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95-Year-Old Woman With Sudden-Onset Dyspnea

      A 95-year-old woman presented with sudden-onset dyspnea of 4 hours' duration, which was soon followed by respiratory failure requiring high-flow supplemental oxygen. She denied having chest pain, back pain, or palpitations. She had completed a course of amoxicillin 2 months previously for acute sinusitis and had no residual symptoms. Results of a complete review of systems were otherwise unremarkable.
      Her medical history was notable for systemic hypertension, pulmonary hypertension, chronic severe mitral regurgitation related to degenerative mitral valve disease with prolapse, and moderate functional tricuspid regurgitation. She had no personal history of coronary artery disease or congestive heart failure. Medications included amlodipine, atenolol, chlorthalidone, fluticasone, and dicyclomine.
      On arrival at the emergency department her vital signs were as follows: blood pressure, 194/110 mm Hg; pulse, 137 beats/min; temperature, 36.5°C; respiratory rate, 36 breaths/min; and oxygen saturation while receiving 15 L of oxygen per minute by closed face mask, 91%. She had markedly increased work of breathing. Cardiovascular examination demonstrated jugular venous distention to the ear with a prominent v wave, irregularly irregular tachycardia, right ventricular lift without thrill, an S3 gallop at the apex, a blowing holosystolic murmur appreciated throughout the precordium, and 2 mm of pitting edema of the mid shins bilaterally. Pulmonary examination revealed coarse crackles throughout the basilar half of both lung fields. Abdominal, musculoskeletal, neurologic, and integument findings were unremarkable. Chest radiography demonstrated the new findings of pulmonary venous congestion and bilateral effusions.
      • 1
        Which one of the following is the most likely cause of this patient's dyspnea?
        • a
          Flash pulmonary edema (FPE)
        • b
          Pneumonia
        • c
          Acute respiratory distress syndrome
        • d
          Chronic obstructive lung disease (COPD)
        • e
          Pulmonary embolism
      The radiographic findings, taken in clinical context, suggest rapid onset of left-sided congestive heart failure (ie, FPE).
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Although community-acquired pneumonia may present with highly nonspecific symptoms in the elderly, this is an unlikely diagnosis, given the absence of cough, fever, chills, or isolated focal infiltrate.
      • Ray P.
      • Birolleau S.
      • Lefort Y.
      • et al.
      Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis.
      This patient does not meet criteria for acute respiratory distress syndrome because cardiogenic pulmonary edema cannot be excluded.
      • Villar J.
      • Blanco J.
      • Kacmarek R.M.
      Acute respiratory distress syndrome definition: do we need a change?.
      Exacerbation of COPD is unlikely, given the absence of smoking or COPD history and other hallmarks, such as increased sputum volume or purulence.
      • Ray P.
      • Birolleau S.
      • Lefort Y.
      • et al.
      Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis.
      Radiographic findings by plain radiograph of pulmonary embolism may be nonspecific or completely absent but do not typically include pulmonary edema.
      • Srivastava S.D.
      • Eagleton M.J.
      • Greenfield L.J.
      Diagnosis of pulmonary embolism with various imaging modalities.
      The patient was transiently treated with positive airway pressure (PAP) in the emergency department. Electrocardiography revealed atrial fibrillation with a rapid ventricular rate (137 beats/min). She received intravenous (IV) diltiazem and enalapril, and her heart rate and blood pressure improved to 85 beats/min and 115/56 mm Hg, respectively. Her initial troponin value was less than 0.01 ng/mL. Her N-terminal pro-B-type natriuretic peptide level was elevated to 3223 pg/mL (reference range, 5-263 pg/mL).
      On arrival at the ward, the patient still reported considerable dyspnea. Her oxygen saturation while receiving 10 L of oxygen per minute by closed face mask was 90%.
      • 2
        Which one of the following is the most appropriate next step in the management of this patient?
        • a
          Administer IV furosemide
        • b
          Transesophageal echocardiography–guided cardioversion
        • c
          Administer IV levofloxacin
        • d
          Cardiothoracic surgery consultation
        • e
          Transfer to intensive care unit setting for bilevel positive airway pressure (BiPAP)
      To address the patient's impending respiratory failure and off-load atrial stretch, pulmonary edema should be addressed first. This involves administration of IV diuretic therapy in addition to judicious use of agents for afterload reduction as necessary.
      • Follath F.
      • Yilmaz M.B.
      • Delgado J.F.
      • et al.
      Clinical presentation, management and outcomes in the Acute Heart Failure Global Survey of Standard Treatment (ALARM-HF).
      Transesophageal echocardiography–guided cardioversion is premature at this point, given the absence of hemodynamic instability or failure of conservative measures.
      • Aronow W.S.
      Management of atrial fibrillation in the elderly.
