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  1. Treatment of HF depends on accurate phenotyping based on the principles in Part 1. First critical inquiry is if malperfusion or CS is present, which requires rapid triage and escalation of medical support, and if appropriate consideration of mechanical circulatory support, with the intent to prevent multisystem organ failure.
    1. Treatment goals in HF: One can think about treating HF in the ICU based on what physiologic parameters we can adjust and intervene upon (independent variables) (see Table 18.5).
    2. Acute decompensated HF (ADHF), without malperfusion (“warm and wet” phenotype), typically treatment relies on:
      1. Adjusting preload: Intravenous diuretics targeting filling pressure goals, urine output, pulmonary edema, and clinical signs of congestion including JVP. Serial assessment of NT-proBNP may also guide diuresis when approaching euvolemia. The amount of daily diuresis tolerated will vary based on the patient and degree of congestion, but most clinicians consider net 1 to 2 L negative per day adequate for routine ADHF, and the average weight loss across HF hospitalizations is about 4 kg. Careful attention to avoid overdiuresis on a day-to-day basis; meaning patients may remain total volume up but do not tolerate rapid shifts in intravascular volume due to rapid diuresis and become intravascularly hypovolemic. This may manifest as hypotension or AKI. If this occurs, then provide a “diuresis holiday” where diuretics are typically held for 24 hours to allow the patient’s intravascular and extravascular volume to equilibrate before resuming diuretics.
        1. Agents like nitrates may also reduce venous return (as well as provide modest LV afterload reduction and coronary vasodilatation).
        2. Morphine is used in myocardial infarction in part for reduction of symptoms but also impacts preload and myocardial oxygen demand. Caution as opiates can impair absorption of enteral P2Y12 agents.
      2. Adjusting afterload: A ventricle that has difficulty ejecting against a high afterload will be encouraged to eject blood antegrade by reducing the force against which it has to pump. As a result, by reducing LV afterload, systemic vasodilators may increase blood pressure by increasing cardiac output in a patient with LV systolic HF. Analogously, RV afterload reduction can be achieved with pulmonary vasodilators.
      3. Pay attention to offending medications: Beta blockers and calcium channel blockers, with negative inotrope effects, for example, may precipitate ADHF and need to be dose adjusted or held in the acute setting.
    3. Advanced HF (ADHF), including LCOS and CS: More advanced strategies are required when malperfusion is an issue. Some of these patients will not respond to diuresis without support of perfusion and/or may be unable to tolerate a trial of vasodilators.
      1. Various tools assist the ICU clinician in treating advanced HF:
        1. Central line: transduce central venous pressure (CVP) to assess venous congestion, as a surrogate for volume status and RV filling pressures. Trend central venous oxygen saturation (proxy for cardiac output)
        2. Pulmonary arterial line: (also called right heart catheter, or Swan- Ganz catheter; see Chapters 1 and 6): can assess LV filling pressures, measure mixed venous oxygen saturation (thereby also used to calculate Fick cardiac output), and thermodilution cardiac output. Hemodynamic data obtained from PA lines is helpful in cases of isolated cardiogenic and mixed shock including cases of complex biventricular disease, severe valvular disease, pericardial disease, uncertain volume status, pulmonary hypertension, or when pharmacologic or mechanical circulatory support are needed.
        3. Venous oxygen saturation: Central venous and mixed venous oxygen saturations differ in that the first is measured from the superior vena cava (or central vein) whereas that the latter is measured from the proximal pulmonary artery and includes blood return mixing from the inferior vena cavae and the coronary sinus, which is the most deoxygenated blood in the body after the heart extracts oxygen. Mixed venous saturation will therefore typically be lower than central venous saturation by 5% to 10%.
        4. Arterial line: for invasive hemodynamic monitoring while titrating vasoactive medications
        5. POCUS/critical care echo: Evaluation of biventricular function, valvular disease, LVOT obstruction, pericardial effusion. Particularly helpful if rapid clinical change occurs, as ultrasonography can be repeated quickly at bedside. Be aware of what is not evaluated on bedside ultrasound and the negative and positive predictive values (see Chapter 3). Thoracic POCUS to evaluate for B-lines (pulmonary edema), lung sliding (for pneumothorax), and pleural effusions.
      2. “Tailored therapy”: Describes a targeted approach to optimize the ICU patient with advanced HF, by titrating medications to optimize preload, afterload, and cardiac output through serial hemodynamic measurements; tailored therapy works toward a goal cardiac index >2.2 L/min/m2, SVR 800-1200 dynes/sec/cm-5, MAP typically > 60-65 mm Hg, and specific ventricular filling pressures.
