the HR or the SV. SV is a measure of myocardial performance, and is dependent on preload,contractility and afterload. These relationships are shown below.

HR and myocardial contractility are strictly cardiac factors. They are characteristics of the cardiac tissues, although they are modulated by various neural and humoral mechanisms. Preload and afterload, however, depend on the characteristics of both the heart and the vascular system. Preload and afterload may be designated as coupling factors because they constitute a functional coupling between the heart and blood vessels.

A. Heart Rate(chronotropy):

Autonomic nervous system is almost the main regulator of the HR.

Tachycardia: the maximum sinus rate is estimated as (220 minus age). The impact of tachycardia on the ‘CO’ is not uniform. During physiological stress response, tachycardia often results in augmentation of ‘CO’. However severe tachycardia may lead to decreased ‘CO’ due to reduced diastolic filling time.

Bradycardia: the impact of bradycardia on ‘CO’ is more uniform, that is pulling down the ‘CO’ within the whole range of its severity.

B. Determinants of stroke volume:

1. Contractility (inotropy)

True contractility is defined as the inherent capacity of myocardium to contract independently to loading conditions (preload or afterload).Since in practice,it is not possible to separate the impact of HR, and loading condition on contractility; the true contractility is not measurable.

Contractility is increased in the healthy heart by adrenergic stimulation (via β1 and β2 receptors), digitalis, and other inotropic agents. Optimizing preload within physiologic range, and lowering afterload can increase contractility as well. 4

2. Preload: Represents the extent of precontraction myocardial fiber stretch, which is determined by the resting force, myocardial compliance, and the degree of filling. In vivo, it is the end-diastolic ventricular volume 9; however due to its complexity in practice, intracardiac pressure is substituted which can be determined more easily.

Starling curve (figure below) shows the relation of stroke volume to preload. In a normal heart, if the ventricles are operating on a steep part of the curve, then increasing preload (point A to B) results in increasing stroke volume (called preload-dependent state). However, if the ventricles are operating on a flat part of the curve (point C), increasing preload does not result in increasing stroke volume (called preload-independent state).

As mentioned before, cardiac output not only depends on preload, but also contractility, and afterload are other players on the table. Therefore the slope of the curve is determined by these two parameters as shown in the following figure.

What factors can impact RV preload?

Compliance of the right atrium and ventricle, filling pressure, heart rate and rhythm can influence the RV preload. In terms of compliance, the right ventricle is more compliant than the left ventricle.

Chamber compliance:

Compliance is the ability of a hollow organ to distend and increase volume with increasing transmural pressure. This concept is illustrated in the following examples.

#1: You have a beach ball and a balloon. Which one is easier for blowing up?

True. For sure the balloon is easier as it’s soft, thinner and more extensible.

In hypertensive heart disease, the left ventricle becomes thickened and muscularized as an adaptation response to the high systemic vascular resistance. This makes the LV less distensible (like the beachball), and therefore for the same amount of volume in the diastole, the end-diastolic pressure would be higher. That is to say, the LV is noncompliant as shown below.10

#2: In another example, you have two balloons, but one in the bottle. Which one is easier for blowing up?

The balloon in the bottle is more difficult, since you should blow up against the opposite force that the bottle is exerting on the balloon. Likewise in pericardial disease, the distensibility of the cardiac chamber is limited due to the impact of pericardial constraint. In pericardial disease, the intracardiac pressure (end-diastolic pressure) is increased to stand against the raised intrapericardial pressure.

3. Afterload: Refers to the total resistance to ejection of blood from the ventricle during contraction. Increasing afterload results in decreased extent and velocity of myocardial contraction. The heart is a double power generator, The RV, and the LV both propel blood into circulation, and each is well adapted to their respected outflow system, called ventriculoarterial coupling. Under normal conditions RV is coupled to the low impedance pulmonary vascular system and the right sided pressures are lower than the left sided pressures.1 11

These unique physiologic and anatomic features of the right heart make it extremely poor-tolerant to pressure overload states e.g. pulmonary embolism(especially if sudden). This is in contrast to biologic design of the left heart which is intended for a distinct purpose. The LV myocardium is thick, and well-adapted to a high pressure system on an evolutionary scale, making it tolerable to pressure overload. The response of the RV and LV to an experimental increase in afterload is shown below.11

Ventricular Interdependence

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Ventricular interdependence refers to the concept that the size, shape and compliance of 1 ventricle may affect the other ventricle through direct mechanical interactions.8

Since the heart is enclosed by pericardium, there’s limited space for distension during diastole. In simple words, the ventricles compete for diastolic filling as illustrated below!

