SCAPE

 

Acute heart failure (AHF) is a common emergency routinely seen in clinical practice. The timely recognition and intervention by an emergency physician (EP) is important to prevent mortality and further morbidity in such patients.

Hypertensive AHF is a distinct subgroup where there is increase in afterload and decrease in venous capacitance, leading to a shift of fluid from splanchnic circulation to pulmonary circulation. Sympathetic crash acute pulmonary oedema (SCAPE) is a life-threatening condition due to the increased systemic vascular resistance and rapid redistribution of fluid caused by a sympathetic surge.

Pathophysiology

Sympathetic activity that causes an abrupt increase in catecholamine release, subsequently increasing venous and arterial tone, SCAPE is a subset of acute hypertensive heart failure syndromes (AHFS) and is a hypertensive emergency with acute heart failure,

• Left Ventricular Dysfunction leads to an abrupt increase in sympathetic tone and the release of catecholamines.
• Intense sympathetic activity causes both venous and arterial tone to increase significantly, resulting in diastolic failure.
• Increased catecholamines cause an elevated heart rate and decreased diastolic time.
• Activation of the renin–angiotensin–aldosterone system (RAAS) further worsens diastolic stiffening and increased diastolic pressures, leading to pulmonary fluid overload.
• Increased sympathetic tone adversely affects the pulmonary circulation by increasing permeability and/or provoking stress failure of the pulmonary capillaries.

• SCAPE occurs due to a vicious spiral involving increasing sympathetic outflow, excessive afterload, and progressively worsening heart failure. 
• SCAPE patients may be euvolemic or hypovolemic. The problem is a shift of fluid into the lungs, rather than hypervolemia.

 Nomenclature

• SCAPE is known by a variety of different terms throughout the scientific literature, most notably:
• Flash pulmonary edema (this is becoming less popular).
• Hypertensive acute heart failure (preferred terminology in hypertension journals).
• SCAPE (increasingly utilized in emergency medicine and critical care journals).
• SCAPE is currently the preferred terminology, since it is clear and unique

 

 

 

Diagnosis

Diagnosis of SCAPE is clinical.

Abrupt onset of shortness of breath which progresses over minutes‑to‑hours into life‑threatening pulmonary edema. Patients present with extremely severe respiratory distress. They are restless, diaphoretic, and hypoxic on arrival to the ED. There are tachycardia and marked hypertension, suggesting elevated sympathetic activity in vivo.SCAPE is a subset of hypertensive heart failure, and hence almost always presents with high systolic blood pressure. Extensive bilateral crepitations are present of chest auscultation. These patients are too unstable and orthopneic to lie down for performing a 12‑lead ECG at the time of arrival

 

Diagnostic criteria of Sympathetic Crashing Acute Pulmonary Edema (SCAPE):

Diagnostic Criteria	Description
1. Sudden Onset of Severe Shortness of Breath	·       Rapid and intense difficulty in breathing, occurring within minutes to hours. (<6 hours)
2. Hypoxia	·       Oxygen saturation (SpO₂) <90%.
3. Blood Pressure	·       Either systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥100 mmHg ·       mean arterial pressure >120 mmHg).
4. Lung Findings	·       Crepitations: Abnormal lung sounds (crackles) heard on auscultation in all lung fields. ·       B Profile: Abnormal lung ultrasound pattern (B-lines) observed in all lung zones.
5. Features of Sympathetic Over-Surge	·       Diaphoresis: Excessive sweating. ·       Agitation: Restlessness or anxiety. ·       Tachycardia: Elevated heart rate.

POCUS

·       Diffuse B-lines throughout the chest, with a thin pleural interface

·       Small bilateral pleural effusions may further support the diagnosis of cardiogenic pulmonary edema.

·       Cardiac ultrasonography may show

o   Systolic heart failure, with reduced left ventricular ejection fraction.

o   Diastolic heart failure may be suggested by left ventricular hypertrophy and a dilated left atrium.

·       ⚠️ Note that SCAPE patients may be hypovolemic, hypervolemic, or euvolemic. Therefore, the IVC will not necessarily be distended (nor will the patient necessarily have distended jugular veins).

Chest X Ray

• Bilateral, fluffy infiltrates centered in the hila (“bat wing pulmonary edema”).
• Kerley B lines (fluid in the interlobular septa causing fine lines perpendicular to the pleura).
• Pleural effusion(s).
• Lack of an alternative diagnosis (e.g., absence of pneumothorax or lobar pneumonia).

Brain natriuretic peptide (BNP)

There is no evidence that BNP testing adds clinical information above and beyond the combination of clinical judgement and POCUS for patients with heart failure.

BNP test is too long to be clinically useful for the immediate bedside management of SCAPE.

·       💡 SCAPE is a bedside clinical diagnosis which must be reached within minutes (on the basis of history, examination, and POCUS).

 

Treatment

SCAPE is not a diagnostic dilemma. Early recognition and prompt initiation of treatment is the key to preventing morbidity and mortality. Immediate ED management of severe pulmonary edema has its impact on subsequent clinical course, rates of invasive mechanical ventilation, and rates of Intensive Care Unit (ICU) admissions.

 

Non-invasive ventilation

• Acute pulmonary edema is a class 1 indication for NIV
•  NIV provides oxygenation.
•  Stents open the flooded alveoli.
• Decreases dead space ventilation.
• Decreases preload and afterload, thereby decreasing cardiac oxygen demand workload.