      Antibiotic therapy is not indicated in the absence of clinical suspicion of pneumonia. No acute surgical concerns, such as acute mitral regurgitation or ventricular rupture, have been identified at this juncture to warrant emergent consultation. Although continuous positive airway pressure (CPAP) decreases intubation rates and improves survival in respiratory failure due to pulmonary edema, there is insufficient evidence to recommend use of its bilevel counterpart (BiPAP) in the absence of documented hypercapnia.
      • Agarwal R.
      • Aggarwal A.N.
      • Gupta D.
      • Jindal S.K.
      Non-invasive ventilation in acute cardiogenic pulmonary oedema.
      Given that the patient's condition stabilized with PAP in the emergency department, it is reasonable to attempt diuresis before escalation of care.
      The patient had a brisk response to intermittent loop diuretic therapy with improvement in respiratory status. Her oxygen requirement was weaned to 1 L/min by nasal cannula. β-Blocker therapy was titrated to maintain an acceptable resting heart rate. Intravenous heparin was continued because of persistent atrial fibrillation. Serial troponin values were 0.03 and 0.03 at 3 and 6 hours, respectively.
      • 3
        Given these findings, which one of the following is the most likely cause for acute decompensation in this patient?
        • a
          Advanced age
        • b
          Infective endocarditis
        • c
          Dietary indiscretion
        • d
          Nonadherence to diuretic therapy
        • e
          Atrial fibrillation with rapid ventricular rate
      Advanced age is a risk factor for multiple precipitants of decompensated heart failure but is not a sufficient single explanation.
      • Michalsen A.
      • Konig G.
      • Thimme W.
      Preventable causative factors leading to hospital admission with decompensated heart failure.
      No case information provided thus far meets criteria for infective endocarditis such as fever or evidence of systemic embolism or immunologic phenomena.
      • Baddour L.M.
      • Wilson W.R.
      • Bayer A.S.
      • et al.
      Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America.
      Dietary indiscretion and medication nonadherence are very common forms of noncompliance and represent the leading cause of acute decompensation of heart failure.
      • Michalsen A.
      • Konig G.
      • Thimme W.
      Preventable causative factors leading to hospital admission with decompensated heart failure.
      However, there is no patient history of noncompliance, and the finding of rapid atrial fibrillation with years of preexisting severe mitral regurgitation provides a more ready explanation.
      The care team sought to reassess the patient's valvular disease in order to further define the reason for acute decompensation. Specifically, the possibility of a flail mitral leaflet had been posed earlier in the course and required further evaluation.
      • 4
        Which one of the following is the most appropriate modality for reassessment of the patient's mitral valve?
        • a
          Electrocardiography
        • b
          Transthoracic echocardiography
        • c
          Transesophageal echocardiography
        • d
          Cardiac magnetic resonance imaging
        • e
          Cardiac computed tomography
      Although sequelae of mitral regurgitation such as left atrial enlargement and left ventricular hypertrophy can be observed on electrocardiography,
      • Carabello B.A.
      Progress in mitral and aortic regurgitation.
      alternative modalities are superior and are required for visualization of the valves. Transthoracic echocardiography is sufficient for nonoperative evaluation of the mitral valve.
      • Monin J.L.
      • Dehant P.
      • Roiron C.
      • et al.
      Functional assessment of mitral regurgitation by transthoracic echocardiography using standardized imaging planes: diagnostic accuracy and outcome implications.
      Transesophageal echocardiography, cardiac magnetic resonance imaging, and cardiac multidetector- row computed tomography can play important roles in perioperative imaging but are not indicated here.
      • Monin J.L.
      • Dehant P.
      • Roiron C.
      • et al.
      Functional assessment of mitral regurgitation by transthoracic echocardiography using standardized imaging planes: diagnostic accuracy and outcome implications.
      The transthoracic echocardiogram revealed severe mitral valve regurgitation due to an unsupported posterior leaflet, severe tricuspid regurgitation, severely increased right ventricular systolic pressure (78 mm Hg at a systolic blood pressure of 121 mm Hg), and severe biatrial enlargement. The left ventricular ejection fraction was preserved (74%).
      The mounting dilemma of cardiac surgical intervention in patients of very advanced age requires careful assessment of health-related quality of life.
      • Rumsfeld J.S.
      Valve surgery in the elderly: question of quality (of life)?.
      After considerable discussion and given the patient's age and preference, surgical considerations for definitive management of mitral regurgitation were not judged reasonable. Transcatheter mitral valve clip devices were not available at our institution at the time of her presentation. We therefore elected to proceed with medical management.
      • 5
        Which one of the following dismissal medications is least indicated in this patient?
        • a
          Metoprolol succinate
        • b
          Furosemide
        • c
          Lisinopril
        • d
          Coumadin
        • e
          Spironolactone
      β-Blockade provides a mechanism of rate control for atrial fibrillation and has been found to improve survival in patients with severe mitral regurgitation and normal ejection fraction.
      • Varadarajan P.
      • Joshi N.
      • Appel D.
      • Duvvuri L.
      • Pai R.G.
