Patients with simple volume overload present subacutely over days to weeks and are more likely to be younger, have heart failure with reduced ejection fraction, or have established coronary artery disease [5]. Nonadherence to diet and medical therapy is thought to be the primary contributor to their weight gain and peripheral edema.

Rates of nonadherence are estimated as high at 60% [3]. Heart failure exacerbations with simple volume overload are nonetheless associated with poor prognosis and high near-term mortality [1].

Heart failure manifesting as cardiogenic shock, with hypotension and signs of extensive end organ failure or hemodynamic instability is the most rare manifestation of decompensated heart failure, comprising less than 5% of presentations [2]. High suspicion should be held for acute cardiac insults such as myocardial infarction, tachydysrhythmias, or valvular pathology (e.g., acute mitral regurgitation) as precipitants of acute systolic failure.

Flash pulmonary edema can instead be viewed as a mismatch between acute increases in systemic vascular resistance (SVR), creating discordance with cardiac contractility. Patients presenting acutely hypertensive with fluid shifts, rather than retention, as a consequence [3].

Risk factors creating the contractility-afterload mismatch and resulting pulmonary edema include increased arterial stiffness (with older age), states of acute inflammation (e.g., sepsis) [3], and sympathetic activation (e.g., pheochromocytoma, stimulant abuse) [6]. If patients have no evidence of valvular disease or preexisting cardiomyopathy causing increased left ventricular filling pressures, a likely culprit may be renal artery stenosis causing activation of the renin-angiotensin-aldosterone axis and elevated SVR [7]. Even unilateral renal artery stenosis, in the setting of acute volume contraction, appears capable of causing flash pulmonary edema due to sympathetic activation [8].

A study of patients with acute hypertensive crises and flash pulmonary edema undergoing echocardiogram demonstrated that, compared to controls, global systolic function in these patients was preserved, but that they had worse left ventricular diastolic stiffness, ventricular-arterial coupling, and overall adaptive capacity to respond to high filling pressures [9]. Other observations of heart failure patients experiencing flash pulmonary edema have not demonstrated weight gain as a predictor of acute exacerbations [10].

As hypertension and increased afterload increases left ventricular pressures, they are translated to the left atrium, and pulmonic veins undergo recruitment and distension in response. This causes intracapillary hypertension in the alveolar vascular bed, and increases transcapillary filtration normally balanced by hydrostatic pressure, oncotic pressure, and vascular flow. Once intracapillary pressure exceeds 20–25 mmHg, fluid floods the alveoli and impairs gas exchange, with resultant hypoxia, tachypnea, and severe dyspnea experienced by the patient [6].