Heart Failure - Clinical Tree

KEY CONCEPTS

Heart failure (HF) is the clinical syndrome defined by signs and symptoms of elevated intracardiac pressures or depressed cardiac output, which in turn are due to either functional or structural cardiovascular (CV) abnormalities. By definition, HF presentations managed in the emergency department (ED) are acute heart failure (AHF) (ie, HF in which the signs and symptoms require unscheduled care).
AHF is a multiorgan, multifactorial, and multiple phenotype disease state. Abnormalities in renal function, central venous volume and fluid shifts, arterial vascular tone, neuroendocrine overactivity, microvascular dysfunction, respiratory failure, or myocardial ischemia have bidirectional relationships with AHF as both potential causes and effects.
Central congestion without hypervolemia is typically due to intercompartmental fluid shifts to the central circulation from venous reservoirs with reduced capacitance (increasing preload) or abrupt increases in central arterial tone (ie, increasing afterload).
Emergency physician (EP) clinical gestalt based on history and physical exam is inaccurate for AHF diagnosis as often as a quarter of the time.
The most useful diagnostic test for identifying lung congestion due to AHF is an 8-point lung ultrasound B-line scan, which is more sensitive than chest x-ray for pulmonary edema, and has a higher positive predictive value for AHF than natriuretic peptides.
Focused cardiac ultrasound (FOCUS) for detecting reduced ejection fraction (EF) misses the 40% to 50% of AHF presentations with preserved EF. It adds little information to risk stratification because EF does not typically change with dynamic worsening of cardiac function or improvement after treatment.
A useful clinical classification of AHF distinguishes between a vascular phenotype and a cardiac phenotype, though overlap can exist. Distinguishing between systolic and diastolic dysfunction is less helpful in the ED, because EF is preserved in about half of AHF cases, and most AHF patients have both systolic and diastolic dysfunction regardless of their EF.
The “vascular phenotype” describes an AHF presentation where functional (ie, reversible) CV abnormalities such as increased vascular tone and fluid shifts predominate over structural (ie, irreversible) ones. These patients tend to be hypertensive, less likely to be hypervolemic, respond favorably to intravenous (IV) nitroglycerin, and have a better prognosis despite more abrupt symptom onset.
The “cardiac phenotype” of AHF involves a predominance of structural (ie, irreversible) CV abnormalities such as more severe chronic myocardial disease, myocardial ischemia, and more complex multiorgan interactions (eg, cardiorenal syndrome). These patients are often hypervolemic and require high-dose IV diuresis. They typically present with a more indolent symptomatic progression, but paradoxically are at higher risk for worse outcomes.
Noninvasive positive-pressure ventilation is the first-line approach for respiratory distress in AHF and may obviate a need for intubation in most cases.
The initial dose of furosemide in the ED for AHF is 1 to 2.5 times the patient’s total daily oral dose (or 40–80 mg if loop-diuretic naïve) and should be given IV. Although creatinine may rise after IV furosemide, it is rarely indicative of iatrogenic acute kidney injury, and patients with acute cardiorenal syndromes typically benefit from aggressive diuresis.
Inotropes are only indicated in cases of cardiogenic shock (CS), because they may increase mortality as a pharmacologic class.
Resuscitation and stabilization of CS should be followed by rapid evaluation from interjectional cardiology or cardiac surgery. While STEMI was traditionally the predominant cause of CS, it may only account for 30% of contemporary cases due to improvements in coronary intervention.
Numerous high-moderate risk features in AHF define which patients likely require admission or observation, however, low-risk factors (ie, for discharge) are less well defined. When high or moderate risk factors are absent, the patient is adherent to the appropriate guideline-directed medical therapy, and can secure close outpatient follow-up (≤1 week), a shared decision-making discussion regarding discharge from the ED may be appropriate.

