© Springer-Verlag London 2017
Howard Eisen (ed.)Heart Failure10.1007/978-1-4471-4219-5_88. Acute Decompensated Heart Failure: Classification, Epidemiology and Pathophysiology
(1)
University of Washington Medical Center, Department of Medicine, Division of Cardiology, 1959 NE Pacific Street, #356422, Seattle, WA 98195, USA
Keywords
Acute Heart FailureAcute Decompensated Heart FailureHospitalizationLoop DiureticsCongestionPulmonary CongestionGuideline Directed Medical TherapyDiuretic ResistanceIntroduction
Hospitalization for heart failure (HF) has emerged as major worldwide public health problem over the last three decades. Heart failure is the most common cause for hospitalization in patients over the age of 65 years in the United States. There are an estimated one million hospitalizations annually in the US with a primary diagnosis of heart failure accounting for 5–10 % of all hospitalizations. Three million patients are hospitalized annually with a primary or secondary diagnosis of heart failure. Approximately 5.1–5.8 million Americans have HF and it is estimated that the prevalence of heart failure will increase by 46 % from 2012 to 2030 [1–4]. The European Society of Cardiology represents 51 countries with a population of > 900 million people. At least 15 million Europeans have heart failure and an equal number have asymptomatic left ventricular dysfunction [2].
The direct and indirect costs associated with HF in the US in 2009 are estimated to exceed $37 billion. Most of these costs are attributable to hospitalization for HF. The number of hospitalizations for HF has triple in the last three decades. The increase in the prevalence of heart failure appears to be due to a number of factors including: the aging of the U.S. population in association with the increased incidence of heart failure with advancing age; improved survival after myocardial infarction resulting in more patients living with left ventricular dysfunction; and better prevention of arrhythmia-related death in patients with chronic left ventricular systolic dysfunction [5].
Definition
Acutely Decompensated Heart Failure (ADHF) can be defined as the new onset or recurrence of heart failure signs and symptoms that require urgent or emergent treatment and that result in hospitalization. A number of other terms have been used in the literature including: Acute Heart Failure Syndromes (AHFS), Acute Heart Failure (AHF) and Acute Decompensation of Chronic Heart Failure (ADCHF). The number of terms used in the literature reflects that ADHF is not a single diagnosis but rather, a group of related syndromes caused by a number of different primary underlying cardiovascular diseases that may be made worse by a variety of cardiac and non-cardiac conditions.
In patients with ADHF, there is significant heterogeneity in the underlying pathophysiology, precipitants, time course, clinical presentation and underlying cause of heart disease. However, pulmonary congestion due to elevated left atrial pressure with associated symptoms of dyspnea with or without clinical evidence of low cardiac output is a consistent finding in patients with this syndrome.
Approximately 80 % of patients hospitalized with ADHF have a previous diagnosis of heart failure, 15 % have new onset heart failure, and 5 % have advanced or refractory heart failure. Underlying cardiovascular diseases including coronary artery disease, hypertension, valvular heart disease and cardiomyopathy are often present. Non-cardiac conditions including kidney dysfunction, pulmonary disease, diabetes, thyroid disease, anemia, substance abuse, obesity, sleep apnea, and infection are often present and may contribute to heart failure decompensation [6].
Epidemiology
The number of hospitalizations with heart failure as a primary or secondary diagnosis tripled from 1979 to 2004, increasing from 1,274,000 in 1974 to 3,860,000 in 2004. Heart failure was the primary diagnosis in 30–35 % of these admissions. Age-adjusted hospitalization rates also increased during this period. More than 80 % of these hospitalizations were in patients age 65 years or older and were paid by Medicare or Medicaid [7].
There has, however, been a recent decline noted in hospitalization rates for ADHF. In an analysis of inpatient National Claims History files from the Centers for Medicare & Medicaid Services (CMS) which identified all fee-for-service Medicare beneficiaries who were hospitalized for HF from 1998 to 2008, the heart failure hospitalization rates adjusted for age, gender and race declined from 2845 per 100,000 person-years in 1998 to 2007 per 100,000 person-years in 2008 (a decline of 29.5 %; p < 0.001). Black men had the lowest rate of age-adjusted decline for all race-gender categories. Importantly, risk-adjusted 1-year mortality after hospitalization decreased from 31.7 % in 1999 to 29.6 % in 2008 (a decline of 6.6 %; p < 0.001) [8].
