Valvular rupture or disease

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dysfunction defined as an EF < 40%. Systolic dysfunction is most commonly the result of ischemic heart disease, although many other causes exist. The pathologic feature of systolic dysfunction is a ventricle that has difficulty ejecting blood. Impaired contractility leads to increased intracar-diac volumes and pressure, and increasing after-load sensitivity. Consequently, these patients are sensitive to hypertension, and maintaining blood pressure (BP) to as low as is tolerated becomes an important management goal.

PSF HF is defined by preserved mechanical contractile function. When measured, the EF is normal or higher. The pathologic deficit is a ventricle with impaired relaxation, which results in an abnormal diastolic pressure-volume relationship. In this situation, the left ventricle (LV) has difficulty in receiving blood. Decreased LV compliance necessitates higher atrial pressures to ensure adequate diastolic LV filling. The hemody-namic consequence of a stiffened noncompliant ventricle is preload sensitivity, where excessively lowered preload may result in hypotension because of a lack of ventricular filling. The frequency of diastolic dysfunction increases with age. Chronic hypertension and LV hypertrophy are often responsible for this syndrome. Coronary artery disease (CAD) also contributes, and di-astolic dysfunction is an early event in the ischemic cascade. It has been reported that as many as 30% to 50% [6] of HF patients have circulatory congestion on the basis of diastolic dysfunction.

The pathologic distinctions based on EF are less important in the acute care setting of the ED and OU. In these environments, volume overload with excessive filling pressures are the most common ED presentation. Irrespective of the EF, the treatment approach is therefore similar. However, once hemodynamics are stabilized, and volume status approaches euvolemia, recognition of the underlying EF and the etiology of HF should be considered. In patients with PSF, excessive diuresis or venodilation may exacerbate the underlying deficit in ventricular filling and result in hypotension.

Determining HF type is difficult using the history and physical examination; consequently, an ECG becomes necessary. Some differentiate between left- and right-sided HF. Left-sided HF has dyspnea, fatigue, weakness, cough, paroxysmal nocturnal dyspnea, and orthopnea in the absence of peripheral edema, jugular venous distention (JVD), or hepatojugular reflux (HJR). Right-sided HF has peripheral edema, JVD, right upper quadrant pain, and HJR, without pulmonary symptoms. Because the cardiovascular system is mechanistically closed and abnormal pressure and chamber volumes are eventually reflected to the contralateral side, this distinction has greatest applicability when there is suspicion of valvular heart disease.

Role of neurohormones

Before the natriuretic peptides (NPs) were identified, extracellular fluid regulation was believed to be controlled by the kidneys, adrenal glands, and sympathetic nervous system via the renin-angiotensin system and other neuroendocrine mechanisms [7]. When arterial BP declines, renin is released by the kidneys. Renin splits hepati-cally synthesized angiotensinogen to form angio-tensin I. Angiotensin I is a biologically inactive decapeptide that is cleaved by angiotensin-convert-ing enzyme (ACE) to form active angiotensin II (AII). AII, a potent vasoconstrictor, increases peripheral vascular resistance and causes an increase in systolic BP. AII also has direct kidney effects that result in salt and water retention and stimulates adrenal aldosterone release. Increased aldo-sterone causes renal tubular absorption of sodium and results in water retention. Ultimately, extracellular volume and BP increase [7].

Natriuretic peptides are important in both BP and fluid balance. Physiologically, atrial NP (ANP) and B-type NP (BNP) function as a counter-regulatory arm to the renin-angiotensin system in regard to BP and volume maintenance. Three types of natriuretic peptides are recognized. ANP is primarily secreted from the atria. BNP is secreted mainly from the cardiac ventricle. Finally, C-type natriuretic peptide (CNP) is localized in the endothelium. The clinical effects of NPs are vasodilation, natriuresis, decreasing levels of endothelin, and inhibition of both the renin-angiotensin-aldosterone system and the sympathetic nervous system. BNP is synthesized as a prohormone, which is cleaved to inactive N-terminal pro-BNP, with a half-life of approximately 2 hours, and physiologically active BNP with a half-life of about 20 minutes [8].