Foundations

Background and Importance

Heart failure (HF) is a clinical syndrome defined by three components ( Fig. 67.1 ) :

Structural or functional cardiovascular abnormalities
Elevated intracardiac pressures or depressed cardiac output (CO) due to these abnormalities
Clinically recognizable signs or symptoms (eg, dyspnea, edema, fatigue, exertional intolerance, or others) due to the elevated intracardiac pressures or depressed cardiac output

Fig. 67.1, Flowchart algorithm for clinical definition and classification of heart failure (HF). Three criteria define HF in general: cardiovascular structural or functional abnormalities, which cause decreased CO or increased intracardiac pressures, and clinical symptoms resulting from these physiologic derangements. Examples of cardiovascular structural (ie, fixed, anatomic) abnormalities include cardiomyopathies, valvular disease, myocardial scar and fibrosis, etc. Functional (ie, dynamic) abnormalities include arterial vasoconstriction, acute volume shifts and redistribution, transient ischemia without infarction, toxicologic or reversible metabolic myocardial dysfunction, and numerous others. In most cases, both structural and functional abnormalities coexist to cause depressed CO, increased intracardiac pressures, or both. HF is also by definition symptomatic, and does not include subclinical myocardial dysfunction (which nevertheless may progress to clinical HF with time or acute physiologic stressors). The three most common presenting signs/symptoms in the ED setting are (in order) dyspnea, edema/swelling, and fatigue. HF is further subdivided into chronic and acute (AHF), based on whether or not the symptoms lead a patient to seek urgent or emergent management in an acute setting such as the ED. When HF is treated in the ED, it is therefore (by definition) AHF. Many AHF patients will have a chronic HF history (ADHF), but a significant proportion will not (de novo AHF). For emergency medicine this distinction has mostly prognostic significance for disposition. HF , heart failure; ED , emergency medicine; CO , cardiac output; S/Sx’s , signs and symptoms; AHF , acute heart failure; ADHF , acutely decompensated heart failure.

Management of clinical manifestations of HF with scheduled care is classified as chronic HF. Conversely, HF symptoms that require unscheduled care define the presentation of acute HF (AHF). Thus, when HF is managed and treated in the ED, it is, by definition nearly always AHF. Some exceptions exist (eg, a stable chronic HF patient presenting to the ED for a medication refill), however, these are relatively few, and AHF is therefore the primary focus of this chapter.

AHF may further be subdivided as decompensated chronic HF versus “de novo HF.” ^, The former describes AHF occurring in a patient with known chronic HF history, while in the latter the AHF episode is the patient’s first known clinical presentation of HF. De novo AHF accounted for over 50% of presentations in a large AHF registry study of Asia and Europe, but is a less common ED presentation in North America. Epidemiologic registry data from 2005 to 2014 suggest that around 28% of ED AHF presentations in the United States (US) are de novo .

It is important to note that many HF terms commonly used in the past are now considered outdated, inaccurate, or clinically misleading. “Congestive heart failure,” for instance, is no longer favored given that volume profiles in HF are heterogeneous and include many patients with normal or even hypovolemic total body water profiles. Also, the terms “systolic HF” and “diastolic HF” are no longer used to describe patient phenotypes. The following, more accurate terms are preferred: “HF with reduced ejection fraction” when the ejection fraction (EF) is less than 40%; “HF with midrange EF” when the EF is 40% to 50%, and “HF with preserved EF” when EF is greater than 50% (HFrEF, HFmrEF, and HFpEF, respectively). The terms “systolic dysfunction” (ie, decreased inotropy) and “diastolic dysfunction” (ie, impaired relaxation) still apply as physiologic concepts but are often overlapping and do not describe clinical phenotypes that warrant particular approaches to management. Combining terms to summarize a patient’s presentation, such as “acutely decompensated chronic HF with reduced EF,” is useful.

Epidemiology

Chronic HF is highly prevalent (≈2.5% of the US population) and is strongly associated with common cardiovascular risk factors. Onset increases sharply with advancing age, such that, by age 65, the annual incidence of new chronic HF diagnosis approaches 2.1%. Other risk factors observed in population-based samples include obesity, hypertension, diabetes mellitus (DM), tobacco smoking, hyperlipidemia, low socioeconomic status, and ischemic heart disease.