NIV is associated with decreased rates of invasive mechanical ventilation and decreased mortality in patients with cardiogenic pulmonary edema, thereby decreasing the rates of associated complication.

• One effective way of using NIV pressures in treatment of SCAPE is to begin with expiratory pressures (CPAP/expiratory positive airway pressure) of 6 cmH2 O which is rapidly increased to 12–14 cmH2 O. Once there is a clinical improvement, pressures are then sharply decreased to 6–8 cmH2 O and then titrated to patient’s requirements.
• ⚠️ Perhaps the most common pitfall in management of SCAPE is failure to up-titrate CPAP or BiPAP settings. Up titrating the airway pressure will cause an instantaneous reduction in preload and afterload, which might be faster and more reliably effective than any medication.

 

Nitrates

Use of nitrates in SCAPE differs from that of other varieties of AHFS. Intense sympathetic activity causes both venous and arterial tone to increase significantly causing diastolic failure. Hence, the aim is to decrease the afterload at the earliest to cut the vicious cycle caused by sympathetic upsurge. Thus, initiating the treatment with low‑dose nitrates (vasodilatory doses) with gradual titration does little to target the underlying pathophysiology.

The treatment of choice for SCAPE is a combination of high-dose NTG bolus (600 – 1000 mcg over 2 mins) followed by an infusion (100 mcg/min) and NIPPV.

sublingual nitroglycerine

• This may be utilized if a patient experiences SCAPE in a location unable to provide IV nitroglycerine (e.g., a medicine ward).
• To bridge the patient until they are able to receive IV nitroglycerine – not as an alternative to  IV nitroglycerine.
• The optimal dose is unclear, but 3-5 sublingual 400-mcg tablets q5 minutes might be reasonable. (Note that the bioavailability of sublingual nitroglycerine is only ~40%.
• Consider using the following protocol to identify which doses may be best for specific patients based on initial systolic blood pressure.
• 
  
  

 

 Fluid management

• Diuresis isn't a front-line intervention for SCAPE.
•  The key pathophysiologic problem with SCAPE is uncontrolled sympathetic outpouring and increased afterload.
• Many patients with SCAPE may be euvolemic or even hypovolemic (merely experiencing a maldistribution of fluid that shifts into the lungs)

·        The initial therapies are positive pressure ventilation and afterload control (usually with high-dose nitroglycerine). These should be instituted immediately, prior to consideration of diuretics.

• Assess the patient clinically - If there is evidence of hypervolemia, then volume removal may be beneficial (either with diuresis or dialysis).
• A benefit from volume removal is particularly supported if there is a clinical history suggestive of volume overload (e.g., nonadherence with diuretics, or missed haemodialysis sessions).

Blood pressure Control

• Excessively high blood pressure increases the afterload on the left ventricle, promoting fluid backup into the lungs.
• This is fundamental to the pathophysiology of SCAPE. Therefore, one of the essential goals of treatment is to rapidly reduce the blood pressure.
• There is no well-defined blood pressure goal, but a common target may be to reduce the systolic Bp to <~140 mm rapidly.
• maximize BiPAP/CPAP pressure and to maximize the nitroglycerine infusion dose. The vast majority of SCAPE patients can be rendered normotensive with optimization of these two therapies.
• Nicardipine or Clevidipine are useful in refractory hypertension:
• These are potent arterial vasodilators than nitroglycerine, so they may work in patients who are failing to respond to nitroglycerine.
• Useful options in patients on phosphodiesterase type-5 inhibitors (e.g., sildenafil), who have contraindications to nitroglycerine.

·       Clevidipine is ideal, due to its shorter half-life and stronger evidentiary basis in acute heart failure.

·       Nicardipine has a longer half-life, so there is a risk of causing overshoot hypotension (especially when the underlying SCAPE abates).

Opiods

• Retrospective studies have correlated the use of morphine with worse outcomes among patients with pulmonary edema.
• This shouldn't be surprising.
• morphine could mask the symptoms of pulmonary edema, prompting providers to be less aggressive with other therapies (e.g., patient doesn't look sick enough to need CPAP).
• The MIMO prospective RCT compared morphine (up to 8 mg IV) with midazolam (up to 3 mg) among patients with acute pulmonary edema.
• The study was stopped prematurely due to harm, with patients in the morphine group accruing higher rates of cardiovascular adverse events (including cardiac arrest and shock). This is only a single, relatively small trial – but it represents the highest quality data available.
• As such, opioids should arguably be avoided in the context of SCAPE (at least pending the availability of higher-quality evidence).

 

Intubation 

Intubation and use of invasive mechanical ventilation can be averted if high‑dose NTG and NIV are rapidly initiated in the emergency room.

References

1.  Agrawal N, Kumar A, Aggarwal P, Jamshed N. Sympathetic crashing acute pulmonary edema. Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit Care Med. 2016;20 (12):719–23. 
2. Paone S, Clarkson L, Sin B, Punnapuzha S. Recognition of sympathetic crashing acute pulmonary edema (SCAPE) and use of high-dose nitroglycerin infusion. Am J Emerg Med. 2018;36(8) (1526.e5–1526.e7). 
3. Mathew R, Kumar A, Sahu A, Wali S, Aggarwal P. High-dose nitroglycerin bolus for sympathetic crashing acute pulmonary edema: a prospective observational pilot study. J Emerg Med. 2021;29(61):1–7
4. Sympathetic Crashing Acute Pulmonary Edema (SCAPE) - EMCrit Project