Perioperative Considerations for Heart Failure

Pharmacological treatment of SysHF

Management of HF by pharmacological or nonpharmacological interventions aims to improve functional capacity by producing symptomatic relief, improving the quality of life, and reducing the death rate. In multiple trials, the use of statins has prevented adverse cardiovascular events in patients with MI, acute coronary syndrome, and those with elevated cardiovascular risk.^[14] Improved survival has been seen in patients with SysHF by the use of β-blockers, angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs), and mineralocorticoid receptor antagonists. β-blocker therapy, in the form of bisoprolol, carvedilol, metoprolol succinate, and nebivolol, can potentially reduce mortality in patients with SysHF.^[10] If the patient has a sinus rhythm, a resting heart rate of ≥70 beats/min, and an LVEF of ≤35%, ivabradine can be used.^[15] For patients with LV dysfunction, irrespective of symptoms, ACEi is considered the first-line therapy. ACEi can reduce the risk of MI and death rate if the patient has HF.^[15] In the perioperative period, the continuation or stoppage of ACEi therapy must be decided on a case-to-case basis. The use of ACEi should be continued if indicated to prevent cardiac remodeling. ACEi therapy should be discontinued when major blood loss, hypovolemia, or renal dysfunction is anticipated. If the patient develops an intolerable cough or angioedema, ACEi can be replaced with an ARB. A combination of sacubitril, a neprilysin inhibitor, and an ARB (valsartan), called angiotensin-receptor neprilysin inhibitor (ARNI), has shown a reduction in hospitalization from HF and mortality rate.^[16] In the PARADIGM-HF trial, a randomized controlled trial, the ARNI, when compared with enalapril in symptomatic patients with SysHF, caused a significant reduction in the composite endpoint of cardiovascular death or HF hospitalization by 20%.^[17] Sodium-glucose cotransporter-2 inhibitors (SGLT2i) such as dapagliflozin or empagliflozin have shown reduced hospitalization and mortality rates in both diabetic and non-diabetic patients with SysHF.^[18] SGLT2i causes osmotic diuresis and natriuresis, leading to a reduced preload and afterload, which favors myocardial remodeling.^[19,20] Due to the potential risk of perioperative normoglycemic ketoacidosis, it is recommended to stop SGLT2i, preferably 3 days (or five half-lives) or at least 24 h before elective surgery. Despite the availability of a wide range of therapeutic agents, there is a need to develop newer, innovative therapies that are effective and well tolerated, with no concern for renal toxicity, hyperkalemia, or hypotension. Newly diagnosed SysHF patients should receive medical therapy for at least 3 months before elective surgery.^[21]

Non-pharmacological treatment of systolic HF

Cardiac implantable electronic devices (CIEDs) are the cornerstone of non-pharmacological therapy for patients with SysHF. CIEDs help prevent sudden cardiac death and treat dyssynchrony. An implantable cardioverter defibrillator reduces the risk of sudden death caused by arrhythmias in patients with SysHF. Cardiac resynchronization therapy (CRT) has the potential to reduce hospitalizations and mortality and improve symptoms and quality of life for patients who have a LVEF ≤35%, a sinus rhythm, left bundle branch block with a QRS duration ≥150 ms, and New York Heart Association (NYHA) class II-IV symptoms.^[22,23] MCS therapy is reserved for patients with SysHF who continue to have symptoms despite optimal medical therapy. The short-term MCS devices include the intra-aortic balloon pump (IABP), extracorporeal life support, and extracorporeal membrane oxygenation. An IABP supports the circulation in patients with myocardial ischemia undergoing percutaneous or surgical revascularization or to treat cardiogenic shock. Indications for durable MCS include recurrent hospitalizations for HF, NYHA class III-IV symptoms, rising need for diuretics, inability to taper off inotropes, persistent symptoms despite CRT, and end-organ dysfunction caused by low CO. Cardiac transplant is advised for patients with end-stage HF (stage D) to improve survival and quality of life.

Treatment of DiastHF

Non-pharmacological management of patients with DiastHF consists of moderate exercise, abstinence from smoking, weight control, dietary modifications such as restricting fluid intake (≤1.5–2 L/d) and sodium (2–3 g/d), and management of comorbidities. Diuretics are recommended for fluid overload and systemic/pulmonary congestion. Anticoagulation should be considered in patients with chronic HF who can develop thromboembolism. Control of heart rate can be achieved with oral β-blockers therapy in patients with chronic AF, while intravenous amiodarone is used for NYHA class IIIIV patients.^[24] ACEi and ARBs are the preferred choices for control of BP in patients with hypertension and DiastHF. SGLT2i has the potential to reduce the hospitalization rate and mortality rate in patients with DiastHF.^[25]

