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Ultrasound Corner |

A Woman in Her 20s With Cardiopulmonary Failure FREE TO VIEW

Anton Lishmanov, MD, PhD; Tara T. Bellamkonda, DO; Ariel L. Shiloh, MD
Author and Funding Information

Division of Critical Care Medicine, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY

CORRESPONDENCE TO: Ariel L. Shiloh, MD, Division of Critical Care Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, 111 E 210th St, Critical Care Administration, Bronx, NY 10467


Copyright 2017, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(6):e123-e125. doi:10.1016/j.chest.2017.01.040
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An African American female in her 20s with sickle cell disease, complicated by previous episodes of acute chest syndrome, was admitted for a planned termination of pregnancy at 18 weeks of gestation. One day post-procedure, in the setting of vaginal bleeding, the patient developed chest pain and hypoxia. Critical care consultation was requested for suspected acute chest syndrome.

Initial evaluation of the patient was notable for significant distress, tachycardia, and severe chest pain, which worsened with respirations and exertion. Physical examination was limited because of her level of distress and pain. Vital signs were as follows: heart rate, 130 beats/min; blood pressure, 115/65 mm Hg; pulse oximetry, 89% on room air; and respiratory rate, 30 breaths/min. An electrocardiogram showed sinus tachycardia at 130 beats/min, with nonspecific T-wave changes in the anterior precordial leads. Laboratory results were significant for the following: hemoglobin level, 6 g/dL (baseline, 8-9 g/dL); leukocytosis (white blood cell count, 22,300/μL), troponin-T, 0.19 ng/mL; and N-terminal pro-B-type natriuretic peptide, 3,560 pg/mL. Chest radiography demonstrated mild cardiomegaly and a suggestion of a retrocardiac opacity (Fig 1). Fluid resuscitation and red cell transfusion were initiated. The patient was transferred to the ICU for further treatment.

Figure Jump LinkFigure 1 Chest radiography demonstrating mild cardiomegaly and a suggestion of retrocardiac opacity.Grahic Jump Location

In the ICU there was a rapid development of multiorgan failure that included a shock state, acute renal failure with hyperkalemia, coagulopathy, and severe lactic acidosis (13 mM). Arterial blood gas analysis was as follows: pH, 7.062; pCO2, 22.6 mm Hg; Pao2, 120 mm Hg on 100% nonrebreather mask. The patient required mechanical ventilation and vasopressor support. Despite aggressive support the patient continued to decompensate. The intensivist team performed point-of-care ultrasonography to further evaluate the cause of decompensation (Video 1).

Question: Based on the clinical scenario and the findings of point-of-care ultrasonography, what is the most likely cause of cardiopulmonary failure in this patient?

Answer: Acute right ventricular failure

Without sonographic evidence (Video 2), acute right ventricular (RV) failure is difficult to diagnose. The clinical findings and organ failures that result from RV failure (circulatory collapse, renal failure, elevated lactate and liver test results, and coagulopathy) are often initially attributed to, or overlapping with, severe sepsis and septic shock. As a result, reflexive volume resuscitation is administered—ultimately worsening RV failure. Similarly, initial therapy for patients with sickle cell hemolytic crisis includes fluid resuscitation and red cell transfusion. When sickle cell crisis is complicated by acute chest syndrome, pulmonary vaso-occlusive disease, and resultant acute pulmonary hypertension/cor pulmonale, large-volume resuscitation is detrimental; it produces a downward spiral of RV failure and clinical deterioration.

Goal-directed echocardiography is essential in determining the cause of cardiopulmonary failure and includes assessment of the right ventricular size and function. Echocardiographic guidelines used in the evaluation of right ventricular failure are complex., Simplified parameters are found in Table 1. Furthermore, in the majority of severe shock states, visual assessment of the RV alone is often adequate to determine RV function. Visual markers of failure include the following:

  • RV size comparable to or larger than left ventricular size in the apical four-chamber view

  • Paradoxical septal motion

  • “D-shaped” septum

Table Graphic Jump Location
Table 1 Simplified Echocardiographic Findings Used in the Evaluation of Right Ventricular Failure

These findings, in combination with a dilated inferior vena cava and minimal respiratory variation (indicating elevated right atrial pressures), should raise the suspicion for RV failure.,

In addition to gross visual markers, RV wall thickness and closer analysis of ventricular septal motion can further delineate the chronicity and pathology associated with RV failure. RV free wall thickness greater than 0.5 cm, measured at end-diastole in the subcostal or parasternal long-axis view, indicates RV hypertrophy; this suggests an element of chronic RV overload or pulmonary hypertension (Fig 2). Isolated RV volume overload results in a “D-shaped” septum most pronounced at end-diastole, with grossly normal septal geometry at end-systole. RV pressure overload results in a leftward shift throughout systole and diastole, most pronounced at end-systole. Although the RV free wall views are limited, the patient had a slightly thickened wall measuring 0.59 cm and a leftward shift throughout the cardiac cycle—demonstrating an acute on chronic right ventricular process with both volume and pressure overload.