Several large multicenter observational registries in the United States and Europe have significantly improved our understanding of the demographics, clinical characteristics, comorbidities, management patterns and outcomes of patients admitted with ADHF. Prior to these registries, our understanding of ADHF came largely from studies of younger patients with moderate to severe systolic dysfunction that were enrolled in single-center or multicenter randomized controlled clinical trials conducted predominantly at academic heart failure centers. The observational registries were designed to enroll a more representative sample of patients with ADHF that included all patients admitted with heart failure at geographically diverse academic and non-academic medical centers.
The Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) used HF case ascertainment methods to identify 48,612 patients hospitalized at 259 centers in the United States for new or worsening HF as the primary cause of admission or who developed significant HF symptoms during hospitalization for a different diagnosis. Using a web-based registry, detailed data were collected including demographics, medical history, signs and symptoms, medications, laboratories, diagnostic testing procedures, discharge status, outcomes and adherence to performance indicators. A pre-specified subgroup that was ≥ 10 % of the total number of patients was followed for 60–90 days after discharge for the collection of outcomes data [9].
The Acute Decompensated Heart Failure National Data Registry (ADHERE) database was a prospective observational registry that was developed to provide a large national database to describe clinical characteristics, management and outcomes of patients hospitalized with heart failure at 285 hospitals in the United States. Thirty one percent of the participating institutions were academic hospitals. From 2002 to 2004, data were collected from 159,168 hospitalizations beginning with the point of initial care and ending with the patients’ discharge or in-hospital death [10–12].
The EuroHeart Failure Survey I (EHFS I) was a retrospective registry in which deaths or discharges from 115 hospitals (50 % university hospitals) from 24 European countries were screened to identify patients with known or suspected heart failure. Demographics, clinical characteristics, evaluation, treatment and outcomes were assessed [13–15]. The EuroHeart Failure Survey II (EHFS II) was a prospective observational registry that recruited 3580 patients hospitalized for HF at 133 centers (47 % university hospitals) in 30 European countries. Using a web based registry, detailed data were collected including demographics, clinical characteristics, etiology, treatment and outcome [16].
The findings from the U.S. and European trials are largely concordant. ADHF disproportionately affects the elderly; the mean age in the registries was 73 years. One quarter of the patients in OPTIMIZE-HF were more than 83 years old [17]. Men and women were equally represented in the U.S. registries while men represented two thirds of the hospitalized patients in EHFS II [16]. Women with ADHF tend to be older, are less likely to have coronary artery disease and are more likely to have hypertension and preserved systolic function [17].
Over 70 % of patients with ADHF in the U.S. registries had a history of hypertension. A history of hypertension was reported in 63 % of patients in EHFS II [16]. Elevation of systolic blood pressure is common at the time of presentation to the emergency department (ED). Mean initial systolic blood pressure on presentation to the emergency department (ED) was 143 mmHg in OPTIMIZE-HF and 144 mmHg in ADHERE. Half of the patients in ADHERE and OPTIMIZE-HF had an initial systolic pressure of greater than 140 mmHg [10, 18]. Renal dysfunction is common. The mean serum creatinine was 1.8 mg/dL in both ADHERE and OPTIMIZE; 20 % of patients in ADHERE had a serum creatinine of greater than 2.0 mg/dL [10, 18].
Approximately half of patients in ADHERE and OPTIMIZE had normal or near normal systolic function defined as a left ventricular ejection fraction (LVEF) ≥ 40 % [19, 20]. Patients with heart failure with preserved ejection fraction (HFpEF) were more likely to be older, female, Caucasian, and have a higher systolic blood pressure on admission and less likely to have had a prior myocardial infarction when compared with patients with heart failure with reduced ejection fraction (HFrEF). In-hospital mortality was lower in patients with HFpEF compared to patients with HFrEF in both ADHERE (2.8 % vs. 3.9 %) and OPTIMIZE-HF (2.9 % vs. 3.9 %). In ADHERE, patients with HFpEF had a similar length of stay and duration of intensive care unit stay when compared with patients with HFrEF [19]. In OPTIMIZE-HF, patients with HFpEF and HFrEF had similar 60–90 day post-discharge mortality (9.5 % vs. 9.8 %, respectively) and rehospitalization rates (29.2 % vs. 29.9 %, respectively). Findings were similar when patients with an LVEF between 40–50 % were compared with patients with an LVEF ≥ 50 % [20]. In an analysis of the data from EHFS I, mortality during the 12-week post-discharge follow-up period was higher in patients with HFrEF compared to patients with HFpEF (12 % vs 10 %). There were no differences in readmission rates during the 12 week follow up period [21].