Preoperative assessment

The history, including the assessment of the NYHA functional class, gives a reasonable estimate of the severity of HF. Patients with congestive HF, especially those with a history of recent decompensation, must be identified in the pre-operative period. History of ADHF in the past 6 months is associated with adverse perioperative outcomes. The presence of HF at the time of major vascular surgery is related to a 12-fold higher risk of perioperative mortality.^[23] The chances of perioperative complications rise if the patient is unable to sustain 4 “metabolic equivalents” of exercise.^[26] Worsening exercise tolerance or the recent use of additional pillows may indicate disease progression. Physical evaluation can detect peripheral and pulmonary edema, as well as an S₃ heart sound. Anemia, infection, electrolyte abnormality, and involvement of other organ systems such as liver and kidney by appropriate testing should be detected and managed. Any structural or functional anomaly of the heart should be ruled out by echocardiography. Significant CAD, as an etiology for HF, can be diagnosed by cardiac catheterization. Risk assessment involves awareness of the etiology of HF, the magnitude of symptoms of HF, concomitant cardiac or non-cardiac risk factors for morbidity/mortality, and the urgency and type of surgery.

Optimization of treatment

Optimization of medical therapy is aimed at providing symptomatic relief from HF and improving functional capacity. The medical therapy for HF often consists of diuretics, β-blockers, and ACEi or ARBs. These medications help in decongestion, control of heart rate, and reduction of afterload, respectively, consequently decreasing the myocardial work. Most anesthesiologists omit ACEi and ARBs on the morning of surgery to avoid the chances of perioperative hypotension. The probable mechanism is volume depletion and the inability to activate the sympathetic nervous system. Hypotension is treated with careful volume expansion and/or administration of vasopressor or inotropic agents. Other medications to treat HF are generally continued in the intraoperative and post-operative period. The heart rate is aimed at around 80 beats/min, and symptomatic arrhythmia, if any, should be treated. Administration of digoxin is known to reduce the frequency of postoperative supraventricular arrhythmias, although its perioperative role is not clearly defined. A recent systematic review and meta-analysis on rhythm versus rate control in postoperative atrial fibrillation after cardiac surgery suggests no clear advantage to either rhythm or rate control.^[27] External defibrillation pads should be placed in patients with ADHF, since defibrillation, cardioversion, or pacing may be required if the patient develops hemodynamically unstable arrhythmias. Elective surgery should be performed after optimization of medical management and thorough assessment of the risk-benefit ratio. Pre-operative stabilization and optimization in the intensive care unit (ICU) is reserved for high-risk patients undergoing elevated-risk surgery.

Intraoperative management

The goals of anesthesia for patients with HF undergoing surgery include (i) control of heart rate by avoiding tachycardia and maintaining sinus rhythm, (ii) maintenance of preload with careful titration to avoid fluid overload, (iii) avoidance of an increase in afterload, and (iv) maintenance of contractility. Peripheral, minor procedures can be performed under local or regional anesthesia. For major surgery, both general and regional anesthesia have shown equal outcomes. Irrespective of the anesthetic technique, the CO should be preserved, and the myocardial work should be minimized during the perioperative period.

Invasive arterial BP monitoring is used when beat-to-beat monitoring of BP is required, for example in patients with prior LV dysfunction, hemodynamic instability, on vasopressors, or at risk of rapid blood loss or large fluid shifts. Central venous pressure (CVP) monitoring is required when there is potential for blood loss and/or large fluid shifts, as well as the likelihood of administration of vasoactive drug infusions. CVP, however, is a poor indicator of fluid responsiveness and is not reliable in patients with pulmonary vascular disease, valvular heart disease, RV dysfunction, and chronic airflow limitation. For volume responsiveness, dynamic indices such as systolic pressure variation, pulse pressure variation, or stroke volume variation, derived from many available technologies are more useful. Pulmonary artery (PA) catheter should not be used routinely, since the studies have not shown any benefit, but possible harm from its use.^[28] In selected patients (e.g. severe HF, pulmonary hypertension, large fluid shifts), it is reasonable to insert a PA catheter to measure PAP and CO, if the practice setting is appropriate. The PA catheter seems particularly valuable in critically ill high-risk patients with circulatory dysfunction. The measurement of CO can differentiate shock states into hypovolemic etiology (low CO with low filling pressures), cardiogenic etiology (low CO and high filling pressures), and distributive etiology (high CO and low systemic vascular resistance). Furthermore, the measurement of CO and filling pressures allows the distinction between LV or RV dysfunction or global dysfunction. For RV dysfunction, the PA catheter (PAC) can further differentiate between RV dysfunction predominantly related to increased afterload (high PAP) and dysfunction related to pump failure (high CVP and low PAP). Intraoperative transesophageal echocardiography (TEE) is a useful asset to establish the etiology of any unexplained, sustained, or life-threatening hemodynamic instability. TEE may identify 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.

