An alternate way of defining this would be by the effect on ejection fraction . HF with preserved EF refers to patients with an EF > 50%, while HF with reduced EF refers to patients with an EF < 40%. Borderline preserved EF is defined by HF with an EF of 41-50%.The most common form is HF with reduced EF, which is primarily related to a decrease in the functional myocardium .Additional causes include excessive pressure overload from hypertension, valvular incompetence, and cardiotoxic medications. HF with preserved EF occurs due to impaired ventricle relaxation and filling, which accounts for 30-45% of all HF cases.This form of HF results in increased end-systolic and diastolic volumes and pressures and is most commonly associated with chronic hypertension, coronary artery disease, diabetes mellitus, cardiomyopathy, and valvular disease. Both systolic and diastolic HF can present with similar symptoms due to elevated, left-sided intracardiac pressures and pulmonary congestion.Right ventricular failure most commonly results from LV failure. As the right side of the heart fails, increased pressure in the venacaval system elevates pressure in the venous system of the gastrointestinal tract, liver, and extremities, resulting in edema, jugular venous distension, hepatomegaly, bloating, abdominal pain, and nausea.High-output HF is associated with normal or greater-than-normal cardiac output and decreased systemic vascular resistance.The associated decrease in after load reduces arterial blood pressure and also activates neurohormones,cannabis growing which increase salt and water retention.
Diseases that may result in high-output HF include anemia, large arteriovenous fistula or multiple small fistulas, severe hepatic or renal disease, hyperthyroidism, beriberi disease, and septic shock.In AHF, peripheral vascular flow and end-organ perfusion decrease, causing the body to compensate by neurohormonal activation , ventricular remodeling, and release of natriuretic peptides.These mechanisms are chronically activated in HF, but worsen during acute exacerbations, resulting in hemodynamic abnormalities leading to further deterioration. Continued progression can result in a critical reduction to end-organ blood flow, leading to severe morbidity and mortality.Patients with HF are classified into one of four classes, primarily determined by daily function, using the New York Heart Association, American College of Cardiology/American Heart Association, or European Society of Cardiology Guidelines.These systems help determine the appropriate interventions to reduce the likelihood of developing severe LV dysfunction, thereby reducing the patient’s potential morbidity and mortality.Other means of classification depend on the presence of cardiomyopathy or acute coronary syndrome . The Nohria-Stevenson classification for decompensated HF in the setting of cardiomyopathy uses perfusion and congestion, while the Killip and Forrester classification systems evaluate AHF in the setting of ACS.In general, short-term mortality is low for well-perfused groups and is higher in poorly-perfused patients.Unfortunately, these classification systems are not as useful for acute exacerbation of HF, thereby limiting their applicability in the ED setting. In the ED, classification is based upon the patient’s hemodynamic status, perfusion, and blood pressure.This differentiation can guide therapy and provides important prognostic information.
Most patients are hypertensive or normotensive upon presentation.The hypertensive form is commonly associated with pulmonary edema, which may occur rapidly .In the normotensive progressive form, systemic edema is predominant.Hypotensive AHF is associated with end-organ hypoperfusion, while systemic and pulmonary edema is minimal. ACS can occur simultaneously with or exacerbate HF and requires emergent coronary angiography.Right-sided HF is associated with right ventricular dysfunction, leading to systemic venous congestion without pulmonary edema if the LV is not involved.Due to the complex pathophysiology involved in HF and multiple phenotypes , the history and physical examination may vary. Patients with HF are heterogeneous in terms of the cardiac structure and function, the etiology of their HF, the precipitant of the AHF exacerbation, comorbidities, and current medications. Early diagnosis is vital, as a delay or misdiagnosis has been associated with an increased risk of adverse outcomes and death.Misdiagnosis occurs in up to one-third of patients upon initial presentation.While no single historical factor or examination finding can significantly reduce the likelihood of HF in isolation, initial clinical gestalt has been shown to have a sensitivity of 61% and specificity of 86% for the diagnosis.Risk factors for HF include hypertension, renal disease, heart disease, diabetes, male gender, older age, and obesity.58-61 In particular, advanced age, renal disease, and lower blood pressure are associated with increased mortality in AHF.Precipitating factors for AHF exacerbation can include cardiac and non-cardiac causes.Cardiac causes include uncontrolled hypertension, dietary or medication noncompliance, aortic dissection, dysrhythmias, and cardiac ischemia.Noncardiac causes include pulmonary disease, endocrine disease, infection, worsening renal function, anemia, and medication side effects.Patients who are noncompliant with their diet and medications have been found to have a lower EF, higher brain-type natriuretic peptide levels, and greater congestion when compared with their counterparts.
