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\begin{document}

\title{Flash pulmonary edema in the cardiac catheterization laboratory: A case
report}



\author[1]{Maryam Mehrpooya}%
\author[1]{Mohammad Reza Eftekhari}%
\author[1]{Tara Moghaddasfar}%
\affil[1]{Tehran University of Medical Sciences}%


\vspace{-1em}



  
  \date{May 25, 2024}


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\selectlanguage{english}
\begin{abstract}
We report a 51-year-old female with a history of a degenerated aortic
bioprosthesis and severe valvular dysfunction who was admitted for redo
valve surgery and unexpectedly developed acute flash pulmonary edema, a
dramatic form of cardiogenic pulmonary edema before coronary angiography
and was managed by timely and proper treatment.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Flash pulmonary edema (FPE) is a remarkable and life-threatening
condition caused by an imbalance in the fluid homeostasis in the
pulmonary vascular bed, which results from elevated left-sided cardiac
filling pressures along with endothelial dysfunction and increased
permeability of pulmonary capillaries.\textsuperscript{(1, 2)}

Common causes of FPE are myocardial ischemia, hypertensive emergencies,
tachyarrhythmias, and acute mitral or aortic valve regurgitation.
Bilateral atheromatous renovascular disease and pheochromocytoma are
also other predisposing factors.\textsuperscript{(3)}

FPE can occur during cardiac catheterization procedures at any time. The
immediate diagnosis and management of this critical condition are
imperative to stabilize the patient as soon as possible and prevent
unfortunate consequences.

This report presents a 51-year-old female with a history of
hypertension, degenerated bioprosthetic aortic valve, and severe
valvular dysfunction who was a candidate for redo valve surgery and
developed acute FPE before coronary angiography.

\textbf{Case Presentation}

The patient was a 51-year-old female with a history of hypertension and
biological aortic valve replacement surgery 21 years ago who was
referred to our hospital for dyspnea. Electrocardiogram revealed sinus
rhythm and incomplete left bundle branch block. Transthoracic
echocardiography demonstrated normal left ventricular (LV) systolic
function and severe LV diastolic dysfunction. Mild LV hypertrophy was
also observed. There was a flail bioprosthetic leaflet due to the
degeneration of aortic bioprosthesis resulting in severe aortic
regurgitation and severe aortic stenosis (Video S1, Video S2, Video S3).
Furthermore, severe posteriorly directed mitral regurgitation was
detected. The patient was admitted for redo aortic valve replacement and
mitral valve surgery, and she was submitted to coronary angiography
before the surgery due to chest discomfort and electrocardiographic
changes. In the catheterization laboratory, she had a blood pressure of
about 160 over 90 mmHg after placing the sheath in the right femoral
artery. Prior to the procedure, the patient gradually developed dyspnea
and severe orthopnea. Her blood pressure rose to 270 over 130 mmHg
(Figure 1), and she had a respiratory rate of 30 per minute, a heart
rate of 120 per minute, and an oxygen saturation of 89 percent in the
room air. Diffuse rales were heard in both lungs. Her situation suddenly
exacerbated, and clinical evidence of FPE was apparent. She was placed
in a semi-setting position, and supplemental oxygen therapy with a mask
was started. Resuscitation equipment was prepared. ECG was obtained, but
it did not show any new changes. Intravenous nitroglycerine and
furosemide were soon administered. Nitroglycerin infusion was started at
a rate of 30 micrograms per minute and the dose doubled every 15 minutes
up to 90 micrograms per minute. She also received three doses of 40
milligrams of furosemide at 20-minute intervals. After about an hour
with the continuation of the vasodilator, loop diuretic therapy, and
respiratory support under hemodynamic monitoring, the patient's
condition improved clinically, and she was stabilized. Coronary
angiography was performed and showed no significant lesion. Two days
later, she underwent aortic and mitral valve replacement surgery. The
timeline of the events is shown in Table 1.

\textbf{Discussion}

We discussed the case of a middle-aged female with acute respiratory
distress and elevation of blood pressure in the cardiac catheterization
laboratory in favor of FPE.

Acute cardiogenic pulmonary edema is a common and critical condition
caused by increased LV end-diastolic and left atrial (LA) pressures,
which are retrogradely transmitted to the pulmonary venous and the
capillary system. It consequently increases the hydrostatic pressure
across pulmonary capillaries, resulting in fluid accumulation within the
lung interstitium and alveoli.\textsuperscript{(1)} FPE is a
life-threatening and extreme form of cardiogenic pulmonary edema which
develops within minutes. It is related to a sudden rise in cardiac
filling pressures as well as endothelial dysfunction and increased
permeability of pulmonary capillaries, which are the key features to
distinguish FPE from cardiogenic pulmonary edema where we solely have
elevated filling pressures.\textsuperscript{(2)}

Exaggerated sympathetic activity and increased activity of the
renin-angiotensin-aldosterone system (RAAS) are etiologies known to play
essential roles in developing FPE.\textsuperscript{(2)} Catecholamines
increase heart rate and reduce diastolic filling time of the LV, which
notably in patients with diastolic dysfunction results in impaired
diastolic filling and therefore elevation of LA and pulmonary venous
pressures.\textsuperscript{(4)} Both sympathetic hyperactivity and
activation of RAAS caused by catecholamines raise systemic vascular
resistance and precipitate acute elevation of blood pressure. The
augmented afterload results in increased LV wall stress and the
imbalance between oxygen demand and supply, leading to even more
diastolic dysfunction and elevation of filling
pressures.\textsuperscript{(2)} Endothelial dysfunction and excessive
permeability of the pulmonary capillaries are other consequences of
catecholamines.\textsuperscript{(2, 4)} Besides systemic RAAS,
activation of intrapulmonary RAAS contributes to fluid accumulation
within pulmonary interstitial and alveolar areas by increasing pulmonary
capillary permeability.\textsuperscript{(2)}