Eighteen percent of patients in OPTIMIZE-HF and 20 % of patients in ADHERE were African American. African American patients in OPTIMIZE-HF were younger (mean age 63.6 years compared with 75.2 years for non-African American patients), were more likely to have systolic dysfunction and a hypertensive etiology of heart failure and significantly less likely to have ischemic heart disease than non- African American patients. African American patients were more likely to receive evidence-based medications but less likely to receive discharge instructions and smoking cessation counseling. African American race was an independent predictor of lower in-hospital mortality but not of hospital length of stay or multivariable adjusted post-discharge outcomes [22].
In ADHERE, 75 % of patients had a prior history of HF and 33 % had a HF admission within the prior 6 months. Eighty eight percent of patients in OPTIMIZE-HF had a prior history of heart failure. Thirty seven percent of patients in EHFS II had new onset HF; 42 % of these patients presented with an acute coronary syndrome [10, 16, 17].
Comorbid conditions are common in patients admitted with ADHF. A history of hypertension was present in over 70 % of patients in the U.S. registries and 53 % and 62.5 % in EHFS I and II, respectively. Over 40 % of patients had diabetes in the U.S. registries (27 % and 32.8 % in EHFS I and II, respectively). Renal insufficiency was present in 30 % of patients and chronic lung disease was present in 30 % of patients in the U.S. registries.
Outcomes
There are significant differences in length of stay, in-hospital mortality, rehospitalization rates and post-discharge mortality when registry data from the US and Europe are compared. Median length of stay is 4 days in the U.S [10, 17] compared with 9–11 days in Europe [13, 16]. In-hospital mortality is approximately 4 % in the U.S. [10, 17] and 6.7 % in Europe [16].
The 60–90 day post-discharge mortality reported in OPTIMIZE-HF was 10.4 % [17]. In EHFS I, 13 % of patients died between admission and the 12-week follow-up visit. 6.9 % of patients died during the index hospitalization [13]. Readmission rate 60–90 days after discharge was approximately 30 % in OPTIMIZE and 24 % in EHFS I. An analysis of Medicare claims data found that 26.9 % of Medicare beneficiaries who were hospitalized for heart failure were rehospitalized within 30 days. However, only 37 % of patients who were rehospitalized were rehospitalized for heart failure [23].
Two large, retrospective observational studies have demonstrated reductions in hospital length of stay, in-hospital mortality, and 30-day mortality and an increase in 30 day readmission rates. An analysis from the Veterans Affairs Health Care System of 50,125 patients with a first hospitalization for HF from 2002–2006 showed a decrease in in-hospital, 30 day and 1 year mortality from 4.7, 7.1, and 27.7 % in 2002 to 2.8, 5.0, and 24.3 % in 2006, respectively (p < 0.0001). Thirty-day readmission rate for heart failure increased from 5.6 in 2002 to 6.1 % in 2006 (p = 0.11) [24]. Another analysis of 6,955,461 Medicare fee-for-service hospitalizations for heart failure between 1993 and 2006 demonstrated a decrease in in-hospital mortality from 8.5 % in 1993 to 4.3 % in 2006 and a decrease in 30-day mortality from 12.8 to 10.7 % over the same time period. Thirty-day readmission rates increased from 17.2 to 20.1 % over the same time period. The risk adjusted 30-day mortality risk ratio was 0.92 and the 30-day readmission risk ratio was 1.11 in 2005–2006 compared with 1993–1994 [25].
A large prospective observational study reported outcomes in 69,958 beneficiaries of the French national health insurance general scheme who were hospitalized with heart failure in 2009 [26]. Patients who were hospitalized for heart failure and did not have a previous diagnosis of HF or prior HF hospitalization were included in the analysis. The in-hospital mortality was 6.4 %. The 1-month, 1-year and 2-year survival rates were 89 %, 71 %, and 60 %, respectively. Heart failure and all-cause readmission free rates were 55 % and 43 % at 1 year and 27 % and 17 % at 2 years, respectively. Factors associated with a better 2 year survival rate in patients less than 70 years who survived 1 month after discharge were: female gender, age < 55 years, absence of comorbidities, and use of an angiotensin converting enzyme inhibitor or angiotensin receptor blocker, beta-blocker, lipid-lowering agent or oral anticoagulant during the month following discharge.