In acute RV pressure or volume overload states, dilatation of the RV shifts the interventricular septum toward the left. As a consequence, the LV distensibility during diastole is impaired which potentially leads to a decreased LV preload, or low cardiac output states.

Heart-Lung Interaction

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With each inspiration, the small change in intrapleural pressure (more negative pressure) leads to significant increase in venous return, RV preload and consequently RV cardiac output.8

During positive pressure ventilation, as the mean airway pressure is increased, there is a fall in RV cardiac output due to two factors; reduced venous return and secondly worsening RV systolic function (this explains the afterload dependency of the RV contractile performance). That is to say, when the lungs are under pressure, the heart is under pressure too as illustrated below.

Perfusion of the Right Ventricle

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Why is it so crucial to understand the RV perfusion principle?

The basic principle of pathogenesis of RV failure is that regardless to the types of the inciting etiology (e.g. volume/pressure overload, or ischemia), a Vicious Cycle(RV spiral of death) is started and RV Malperfusion is reinforced through complex chains of events, culminating to cardiogenic shock and death. This principle underlies the fact that management of patients with ‘acute right heart failure’ is challenging and inappropriate therapeutic interventions are unforgivable.12

The heart is supplied by coronary arteries. When oxygen supply does not meet the demand, myocardial ischemia occurs and cardiac performance is threatened.

The left ventricle is a pressure pump, i.e. the LV end-systolic pressure is high, therefore LV perfusion occurs during diastole alone, whereas the right ventricle is a volume pump, and the end-systolic and diastolic pressure within the RV are low enough for making perfusion possible during Both Systole and Diastole.13

Perfusion pressure within the right coronary artery is equal to (aortic pressure minus pulmonary arterial pressure).14 The aortic and pulmonary arterial pulse wave are illustrated below.The gap between these two represent the perfusion pressure within the right coronary artery. In hemodynamic management of patients with acute right heart failure, an essential goal is to maintain systemic blood pressure above pulmonary arterial pressures, thereby preserving right coronary blood flow.

Etiology and Pathophysiology of RV Failure

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The RV function integrates preload, afterload, contractility (figure below). RV mechanics and functions are altered in the setting of pressure, and or volume overload as well as in primary reduction of myocardial contractility. 15

The most common cause for RV dysfunction/failure is pressure overload with decreased contractility at second place. The prevalence of acute RV failure is difficult to estimate but the predominant causes are left-sided heart failure, acute pulmonary embolism, acute myocardial ischaemia.15

Other etiologies for RV failure are mentioned in figure 23.

The pathophysiology of the primary insults to the right heart, and their relevant evolution within the course of the disease process are illustrated below (figure 25).

Any type of primary insults will further deteriorate RV performance via downward complex chains of events that reinforce themselves through a feedback loop (Vicious Cycle),16 and if not timely intervened, cardiovascular collapse and death will be the final outcome.

Pressure overload: The thin-walled RV is not built to handle large or sudden increase in pulmonary arterial pressure.16

  • In the setting of acutely increased afterload, the RV responds by increasing its Contractility, but RV failure may occur rapidly if these mechanisms prove unable to generate sufficient pressure to maintain flow.
  • In chronically evolving pulmonary hypertension, the RV responds to increasing afterload with progressive hypertrophy, which allows it to maintain cardiac output at rest over long periods of time. Finally the RV dilates in end-stage disease, leading to tricuspid regurgitation and, ultimately, decreased cardiac output. Acute decompensation of chronic pulmonary hypertension may lead to a clinical presentation barely distinguishable from that of ‘truly’ acute RV failure as, for example,in acute pulmonary embolism.
  • The consequence of pulmonary hypertension for the right ventricle is illustrated in the figure below.