      3. Preload optimization: Goal is optimization of LV end-diastolic volume and pressure. Because we cannot measure LVEDP directly at the bedside, we measure the pulmonary capillary wedge pressure (PCWP) which acts as a surrogate for LA pressure which itself approximates left ventricular end-diastolic pressure. These assumptions may be confounded depending on which West lung zone the right heart catheter tip is in, by intrinsic pulmonary disease (fibrosis, veno-occlusive disease, pulmonary vein stenosis), mitral valve disease, ventricular interdependence, and noncompliant LV.
        1. Typical PCWP goal 10-12, but higher in patients with acute MI or restrictive heart disease where the ventricle compliance is lower. Targeting a higher PCWP is also favored in patients who require higher LV preload to maintain a normal cardiac output, including patients with severe AS and those with severe LV systolic dysfunction. In the ICU, clinicians can utilize pulmonary artery line hemodynamics to assess stroke volume and cardiac output at different filling pressures.
        2. Many patients with advanced HF are operating at filling pressures higher than optimal by their Starling curve and may need diuretic drips or renal replacement therapy to achieve euvolemia if diuretic nonresponsive (see Chapters 3 and 25).
        3. RV filling pressure is assessed by CVP, and patients with noncompliant RV may require CVP goals that are higher.
        4. Closely monitor input fluid and output fluid balance in the ICU. Many medications require high infusion rates that may contribute to volume overload; work with the ICU pharmacist to concentrate or change agents to avoid obligate fluid inputs.
      4. Afterload optimization: Goal is optimization of LV myocardial oxygen demand and reduction in wall stress. Systemic vascular resistance (SVR) is given by the formula (MAP - CVP)/CO × 80. SVR can be useful but must be considered in context of the patient’s MAP and also with some caution because estimates of CO may bring their own sources of error to the SVR calculation. A typical SVR goal range is 800 to 1200, and patients with advanced HF will have calculated SVR much higher. By reducing the SVR, the intent is to allow the ventricle to eject. Various parenteral vasodilators can be used for this purpose. However, in patients who are in shock, the first goal must be maintaining a MAP for adequate end-organ perfusion (MAP > 60-65). Some patients with decompensated advanced HF present with hypotension caused by low cardiac output resulting in compensatory sympathetic activation leading to elevated SVR; despite an elevated SVR, their hypotension must initially be treated with vasopressors. As there is improvement in hemodynamics, a switch from vasopressor to vasodilator can be considered, often guided by PA line hemodynamics.
      5. Contractility optimization: In the ICU, contractility can be directly augmented with inotrope infusions. Inotropes have a variable effect on MAP and SVR, as some are inopressors and some are inodilators. Inotropes are also generally positive chronotropes, and thus tachyarrhythmia is a common side effect. Contractility is not routinely measured directly in ICU clinical care. Typical goal is improvement in the cardiac index (which summates contributions from all of the aforementioned interventions) to more than 2.2 L/min/m2. If pharmacologic intervention is insufficient, mechanical circulatory supports are available in contemporary practice; consult with your hospital HF service, at an early stage, before metabolic dysfunction due to CS becomes severe or irreversible.
      6. Mechanical circulatory support: See Chapter 19. Devices in contemporary practice include:
        1. Intra-aortic balloon pump
        2. Percutaneous ventricular assist device (LV, RV, or both)
        3. Paracorporeal ventricular assist device (LV, RV, or both)
        4. Veno-arterial extracorporeal membrane oxygenation
        5. Durable ventricular assist device (primarily LV)
    4. Medications: Tenets of HF treatment in ICU as well as inpatient and outpatient contexts. Specific classes and their medications include:
      1. Diuretics
        1. Intravenous loop diuretics (furosemide, bumetanide)
          1. DOSE trial found no significant differences in symptoms, weight loss, net diuresis, or renal function with bolus versus continuous infusion diuretic in ADHF. However, intensification of bolus dosing was associated with weight loss, symptom reduction, and net diuresis.
          2. In practice, diuretic infusions are often employed as they allow patients to maintain a continuous diuresis without relying on clinicians to reorder or adjust bolus dosing in a timely manner. Some data from ICU literature suggests that continuous infusion may be more effective in patients in the ICU.
        2. Diuretic resistance: Loop diuretic alone may be inadequate especially in older patients, advanced HF, and renal dysfunction. Adjunct blockade may be useful and may include thiazide-type diuretics (intravenous chlorothiazide, oral metolazone) that target the distal renal tubule. Newer data suggest acetazolamide may be an adjunct in ADHF.
