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A 37-Year-Old Woman With Diabetes Mellitus, Systemic Hypertension, and Chronic Kidney Disease Admitted With Multifocal Pneumonia and EmpyemaMultifocal Pneumonia and Empyema FREE TO VIEW

J. Terrill Huggins, MD; Nithin Karakala, MD; Ruth Campbell, MD; Carlos Kummerfeldt, MD; Jennings Nestor, MD; Nicholas J. Pastis, MD, FCCP; Peter Doelken, MD
Author and Funding Information

From the Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine (Drs Huggins, Kummerfeldt, Nestor, and Pastis) and the Division of Nephrology (Drs Karakala and Campbell), Medical University of South Carolina, Charleston, SC; and the Division of Pulmonary and Critical Care (Dr Doelken), Albany Medical Center, Albany, NY.

CORRESPONDENCE TO: J. Terrill Huggins, MD, Medical University of South Carolina, Pulmonary, Critical Care, Allergy and Sleep Medicine, 96 Jonthan Lucas St, Charleston, SC; e-mail: hugginjt@musc.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(2):e41-e46. doi:10.1378/chest.13-2711
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Published online

A 37-year-old woman with a medical history of type 1 diabetes mellitus, systemic hypertension, and chronic kidney disease due to glomerulosclerosis was admitted with multifocal pneumonia and empyema. She underwent a small-bore tube thoracostomy placement and rapidly developed respiratory failure and shock. She was intubated and started on norepinephrine. Table 1 is a summary of the daily urine output (UOP), fluid balance per day, and corresponding serum creatinine level during the initial ICU stay. Mechanical ventilator settings were as follow: pressure-regulated volume control; tidal volume, 450 mL; respiratory rate, 20 breaths/min; positive end-expiratory pressure (PEEP), 8 cm H2O; and Fio2, 50%. Urinary sediment was positive with granular casts. The calculated plateau pressure (PP) was 32 cm H2O. On day 4, consultation requested a point-of-care echocardiography (POCE) to be performed. Video 1A shows the subcostal longitudinal view of the inferior vena cava (IVC), and Figure 1 shows the corresponding M mode of the IVC. Figure 2 shows an apical 5C view of the pulse-wave Doppler of the left ventricular (LV) outflow tract (LVOT) and Video 1B, an apical 4C view. Video 1C shows the lung ultrasound (abnormal lung finding seen diffusely). Pulse-wave Doppler of the mitral inflow showed an impaired relaxation pattern with E to A wave reversal. Calculated E/e′ was < 8 (not shown).

Video 1A

Subxiphoid Long-axis IVC

Running Time: 0:02

Video 1B

Apical 4-C view ACP

Running Time: 0:06

Video 1C

Lung Utraound with Diffuse B-line Pattern

Running Time: 0:06

Table Graphic Jump Location
TABLE 1 ] UOP, Fluid Balance Per Day, and Corresponding Serum Creatinine During the Initial ICU Stay

Cr = creatine; CRRT = continuous renal replacement therapy; UOP = urine output.

a 

CRRT.

Figure Jump LinkFigure 1  M-mode of the inferior vena cava (IVC) obtained from a subcostal longitudinal view. The IVC maximal diameter measured at 2.69 cm.Grahic Jump Location

Figure Jump LinkFigure 2  Apical 5C view of the pulse-wave Doppler of the left ventricular outflow tract (LVOT). The velocity time integral of the LVOT was calculated to be 23.2 cm2.Grahic Jump Location
What is the clinical diagnosis supported by the POCE findings?
Answer: Acute cor pulmonale due to the effects of positive pressure ventilation and ARDS

Discussion Video

Discussion Video

The following interventions were undertaken immediately:

  • 1. Adaptive mechanical ventilation strategies (tidal volume decreased to 400 mL, PEEP reduced to 6 cm H2O, and respiratory rate increased to 25 breaths/min; this resulted in a reduction of PP to 26 cm H2O)

