Acute Heart Failure



Acute Heart Failure


Nicholas S. Hendren

Justin L. Grodin

Mark H. Drazner



INTRODUCTION

Acute decompensated heart failure (ADHF) is defined as new or recurrent symptoms and signs of heart failure (HF) requiring unscheduled care for impromptu therapies. Clinically, this is manifest by typical symptoms (eg, orthopnea) that may also be accompanied by signs of increased intracardiac pressure (eg, rales). HF is a clinical diagnosis based on a combination of symptoms, physical exam findings, radiographic, and/or laboratory abnormalities. Left ventricular ejection fraction (LVEF) is a key descriptor of HF. Heart failure with reduced ejection fraction (HFrEF) is typically defined as an LVEF less than or equal to 40%, and heart failure with preserved ejection fraction (HFpEF) as an LVEF greater than or equal to 50%. Heart failure with mildly reduced ejection fraction (HFmrEF) represents an LVEF of 41% to 49%. Differentiation based on LVEF is important owing to different underlying etiologies, demographics, comorbidities, and responses to therapy.


Epidemiology

ADHF remains a common reason for hospitalization. In the United States, the total estimated annual cost of HF is projected to increase to nearly $70 billion by 2030.1 An aging population, increasing rates of obesity, lower myocardial infarction mortality, and improved survival with chronic left ventricular (LV) systolic dysfunction have all resulted in a larger population with chronic HF at risk for acute decompensation.12,13


Disease Burden, Incidence, and Trends

Based on data from the U.S. National Inpatient Sample, between 2001 and 2014 more than 57 million admissions occurred for ADHF as the primary or secondary diagnosis.2 Approximately 25% of these admissions were caused by a primary HF diagnosis.2 From 2001 to 2014, the rate of hospitalization for the primary diagnosis of HF declined 3% annually from 563/100,000 U.S. adults in 2001 to 398/100,000 U.S. adults in 2014.2 This is in contrast to the rates of hospitalization for a secondary diagnosis of HF, which remained stable between 2010 and 2014 at approximately 1388/100,000 U.S. adults.2 From 2013 to 2017, on the other hand, an increase in primary HF admissions was observed, including increases in crude rates of overall and unique patient hospitalizations (JAMA Cardiol. 2021 Feb 10;e207472. doi:10.1001/jamacardio.2020.7472, PMID: 33566058).). Owing to an expanding population, the absolute number of hospitalizations for ADHF is anticipated to increase.


Hospitalization and Outcomes

Large HF registries such as the Acute Decompensated Heart Failure National Registry (ADHERE), Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) and EuroHeart Failure Survey II (EHFS II) have helped to inform our understanding of ADHF. Registries have observed that new onset HF represents 12% to 37% of admissions while patients with a known HF history represent 63% to 88% of admissions.3,4,5 These registries have demonstrated that despite declining primary HF admissions, the proportion of admissions for HFpEF is increasing. Data from Olmstead County, Minnesota, observed that admissions for HFpEF relative to HFrEF increased at a rate of 1% per year from 1987 to 2001.6 Similarly, the Get With The Guidelines-Heart Failure (GWTG-HF) registry demonstrated that the proportion of patients hospitalized with ADHF and HFpEF increased from 33% in 2005 to 39%, and those with HFrEF decreased from 52% to 47% in 2010.7 Presently, the proportions of hospitalizations for ADHF with HFrEF versus HFpEF are roughly equivalent.8,9


Demographics and Risk Factors

ADHF is the most common cause of hospitalization for patients greater than or equal to 65 years, and about 75% of HF admissions occur in patients greater than or equal to 65 years old (Figure 75.1A).2 Although the lifetime risk for HF is equal for men10 and women,2 women hospitalized for ADHF are more likely to present with HFpEF and are typically older than men.14,15,16 Women with HF are less likely to have coronary artery disease (CAD) and are more likely to have hypertension and diabetes.14,15,16 In the absence of CAD, the lifetime risk of HF is 11.4% for men and 15.4% for women, suggesting differences partly attributable to hypertension.11