Nearly 1 million admissions for AHF occur each year in the United States, and more than 80% of these originate from the ED with a nearly 50/50 split between HFpEF and HFrEF. Outcomes are poor with 30-day and 1-year mortality of 10% and 30%, respectively, after an AHF episode, and appear to be similar regardless of EF. After hospital discharge, roughly 20% of AHF patients will be readmitted within 30 days.

Myocardial Physiology and the Cardiac Cycle in Heart Failure

The cardiac cycle ( Fig. 67.2A ) and its relationship to CO is often described by three physiologic parameters: chronotropy, inotropy, and lusitropy. CO is the mathematical product of heart rate (HR; ie, chronotropy) and the stroke volume (SV). SV is itself the product of end diastolic volume (EDV; ie, lusitropy) and EF (ie, inotropy). Thus, mathematically

C O = H R \times E D V \times E F

$C O = H R \times E D V \times E F$

$Fig. 67.2, Pressure-volume (PV) loop concept diagrams demonstrating the relationship between underlying cardiac function, SV, and changes in preload or afterload. Each loop is delimited by underlying limits to inotropy (top limit line) and lusitropy (bottom limit line). Stroke volume alterations (by changes in preload and afterload) are limited to these confines. (A) Baseline PV loop of a hypothetical healthy heart. (B) Isolated increases in afterload ( red dotted line ) or preload ( blue line ) under healthy conditions lead to decreased or increased SV, respectively. (C) Isolated impairment of lusitropy (ie, diastolic dysfunction) decreases SV by reducing EDV for a given EDP, ESP, and ESV ( dotted line ). This is representative of many, but not all, cases of HFpEF (since diastolic dysfunction may be isolated or may coexist with systolic dysfunction, even in HFpEF; see panel E). (D) Isolated impairment of inotropy (ie, systolic dysfunction) decreases SV by reducing ESV for a given EDP, ESP, and EDV ( dotted line ). EF is observed to decrease, though the reduction in SV is just as severe as isolated diastolic dysfunction in panel C. This curve is mostly hypothetical because in reality systolic dysfunction is nearly always accompanied by diastolic dysfunction in both HFrEF and HFpEF. (E) Combined inotropic and lusitropic impairment decreases SV by reducing ESV and EDV for a given EDP and ESP. This represents nearly all cases of HFrEF and many cases of HFpEF. (F) Compared to the healthy heart in panel B, preload ( blue dotted line ) has only marginal effects on SV in HF (ie, decreased preload tolerance). For afterload, the direction of effect is the same as the healthy heart: increased afterload reduces SV ( red dotted line ) when all other parameters are held constant. SV , stroke volume; EF , Ejection fraction; EDP/ESP/EDV/ESV , end-diastolic/systolic pressure/volume; HF , heart failure; HFpEF , HF with preserved EF; HFrEF , HF with reduced EF.$

and conceptually

CO=Chronotropy × Lusitropy × Inotropy.

Recall that the second criterion of the HF definition requires that CO be reduced or intracardiac cardiac pressures be increased; however, these two defining hemodynamic insults tend to coexist and are distinctly related.

Lusitropy and inotropy ( Fig. 67.2 C–E) may be chronically depressed due to underlying chronic structural or functional cardiac changes, as in the setting of ischemic heart disease or hypertensive heart disease, or acutely impaired by a new hemodynamic stressor such as hypertensive emergency, infection, volume redistribution or overload. As shown in Figure 67.3 , AHF is also an inherently multiorgan process, with bidirectional feedback between cardiac dysfunction, vascular tone, and multiple organ involvement.