  • 2. A single dose of bumex, 1.5 mg, given with no change in UOP at 6 h

  • 3. Continuous renal replacement therapy started with a goal to ultrafiltrate

Video Figure File Set illustrates the results of adaptive ventilation and after a 1-L ultrafiltration was achieved. The pulse wave Doppler shows a velocity time integral of 22.0 cm and a calculated stroke volume (SV) of 86 mL (Fig 3). Video 2A is an apical 4C view showing resolution of acute cor pulmonale (ACP), with a normal-appearing right ventricular (RV) end-diastolic surface area to LV end-diastolic surface area (RVEDSA to LVEDSA) ratio. Compare this finding to Video 1D, which demonstrates ACP with an RVEDSA to LVEDSA > 1.0. Tricuspid annular plane systolic excursion (TAPSE), previously measuring 1.6 cm, has now increased to 2.5 cm (Fig 4). The lung ultrasound showed B lines, which were noted diffusely (Video 1C). The presence of B lines was caused by the presence of interstitial edema, which could be attributed to either cardiogenic or noncardiogenic pulmonary edema. With the use of Doppler echocardiogram (ECHO), one can estimate the left-side filling pressures. As in this case, the mitral E/E′ was < 8 and was consistent with normal left-sided filling pressures and helpful in excluding a cardiogenic cause for the patient’s respiratory failure.

Video 2

Apical 4-C resolution of ACP

Running Time: 0:06

Figure Jump LinkFigure 3  Apical 5C view of the pulse-wave Doppler of the LVOT. The velocity time integral of the LVOT was calculated to be 21.4 cm2. See Figure 2 legend for expansion of abbreviation.Grahic Jump Location
Figure Jump LinkFigure 4  Tricuspid annular plane systolic excursion (TAPSE) obtained on M-mode for an apical 4C view. TAPSE was 2.5 cm.Grahic Jump Location

Figure 5 shows a static image of the apical 4C view showing the cardiac anatomy, and Figure 6 shows a static image of the apical 5C view showing the cardiac anatomy, with corresponding pulse-wave Doppler of the LVOT. Figure 7 also shows a static image of a subcostal longitudinal view of the IVC, with the corresponding M mode of IVC.

Figure Jump LinkFigure 5  Cardiac anatomy shown in an apical 4C view.Grahic Jump Location
Figure Jump LinkFigure 6  Cardiac anatomy of an apical 5C view with corresponding PW Doppler of the LVOT. Please note that the aortic valve closure occurring at the end of Doppler signal signifies proper positioning of the gate of the Doppler in the LVOT. PW = pulse wave. See Figure 2 legend for expansion of other abbreviation.Grahic Jump Location
Figure Jump LinkFigure 7  Anatomy shown for a subcostal longitudinal view of the IVC with the corresponding M-mode of the IVC. Please note placement of M-mode cursor is 2 cm below the junction of the right atrium. See Figure 1 legend for expansion of abbreviation.Grahic Jump Location

As shown in Table 1, these interventions and correcting a state of severe venous congestion and ACP had dramatic effects on the UOP without a significant change in the required dose of norepinephrine. Within a day, a robust response in the patient’s UOP was noted by as much as a 20-fold increase. On days 6 to 8, a positive fluid balance was instituted in an attempt to resolve the need for vasopressors, which resulted in a UOP similar to that which was seen before, without correcting the need for norepinephrine.

RV dysfunction is an often underappreciated clinical entity when echocardiography is not used by the intensivist. RV dysfunction may present as (1) ACP due to acute pulmonary embolism, ARDS, inappropriate ventilator support, systemic acidemia, fat emboli, or gas emboli; (2) acute RV dysfunction secondary to sepsis; (3) RV infarction; or (4) acute chronic cor pulmonale. Echocardiography is the only modality available to allow the intensivist to diagnose and monitor right-sided heart function, and more importantly, to assess RV function response to implemented therapies.