Volume overload: By enlarge, the RV is more tolerant to volume overload (relative to pressure overload). However following RV dilation, myocardial perfusion is impaired (purple arrows in figure 25), and consequently a vicious cycle is inevitable if not timely intervened.16

Definition: Heart failure vs. Cardiac Dysfunction

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The term Heart failure should not be conflated with cardiac dysfunction. Heart failure is a clinical syndrome in which symptoms and signs are caused by impaired ventricular filling or reduced ventricular flow output.

Cardiac dysfunction refers to abnormalities in intrinsic chamber performance e.g. diastolic dysfunction, systolic dysfunction, however patients may have RV, or LV dysfunction but do not manifest symptoms and signs of poor tissue perfusion, or congestion.17

Clinical Presentation of RV Failure

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The clinical presentation of acute RV failure varies depending on the underlying cause, severity and acuity of the disease as well as presence of comorbidities.16 For the purpose of this post, clinical presentation and diagnostic evaluation are summarized here (table 1).

Differential Diagnosis

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DDx of shortness of the breath with dry lungs:

  • ACS
  • PE
  • Cardiac tamponade
  • Pre-capillary pulmonary hypertension
  • Anemia, metabolic disorder e.g. DKA

DDx of shortness of the breath with dry lungs but in the presence of peripheral congestion

  • Precapillary pulmonary hypertension
  • Cirrhosis
  • Nephrotic syndrome
  • Constrictive pericarditis
  • Superior vena cava syndrome

DDx of shortness of the breath with wet lungs

  • Postcapillary pulmonary hypertension
  • Combined pulmonary hypertension
  • HFrEF
  • HFpEF
  • Pneumonia
  • ARDS

Approach To Diagnosis: Bedside US

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Patients with acute right heart failure are critically ill and often have multiple comorbidities. Oftentimes definitive diagnosis and implementation of specific treatment is time consuming. While the simultaneous employment of resuscitative and diagnostic measures(table above) are warranted for critically ill patients, the crucial role of bedside echocardiography cannot be overemphasized.It can facilitate the diagnostic process and often is helpful in therapeutic decision making. It can be used to exclude extrinsic causes of acute RV failure, especially those which require immediate treatment (such as pericardial tamponade which mimics acute RV failure).

The recommended conventional echocardiographic measures for the evaluation of right heart structures and function are summarized below (table 2 and figure 26).

Performance of bedside ultrasound/echo can shift the paradigm in the patient management, if used appropriately in the clinical context.25 Therefore the focus of the following discussion is to frame the following fundamental questions:

  • What are the clinical questions are you trying to answer with US/echo?
  • How do you interpret your finding in clinical context?

Case scenario #1

A 40-year old obese woman with a history of breast cancer presented to the hospital with watery diarrhea following her last chemo this morning. She looked pale and irritable.

HR135, BP 95/60, RR28, T37.3 C, SO2 90% room air, BS127. Subcostal echo showed hyperdynamic, underfilled LV. IVC measured 1.8 cm with >50% respiratory collapse.Other ultrasonographic findings were unremarkable including 3-point US examination of lower extremities which showed no evidence for venous clot. She received a 2L crystalloid solution, antibiotic, supplemental oxygen via non-rebreather mask and monitored closely. After 1 hour; she complained of worsening shortness of the breath. Upon further questioning, she opened up that her breathing difficulties started yesterday which she ignored. The subsequent US exams are shown below.

Courtesy of M.Chardoli, MD.

On the second exam hyperdynamic, underfilled LV, RV enlargement (shown above) and IVC with <50% respiratory collapse seen.

Hyperdynamic underfilled LV can be seen with two conditions:

  1. Right-sided low pressure state with normal sized RV and a normal IVC. The DDx might include hypovolemia, early sepsis among the list.
  2. Right-sided high pressure state with dilated RV and IVC. The LV is hyperdynamic and underfilled since it is not receiving enough volume from the right side. The DDx would be hemodynamically significant PE, RVMI, and possibly other causes for acute RV failure.

Hyperdynamic LV should always be interpreted in the context of RV status.

Remember that in a patient with frank volume loss, a normal IVC is not reliable for ruling out massive PE. It is worth mentioning that absence of DVT does not rule out the presence of PE too. In a study using venography, DVT was found in 70% of patients with proven PE.25

In this patient, CTPA study was performed and showed total occlusion of the right main pulmonary artery.