      Effect of Beta-blocker therapy on survival in patients with severe mitral regurgitation and normal left ventricular ejection fraction.
      Diuretic therapy is indicated for management of volume and symptoms but has not been found to result in survival benefit.
      • Ramani G.V.
      • Uber P.A.
      • Mehra M.R.
      Chronic heart failure: contemporary diagnosis and management.
      By the reduction of left ventricular afterload, angiotensin-converting enzyme inhibition improves exercise tolerance and echocardiographic indices in severe mitral regurgitation, and is particularly beneficial in the setting of concomitant systemic hypertension,
      • Sekuri C.
      • Utuk O.
      • Bayturan O.
      • Bilge A.
      • Kurhan Z.
      • Tavli T.
      Effect of losartan on exercise tolerance and echocardiographic parameters in patients with mitral regurgitation.
      but it has yet to be found to confer a definite survival benefit. The patient's CHA2DS2-VASc score is 5, with points assigned for heart failure, hypertension, age, and sex. This confers an ischemic stroke risk of 6.7% per year without anticoagulation.
      • Olesen J.B.
      • Lip G.Y.
      • Hansen M.L.
      • et al.
      Validation of risk stratification schemes for predicting stroke and thromboembolism in patients with atrial fibrillation: nationwide cohort study.
      It should be noted that both CHADS2 and CHA2DS2-VASc risk stratification schemes were validated for nonvalvular atrial fibrillation. Age alone in an otherwise highly functional patient is not a contraindication. Spironolactone is recommended only in symptomatic patients with depressed left ventricular ejection fraction.
      • Ramani G.V.
      • Uber P.A.
      • Mehra M.R.
      Chronic heart failure: contemporary diagnosis and management.
      The patient was transitioned from IV to oral furosemide. Amlodipine was discontinued in favor of lisinopril with addition of metoprolol succinate (instead of atenolol) for rate control therapy of atrial fibrillation. With incremental β-blockade and diuresis, the patient's atrial fibrillation was rate-controlled well and her symptoms resolved promptly. Because of this response, rate control therapy with anticoagulation, rather than attempts to restore sinus rhythm, was pursued. Lisinopril was judged a reasonable choice, given low suspicion for bilateral renal artery stenosis. After safety evaluation, anticoagulation with warfarin was started. The patient was dismissed to home in stable condition.

      Discussion

      Flash pulmonary edema is a term used to describe rapid accumulation of fluid within the lungs due to acute elevation in left ventricular end-diastolic pressure.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Clinically, 3 distinct stages are observed, beginning with distention of small pulmonary vessels as a consequence of elevated left atrial pressure. This pressure increase is transmitted across the pulmonary venous bed to the pulmonary capillaries, resulting in pulmonary edema (stage 2). Initially, fluid accumulates in the interstitial space but invades the alveolar space once the epithelial barrier is compromised.
      • West J.B.
      Invited review: pulmonary capillary stress failure.
      Stage 3 is marked by hypoxia and dyspnea due to diminished alveolar gas exchange.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Causes of FPE are similar to those of acute decompensated heart failure, including myocardial ischemia, uncontrolled hypertension, atrial arrhythmia, and volume overload.
      • Michalsen A.
      • Konig G.
      • Thimme W.
      Preventable causative factors leading to hospital admission with decompensated heart failure.
      Patients with FPE, however, are felt to have higher susceptibility to the same pathophysiologic insults. This may result from patient factors such as increased renin-angiotensin-aldosterone system activity, impaired nitric oxide synthesis, or increased sympathetic activation.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Flash pulmonary edema can occur without baseline predisposition if there is an acute process such as chordae tendineae rupture.
      In the present case, the patient's rapid decompensation is consistent with FPE. The precise cause is unclear. The episode was likely precipitated by spontaneous conversion into atrial fibrillation with rapid ventricular rate. Acute spontaneous rupture of chordae tendineae was unlikely the precipitating event because the patient already had chronic severe mitral regurgitation. Hypertensive urgency likely represented a sympathetic response to respiratory distress because acute systemic hypertension is a classic feature of FPE.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Acute treatment of FPE is aimed at hemodynamic stabilization and symptomatic relief. Loop diuretics are widely regarded as initial therapy with roles in both volume removal and vasodilation.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.
      Additional vasodilators, such as nitroglycerin, are helpful to relieve pulmonary congestion and reduce both left ventricular preload and afterload.
      • Follath F.
      • Yilmaz M.B.
      • Delgado J.F.
      • et al.
      Clinical presentation, management and outcomes in the Acute Heart Failure Global Survey of Standard Treatment (ALARM-HF).
      This patient's management was unique in that initial management also involved rate control of rapid atrial fibrillation. Flash pulmonary edema is a common clinical entity that requires rapid recognition because of its high mortality. Identification of triggers and prompt intervention are critical.
      • Rimoldi S.F.
      • Yuzefpolskaya M.
      • Allemann Y.
      • Messerli F.
      Flash pulmonary edema.

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