Classification of ADHF
Heart failure is the final common pathway for a broad range of cardiovascular disorders. Patients with ADHF have diverse underlying causes of cardiac dysfunction, time course of symptom development, co-morbid conditions and precipitants, and underlying pathophysiology. A number of attempts have been made to classify ADHF based on onset, underlying heart disease, underlying hemodynamic abnormalities and clinical profiles.
The International Working Group on Acute Heart Failure Syndromes [6] emphasized the time course of development of HF and the American College of Cardiology/American Heart Association (ACC/AHA) stage in their classification of ADHF:
- 1.
Worsening chronic heart failure: with reduced or preserved LVEF. ACC/AHA Stage C heart failure. Seventy percent of all admissions.
- 2.
De novo heart failure: most commonly caused by acute coronary syndrome (ACS); also, acute myocarditis or sudden increase in blood pressure in a patient with a non-compliant left ventricle. Many with either ACC/AHA Stage A (risk factors but no structural heart disease) or Stage B (pre-existing structural heart disease but without signs or symptoms of heart failure). Twenty five percent of all admissions.
- 3.
Advanced heart failure: severe LV systolic dysfunction, associated with progressively worsening low output state, refractory to conventional heart failure therapy and requiring specialized therapies (LVAD, heart transplant, hospice). ACC/AHA Stage D 5 % of all admissions.
The 2009 ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults [27] have described three clinical profiles of patients with ADHF that focus on clinical manifestations of congestion and systemic perfusion:
- 1.
The patient with volume overload, manifested by pulmonary and/or systemic congestion, frequently precipitated by an acute increase in chronic hypertension
- 2.
The patient with profound depression of cardiac output manifested by hypotension, renal insufficiency, and/or shock syndrome
- 3.
The patient with signs and symptoms of both fluid overload and shock.
The European Society of Cardiology (ESC) has described six clinical scenarios for patients presenting with ADHF in their 2008 Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure [2]. EHFS II used a modification of the ESC scenarios to characterize patients included in the registry [16]:
- 1.
Worsening or decompensated chronic heart failure: history of progressive worsening of known chronic heart failure. Signs and symptoms of worsening heart failure with evidence of pulmonary and systemic venous congestion. Patients can have either reduced or preserved ejection fraction. (65 % of patients in EHFS II).
- 2.
Pulmonary edema: Patients who present with severe respiratory distress, tachypnea with diffuse pulmonary rales, hypoxia with oxygen saturation < 90 % (without supplemental oxygen) with alveolar edema on chest X-ray. (16 % of patients in EHFS II)
- 3.
Hypertensive heart failure: Patients have signs and symptoms of heart failure with high blood pressure (generally ≥ 180/100 mmHg). There is commonly evidence of high sympathetic tone with tachycardia and signs of vasoconstriction. Patients are more likely to have preserved systolic function. Frequently, these patients present with evidence of pulmonary congestion without signs of systemic congestion. The response to HF therapy is generally rapid and the in-hospital mortality is low (1.5 % in EHFS II). (11 % of patients in EHFS II).
- 4.
Cardiogenic shock: Patients with evidence of end-organ hypoperfusion due to heart failure with adequate or elevated LV end-diastolic pressure. Typically, these patients have a reduced systolic blood pressure (<90 mmHg), oliguria, and low cardiac index (<2.2 L/min/m2). Many patients will also have severe pulmonary congestion. Mortality in this population is high. (4 % of patients in EHFS II)
- 5.
Isolated right heart failure: evidence of systemic venous congestion, elevated jugular venous pressure and low cardiac output without evidence of pulmonary congestion.
- 6.
Acute coronary syndrome complicated by heart failure: (This was not included as a separate classification in EHFS II) heart failure with a clinical picture and laboratory evidence of an acute coronary syndrome. Approximately 13.6 % of patients with ACS have associated signs and symptoms of heart failure [28, 29]. In EHFS II, ACS was the precipitating factor in 42 % of patients who presented with new onset or de novo heart failure and 23 % of patients who had preexisting heart failure.
A recent American Heart Association Scientific Statement on Acute Heart Failure Syndromes has also emphasized the concept of clinical profiles of patients presenting with ADHF [30].
ADHF has also been characterized by the presence or absence of systolic dysfunction. Patients with heart failure with normal or near normal left ventricular ejection fraction are described as having heart failure with preserved ejection fraction (HFpEF). Patients with heart failure with significant reduction in LVEF (and generally with left ventricular dilation) are characterized as having heart failure with reduced ejection fraction (HFrEF). Patients with HFpEF are more likely to be female, older, Caucasian, have hypertension and atrial fibrillation and less likely to have coronary artery disease. Length of stay for patients with HFpEF is similar to patients with HFrEF but in-hospital mortality is lower. Long-term survival is somewhat better in patients with HFpEF but readmission rates and functional class are similar in patients with HFpEF compared with patients with HFrEF [20, 21, 31].