Case scenario #2

A 38-year old woman with no significant past medical presented to the hospital with ischemic chest pain and dyspnea. Upon entry, she looked pale,diaphoretic. BP100/80mm Hg, HR140, RR 25, SO2 91% room air. EKG showed STE in inferior and anteroseptal leads. Troponin was positive. Upon initial resuscitation (1L crystalloid fluid, anti-ischemic, antiplatelet meds), her hemodynamic deteriorated. She was taken for cardiac catheterization, which demonstrated no significant coronary arterial disease. After cardiac catheterization, TTE was performed (shown below).

©European Journal of Heart Failure, 15 March 2016.

Angiography has ruled out atherosclerotic coronary arterial lesions despite presence of inferior and anteroseptal STE on EKG. Echo (A4C view) showed interventricular and interatrial septal shift to the left, as well as McConnel’s sign. IVC shows no respiratory collapse.

All these findings can be seen in both RV myocardial infarction (type I MI) as well as acute PE. Not to mention the fact that ‘TAPSE’ can be abnormal in both situations. Therefore the above information is not helpful in differentiating between AMI (type I), and PE.

The primary problem in AMI (type I) is pump failure while in acute massive PE the pulmonary vascular resistance is increased.

The helpful echocardiographic parameter that can differentiate these two disease entities is PAP, which is increased in acute massive PE, but is fairly low in RVMI.

In this case estimated PASP was 41 mmHg (shown below). CTPA study was performed and showed bilateral total occlusion of the main pulmonary artery and decision was made for administration of thrombolytics.

The echo findings in the clinical settings of acute right heart failure is mentioned in the following table.

Case scenario #3

A 36-year old man with no remarkable past medical history is presented with flu-like symptoms and mild chest discomfort.He is tachypnic but not in respiratory distress. HR 90, BP 95/55, RR26,T38.5C,SO2 85% room air. EKG showed ‘incomplete RBBB’.

Physical exam was remarkable for central cyanosis,clubbing and dry mucous membrane. No peripheral edema was detected. Lung US revealed A-profile. No evidence for DVT on US exam of lower extremities was found. The echo exam at A4C is shown below. Patient received supplemental oxygen, 500 cc of crystalloid solution.

Courtesy of M.Chardoli, MD.

The RA, RV obviously are enlarged with interatrial and interventricular septal flattening. On A4C TTE an interatrial septal defect was noted raising suspicion for ASD. This was confirmed on subcostal view.

Color doppler as well as contrast study with saline injection were performed to detect for the shunt.

Courtesy of M.Chardoli, MD.

Right to left shunt was shown on the color doppler. Following saline injection, complete opacification of RA,RV with early crossing bubbles into the LA,LV consistent with intracardiac shunt was demonstrated.

The hemodynamic effects of ASD are primarily related to the direction and magnitude of shunting. In most

patients, the greater compliance of the RV compared with the LV, and the lower resistance of the pulmonary compared with the systemic circulation, results in a net left-to-right shunt, leading to RV dilation. The pulmonary vasculature normally accommodates the increased volume of flow secondary to ASD without a significant increase in PA pressure. With continued RV volume overload and increased PA flow over time, some patients will develop pulmonary hypertension (PH). Development of PH is associated with right-to-left shunt as well as interventricular flattening during systole.26

Eisenmenger syndrome is the triad of congenital systemic-to-pulmonary communication, pulmonary arterial disease, and cyanosis. It implies that the development of pulmonary arterial disease is a consequence of increased pulmonary blood flow, and requires exclusion of other causes of PH.27

In this case CTPA was negative for pulmonary embolism.

Case scenario#4

A 65-year old man with past medical history of HTN, COPD, and atrial fibrillation presented to the hospital with acute shortness of the breath. He looked diaphoretic with respiratory discomfort. Initial set of vitals showed BP160/100, HR irregular, ranging 70-90, RR 30, SO2 90% room air. EKG shown below. While initial resuscitative measures were ongoing, bedside echocardiography was performed (shown below). RV free wall diastolic diameter in subcostal view read at 8 mm. IVC measured 23 mm with < 50% collapse with a sniff. US exam of right lower extremity at popliteal vein shown below.