ACP is caused by a sudden increase in RV afterload, which occurs in the setting of ARDS and acute pulmonary embolism. An untoward afterload increase on the right ventricle is commonly seen as a deleterious effect of positive pressure ventilation. ACP is characterized by both systolic and diastolic overload. Septal dyskinesia is the echocardiographic hallmark of RV systolic overload. Septal dyskinesia occurs with a sudden increase in RV afterload, prolonging RV contraction longer than LV systole. Because the right ventricle is still contracting while the left ventricle is beginning to relax at the end of systole, RV pressures exceed LV pressures, resulting in the intraventricular septum bulging into the LV cavity. Simply identifying septal dyskinesia and the paradoxical septal motion by echo are the only steps necessary in the diagnosis of ACP.1-3

RV diastolic overload is synonymous with RV dilation. Vieillard-Baron and colleagues4 proposed a semiquantitative method to assess RV diastolic overload. On an apical four-chamber view, measurement of the end diastolic area by tracing the endocardium of both ventricles was performed. They found an RVEDSA to LVEDSA ratio correlated to RV dilatation. A normal RVEDSA to LVEDSA ratio was found to be between 0.36 and 0.6. Moderate dilation was defined as a ratio of 0.7 to 0.9. Severe dilation was defined as a ratio ≥ 1.0.4

Another way to assess RV function is to evaluate TAPSE. Systolic excursion of the lateral tricuspid annulus represents the global RV systolic function.5 RV SV is generated more from longitudinal than circumferential shortening. This longitudinal shortening is best seen on an apical 4C view with the movement of the lateral tricuspid annulus toward the cardiac apex. TAPSE is measured on M mode with the cursor aligned through the lateral tricuspid annulus; it is reported in millimeters and is considered normal when it is ≥ 16.

Doppler ECHO, which requires an advanced ECHO skill set, is not performed routinely by most intensivists. However, we believe the acquisition of Doppler skill sets is obtainable by most physicians who are already adept at basic echocardiography. With the use of Doppler ECHO, important parameters can be obtained in the critically ill. These parameters include SV/cardiac output, and, more importantly, they allow one to have a better understanding of left-sided filling pressures in cases of “white-lung” syndrome.

Doppler ECHO-derived measurement of SV and carbon monoxide are highly correlated to the thermodilution technique. To obtain SV by ECHO, we simply obtain the volume of the cylinder (in this case, the cylinder is the LVOT). We begin with a parasternal long-axis view to acquire the LVOT diameter, which is measured at the base of the aortic valve when the aortic valve is open. The normal LVOT diameter is 1.8 to 2.2 cm. We can now calculate the cross-surface area of the cylinder (πr2). Next we need to know the height of the cylinder, which is obtained by pulse-wave Doppler of LVOT. From an apical 4C view, we simply angle the transducer into the LVOT (apical 5C view). Then we place the pulse-wave Doppler gate in the LVOT, which is typically a couple of millimeters below the aortic valve. The velocity time integral of the Doppler signal from the LVOT is obtained and is reported in centimeters. We multiply the cross surface area of the LVOT and the velocity time integral of the LVOT to obtain SV.2,3

A less precise and more difficult skill set is involved in performing Doppler measurements of the mitral inflow to characterize the diastolic function and to estimate the left-sided filling pressures. The diastolic velocities of the mitral inflow (E and A wave) are preload dependent and are affected by the effects of positive-pressure ventilation. Tissue Doppler mitral annulus can be obtained at the lateral or medial mitral annulus, usually the lateral if it is not obscured by the lung; it is expressed as E′. The E/E′ ratio can yield an estimate of LV end diastolic pressure. Normal is < 10, indeterminate is 10 to 15, and > 15 is indicative of increased LV end diastolic pressure. These measurements are obtained from an apical 4C view. Pulse-wave Doppler is used to obtain the mitral inflow, with the gate positioned at the tips of the mitral leaflets when fully open; the E and A velocities then can be measured. Tissue Doppler is then activated, and the pulse-wave gate is positioned over the medial mitral annulus.