Fig. 67.3, A multiorgan, multidirectional concept chart of AHF. Increased intracardiac pressures or reduced CO (ie, a sine qua non of AHF) can be the result or the cause of other organ system dysfunction. Activation of the sympathetic and RAAS neurohomonal axes, for instance, can be a precipitant of AHF. However, depressed CO also will activate these neurohormonal mechanisms both directly and indirectly. Certain bidirectional relationships have been described as distinct and important syndromes, such as the cardiorenal syndrome. Not every cardiac to end-organ relationship pictured here is a key component of every AHF presentation, underlining the importance of AHF phenotypic heterogeneity and the fact that therapeutic approaches should be tailored to phenotype when possible. Also, many relationships not pictured are likely important in some cases since understanding of AHF physiology is continuously changing. AHF , acute heart failure; CO , cardiac output; RAAS , renin-angiotensin aldosterone system; RV , right ventricle; PA , pulmonary artery.

SV is classically modeled by the Frank-Starling mechanism, which describes a relationship between stroke volume and EDV ( Fig. 67.4A ). In the idealized scenario, increasing EDV leads to increasing SV because stretching myocardial sarcomeres further apart in diastole allows them a further distance to contract during systole, increasing inotropy. This model describes the preload-SV relationship well under conditions where EDV is far below the heart’s maximum capacity. Eventually, an inflection point is reached where sarcomeric stretch is maximized and increases in inotropy level-off despite further increases in EDV, noted as the flat portion of a Starling curve. If EDV increases even further, sarcomeres are stretched into abnormal configurations that inhibit inotropy and produce systolic dysfunction. Even brief and transient exposure to excessive left ventricular (LV) EDV can trigger a cascade of stretch-related insults to myocardial function, including subendocardial ischemia with cardiomyocyte injury and necrosis with associated cardiac troponin [cTn] release. Further or sustained stretch results in myocardial stunning and sarcomere proteomic remodeling, culminating in clinical deterioration that manifests as AHF. ^, ^, ^,

Fig. 67.4, SV versus preload curves describing the Starling mechanism in the context of AHF versus health. (A) Curves I through V represent progressive worsening of baseline cardiac function. Increased preload leads to increased SV early because of more favorable sarcomeric configurations in myocytes. Once all sarcomeres are at a maximal degree of stretch the ability to increase SV by preload is exhausted, and the curve levels off. At severe degrees of stretch, sarcomere configurations become disorganized and stretch-related myocyte injury mechanisms are activated, causing the curve to potentially invert with more preload (“falling off the Starling curve”). The inflection points of leveling off and then of curve inversion occur at less extreme levels of preload as cardiac pump function worsens. (B) For any given preload, patients with cardiac pump dysfunction (IV–V) are more likely to be in the flat or inverted part of the Starling curves ( yellow and red zones , respectively) compared to those with normal or excellent pump function (I–III), and far less likely to be in the preload responsive part of the Starling curve ( blue zone ). Common ED treatment strategies for AHF either push the patient’s preload “backwards” to a more favorable zone along the same Starling curve (IV diuretics only, orange arrow ), move the patient “up” to a curve with improved cardiac performance (inotropes only, red arrow ), or both (vasodilator only, blue arrow ; vasodilator plus diuretic, green arrow ; vasodilator, diuretic, and inotrope, purple arrow ). (C) Preload tolerance is a conceptualization of whether a patient will benefit, have no change, or sustain harm from a fixed change in preload (intervals/arrows 1, 2, and 3). In AHF, relatively rapid increases in preload occur from intercompartmental fluid shifts, while slower increases occur from progressive volume overload. Interval 1 shows a severely hypovolemic state, in which all 5 patient curves benefit from an increase in preload (eg, a fluid bolus), though SV augmentation is only modest with cardiac dysfunction IV–V. Interval 2 represents a state in which increased central venous volume pushes patients IV–V closer to falling off the Starling curve (while achieving no change in SV), whereas SV is augmented in I–III. In interval 3, further increased central venous volume pushes the patients with myocardial dysfunction “off” the Starling curve, but given the same preload has neutral-to-positive effects for patients I– III. AHF , acute heart failure; SV , stroke volume.