©European Journal of Heart Failure, 15 March 2016.

Is this clinical presentation and information obtained from bedside US suggestive for PE?

Echo is remarkable for the enlarged RA, RV with septal shift to the left and severe TR. Pericardial effusion without diastolic chamber collapse is noticed as well. Echogenicity within the right popliteal vein is in favour of DVT.

The past medical history, presence of RV free wall hypertrophy and a severe TR (4m/s) with estimated PASP about 74 mmHg all are indicative for the presence of chronic pulmonary hypertension. Presence of lower extremity DVT will increase the pretest probability for PE, however none of the above findings are diagnostic for acute PE in this case.

Acute decompensation of chronic pulmonary hypertension can occur due to multiple problems as well as new onset superimposing PE. Unfortunately No bedside US findings is definitively diagnostic for PE in such cases, unless ‘CLOT IN TRANSIT’ is seen. In patients with acute decompensation of chronic pulmonary hypertension, CTPA,or V/Q lung scan are diagnostic.

In this case, CTPA revealed no evidence of pulmonary embolism, and the patient was treated for acute decompensation of pulmonary hypertension and DVT.

Pearl: As mentioned in table 3, presence of pericardial effusion in patients with chronic pulmonary hypertension carries poor prognosis. 28

Echocardiographic findings in Acute Pulmonary embolism (PE):29

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Overall, the sensitivity of TTE for the diagnosis of PE is about 50-60% while the specificity is around 80-90%. TTE is normal in about 50% of unselected patients with acute PE, but it can provide direct and/or indirect evidence for the diagnosis.

Direct signs for PE: Clot in transit defined as a large, mobile (i.e unattached to any intracardiac structure), serpentine echogenicity trapped in the right heart chambers or pulmonary artery is rare, but makes the diagnosis evident.

Large,mobile,snake-like clot in the right atrium.

Courtesy of M.Chardoli, MD.

Indirect signs for PE (though nonspecific): 30

  • Systolic/diastolic septal shift (D-shaped left ventricle).
  • Dilatation of RA,RV (end-diastolic RV/LV diameter 0.6 or area 1.0)
  • Global RV hypokinesia
  • McConnell sign: RV hypokinesia sparing the apax. It is not specific for PE and can be seen with RVMI as well. It has poor sensitivity (77%).
  • Pulmonary hypertension around 40-50 mmHg (>60 mmHg in the case of pre-existing pulmonary hypertension)
  • Mild to severe TR: Secondary TR is frequent in patients with intermediate to high risk PE allowing estimation of systolic pulmonary arterial pressure (sPAP). As the RV is only able to generate a sPAP of up to 60 mmHg acutely, in the acute setting the TR jet velocities are expected to be no higher than 2.5-3.5 m/s, corresponding to a sPAP of about 40-50 mmHg in acute PE. Conversely, a sPAP 60 mmHg may suggest a more chronic process, relating to repeated episodes of PE, or chronic pulmonary parenchymal disease and/or superimposed PE.
  • Pulmonary acceleration time < 60 ms is in favour of PE.
  • Pulmonary systolic notch: Normal pulmonary systolic flow pattern has no notching. As pulmonary vascular resistance is increased, doppler flow wave will reflect backward to the RV during systole, which impedes RV ejection and causes doppler envelope notching.Presence of early systolic notching (ESN) indicates mildly elevated mean PAP (notch is defined early, if it falls within initial 50% of the ejection time). Moreover the presence of ‘ESN’ identifies patients with Massive or submassive PE.

In patients with suspected high-risk PE presenting with shock or hypotension, the absence of echocardiographic signs of RV pressure overload and/or dysfunction virtually excludes massive PE as a cause of hemodynamic instability.

Where PE is diagnosed, echocardiography can be used to differentiate those patients not at high risk into intermediate risk (evidence of RV dysfunction) vs. low risk (no RV dysfunction).

Echocardiographic findings in acute PE are illustrated in figure 36.29

Case scenario #5

A 65-year old woman was presented to the hospital with syncope. During initial evaluation in the triage, she became unresponsive and pulseless.CPR immediately started and the patient was transferred to the resus bay. While the resuscitation was undergoing her husband mentioned that she has a history of HTN, stroke (s/p 8 months), lower extremity DVT, and GI bleeding. Monitor showed rapid irregular narrow complex tachycardia, Focused Echo (FE) showed no cardiac wall/valve motion (shown below).