Disparities for HF among different races have also been observed. The U.S. National Inpatient Sample from 2001 to 2014 observed that White patients comprised the majority of primary HF hospitalizations (˜65%), followed by Black (˜20%), Hispanic (˜10%), Asian (˜2%) patients and other races (˜3%).2 In the Multi-Ethnic Study of Atherosclerosis (MESA), incident HF was highest in Black Americans, followed by Hispanic, White, and Chinese Americans (4.6, 3.5, 2.4, and 1.0 per 1000 person-years, respectively) (Figure 75.1B).17 Black Americans have a higher rate of hospitalization and HF death, at least partially attributed to increased comorbid conditions and lower socioeconomic status.17,18 Payer status and
socioeconomic status are strongly associated with clinical outcomes in ADHF.19 HF patients without insurance are typically younger with fewer comorbidities; however, the absence of insurance is associated with longer hospitalization for ADHF, lower rate of implantable cardioverter defibrillator (ICD) implantation, lower rate of beta-blockade, decreased quality of care, and a trend toward increased in-hospital mortality compared with private payer status.19 Medicaid insurance is associated with increased risk of rehospitalization or death and repeated hospitalization compared with private payer status.20 Decreased quality of care and modest increases in adjusted length of stay for HF have also been observed for Medicare groups compared with private payer status.19 Limited data also suggest that HF may disproportionately affect lower socioeconomic classes. Approximately one-third of the admissions have been reported to occur among patients within the lowest quartile of household income.2 Lower socioeconomic status has been associated with increased mortality and higher risk of readmission for ADHF.20,21,22






Finally, patients admitted for ADHF are increasingly complex with comorbidies including CAD (50%-60%), chronic obstructive pulmonary disease (20%-30%), chronic renal disease (20%-30%), atrial arrhythmias (30%-35%), and other medical problems.2,6,15 Frailty is increasingly identified as a comorbidity (18%-54% in the elderly)23 and has been associated with a higher rate of hospitalization for ADHF, worse prognosis, and higher mortality compared with nonfrail elderly patients with HF.23




CLINICAL PRESENTATION AND DIAGNOSTIC EVALUATION

The initial evaluation of the patient with suspected ADHF should focus on an efficient and expeditious diagnosis of HF, defining the clinical profile of the patient, triaging to an appropriate level of care, and providing urgent therapies for potentially life-threatening conditions.



Physical Examination

Despite advancements in biomarkers, imaging and labs, the clinical exam remains fundamental to identifying the hemodynamic status of the patient (Table 75.2). Heart rate and blood pressure are important assessments in patients with ADHF. Tachycardia is often present either owing to arrhythmias or as a compensatory mechanism to maintain cardiac output with a reduced stroke volume. Most patients presenting with ADHF are normotensive or hypertensive. Based on the ADHERE registry, about 50% of patients presenting with ADHF have a systolic blood pressure greater than 140 mm Hg, and about 15% of patients have a systolic blood pressure greater than 175 mm Hg.38 Hypotension with a systolic blood pressure less than 90 mm Hg occurs in a minority of patients admitted with ADHF but is strongly associated with worse outcomes.3 Pulse pressure (difference between systolic and diastolic blood pressure) and proportional pulse pressure (pulse pressure/systolic blood pressure) are useful indirect crude assessments of LV stroke volume and, thus, cardiac index. For acute and chronic systolic HF, a proportional pulse pressure less than 25% is associated with a cardiac index (CI) less than 2.2 L/min/m2. 39,40,41 Increased pulse pressure may indicate underlying anemia, aortic insufficiency, thyroid abnormalities, and/or poor vascular compliance.








Jugular venous distention (JVD) is a useful estimate of right atrial pressure, but accurate assessment is highly dependent on the skills of the examiner. For most patients, higher right atrial pressure is related to a higher pulmonary capillary wedge pressure (PCWP).42 However, this association may not be true in the setting of significant tricuspid regurgitation, isolated right ventricular failure, pericardial constriction, restrictive cardiomyopathy, or a large pulmonary embolism.