Mechanical ventilation markedly affects pulmonary circulation and is more pronounced in the setting of reduced lung compliance. Several studies have correlated a reduced ARDS survival to the development of ACP.6,7 PP, which is a reflection of transpulmonary pressure, has direct effects on pulmonary capillaries with alterations on RV afterload. In a study of 352 patients with ARDS who were mechanically ventilated, an ACP incidence of 13% was noted in PP < 27 cm H2O, 30% for PP range 27 to 35 cm H2O, and 60% for PP greater than > 35 cm H2O. Corresponding mortality rates for these three PP ranges were 30%, 40%, and 80% respectively. Similarly, the application of high extrinsic PEEP also has deleterious effects on RV function and results in overloading the right ventricle.7 Limiting tidal volumes is ideal in reducing PP, but it is also responsible for the development of hypercapnia. Hypercapnia likewise will induce pulmonary arterial vasoconstriction and worsen ACP. To control for the development of hypercapnia in the treatment of ACP, one should not increase the tidal volume, but should correct by increasing the respiratory rate and avoiding the development of intrinsic PEEP.

Cardiorenal syndrome (CRS) is a disorder of the heart and kidneys whereby an acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. Five subtypes of CRS exist: (1) CRS type 1 = acute worsening of heart function leading to kidney injury; (2) CRS type 2 = chronic heart abnormalities in heart function leading to kidney injury; (3) CRS type 3 = acute worsening of kidney function leading to acute heart dysfunction; (4) CRS type 4 = chronic kidney disease leading to heart injury/dysfunction; and (5) CRS type 5 = systemic conditions leading to simultaneous injury or dysfunction of the heart and kidneys.

Different pathophysiologic mechanisms are involved in the combined dysfunction for the five subtypes of the CRS described. POCE is an excellent modality to assist the physician in identifying CRS subtype and instituting the proper management to correct the pathophysiologic consequence of CRS.8-10

  • 1. Echocardiography is the only modality to diagnose ACP.

  • 2. The development of ACP is common in the setting of ARDS and sepsis, which warrants a need to aggressively screen these patient populations.

  • 3. Diagnosis of ACP by ECHO requires the presence of RV systolic and diastolic overload. The echo correlation of ACP is septal dyskinesia and RV dilation.

  • 4. Therapeutic strategies for ACP management include (1) an adaptive mechanical ventilation strategy to lower PP and minimize PEEP without worsening hypercapnia; (2) a complete avoidance of IV fluids; (3) an appropriate use of inotropes/vasopressors if clinically indicated; (4) a consideration of pulmonary artery vasodilators, such as nitric oxide or inhaled prostacyclin derivatives; and (5) prone positioning as a measure to unload the right ventricle.

  • 5. Dynamic measures to predict preload dependency will be universally positive in patients who develop ACP and will always lead to an inappropriate use of IV fluids and increase mortality.

  • 6. POCE can be used safely at the bedside to establish the type of CRS present and to help the physician with fluid challenges and the need to aggressively remove volume in the setting of RV failure.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Additional information: The Videos can be found in the “Supplemental Materials” area of the online article.

Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997;111(1):209-217. [CrossRef] [PubMed]
 
Narasimhan M, Koenig SJ, Mayo PH. Advanced echocardiography for the critical care physician: part 1. Chest. 2014;145(1):129-134. [CrossRef] [PubMed]
 
Narasimhan M, J Koenig S, Mayo PH. Advanced echocardiography for the critical care physician: part 2. Chest. 2014;145(1):135-142. [CrossRef] [PubMed]
 
Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F. Echo-Dopler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med. 2002;166(10):1310-1319. [CrossRef] [PubMed]
 
Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J. 1984;107(3):526-531. [CrossRef] [PubMed]
 
Vieillard-Baron A, Schmitt JM, Augarde R, et al. Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis. Crit Care Med. 2001;29(8):1551-1555. [CrossRef] [PubMed]
 
Jardin F, Vieillard-Baron A. Is there a safe plateau pressure in ARDS? The right heart only knows. Intensive Care Med. 2007;33(3):444-447. [CrossRef] [PubMed]
 
Schrier RW. Cardiorenal versus renocardiac syndrome: is there a difference? Nat Clin Pract Nephrol. 2007;3(12):637. [CrossRef] [PubMed]
 