Pathophysiology
ADHF is a syndrome due to a broad range of cardiovascular disorders. The underlying pathophysiology is heterogeneous and depends on the nature, time course and severity of the underlying cardiac disease and the presence and severity of non-cardiac precipitating factors. The heterogeneity of patients with ADHF makes it difficult to develop a single pathophysiologic model. Despite this heterogeneity, there are some important themes in patients with ADHF that guide the approach to patient management.
Neurohormonal Activation and Salt and Water Retention
In heart failure, there is a decrease in cardiac output that results in activation of baroreceptors in the central circulation in response to “vascular under-filling”. This causes activation of the sympathetic nervous system resulting in an increase in sympathetic outflow to the kidney and systemic vasoconstriction.
Decreased renal blood flow and sympathetic stimulation of the kidney cause release of renin from the juxtaglomerular apparatus which, in turn, results in conversion of angiotensinogen to angiotensin I which is converted to angiotensin II by angiotensin converting enzyme (ACE) and other tissue proteases. Angiotensin II is a potent vasoconstrictor that causes systemic vasoconstriction, renal arterial efferent > afferent vasoconstriction, activation of the sympathetic nervous system, stimulation of sodium retention in the proximal tubule of the kidney, release of aldosterone, release of arginine vasopressin, and stimulation of thirst centers in the brain.
Aldosterone increases sodium and water reabsorption in the distal tubule and collecting duct contributing to extracellular fluid expansion and systemic congestion. Aldosterone also increases sodium and water absorption in the colon. Hepatic congestion in the setting of elevated right atrial pressure decreases aldosterone metabolism leading to higher aldosterone levels. In heart failure, patients do not have “aldosterone escape” so that, unlike patients with isolated hyperaldosteronism, the distal tubule continues to reabsorb sodium in response to elevated aldosterone levels.
Stimulation of central baroreceptors and increased angiotensin II levels stimulate the non-osmotic release of arginine vasopressin from the posterior pituitary gland. This leads to increased free water reabsorption in the collecting ducts which worsens volume overload and leads to the development of hyponatremia.
In heart failure, retention of sodium and water is mediated by decreased systemic and renal perfusion, activation of the sympathetic nervous system and activation of the renin angiotensin aldosterone system (RAAS). In many patients, salt and water retention cannot be reversed by pharmacologic blockade of the RAAS and sympathetic nervous system suggesting that neurohormonal activation is not the only mechanism responsible for salt and water retention [32–34]. Increases in sodium and water intake are mediated by an increase in thirst caused by stimulation of central thirst centers mediated by activation of baroreceptors in the central circulation and excessive production angiotensin II. Systemic congestion is a result of an increase in total body salt and water mediated by a decrease in sodium and water excretion and an increase in intake.
Activation of the sympathetic nervous system and RAAS cause systemic vasoconstriction and an increase in systemic vascular resistance (SVR). Increases in SVR result in a decrease in stroke volume and cardiac output in patients with systolic dysfunction and an increase in functional mitral regurgitation in patients with ventricular dilation.
Pulmonary Congestion
Most patients with ADHF present with the primary symptom of dyspnea either at rest or with activity. This is true for patients with new-onset or chronic heart failure and for patients with and without systolic dysfunction. Many patients have evidence on physical exam of pulmonary and systemic venous congestion [10, 17].
Dyspnea in patients with ADHF is caused by an elevation in left atrial and pulmonary capillary pressure. The movement of fluid from the pulmonary capillary space to the pulmonary interstitium is determined by a balance between hydrostatic and oncotic pressures in the pulmonary capillary and the pulmonary interstitial space. The major factor that causes fluid to move out of the capillary is a difference between the higher hydrostatic pressure within the pulmonary capillary and the lower hydrostatic pressure in the surrounding interstitium. This movement of fluid is opposed by the difference between the colloid osmotic pressure (which is mainly provided by the concentration of albumin) in the capillary space and the interstitium, which reduces the transudation of fluid out of the capillary. In normal physiology, lymphatic washout of albumin that enters the interstitium results in an increase in the osmotic gradient between the interstitium and pulmonary capillary which reduces transudation of fluid. In normal physiology, fluid continuously moves from the capillary space into the interstitium and is then removed by the lymphatic system. When hydrostatic pressure in the pulmonary capillary significantly increases, transudation of fluid into the interstitium increases with potential for “spillover” into the alveolar space [35].