Courtesy of Sonostuff

Does RV dilation during cardiac arrest is a specific finding for PE?

Absolutely Not! Several recent studies have shown that relative or absolute RV enlargement during cardiac arrest can be seen with other possible causes e.g. hypoxia, hyperkalemia, primary arrhythmia(VF) and is not particularly associated with PE. These findings challenge the paradigm that RV dilatation on ultrasound during CPR is particularly associated with PE.31 32 33 34

Management: Hemodynamic Support of Right Heart Failure29

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Identification and treatment of the underlying cause of RV failure, such as acute pulmonary embolism, acute decompensation of chronic pulmonary hypertension, RV infarction, is the primary management strategy. Oftentimes definitive diagnosis and implementation of specific treatment is time consuming.

Meanwhile hemodynamic support is life saving in clinical care of these patients (figure 37).14 16

Volume optimization

Despite that patients with RV failure may be preload-dependent, vigorous fluid administration results in leftward shift of interventricular septum, decrease LV output, and hypotension through ventricular interdependence; especially in the setting of high intrathoracic pressure and pericardial disease.

Generally fluid administration is often prohibited in acute RV failure unless the patient has frank volume loss e.g. overt GIB, or in the setting of RVMI.16

Why is fluid administration in RVMI relatively safe?

In RVMI, the primary problem is reduced RV contractility but Not the RV afterload (in contrast to PE where RV afterload is the primary problem). Therefore, in RVMI giving fluid will increase the pressure ahead and consequently increase RV cardiac output (RV behaving as a passive conduit).

Diuretics: Patients with certain conditions e.g. postcapillary pulmonary hypertension (chronic right heart failure due to left heart failure) with clinical signs of volume overload may need diuretic treatment.14 Treating left HF will reduce RV afterload by decreasing pulmonary artery pressures.35 Ultrafiltration is an option for patients with refractory volume overload (diuretic-resistant).

Protect Right Heart Coronary Perfusion Pressure:

Right heart is perfused throughout the whole cardiac cycle. As explained in the context of the RV spiral of death (vicious cycle), the inciting events prime the right ventricle for the secondary ischemic insult. Even transient hypotension can be detrimental in such patients. Strategies that improve RV perfusion include maintaining MAP, reducing RV afterload (↓PVR), improving contractility, and possibly eliminating hemodynamically significant brady-dysrhythmias,and tachy-dysrhythmias.

Maintaining MAP: Hemodynamically unstable patients require vasopressor to keep their MAP within the safe range (60 to 65mm Hg).The agent of choice would be the one with optimal systemic vasopressor activity while having the least pulmonary vasoconstriction effect (↓PVR/SVR).13

Norepinephrine, epinephrine36 and vasopressin administration are recommended. The pulmonary vascular properties of commonly used vasoactive agents are summarized in table 4.

Avoid phenylephrine for its potential pulmonary vasoconstriction, and dopamine for its arrhythmogenic properties.13

Inotropes: If the primary problem is decreased contractility e.g. RVMI, then institutions of inotropes can improve contractility, reduce RVEDV, and cause perfusion improvement (table 3 below).

Inhaled Pulmonary Vasodilators: Strategies that decrease pulmonary vascular resistance may include inhaled nitric oxide, epoprostenol, nitroglycerine 38 and milrinone.39

Suggested dosage include:

  • Epoprostenol at 0.05mcg/kg/min
  • Nitric Oxide at 20ppm
  • Milrinone (1mg/ml), inhale 5mg over 15 minutes
  • Nitroglycerin (1mg/ml), inhale 5mg over 15 minutes

Rhythm stabilization: Patients with RV failure are susceptible to alteration in cardiac rhythm and ventricular synchrony.40 Clearly, hemodynamically significant bradycardias or tachyarrhythmias should be corrected.

Supraventricular arrhythmias (especially atrial fibrillation) are more common than ventricular arrhythmias in PAH. Management of tachyarrhythmia is challenging. Most medications which are used for rate control (e.g. beta blockers, calcium channel blockers) have the potential for dropping the blood pressure. Digoxin may be a useful alternative for rate control. In patients with longstanding AF, cardioversion is often unsuccessful. Even after successful cardioversion, the atrial contraction (and cardiac output) is not improved.41

Correction of the underlying conditions will often result in elimination of AF.