Although BNP was named ''brain natriuretic peptide'' because it was first identified in porcine brain [9], in humans the dominant source is myo-cardial. BNP is secreted and stored in cardiac ventricular membrane granule [9]. BNP is continuously released from the heart in response to both volume expansion and pressure overload [10].

BNP is cleared by three pathways: a protein receptor, neutral endopeptidases, and to a lesser extent, the kidney [11]. Both ANP and BNP have natri-uretic and diuretic characteristics that increase sodium and water excretion by increasing glomerular filtration rate and inhibiting renal sodium resorption [12]. They also decrease aldoste-rone and renin secretion, causing both a reduction in blood pressure and extracellular fluid volume [8-12]. Circulating BNP levels increase in direct proportion to HF severity, as based on the New York Heart Association (NYHA) classification, and BNP is detectable even with minimal clinical symptoms. Physiologically, there is a correlation between BNP concentrations and LV end diastolic pressure (LVEDP). This suggests that the natriuretic effects, coupled with neurohormonal antagonism, serve to counterbalance fluid overload and elevated ventricular wall tension [12]. There is also an inverse correlation between BNP and LV function after acute MI. Elevated BNP occurs in the setting of raised atrial or pulmonary wedge pressures, or MI [12]. Ultimately, BNP measurement offers an independent assessment of ventricular function without the use of intravascular pressure monitoring.

Clinical features of decompensated heart failure

HF may present after myocardial infarction as the result of acute pump dysfunction. This is the result of the loss of a critical amount of myocar-dial contractile ability, the consequence of which is immediate symptoms. If there is symptomatic hypotension accompanied by findings of symptoms of inadequate perfusion (eg, mental status change, decreased urine output), cardiogenic shock is diagnosed. Patients with cardiogenic shock require hemodynamic monitoring and arrangements for emergency revascularization. They are therefore inappropriate OU candidates.

HF can present precipitously, as acute pulmonary edema (APE), and also insidiously as the final consequence of a cascade of pathologic events initiated by myocardial injury or stress. After a threat to cardiac output, a cascade of neurohormonally mediated reflexes occurs. These include activation of both the renin-angiotensin-aldosterone system and the sympathetic nervous system. Consequently, the levels of these neurohormones increase and include norepinephrine, vasopressin, endothelin (the most potent vasoconstrictor known), and TNF-alpha. Although not available in routine clinical practice, these hormone elevations are critical and correlate directly with mortality in HF patients.

Neurohormonal activation results in both sodium and water retention and an increase in systemic vascular resistance. Although these reflexes are initially compensatory and function to maintain systemic BP and perfusion, they occur at a cost of increased myocardial workload and cardiac wall tension. HF can be asymptomatic through these initial neurohormonal and hemo-dynamic perturbations. However, these reflexes establish the mechanism that initiates the secondary pathologic process of cardiac remodeling. Neurohormonal activation portends a worse prognosis in HF. Its attenuation forms the theoretical basis for nearly all treatments that decrease morbidity and mortality. This includes ACE inhibitors, angiotensin-receptor blockers, aldoste-rone antagonists, beta-blockers, and nesiritide.

Differential diagnosis

Many diseases mimic HF (Box 2). Because treatment omissions prevent optimal response, and misdirected therapy may have adverse consequences, an accurate diagnosis is important. Acute MI must always be considered as the cause of a HF visit. As many as 14% of ED HF presentations will have a troponin diagnostic for MI [13]. Furthermore, ADHF patients with elevations in troponin have markedly worse acute outcomes [14].

Additionally, because shortness of breath is the most common presenting symptom, other dys-pneic conditions must be considered. A common confounder is coexisting chronic obstructive

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