Careful auscultation can reveal clinical clues about underlying cardiac function and valvular abnormalities. Despite poor interobserver agreement,43 extra heart sounds (S3 or S4) are present in at least 30% of patients admitted for ADHF.44 The presence of a third heart sound and elevated jugular venous pressure (JVP) were independently associated with all-cause death, HF death, and increased HF hospitalization.44 A right ventricular heave, pulsatile liver, or enlarged point of maximal impulse may also provide ancillary information about cardiac function.

The hepatojugular or abdominojugular reflux is an assessment of venous congestion. A positive test is defined as greater than 3 cm H2O sustained increase in JVP after ten continuous seconds of pressure on the abdomen. In the absence of isolated right ventricular failure, a positive result reliably predicts a PCWP greater than 15 mm Hg.45 Bendopnea is a recently described symptom of HF that may be present in at least 50% of patients with ADHF, reliably predicts a PCWP greater than 15 mm Hg, and may be associated with adverse long-term clinical outcomes.42,46 Bendopnea can be tested by having a patient bend at the waist while sitting to touch their feet for up to 30 seconds to assess for dyspnea.42

Rales and peripheral edema are a common physical exam finding present in half to two-thirds of patients presenting with ADHF.36 Lower extremity edema is typically symmetric, pitting and predominates in gravity dependent areas, including the legs, ankles, thighs, sacrum, abdomen, or back. Redness and erythema are often present in patients with ADHF, and bilateral erythema rarely represents cellulitis.47 Visceral congestion is common, and patients frequently report abdominal distention independent of lower extremity edema. Right-sided congestion can also result in hepatomegaly and splenomegaly, leading to right upper quadrant pain, hemorrhoids, and ascites. However, the absence of rales and peripheral edema is also frequent in patients with chronic HF caused by hypertrophy of the lymphatic system to accommodate increased venous drainage. Thus, the absence of rales and edema does not
exclude ADHF. Cool extremities with sluggish capillary refill are frequently invoked as a sign of decreased perfusion and low cardiac output. However, assessment is highly subjective and is neither a sensitive nor a specific sign of cardiac output and is thus not a reliable clinical exam finding.41 For example, in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE), trial cool extremities only had a sensitivity of 20% to detect a CI less than 2.3 L/min/m2.41 We summarize these observations to our trainees by saying, “If patients are cold, they are cold; but if they are warm, they may still be cold.”









Biomarkers

In the context of ADHF, B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are useful for the diagnosis of ADHF when clinical symptoms and exam findings are equivocal. In the Breathing Not Properly study, a sensitivity and specificity cutoff of 100 pg/mL maximized the discriminatory characteristics of BNP. A value less than 100 pg/mL had an 89% negative predictive value to rule out HF, whereas the positive predictive value was more modest, at only 79%.48 NT-proBNP has similar operating characteristics, albeit with different values for sex and age. Like any test, clinical and exam findings must be integrated to most accurately interpret the value. False positives can result from increased age, anemia, arrhythmias, infection, LV hypertrophy, pulmonary embolism, malignancy, renal failure, chemotherapy, illicit drugs, and/or myocardial infarction, among other etiologies8. False negative test results can be related to obesity or HFpEF.8 Importantly, for patients recently started on angiotensin receptor-neprilysin inhibition (ARNI) therapy, BNP may be elevated owing to inhibition of BNP degradation.49 Higher absolute levels of NT-proBNP are associated with increased risk for adverse outcomes, including HF hospitalization or cardiac death.50

With effective decongestion, NT-proBNP or BNP typically declines by >50%, and a decrease of at least 30% by discharge may be associated with better clinical outcomes.51 Studies with natriuretic peptide-guided therapies with serial measurements of natriuretic peptides have not shown clear and consistent evidence for improvement in mortality and cardiovascular outcomes and are therefore not recommended for reducing hospitalization or death in the guidelines.8

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Acute Heart Failure

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