Repeated exposures to increased LVEDV (and resultant LVEDP) cause fibrosis and myocardial hypertrophy that ultimately lead to a stiff, noncompliant ventricle. The net effect is an impairment of lusitropy (ie, diastolic dysfunction) that serves to limit the degree of myocardial stretch during future elevations protecting the myocardium from further stretch-induced myocyte death. However, this comes with a tradeoff, because the ensuing diastolic dysfunction prevents accommodation of increased LVEDV, contributing to onset of symptomatic HF. In the early stages, a certain degree of diastolic dysfunction may be subclinical, or only induced upon stress with exercise, acute hypertension, or hypoxia. ^, As diastolic dysfunction progresses, demand from activities of daily living may be superimposed on diminishing cardiac reserve associated with other physiologic changes, including decreased myocardial oxygen reserve, abnormalities in nitric oxide signaling, decreased aortic and pulmonary artery compliance, decreased ventricular volume, right ventricular dysfunction, and worsening interventricular and ventricular-circulatory coupling, resulting in depressed tolerance of increased preload and afterload. ^,

Depressed SV resulting from acute diastolic or systolic dysfunction can be theoretically compensated for by increased chronotropy. However, the time between systolic cycling sets a “hard stop” on the upper limit of cardiac filling time and, at a certain point, further augmentation of CO through increased chronotropy becomes limited by diminished lusitropy ( Fig. 67.5 ). Thus while increasing heart rate has early adaptive benefits, persistent sinus tachycardia in the setting of AHF is generally an ominous sign that CO has been stressed to its limit. This also explains why increased or decreased chronotropy (as in tachy- or brady-arrhythmias) is a relatively common precipitant of AHF.

Fig. 67.5, Plot of SV ( dotted line ) or CO ( solid line ) versus HR for healthy and impaired myocardial function ( blue line vs. red line , respectively). Myocardial stimulation in response to physiologic demands (eg, sympathetic drive in response to a physiologic stressor), can compensate by augmenting SV up to a ceiling dictated by the optimization of inotropy and lusitropy. Past this SV ceiling, the only way to augment CO to meet even higher physiologic demand is to increase HR (ie, tachycardia in AHF may signify severe mismatch between myocardial function and metabolic demand). After a certain point of tachycardia, SV will worsen due to insufficient time spent in diastole (ie, de-optimized filling time) and further increases in tachycardia will cause CO to decrease (ie, tachydysrhythmias precipitate hemodynamic instability at extremely high HRs in healthy patients, but at lower HRs in acute or chronic myocardial dysfunction). SV , stroke volume; CO , cardiac output; HR , heart rate; AHF , acute heart failure.

Abnormal Loading Conditions and Elevated Filling Pressures

Patients with chronic HF (eg, curves IV and V in Fig. 67.4 ) tend to stay near or beyond the inflection point of the Starling curve (red and yellow zones Fig. 67.4 ) because of their chronically impaired diastolic and systolic dysfunction. Even subtle increases in loading parameters (rightward shifts on the curves) can lead to fulminant AHF. Additionally, with relatively normal baseline cardiac function (curve III Fig. 67.4 , curves I–II Fig. 67.6A ), extremes that impede forward flow (eg, hypertensive emergency) can precipitate AHF through a large rightward shift on the curve. Multiple neurohormonal effects result from and contribute to loading conditions and filling pressures. ^, Natriuretic peptides (NPs) are especially important in this regard and are upregulated in HF where they result in natriuresis and diuresis, vasodilation, and antifibrotic effects that can reverse remodel the heart. Produced directly by the heart, atrial-NP (ANP), B-type NP (BNP), and the N-terminal fragment of BNP’s prohormone (NT-proBNP) are clinically useful for diagnosis and prognosis of HF.