FPE was reported in some other clinical conditions. Several reports
discussed FPE associated with renal artery stenosis and excessive
renin-angiotensin-aldosterone system activity. Symptoms were improved
after revascularization of the renal artery in these
cases.\textsuperscript{(5-7)} Naman Agrawal et al. in 2016 described
sympathetic crashing acute pulmonary edema as the most severe entity of
acute pulmonary edema, which must be treated with noninvasive
ventilation and intravenous nitrate started in
minutes.\textsuperscript{(4)} In a case report by Catrina Patr\selectlanguage{ngerman}ício et
al. in 2014, a 64-year-old woman was reported who was admitted to the
emergency department with FPE due to acute severe aortic
insufficiency.\textsuperscript{(8)}

FPE may develop in the cardiac catheterization laboratory at any time
during the procedure. The diagnosis of FPE is based on clinical
evaluation. Rapid progression of dyspnea and hypoxemia indicates the
necessity of prompt diagnosis and management to avoid the need for
mechanical ventilation and adverse outcomes.

It seems that activation of the sympathetic system secondary to extreme
anxiety in combination with severe valvular dysfunction and severe LV
diastolic dysfunction predisposed our patient to FPE.

History and physical examination are the most valuable tools for better
determination of this event.\textsuperscript{(2)} Patients may have a
history of LV diastolic dysfunction, systemic hypertension, or severe
valvular dysfunction. The presence of bilateral renal artery stenosis or
pheochromocytoma must be noted. Moreover, acute events such as
tachyarrhythmias, acute mitral or aortic valve regurgitation, myocardial
ischemia, and hypertensive crisis commonly predispose patients to
FPE.\textsuperscript{(2, 3)} Patients usually present with respiratory
distress, orthopnea, tachypnea, and diaphoresis. Assessment of blood
pressure, heart rate, and oxygen saturation must be done. Elevated blood
pressure, tachycardia, and hypoxemia are common. Auscultation may reveal
rales, S3 gallop, and valvular murmurs. Jugular venous pressure may be
elevated, although it may be hard to measure. 12-lead ECG and bedside
echocardiography are also helpful.\textsuperscript{(3, 9)}

Immediate initiation of high-dose intravenous nitroglycerine must be
done in the first step because of its vasodilatory effect on the
arterial system. The aim is to reduce the afterload and cut the vicious
cycle of sympathetic and RAAS hyperactivity as soon as
possible.\textsuperscript{(4)} Intravenous loop diuretics may also be
helpful. Since FPE is basically caused by fluid redistribution rather
than volume overload, and the diuretic effect of furosemide starts in 30
minutes at the earliest, the effect of loop diuretics is mostly due to
their vasodilator instead of diuretic activity.\textsuperscript{(2,
4)}Supplemental oxygen therapy should be administered for hypoxemia as
well. Once the patient is stabilized, further evaluation and
determination of the cause of FPE must be
performed.\textsuperscript{(2)}

\textbf{Conclusion}

Flash pulmonary edema is not a rare clinical condition and may happen in
critical situations, especially in the catheterization laboratory. This
case highlights the value of urgent diagnosis and initiation of
appropriate treatment in order to avoid catastrophic consequences.

\textbf{Author Contributions:}

\textbf{Maryam Mehrpooya:~} Conceptualization; data curation;
supervision; validation; writing -- review and editing.

\textbf{Mohammad Reza Eftekhari:~} Software; data curation; writing --
review and editing.

\textbf{Tara Moghaddasfar:} ~Conceptualization; methodology; writing --
original draft; resources; project administration; writing -- review and
editing.\textbf{~}

\textbf{Acknowledgments}

None.

\textbf{References}

1. Ware LB, Matthay MA. Acute pulmonary edema. New England Journal of
Medicine. 2005;353(26):2788-96.

2. Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F. Flash pulmonary
edema. Progress in cardiovascular diseases. 2009;52(3):249-59.

3. Ingbar DH. Cardiogenic pulmonary edema: mechanisms and treatment-an
intensivist's view. Current opinion in critical care. 2019;25(4):371-8.

4. Agrawal N, Kumar A, Aggarwal P, Jamshed N. Sympathetic crashing acute
pulmonary edema. Indian Journal of Critical Care Medicine:
Peer-reviewed, Official Publication of Indian Society of Critical Care
Medicine. 2016;20(12):719.

5. Cimen T, Algul E, Efe TH, Sunman H, Yeter E. Flash pulmonary edema: A
rare cause and possible mechanisms. Turkish Journal of Emergency
Medicine. 2017;17(2):65-7.

6. Planken I, Rietveld A. Rapid onset pulmonary edema (flash edema) in
renal artery stenosis. The Netherlands journal of medicine.
1998;52(3):116-9.

7. Vohra H, Osman F, Singh H, Vohrah A, Dimitri W, editors. Flash
pulmonary edema manifesting for the first time after cardiac surgery:
case report. Heart Surg Forum; 2005.

8. Patrício C, da Silva FP, Brotas V. Pulmonary oedema in the emergency
room: what is hidden beyond an apparently common presentation. Case
Reports. 2014;2014:bcr2014204131.

9. Murray J. Pulmonary edema: pathophysiology and diagnosis. The
International journal of tuberculosis and lung disease.
2011;15(2):155-60.

\textbf{Figure Legend}

Figure 1

Femoral arterial pressure tracing when the patient's condition started
to exacerbate, showing a pressure of about 270 over 130 mmHg.

Table 1

Timeline of clinical events.

\textbf{Hosted file}

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