Correct Hypoxia, Hypercarbia, Acidosis

Hypoxia causes pulmonary vasoconstriction(HPV) and this effect is potentiated in the presence of acidosis.42 43

Adequate oxygenation to avoid HPV is of paramount importance. Administration of pulmonary vasodilators improve lung units with physiologic dead space,and therefore elimination of carbon dioxide is augmented via improvement in alveolar ventilation.

Avoid Intubation as possible:

Patients with acute right heart failure are very sensitive to hypoxia and systemic hypotension as explained before.14 All medications used for RSI have the potential to drop the blood pressure, moreover the transient apnea during intubation procedure is poorly tolerated in these patients.44

Patients with acute right heart failure most commonly succumb to death via cardiovascular collapse.

Except for conditions with primarily involvement of the respiratory system such as pneumonia, ARDS; intubating the patient is not the right decision.

Most patients with right heart failure have tachypnea because of hemodynamic instability. They do not have primary respiratory problems, and as such intubation will not fix their underlying condition. The fact that a patient has severe tachypnea does not necessarily mean that intubation will resolve the problem.

In extreme situations where intubation is required, minimizing apeniec period and correcting the hypotension, acidosis, hypoxia before proceeding to intubation are warranted. Hemodynamically neutral intubation (cardiostable intubation) is advised.

Mechanical Ventilator Setting:

Lung protective mechanical ventilator setting with considering low VT 4-6mL/kg/PBW, low peak pressure, Pplat ≦ 30 mmHg, minimal PEEP is recommended.14

Prone ventilation may unload the RV through effects on airway pressure and improved alveolar ventilation.45


Despite its limited availability, and lack of high-level evidence 46 47 regarding VA-ECMO for potential candidates with acute right heart failure, the mechanical circulatory support of the right ventricle may be considered in certain clinical situations such as RV myocardial infarction (MI), acute PE, following left ventricular assist device implantation, or primary graft failure after heart transplantation.48


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  • Patients with acute right heart failure are critically ill and often have multiple comorbidities. Prompt diagnosis, hemodynamic support and initiation of specific treatment are significantly important to keep your patient alive.
  • Usually there is a time lag between diagnosis and employment of specific treatment. Performance of bedside ultrasound is extremely helpful in making rapid diagnosis, risk stratifying your patients, and guiding therapeutic regimen.
  • Right heart structure and physiology are uniquely different from the left heart. The medications that are used for left heart failure often do not work in right heart failure. Understanding the right heart physiology and pathogenesis of the RV failure make this distinction more clear.
  • The vicious cycle of RV failure makes it unforgiving for any misdiagnosis and mismanagement.

  • Except for certain diseases such as tamponade for which pericardiocentesis may rapidly fix it, there are not such rapidly fixable treatments for almost all other causes of the right heart failure. Appropriate hemodynamic support works as a bridge to employment of specific treatment and onset of their therapeutic effects. During this interim period, the following steps are life saving as can improve RV performance:

  1. Interventions that improve RV perfusion such as increasing MAP(if indicated) by systemic vasopressors, reducing PVR by inhaled pulmonary vasodilator medications, augment RV contractility by inotropes (if indicated).
  2. Correcting other factors which potentially cause pulmonary vasoconstriction such as hypoxia, hypercarbia, and acidosis.
  3. Perform bedside US to evaluate the volume status and optimize it accordingly. In questionable situations err on the side of keeping your patient dry.
  4. Correct hypotension, hypoxia and acidosis, before ever trying to intubate your patients, and Be Prepared. Hemodynamically neutral intubation and minimizing the apneic period are recommended.
  5. Be cautious for the deleterious effects of mechanical ventilation on the RV performance and employ strategies to minimize these adverse effects by using a low tidal volume, PEEP, and keeping Pplat < 30 mmHg.

Going further:

Post Peer Reviewed By: Mojtaba Chardoli. MD, Darab Zohri. MD

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Shahriar Lahouti

Founder, Chief Editor
I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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