There are several protective mechanisms that prevent the development of pulmonary edema (fluid entering the alveolar space). First, the alveolar-capillary unit is composed of a thin and thick side. The thin side is made up of a capillary closely opposed to the alveolar air space. The capillary endothelium and alveolar epithelium are attenuated, the basal laminae of the alveolar epithelium and capillary endothelium are fused and the permeability to salt and water is low. The thick portion of the alveolar capillary unit contains an interstitial matrix with a gel-like protein component that separates the alveolar epithelium from the capillary endothelium. With a rise in capillary hydrostatic pressure, edema first forms in the interstitial compartment away from areas of gas exchange. Second, as fluid enters the interstitial compartment, hydrostatic pressure rises and oncotic pressure falls, which serves to oppose further movement into the interstitial space. Third, fluid that forms in the interstitium travels along a negative pressure gradient to the interlobular septae, the bronchovascular space and the hila. Edema fluid also collects in the pleural space. Lymphatic vessels in the interlobular septae, peribronchovascular sheath and pleura facilitate clearance of lung water. Pulmonary lymphatics are highly recruitable and, over time, are able to increase clearance of lung water by more than tenfold. Fourth, active Na+ transport across the alveolar-capillary barrier by type II alveolar epithelial cells lining the alveoli is responsible for clearance of alveolar edema. Na+ enters the alveolar epithelial cells through apical amiloride sensitive Na+ channels and other Na+ channels and, by a process that consumes energy, is pumped out of the cell by the Na+,K+-ATPase located in the basolateral membrane [35–40].
In patients with HFpEF or HFrEF, the LV filling pressure required to support a given amount of left ventricular work is increased. As left ventricular end-diastolic pressure (LVEDP) rises, so do left atrial and pulmonary capillary pressures. As pulmonary capillary pressure increases, there is an increase in the transmural filtration of fluid into the pulmonary interstitium. There is a point at which the capacity of the lymphatic system to remove fluid from the interstitium is exceeded and fluid begins to accumulate in the alveoli. Animal data suggest that there is a threshold beyond which interstitial fluid begins to accumulate and that the rate of fluid accumulation is linearly related to pulmonary capillary wedge pressure.
The accumulation of extravascular fluid in the pulmonary interstitium and alveoli is associated with symptoms of dyspnea, orthopnea, paroxysmal dyspnea, and impaired gas exchange. Symptoms and pulmonary function are influenced by water content of the lungs. The underlying pathophysiology of dyspnea in ADHF is multifactorial and complex with contributions from: decreased lung volume; airflow obstruction from reflex bronchoconstriction; geometric decrease in airway size from decreased lung volumes, intraluminal edema fluid and mucosal swelling; decreased lung compliance; decreased alveolar-capillary membrane conductance with acute and chronic decreases in DLCO; impaired gas exchange due to alveolar edema; arterial hypoxemia; increased work of breathing; respiratory muscle weakness in the chronically ill patient; activation of chest wall sensors, an increase in the elastic work of breathing due to vascular engorgement and cardiac enlargement with chest wall expansion past the usual or physiologic position; and stimulation of nerve endings in response to vascular distention and interstitial edema [35].
Transition from Compensated to Decompensated Heart Failure
A traditional understanding of why patients with chronic heart failure develope ADHF suggests that patients with chronic heart failure commonly experience a gradual increase in total body salt and water reflected by gradual weight gain and the gradual development of signs and symptoms of pulmonary and systemic venous congestion. While this paradigm occurs in some patients with chronic heart failure, it may not be applicable to the majority of patients with ADHF. A nested case-control study of patients referred to a home monitoring system by managed care organizations matched 134 case patients with HF hospitalization with 134 control patients without HF hospitalization [41]. Case patients experienced gradual weight gain beginning approximately 30 days before hospitalization. Within 7 days of hospitalization, weight patterns between case and control patients began to diverge more substantially with greater weight gain strongly associated with a greater odds ratio for hospitalization for ADHF (>2–5 lbs HR 2.77; >5–10 lbs HR 4.46; >10 lbs HR 5.65). However, only 46 % of case patients hospitalized for ADHF gained more than two pounds suggesting that in approximately half of patients, weight gain was not the precipitating cause of hospitalization.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
