Research Article

The PIEPEAR Workflow: A Critical Care Ultrasound Based 7-Step Approach as a Standard Procedure to Manage Patients with Acute Cardiorespiratory Compromise, with Two Example Cases Presented

Table 2

Applying PIEPEAR workflow to case 1.

OutlinesApplication

1.
Problems emerged?
Acute circulatory compromise emerged—severe dyspnea+abundant flesh-colored endotracheal secretions
Acute respiratory compromise emerged—cardiac arrest +heart rate increase+oliguria+elevated lactate

2.
Information clear?
(1) No evidence of dysfunction of heart and lung before admission
(2) Stable after surgery
(3) Newly presented anxiety and dyspnea after transfusion and cardiac arrest, awake after 20 min’s CPR, ABG showed severe hypoxia and extremely hypercapnia after intubated

3.
Focused exam launched
Heart browse: no circumstances that need immediate life-saving intervention or cardiologist emergency consultation, no signs of valvular diseases 
IVC exam: no fluid responsiveness, maybe hypervolemia because of no collapse during respiration, and hepatic vein enlarged (Figure 2(a)) 
RV exam: no right ventricular failure that may harm the function of left ventricle or misleading the therapy 
Diastole of left heart: Restrictive diastolic dysfunction was presented and PAOP estimated by E/e’ was increased(Figure 2(b))  
Systole of left heart: a filling cavity, mild to moderate dysfunction, no RWMA 
Afterload: increased
Bilateral inferior and lateral B pattern, with posterior atelectasis and plural effusion, indicate diffuse sonographic interstitial syndrome (Figure 2(c))

4.
Pathophysiologic changes reported
Pulmonary edema, hypervolemic and cardiogenic as CCUS indicates; increased-permeability pulmonary edema may also be suspected when involved with the history of transfusion

5.
Etiology explored
(1) (1) Acute hypervolemic and cardiogenic pulmonary edema (2)Transfusion-related acute lung injury?  
(2) Test BNP, WBC, test the albumin of the endotracheal secretions, CXR when possible, repeat ABG are needed

6.
Action
Diuresis to eliminate extra fluid, PEEP increase to reaerate the alveolar, continuing draining the secretions
Continue cortisone, and further using blood products was prohibited

7.
Recheck to adjust
PAOP and B lines decreased after 200ml urine in two hours  
Two hours later, oxygen improved as well as the internal environment (PO2 increased from 56 to 125mmHg, Lac decreased from 16 to 11.8 mmol/l, pro-BNP35000 pg/ml, CXR revealed bilateral symmetrical infiltration, Figure 3(a))  
Confirm: acute hypervolemic edema existed; the current treatment should be continued.  
Ratio of protein in ETA to protein in plasma was 0.8 (31.7/39.6). The strength of ventilator also decreased the next day. Lung ultrasound showed bilateral A-lines(Figure 4) and the second day’s CXR revealed that bilateral pulmonary edema was obviously decreased, as shown in Figure 3(b).  
Final diagnosis: TRALI associated hypervolemic pulmonary edema.

CPR: cardiopulmonary resuscitation; ABG: arterial blood gases; IVC: Inferior vena cava; RV: right ventricle; PAOP: pulmonary artery occlusion pressure; E/e’: early diastolic transmitral velocity to early mitral annulus diastolic velocity ratio; RWMA: regional wall motion abnormality; CCUS: critical care ultrasound; PEEP: Positive End Expiratory Pressure; BNP: brain natriuretic peptide; WBC: white blood cell; CXR: chest X ray; ETA: Endotracheal aspiration; TRALI: transfusion related acute lung injury.