Ronco C. Cardiorenal and renocardiac syndromes: clinical disorders in search of a systematic definition. Int J Artif Organs. 2008;31(1):1-2. [PubMed]
 
Ronco C, McCullough P, Anker SD, et al; Acute Dialysis Quality Initiative (ADQI) consensus group. Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative. Eur Heart J. 2010;31(6):703-711. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1  M-mode of the inferior vena cava (IVC) obtained from a subcostal longitudinal view. The IVC maximal diameter measured at 2.69 cm.Grahic Jump Location
Figure Jump LinkFigure 2  Apical 5C view of the pulse-wave Doppler of the left ventricular outflow tract (LVOT). The velocity time integral of the LVOT was calculated to be 23.2 cm2.Grahic Jump Location
Figure Jump LinkFigure 3  Apical 5C view of the pulse-wave Doppler of the LVOT. The velocity time integral of the LVOT was calculated to be 21.4 cm2. See Figure 2 legend for expansion of abbreviation.Grahic Jump Location
Figure Jump LinkFigure 4  Tricuspid annular plane systolic excursion (TAPSE) obtained on M-mode for an apical 4C view. TAPSE was 2.5 cm.Grahic Jump Location
Figure Jump LinkFigure 5  Cardiac anatomy shown in an apical 4C view.Grahic Jump Location
Figure Jump LinkFigure 6  Cardiac anatomy of an apical 5C view with corresponding PW Doppler of the LVOT. Please note that the aortic valve closure occurring at the end of Doppler signal signifies proper positioning of the gate of the Doppler in the LVOT. PW = pulse wave. See Figure 2 legend for expansion of other abbreviation.Grahic Jump Location
Figure Jump LinkFigure 7  Anatomy shown for a subcostal longitudinal view of the IVC with the corresponding M-mode of the IVC. Please note placement of M-mode cursor is 2 cm below the junction of the right atrium. See Figure 1 legend for expansion of abbreviation.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ] UOP, Fluid Balance Per Day, and Corresponding Serum Creatinine During the Initial ICU Stay

Cr = creatine; CRRT = continuous renal replacement therapy; UOP = urine output.

a 

CRRT.

Video 1A

Subxiphoid Long-axis IVC

Running Time: 0:02

Video 1B

Apical 4-C view ACP

Running Time: 0:06

Video 1C

Lung Utraound with Diffuse B-line Pattern

Running Time: 0:06

Discussion Video

Discussion Video

Video 2

Apical 4-C resolution of ACP

Running Time: 0:06

References

Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997;111(1):209-217. [CrossRef] [PubMed]
 
Narasimhan M, Koenig SJ, Mayo PH. Advanced echocardiography for the critical care physician: part 1. Chest. 2014;145(1):129-134. [CrossRef] [PubMed]
 
Narasimhan M, J Koenig S, Mayo PH. Advanced echocardiography for the critical care physician: part 2. Chest. 2014;145(1):135-142. [CrossRef] [PubMed]
 
Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F. Echo-Dopler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med. 2002;166(10):1310-1319. [CrossRef] [PubMed]
 
Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J. 1984;107(3):526-531. [CrossRef] [PubMed]
 
Vieillard-Baron A, Schmitt JM, Augarde R, et al. Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis. Crit Care Med. 2001;29(8):1551-1555. [CrossRef] [PubMed]
 
Jardin F, Vieillard-Baron A. Is there a safe plateau pressure in ARDS? The right heart only knows. Intensive Care Med. 2007;33(3):444-447. [CrossRef] [PubMed]
 
Schrier RW. Cardiorenal versus renocardiac syndrome: is there a difference? Nat Clin Pract Nephrol. 2007;3(12):637. [CrossRef] [PubMed]
 
Ronco C. Cardiorenal and renocardiac syndromes: clinical disorders in search of a systematic definition. Int J Artif Organs. 2008;31(1):1-2. [PubMed]
 
Ronco C, McCullough P, Anker SD, et al; Acute Dialysis Quality Initiative (ADQI) consensus group. Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative. Eur Heart J. 2010;31(6):703-711. [CrossRef] [PubMed]
 
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