Fig. 67.6, (A) SV versus afterload relationship plotted for 3 levels of decreasing LV function (I–III) and the RV. Increasing afterload for a fixed degree of inotropic and lusitropic function causes a decline in stroke volume. However, resistance to this decline (a flatter slope) is higher with better baseline cardiac pump function. Eventually, regardless of ventricular resilience to afterload, vascular pressure can become high enough to induce a precipitous decline in stroke volume (ie, rapid ventricular-vascular decoupling). The RV is extremely pressure sensitive (but more volume tolerant) compared to the LV. (B) The relationship between the ventricular-vascular pressure difference (“driving pressure” or “delta pressure”) and arterial flow rate ( right ) or time ( left ) for a set afterload. In order to overcome high afterload, cardiac driving pressure must increase to maintain arterial flow. This relationship is linear when flow is laminar, but flow becomes turbulent once the pressure difference reaches or exceeds a critical value. Under turbulent flow, further increases in the pressure difference yield decreasing rates of return in arterial flow despite steadily increasing cardiac MVO 2 . Flow thus becomes highly inefficient as ventricular-vascular decoupling progresses (eg, in severe hypertension), as in the purple curve of the delta pressure versus time. When blood pressure is lowered (post-vasodilator green curve ), a larger proportion of flow is laminar and the driving ventricular-vascular pressure difference is spread more evenly over time, leading to more efficient hemodynamics (ie, lower MVO 2 required to produce similar degree of flow). In AHF the “supply” of myocardial oxygen is lowered while the “demand” is increased, so decreasing MVO 2 for a given SV is physiologically beneficial. In the initial resuscitation of the hypertensive/vascular AHF phenotype this typically means IV bolus vasodilators such as nitroglycerin. SV , stroke volume; LV , left ventricle; RV , right ventricle; MVO 2 , myocardial oxygen consumption rate.

Elevated intracardiac pressures are a defining characteristic in AHF (see Fig. 67.1 ), and even brief episodes can impair the normal cardiac cycle and lead to irreversible systolic or diastolic dysfunction. ^, Thus, episodes of AHF negatively impact the long-term prognosis of patients with chronic HF. This is of particular relevance to ED management, with a physiologic justification for a “time-to-treatment” concept in AHF, similar to many other time-sensitive conditions seen in emergency medicine. Given the potential benefit of limiting myocardial damage through earlier normalization of intracardiac pressures, organizations such as the Heart Failure Society of America (HFSA), the Society for Academic Emergency Medicine (SAEM), the American Heart Association (AHA), and the American College of Cardiology (ACC) have all recommend that AHF treatment be started as quickly as possible after ED arrival. Broadly speaking, the major classes of ED AHF therapies work by targeting the physiology underlying elevated intracardiac pressures either by moving the Starling curve leftward with diuretics or venodilators, moving the curve upward to a higher level of efficiency for a given EDV with inotropes or arterial vasodilators, or both. A simple but useful hemodynamic classification distinguishes between cardiac (ie, primary pump failure predominates) and vascular (ie, acutely increased preload or afterload predominates) phenotypes of AHF. The ED management differs depending on which phenotype predominates.

Congestion and Preload

Congestion in AHF is very specifically the congestion of the central vasculature (ie, the vena cava, great arteries, and proximal organs such as the heart, lungs, and kidneys). Central congestion can occur from true volume overload associated with excessive fluid intake or retention, typical of the cardiac phenotype. Generally, this is an indolent process ( Fig. 67.7A ). When rapid decompensation occurs in AHF, fluid typically shifts from venous reservoirs to the central circulation in a process largely independent of total body water, more typical of the vascular phenotype. This, in part, explains why classic signs and symptoms of fluid overload may be absent in patients with AHF.