Dysrhythmias are another frequent precipitating cause. Among those, atrial fibrillation is the most common.ACS is more commonly associated with de novo HF.Components of the history such as weight gain, dyspnea, chest pain, peripheral edema, substance abuse, new medications, past complications, prior hospitalizations, diet changes , and medication compliance are vital to determine the underlying etiology, and an identifiable trigger can be found in approximately 60% of patients.Acutely, the most common symptoms associated with AHF include paroxysmal nocturnal dyspnea , orthopnea, and edema.The most common manifestation is dyspnea or edema from elevated LV filling pressures.However, the classic symptoms such as PND, dyspnea, and orthopnea demonstrate poor sensitivity and specificity .On examination, an S3 heart sound has the highest specificity, ranging from 97.7–99%, but it has only 12.7% sensitivity.Additionally, an S3 heart sound can be difficult to detect in the ED setting, and inter-rater reliability can be poor.Hepato-jugular reflux and jugular venous distension possess a specificity of 93.4% and 87% and sensitivity 14.1% and 37.2%, respectively, for HF.Lung auscultation is also less reliable, as the presence of rales has a sensitivity of approximately 60% and a specificity approaching 70%.Lower extremity edema has a sensitivity of 50% and specificity 78%.A meta-analysis evaluating various signs and symptoms in patients with dyspnea found that no single sign or symptom was sufficiently able to rule out AHF, chronic obstructive pulmonary disease, asthma, or pulmonary embolism.However, elevated jugular venous pressure,cannabis grow racks third heart sound, and lung crepitations were strongly suggestive of a diagnosis of AHF.Laboratory assessment in the patient with suspected AHF can provide important diagnostic and prognostic information.Testing should include a complete blood count, basic metabolic panel with renal function testing, liver function testing, troponin, and a BNP level.Abnormalities in liver function are found in approximately 75% of patients with AHF and are associated with more severe disease.If the right ventricle is involved, bilirubin and alkaline phosphatase levels may be elevated, while left sided disease is more commonly associated with elevated transaminase levels.Renal function is an important assessment, as it is a predictor of disease severity and mortality.Decreased glomerular filtration rate is associated with increased length of in-hospital stay, short-term mortality, and long-term mortality.In patients with AHF, every 10 mL/minute decrease in GFR is associated with an increase in mortality of 7%.Troponin testing can assist in prognostication and in the detection of underlying ischemia as a potential inciting event for AHF. Elevated troponin levels are associated with higher re-hospitalization rates and 90-day mortality.Troponin elevation is common in AHF, as one study found elevated troponin levels in 98% of patients with diagnosed AHF, with 81% of the levels above the 99th percentile.Other studies have suggested that this may be closer to 30-50%.However, an elevated troponin is not specific for ACS and may be seen with a variety of other causes, including demand ischemia and renal dysfunction.