Figure 2
Figure Jump LinkFigure 2 Measurement of right ventricular free wall thickness in the subcostal long-axis view. RA = right atrium; RV = right ventricle.Grahic Jump Location

The causes of RV dysfunction are extensive, and the presence of acute RV failure or cor pulmonale may not be the sole reason for a patient’s decompensation, but rather a consequence of the ongoing disease process, a manifestation of a secondary disease process, or a consequence of therapy., Patients with severe sepsis syndrome may manifest acute RV cardiomyopathy. Similarly, pulmonary hypertension is prevalent among patients with sickle cell disease, and further vaso-occlusive crisis may exacerbate pulmonary hypertension and RV failure. In a study of patients admitted to the ICU with acute chest syndrome, up to 60% of patients had pulmonary hypertension (as defined by a tricuspid jet velocity > 2.5 m/s), and cor pulmonale occurred in 13% of patients. The pathophysiology of acute pulmonary hypertension and RV failure in acute chest syndrome is multifactorial and attributed to a combination of hypoxic pulmonary vasoconstriction, nitric oxide depletion due to hemolysis, and pulmonary vasculature occlusion.

The presence of RV dysfunction should alter shock management, and consideration should be given to fluid restriction, diuretics, inotropes and vasopressors, pulmonary vasodilators, and limiting tidal volume and positive end-expiratory pressure on mechanical ventilation. In the most severe cases, extracorporeal circulatory support and oxygenation may be implemented.

In our case, veno-arterial extracorporeal membrane oxygenation (ECMO) via the femoral vasculature was implemented. Ultrasound guidance during percutaneous ECMO cannulation assisted with vascular identification, cannula sizing, and cannula deployment. Video 3 demonstrates the use of real-time ultrasound guidance, in accordance with Extracorporeal Life Support Organization (ELSO) guidelines, for the venous limb cannulation. After the guidewire was visualized ascending through the inferior vena cava and into the internal jugular vein, the cannula was deployed and positioned at the cavo-atrial junction (Discussion Video 4).

The signs and symptoms of RV failure mimic, and commonly overlap with, other causes of shock and acute respiratory failure—but the treatment can be markedly different. Without appropriate echocardiographic identification of shock states, empiric therapies can potentially result in further morbidity and mortality.

  • 1.

    Point-of-care ultrasonography assists in differentiating shock states and can evaluate for possible causes of right ventricular failure.

  • 2.

    Pulmonary hypertension is prevalent among patients with sickle cell disease. Clinicians should be vigilant in identifying acute pulmonary hypertension with right ventricular failure in patients with acute chest syndrome.

  • 3.

    Real-time vascular ultrasound and echocardiography assist in percutaneous ECMO cannulation.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Additional information: The videos can be found in the Supplemental Materials section of the online article.

Krishnan S. .Schmidt G.A. . Acute right ventricular dysfunction: real-time management with echocardiography. Chest. 2015;147:835-846 [PubMed]journal. [CrossRef] [PubMed]
 
Rudski L.G. .Lai W.W. .Afilalo J. .et al Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-713 [PubMed]journal. [CrossRef] [PubMed]
 
Mekontso Dessap A. .Leon R. .Habibi A. .et al Pulmonary hypertension and cor pulmonale during severe acute chest syndrome in sickle cell disease. Am J Respir Crit Care Med. 2008;177:646-653 [PubMed]journal. [CrossRef] [PubMed]
 
Extracorporeal Life Support Organization.Ultrasound Guidance for Extra-corporeal Membrane Oxygenation General Guidelines. ELSO website.https://www.elso.org/Portals/0/Files/elso_Ultrasoundguideance_ecmogeneral_guidelines_May2015.pdf. Accessed August 28, 2016.
 

Figures

Figure Jump LinkFigure 1 Chest radiography demonstrating mild cardiomegaly and a suggestion of retrocardiac opacity.Grahic Jump Location
Figure Jump LinkFigure 2 Measurement of right ventricular free wall thickness in the subcostal long-axis view. RA = right atrium; RV = right ventricle.Grahic Jump Location

Tables

Table Graphic Jump Location
Table 1 Simplified Echocardiographic Findings Used in the Evaluation of Right Ventricular Failure

References

Krishnan S. .Schmidt G.A. . Acute right ventricular dysfunction: real-time management with echocardiography. Chest. 2015;147:835-846 [PubMed]journal. [CrossRef] [PubMed]
 
Rudski L.G. .Lai W.W. .Afilalo J. .et al Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-713 [PubMed]journal. [CrossRef] [PubMed]
 
Mekontso Dessap A. .Leon R. .Habibi A. .et al Pulmonary hypertension and cor pulmonale during severe acute chest syndrome in sickle cell disease. Am J Respir Crit Care Med. 2008;177:646-653 [PubMed]journal. [CrossRef] [PubMed]
 
Extracorporeal Life Support Organization.Ultrasound Guidance for Extra-corporeal Membrane Oxygenation General Guidelines. ELSO website.https://www.elso.org/Portals/0/Files/elso_Ultrasoundguideance_ecmogeneral_guidelines_May2015.pdf. Accessed August 28, 2016.
 
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Video 1


Video 2


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Discussion Video 4

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