Heart Failure

Definitions

• AHA defines HF as a complex clinical syndrome with symptoms and signs that result from any structural or functional impairment of ventricular filling or ejection of blood.¹
• Impairment can occur during systole, diastole, or both.
• The most common causes of HF are ischemic heart disease and myocardial infarction, hypertension (HTN), and valvular heart disease, although other causes are listed below (Table 1).¹
• The number of patients with HF in the United States has been increasing, partly due to an aging population, improved survival, and increased recognition and diagnosis.¹

Classifications

• The New York Heart Association (NYHA) classification (Table 2) is widely used to categorize and track patients’ symptoms of cardiac-related congestion and functional capacity. It has been identified as an independent predictor of mortality.²
• The American College of Cardiology and AHA have proposed the terminologies stage A: at risk for HF, stage B: pre-HF, stage C: symptomatic HF, and stage D: advanced HF (Table 2).¹
• Another commonly used classification considers left ventricular (LV) ejection fraction (Table 2).

Systolic vs Diastolic HF

• Systolic HF is characterized by abnormalities in the ventricular pressure-volume relationship during systole that include decreased EF, stroke volume, and stroke work.³
• When HF is accompanied by a predominant or isolated abnormality in diastolic function, this clinical syndrome is called diastolic HF and can occur in the presence or absence of systolic dysfunction.³
• Diastolic HF is characterized by a ventricle that is unable to accept an adequate volume of blood during diastole due to abnormalities in ventricular relaxation (an active energy-consuming process) and/or ventricular stiffness (a passive process).³ This can lead to symptoms even at rest (NYHA IV).
• Ventricular pressure, volume, stress, and strain can change during systolic and diastolic dysfunction.3
• While patients with systolic HF have an overall higher mortality than those with diastolic HF, data show that in patients older than 70 years of age, the mortality rates for systolic and diastolic HF are nearly equivalent.³
• The morbidity rate regarding outpatient visits, hospital admissions, and the expenditure of significant healthcare resources is nearly identical between patients with systolic vs diastolic HF.³

Diagnosis

• In addition to a history and physical examination, routine evaluation of patients with HF includes laboratory testing, electrocardiography, and cardiac imaging.
• Laboratory evaluation includes tests regarding patients’ comorbidities, suitability for and adverse effects of treatments, potential causes or confounders of HF, and severity and prognosis of HF.¹
• Measurement of the biomarkers B-type natriuretic peptide (BNP) and N-terminal prohormone of BNP can be useful in supporting or excluding the diagnosis of HF. Still, there is little evidence to support the use of absolute values for guidance in treatment.¹
• Please see the OA summary on atrial and B-type natriuretic peptides for more details. Link
• Electrocardiography provides information not only on rate and rhythm but also on QRS morphology, potential causes, and prognosis in HF.
• Cardiac imaging can include chest X-ray, echocardiography (transthoracic, transesophageal, and stress echocardiography), cardiac magnetic resonance (CMR), cardiac computed tomography, and radionuclide imaging, including single-photon emission computed tomography (SPECT) and positron emission tomography (PET).
  • Chest x-ray is used to assess for cardiac size and silhouette, evidence of pulmonary congestion, and any other causes of the patient’s symptoms.¹
  • Echocardiography can be the most useful tool for obtaining dynamic diagnostic information. Echocardiography is primarily used to assess cardiac structure and function, to estimate filling pressures, and to identify subclinical LV systolic dysfunction; other imaging modalities can provide additional information. Echocardiography can also be performed serially to monitor trends and surveillance of cardiac structure and function.¹
• In addition to non-invasive imaging (stress echocardiography, SPECT, CMR, PET), invasive angiography or computed tomography coronary angiography can detect coronary artery disease (CAD). This is useful because CAD and myocardial ischemia are the leading causes of HF; thus, detection of myocardial ischemia can guide management.¹
• Myocardial viability can be assessed; however, the STICH trial (Surgical Treatment for Ischemic Heart Failure) showed that myocardial viability did not correlate with greater long-term benefit from surgical revascularization in patients with ischemic cardiomyopathy.⁴
• Invasive evaluations such as right heart catheterization and endomyocardial biopsy have not been proven to provide sufficient helpful information unless there are uncertain hemodynamics, shock states, acute respiratory distress, or a need for histologic diagnosis that will actually influence treatment decisions.¹