Optimization of preload is essential, and the non-compliant ventricle must be allowed to fill in during diastole. To achieve adequate filling, one must avoid tachycardia to increase the duration of diastole, aggressively treat arrhythmias, and maintain higher than usual CVP. The factors that may promote tachycardia include endotracheal intubation, surgical stimulus, hypovolemia, anemia, hypoxia, hypercapnia, postoperative pain, nausea, and vomiting. In patients with HF, atrial contraction’s contribution is significant to the ventricular filling and maintenance of CO. Loss of “atrial kick,” as happens in AF, will decrease the preload and CO significantly. An acute increase in afterload can cause a decrease in CO. Maintenance of myocardial contractility helps maintain an adequate CO. Patients with HF have increased sympathetic tone to maintain CO and can develop circulatory collapse after induction of anesthesia. For patients with severe systolic dysfunction, inotropic therapy might be preferable to fluid administration for ensuring end-organ perfusion. Anesthetic agents causing myocardial depression might be avoided or administered in low doses. If severe diastolic dysfunction in a small non-compliant LV is identified, adequate preload should be maintained. Underfilling the LV may result in decreased CO and concomitant hypotension, even if the LVEF is normal. For acute decompensation in the perioperative period, the use of inotropes may become necessary.

Anesthesia for patients with Stage A and Stage B HF centers around the optimization of drug therapy and the avoidance of drugs that worsen HF. Perioperative fluid balance, analgesia, temperature, and rhythm should be closely monitored. For Stage C and Stage D HF patients, perioperative fluid balance, medical management, and anesthetic management are challenging. The evidence for the superiority of one technique over another is lacking.^[24] Adequate premedication allays anxiety and avoids sympathetic stimulation. A short-acting opioid such as alfentanil attenuates the sympathetic response to intubation. General anesthesia can be induced with a short-acting benzodiazepine such as midazolam, a hypnotic (e.g. etomidate or ketamine, or a low dose of propofol), a moderate dose of an opioid (e.g. fentanyl), lidocaine to obtund the tachycardia response to laryngoscopy and intubation, and a neuromuscular blocking agent with a rapid onset. The clinical relevance of adrenal suppression after a single dose of etomidate for induction is controversial.^[29] Administration of etomidate is associated with higher rates of adrenal insufficiency and mortality in patients with sepsis, whose adrenal function is already suppressed. Keeping the slow circulation in mind, the induction dosages of most anesthetic agents are reduced by 30–50%, and induction may be prolonged in patients with HF.^[30]

Whether the anesthetic agents affect the diastolic function or not, the clinical data are scarce. Sevoflurane preserves diastolic relaxation better than propofol during spontaneous respiration but not during positive pressure ventilation.^[31] Sevoflurane can decrease arterial tone and increase arterial stiffness, thereby leading to a change in the ratio of arterial elastance to ventricular elastance, which is a measure of coupling. Altered ventriculoarterial coupling due to sevoflurane can contribute to reductions in overall cardiac performance, particularly in patients with compromised cardiovascular function. Effective analgesia, by the use of regional techniques or epidural administration of local anesthetics and narcotics, reduces the stress response to surgery. The afterload reduction and vasodilation caused by epidural analgesia reduce the myocardial work. However, the blood flow to the cerebral, renal, and coronary circulations should not be compromised. Diastolic BP must be maintained, as the coronary artery perfusion occurs during diastole, and many patients with HF do have associated CAD. 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.^[32]

Patients with severe diastolic dysfunction and DiastHF are at high perioperative risk due to the persistently elevated LA pressures. Fluid overload and hemodynamic instability make these patients susceptible to pulmonary edema, post-capillary pulmonary hypertension, and RV systolic dysfunction.^[33] In patients with ADHF, fluid overload, and systemic hypertension, the use of vasodilators (e.g. nitroglycerin, nitroprusside) or inodilators (e.g. milrinone) is reasonable to reduce LVEDP and myocardial oxygen consumption. The drugs with positive lusitropic effects, such as phos-phodiesterase III inhibitors (milrinone) and calcium channel sensitizers (levosimendan), play a significant role in the management of circulatory failure. Milrinone acts by increasing calcium ion uptake. Levosimendan is an inodilator that increases the sensitivity of the heart to calcium, thus increasing cardiac contractility. Thus, systolic myocardial contractility is enhanced, while diastolic relaxation is preserved or improved. The 2021 ESC HF guidelines suggest levosimendan (or a phosphodiesterase inhibitor) rather than dobutamine if reversal of the effects of β-blockade is necessary to treat hypoperfusion.^[34-36] However, the vasodilatory effect of levosimendan makes it unsuitable for treating patients with hypotension or cardiogenic shock and may require simultaneous administration of other inotropes or vasopressors. With these hemodynamic goals and the physiology of HF in mind, perioperative invasive monitoring and postoperative care in the ICU should be considered for major surgeries.

Post-operative management

Post-operative complications that may develop in patients with HF include cardiogenic shock, low CO syndrome, pulmonary edema, MI, ventricular fibrillation, acute renal failure, congestive hepatopathy, and cardiac arrest. Monitoring of oxygen saturation, supplemental oxygen, and careful fluid balance is required in the post-operative period. Postoperatively, renal failure can develop due to impaired glomerular filtration rates. If oliguria develops, euvolemia, normal perfusion pressure, and CO should be assured before diuretics are administered. Non-steroid anti-inflammatory drugs can potentiate renal insult. ACEi or ARBs should be restarted at the earliest. Patients of HF with refractory hypotension or pulmonary edema may require inotropic support and post-operative ICU care.