BNP is produced by cardiac myocytes when exposed to significant myocardial stretch. Use of BNP and NTproBNP may be sensitive, but not specific for the diagnosis of AHF. Levels less than 100 picograms per milliliter for BNP have demonstrated a sensitivity and specificity of 93.5% and 52.9%, respectively, with negative likelihood ratio of 0.2.Other conditions associated with elevations in natriuretic peptide levels include pulmonary embolism, pulmonary hypertension, valvular heart disease, and acute respiratory distress syndrome. BNP levels of 100-400 pg/mL and NT-proBNP levels of 300-900 pg/mL are non-specific and may require further testing.Although these biomarkers may assist in differentiation of other conditions, studies have not demonstrated improved patient-centered outcomes with use of natriuretic peptides.Observational trial data suggest natriuretic peptides demonstrate sensitivity over 90%, but specificity is poor.Data from randomized, controlled trials found that knowledge of the BNP levels did not significantly change the ED treatment, mortality, or readmission rates; however, it may decrease hospital length of stay and total cost.Imaging is an important component in the patient with suspected heart failure. The most common modality used is the chest radiograph . Several findings suggest the diagnosis of heart failure on CXR, including cardiomegaly, central vascular congestion, and interstitial edema .However, a normal CXR should not be used to exclude the diagnosis of AHF, as up to 20% of CXRs may appear normal in AHF.4,102-106 Studies evaluating physician accuracy with identifying AHF on CXR have demonstrated sensitivities of 59- 74.5% and specificities of 86.3-96%.While CXR should not be used to exclude AHF, it can be valuable for identifying alternate disease processes that may mimic AHF.Bedside ultrasound can be valuable for diagnosing AHF, with high specificity and positive likelihood ratios . Ultrasound can be used to evaluate for B-lines, pleural effusions, inferiorvena cava size and respiro-phasic variability, and cardiac contractility.B-lines are vertical artifacts that result from sound wave reverberation through fluid-filled pulmonary interstitium. The presence of greater than three B-lines in two bilateral lung zones defines a positive lung ultrasound examination.The number of lung zones examined varies in the literature, with eight thoracic lung zones used in the initial lung ultrasound protocols, while newer studies have used four or six lung zones. B-lines demonstrate high sensitivity and specificity for interstitial edema,while the identification of pleural effusions is not as helpful.Assessment of EF on ultrasound may be assessed with visual assessment or quantitative measurements. Qualitative visual estimation is made by assessing the inward movement of the interventricular septum and inferior wall of the LV during systole.E-point septal separation is a quantitative measurement assessing the distance between the anterior mitral valve leaflet and ventricular septum. An EPSS measurement > 7 mm is suggestive of an EF < 50%.Ultrasound can also estimate intravascular volume through the measurement of inferior vena cava diameter and percentage change during the respiratory cycle. However, diagnostic performance is controversial, with many confounding factors and a wide range of sensitivities and specificities.One study found that by using a combination of lung, cardiac, and inferior vena cava ultrasound, the authors were able to improve diagnostic accuracy by 20%.Others have suggested that combining CXR with ultrasound may increase the sensitivity and specificity for diagnosing AHF.The State of Maryland is at the forefront of healthcare reform in the U.S. The state is unique in its implementation of an all-payers payment system for hospitals. The system is governed by the Health Services Cost Review Commission , which sets hospital rates for all providers for both inpatient and outpatient services.In 1977 the federal government granted the state a Medicare waiver that required government payers to abide by HSCRC hospital rates. Global Budget Revenue is a revision of this waiver and was implemented in 2014. GBR drives a value-based healthcare service by setting global budgets for acute care hospitals, i.e., creating a capitated system for hospitals. In 2011, Maryland implemented the Total Patient Revenue program, a revenue constraint policy designed by the HSCRC. TPR was implemented as a pilot project in 12 Maryland hospitals located primarily in rural and geographically isolated parts of the state. Under TPR, these pilot hospitals were guaranteed a certain annual revenue calculated from a formula based on the prior year’s revenue and reasonable annual adjustments. This structure provided an incentive to control costs by reducing unnecessary hospitalizations and inpatient resources. Communities were rewarded for the development of robust outpatient resources and improving the health of the population. Based on the success of TPR, the state and federal government moved forward with GBR on a statewide basis.On January 1, 2014, the State of Maryland began the GBR program with the main goals of improving the health of communities, improving the patient experience, and lowering the cost of healthcare services for all patients.