Fig. 67.7, (A) Concept flowchart of central circulation congestion in AHF. The splanchnic circulation under normal physiology holds up to half of total circulating volume, with a large residual capacity to buffer the central circulations against acute increases or decreases in total vascular volume. Neurohormonal activation (eg, alpha-adrenergic, RAAS, etc.) causes progressive splanchnic vasoconstriction that reduces the capacitance of the reservoir and decreases its residual capacity (ie, even without a change in total body water). This impairs the splanchnic buffering capacity, meaning that any increase in oral fluid intake more readily “spills over” to the central circulation while any decreases in central circulation fluid elimination (eg, renal impairment, insensible losses) are unable to be buffered against. The result is the “slow pathway” described in the figure, where progressive central congestion occurs over weeks to months. Left uncompensated, this can result in a slow but progressive descent into AHF. Additionally, if an acute stressor (eg, severe hypertension) rapidly and massively activates sympathetic drive and RAAS, fluid shifts from the splanchnic to central circulation will occur much more rapidly (the rapid pathway). (B) Plots of central congestion versus time, benchmarked by key clinical or physiologic events, to illustrate the ramifications of the rapid versus slow physiologies for AHF clinical presentations. In the rapid pathway only, the abrupt fluid shift produces dramatic and rapid symptoms over only a few days but may resolve quickly with appropriate AHF treatment. These patients, typical of the AHF “vascular phenotype,” may present more dramatically by history but ironically have a better prognosis. In the slow pathway only, symptoms develop more indolently but also after significantly more intractable change because symptoms of HF can occur weeks after increases in cardiac pressures and increases in lung water under such conditions. This is typical of a slow decompensation in the “cardiac” AHF phenotype without any overt superimposed physiologic stressor/AHF precipitant to activate the rapid pathway as well. The presentation is less dramatic but prognosis is significantly worse, possibly because lung water and intracardiac pressures have been asymptomatically elevated for a longer period of time and are more intractable. The third curve describes a scenario in which the rapid pathway is superimposed on the slow pathway (in which cardiac and vascular AHF phenotypes are relatively intermixed) such as when a patient with the cardiac phenotype is afflicted by an acute AHF precipitant (infection, hypoxia from other disease, ischemia, etc) activating rapid fluid shifts superimposed on an already chronically reduced splanchnic buffering capacity.

One of the largest and most critical venous reservoirs in the body is the splanchnic circulation, containing 20% to 50% of total blood volume at any given time. The splanchnic vessels dilate or contract in response to central circulation baroreceptors and sympathetic tone, and the renin-angiotensin-aldosterone system (RAAS). Under normal physiologic conditions, regulation of fluid from the splanchnic to central circulation via the hepatic veins acts as a buffer to maintain central volume. In stress situations, volume can be rapidly mobilized from the splanchnic circulation to the central circulation by vasoconstriction. When HF is present, neurohormonal mediators are chronically activated, leading to basal splanchnic vasoconstriction and a reduction in the reservoir’s buffering capacity. As a result, rapid fluid shifts can develop in response to any number of AHF precipitants (eg, infection, acute hypertension, ischemia, etc.), leading to central congestion even when total body water is normal ( Fig. 67.7B , first curve). Experimentally, denervation of the splanchnic vasculature in AHF patients dramatically lowers intracardiac filling pressures while increasing cardiac output.

In contrast, patients with the cardiac pathophysiology typically have gradual fluid accumulation superimposed on long-standing and intractable hemodynamic derangements. AHF patients with slow onset of symptoms tend to have less pronounced pulmonary edema on arrival and delayed dyspnea relief with worse in-hospital and postdischarge outcomes. Thus, clinicians should not rely entirely on a patient’s apparent clinical severity at presentation to determine how much decongestion they may need ( Fig. 67.7B ).

Afterload

Afterload is the pressure against which the ventricle must contract to eject blood. In practical terms, this means the aortic and pulmonary artery (PA) pressures for the LV and right ventricle (RV), respectively. The coupling of ventricular and vascular function is a dynamic relationship. As afterload rises, SV will gradually decline until extremes in ventricular pressure are reached and a precipitous worsening of ventricular function ensues ( Fig. 67.6A ). The RV is significantly more pressure-sensitive and volume-tolerant than the LV, though chronic elevated pressure can cause hypertrophic remodeling similar to the LV. The ratio of oxygen consumption to stroke work increases as afterload rises (a phenomenon referred to as ventricular-vascular decoupling), burdening a heart with already diminished oxygen capacity at baseline. Whether intrinsic or exogenous, rises in afterload are often abrupt. Clinical deterioration rapidly follows, resulting in the onset of “flash” pulmonary edema. Though sometimes described as a distinct entity, flash pulmonary edema is the most severe form of afterload-mediated or hypertensive AHF.