Treatment Options for HF

• Patients with HF or at risk for it are recommended to maintain a healthy lifestyle through diet, physical activity, maintenance of a normal weight, normal blood pressure, normal blood glucose levels, and abstinence from smoking.¹
• Once HF has developed, consideration should be given to management with GDMT, which encompasses evaluation, testing, pharmacologic, and procedural treatments.¹
• The four primary medication classes currently included in GDMT are angiotensin receptor-neprilysin inhibitors, beta blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter 2 inhibitors.¹
• Once GDMT is optimized, further management may include cardiac implantable devices and interventional therapies, such as implantable cardioverter-defibrillators (ICDs) and cardiac resynchronization therapy (CRT). Several trials have shown benefit and a reduction in sudden cardiac death with an ICD in patients with reduced EF.¹ CRT has also been shown to reduce mortality and hospitalizations in patients with prolonged QRS duration regardless of HF stage.¹
• Advanced HF may eventually require surgical intervention.
• When valvular dysfunction is present as a sequelae of HF, transcatheter or surgical repair or replacement may be indicated.
• MCS has been shown to improve survival and function in the short and long term in patients with NHYA class IV symptoms despite optimal GDMT.¹
• Durable left ventricular assist devices have advanced with successive generations and, with appropriate patient selection, can yield significant improvements in mean survival and health-related quality of life.¹ Absolute and relative contraindications are listed below (Table 3).¹
• Please see the OA summary on ventricular assist devices for more details. Link

• Additionally, patients with factors such as elevated central venous pressure, pulmonary HTN, coagulopathy, and inability to tolerate anticoagulation have had poorer outcomes.¹
• MCS can be permanent, also known as destination therapy, or temporary, also known as bridge therapy, to allow for stabilization or temporization until cardiac transplantation.
• Patients presenting in cardiogenic shock can receive temporary MCS via Impella devices, ECMO, and/or intra-aortic balloon pump.
• Cardiac transplantation can be performed for eligible patients with stage D HF that is refractory to GDMT, surgical optimization, and MCS. A heart transplant can confer benefits not only to patients with cardiac origin HF, but also to patients with systemic conditions that are complicated by HF. As in MCS, appropriate patient selection is critical and is described by the International Society for Heart and Lung Transplantation.

Acute HF

• An acute presentation of HF or cardiogenic shock must trigger an evaluation of the severity of congestion and adequacy of perfusion, with consideration for treatment of worsening ischemic disease, acute infection, inflammation, or other reversible precipitating causes.¹
• Symptoms of acute HF include, but are not limited to, pulmonary edema, hypotension, severe HTN, arrhythmia, elevated BNP, elevated lactate, impaired renal function, elevated liver function tests, acidosis, altered mental status, cold extremities, and weak pulses.¹
• Inotropic agents and vasopressors can be used to improve hemodynamics and increase cardiac output. Invasive arterial and filling pressure monitoring should be considered.
• Continuation of GDMT during hospitalization for acute HF, when hemodynamically possible, has been shown to lower the risk of post-discharge death and readmission compared with discontinuation, especially regarding beta blocker therapy.¹
• There should be careful monitoring of fluid status, intake and output, and laboratory results. Diuretic therapy can be initiated and continued despite small changes in serum creatinine.¹
• Patients hospitalized with acute HF are at increased risk of venous thromboembolism (VTE) and therefore should receive VTE prophylaxis.¹
• As previously described, MCS can also be used in acute HF.