Disorganized Contraction

In addition to perturbations in preload and afterload, the heart itself can contribute to AHF through disorganized contraction and relaxation. Each ventricle can be divided into individual myocardial segments (eg, apex to base, anterior/posterior, septal/free wall), which under idealized circumstances all contract and relax simultaneously. In reality, some segments within a single ventricle may contract or relax slightly before others, and even slight asynchrony reduces the mechanical efficiency of contraction. The reasons for segmental asynchrony include relatively fixed myocardial lesions, such as a scar from past MI, and more acute, dynamic causes such as localized demand ischemia, stretch-related myocyte toxicity, coronary microvascular dysfunction, or acute MI. ED treatment of AHF, including noninvasive positive-pressure ventilation (NPPV), diuresis, and vasodilation, can significantly improve segmental contraction synchronization. Failure to improve mechanical synchrony on point-of-care echocardiography (POC echo) after ED AHF treatment is associated with adverse AHF outcomes.

Right Ventricular Dysfunction and Pulmonary Hypertension

Right ventricular dysfunction (RVD) has been increasingly recognized as an important pathologic and prognostic marker in both chronic HF and AHF. RVD identifiable on ultrasound may be present in 28% to 46% of AHF cases and significantly declines in the first 24 hours after initial ED treatment. Missed antihypertensive medication within 7 days, ED PPV, COPD history, LVEF, lung ultrasound congestion severity, and right ventricular systolic pressure (RVSP) are significant predictors of RVD. RVD evident on POC echo is rarely recognized despite a high prevalence and potentially greater prognostic implications than LVEF. RVD in AHF is associated with higher all-cause mortality in AHF even after adjusting for LVEF and other measures of LV function. More importantly, the association between RVD and AHF mortality strengthens when pulmonary hypertension is absent. The relationship between acute RV and LV dysfunction is bidirectional and inextricably interdependent ( Fig. 67.8 ). Although the most common cause of right heart failure is left heart failure, RVD can precede, precipitate, or be concurrent with LV dysfunction in AHF. This is evident given that the path through the right heart, pulmonary circulation, left heart, and systemic circulation is a closed circuit and RV CO must equal LV CO. As a consequence, any hemodynamic derangement within the circuit will, on a beat-to-beat basis, adversely impact biventricular functionality. Additionally, the LV and RV share a common wall (the interventricular septum), meaning acute changes on one side do not occur in isolation.

Fig. 67.8, A physiologic flow diagram of the biventricular nature of AHF. Although LVD has long been the focus of an understanding of AHF, it is now recognized that RVD is common, indicates severity of presentation, and predicts poor prognosis. Because both ventricles share (on average, beat to beat) a CO and a wall (ie, the intraventricular septum), forces affecting the RV affect the LV (and vice versa). RV and LV stroke work, however, is not inherently equal and it has been shown that improvement of the former in response to AHF treatment is associated with better outcomes than improvement in the latter. Disorganization of contraction, ischemia, volume overload, acute ventricular-vascular decoupling, or other insults in one ventricle are transmitted to the other ventricle through complex and somewhat unpredictable ways. LVD causing PHTN and subsequent RVD (the classic understanding of “right heart failure”) is only one of many ways that RVD develops in AHF (ie, PHTN is neither necessary nor sufficient to produce acute RVD in AHF patients). AHF , acute heart failure; LV , left ventricle dysfunction; RVD , right ventricle; LVD/RVD , LV/RV dysfunction; CO , cardiac output; RAAS , renin-angiotensin-aldosterone-system; PHTN , pulmonary hypertension.

RVD in AHF can result from factors intrinsic and extrinsic to the RV itself (see Fig. 67.8 ). Some AHF therapies affect the RV as much as or more than the LV, as suggested by the observation that improvement in RV stroke-work (but not LV stroke-work) during an episode of AHF is associated with decreased rates of death, transplantation, ventricular assist device implantation, or HF-related rehospitalization at 6 months. Moreover, RVD independently predicts hyponatremia, worsening renal function after hospitalization, longer hospital length of stay, and higher rates of myocardial fibrosis.

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