Preoperative Evaluation of HF patients

• Perioperative management of patients with HF can be challenging. Identification of these patients with a thorough history and physical with review of their diagnostic testing, including cardiac imaging, is critical.
• Perioperative complications are more likely in patients with decreased functional capacity, typically defined as less than 4 metabolic equivalents. A history of acute decompensation in HF within the past 6 months is associated with adverse perioperative outcomes and the presence of HF at the time of major vascular surgery is related to a 12-fold higher risk of perioperative mortality.⁵
• Worsening symptoms can indicate disease progression and may warrant further diagnostic workup if prior testing is insufficiently recent.
• Depending on the urgency and type of surgery, all efforts should be made to ensure the patient is optimized regarding their HF prior to proceeding with surgery. Optimization aims to relieve symptoms and improve functional capacity.
• Careful attention must be paid to the patient’s GDMT, pharmacologic therapy, and the timing of their last dose.

Intraoperative Management of HF patients

• Intraoperative management of patients with HF may include local, regional, neuraxial, and general anesthesia. Major surgery has shown comparable outcomes between regional and general anesthesia.⁵
• Irrespective of method, the anesthetic goals are as follows:⁵
  • Heart rate control by maintaining sinus rhythm and avoiding tachycardia
  • Maintaining adequate preload and avoiding fluid overload
  • Maintaining adequate perfusing pressure and avoiding excessive afterload
  • Maintaining contractility, possibly with inotropic therapy
  • Preserving cardiac output
  • Minimizing myocardial work as much as possible
• If regional or neuraxial anesthesia is selected, then this may lead to afterload reduction and decreased myocardial work, but careful management of hemodynamics is required as blood flow must still be adequately maintained for organ perfusion, and diastolic blood pressure must be maintained for coronary perfusion.⁵
• General anesthesia with IV and inhaled anesthetics can also cause vasodilation.
• Inotropes and vasopressors should be selected judiciously based on the patient’s cardiovascular structure and function.
• Additionally, consideration should be given to the reduction in circulation time in patients with HF and the increased time to effect of intravenous agents.⁵
• Careful management of patients at the conclusion of anesthesia may also be required as restoration of sympathetic tone and shifting of blood volume during emergence from general anesthesia or the resolution of the neuraxial blockade can cause decompensated HF.⁵
• Fluid overload and hemodynamic instability at any time can lead to pulmonary edema, pulmonary HTN, and right ventricular (RV) dysfunction. In such patients, vasodilators and inodilators may be useful.⁵
• Strong consideration should be given to using invasive arterial BP monitoring, especially in patients with hemodynamic instability, on vasopressors, and at risk of rapid blood loss or fluid shifts.⁵
• Central venous pressure monitoring may be used as well to guide management, although it is less reliable for indicating fluid responsiveness than dynamic measurements such as systolic pressure variation, pulse pressure variation, and stroke volume variation.⁵
• Premature atrial contraction (PAC) may also be considered, although some studies have shown possible harm rather than benefit from its use.⁵ The value of PACs may be in critically ill high-risk patients with circulatory dysfunction to use pulmonary artery pressures, cardiac output measurements, and filling pressures to differentiate between shock states and guide management.⁵
• Transesophageal echocardiography can also be used to identify states such as hypovolemia, LV and RV dysfunction, myocardial ischemia, pericardial effusion or tamponade, pulmonary embolism, valvular dysfunction, or LV outflow tract obstruction as possible causes of hypotension.⁵
• Patients with advanced HF with cardiac devices such as ICD or CRT require careful attention to the management of these devices; many will need reprogramming for the intraoperative period.
• Management of patients with MCS devices also requires careful planning and vigilant monitoring. Often, perfusionists, VAD technicians, or other specialized personnel may be required to assist in managing the patient and their MCS device.

Postoperative Management of HF patients

• Postoperative complications that can arise are cardiogenic shock, pulmonary edema, myocardial ischemia, malignant arrhythmias, acute renal failure, acute congestive hepatic dysfunction, and cardiac arrest.⁵
• Patients should be managed in facilities knowledgeable about HF and equipped with monitors for cardiac activity, oxygenation, fluid balance, and renal function.⁵
• Inotropic medications may need to be continued, and GDMT medications should be restarted when appropriate.⁵