          1. In states of significant renal congestion (elevated visceral and central filling pressures) limiting adequate renal perfusion, or in the setting of severe kidney injury, renal replacement therapy may be needed.
          2. Consider whether perfusion must be optimized with inotropes first in order to facilitate renal perfusion and diuresis.
      2. Inotropes: Parenteral agents that boost contractility are divided into inodilators and inopressors based on variable effects on blood pressure.
        1. Inodilators: May cause hypotension and could need to be used with vasopressors. Pure inodilators are helpful if SVR is high and patient is normotensive.
          1. Milrinone: Phosphodiesterase inhibitor. Increases contractility and vasodilation. Half-life 2 to 3 hours, longer with renal impairment as renally cleared (up to 20 hours on renal replacement therapy). Provides pulmonary vasodilation, helpful with RV failure. Watch for ventricular arrhythmia and hypotension.
          2. Dobutamine: Beta-1 agonist, increasing contractility and chronotropy, and also β-2 agonist that can cause vasodilatation. Onset 2 minutes, half-life 2 minutes. Increased risk of ventricular arrhythmias
          3. DoReMI trial found no difference on composite CS outcomes with dobutamine versus milrinone.
        2. Inopressors: Provide vasoconstriction along with inotropy and thus may be needed if there is hypotension.
          1. Norepinephrine: Agonist at α-1, α-2, and β-1 receptors. Alpha-1 agonism provides vasoconstriction and β-1 agonism provides inotropy and chronotropy.
          2. Epinephrine: Similar pattern to norepinephrine but provides β-2 agonist activity, and with β effects greater than α effects. Epinephrine can be helpful for RV failure.
          3. Dopamine: targets dopamine, β-1, and α-1 receptors in a dose-dependent manner, providing inotropy and chronotropy at mid-range doses (>5 μg/kg/min) and vasopressor activity via α receptors at high doses (10 μg/kg/min).
          4. SOAP II trial evaluated vasoactive agents across multiple shock phenotypes and found more tachyarrhythmias and increased mortality risk in dopamine group.
          5. Wean inotropes first, as fluid and afterload status are optimized; this is because in general inotropes cannot be continued out of the ICU setting, but oral diuretics and oral vasodilators are available.
        3. Parenteral vasodilators
          1. Nitroprusside: potent arterial vasodilator (NO pathway), caution in renal failure: byproduct cyanide, methemoglobin. Caution with severe unrevascularized CAD, impaired cerebral perfusion (can cause steal).
          2. Nitroglycerin: Venous (2/3) > arterial dilation (1/3). Venodilatation reduces RV preload, improves pulmonary edema. Coronary vasodilator activity. Tachyphylaxis if on continuous infusion.
          3. Other options include nicardipine and clevidipine.
    5. Optimization of ventilator mechanics/positive end-expiratory pressure (PEEP): PEEP decreases LV afterload and preload. Optimal PEEP decreases RV preload and optimizes pulmonary vascular resistance (decreases atelectatic lung, optimizes oxygenation, both of which decrease pulmonary vascular resistance [PVR] and RV afterload), though nonoptimized PEEP can increases RV afterload. Ventilation and correction of hypercarbia decreases PVR and optimizes RV afterload.
      1. Maintaining adequate exogenous oxygenation is important to support oxygen delivery. Analogously, maintaining Hb in terms of oxygen- carrying capacity may be a goal.
    6. Guideline-directed medical therapy (GDMT): In contemporary practice, HF patients with reduced EF use four “pillars” of medication classes, designed to improve EF and reduce HF events:
      1. Renin-angiotensin-aldosterone system (RAAS) In HF patients, low perfusion pressure results in RAAS activation through baroreceptor response and increased sympathetic tone. Initially a compensatory mechanism, RAAS activation progresses to having detrimental effects by increasing both preload and afterload and adverse cardiac remodeling.
        1. Renin-angiotensin inhibitors: (ACEI, ARB, and sacubitril-valsartan): Provides afterload reduction in addition to RAAS inhibition. Side effects include hypotension, acute kidney injury (AKI), hyperkalemia, postoperative vasoplegia (particularly cardiac surgery). Typically hold 48 to 72 hours prior to surgery.
        2. Aldosterone antagonism (spironolactone, eplerenone): Provides diuretic and antihypertensive effect. Side effects include hyperkalemia and hyponatremia.
      2. Beta antagonist: Inhibits the heightened sympathetic tone that is activated in HF patients. Besides hemodynamic effects, these agents impact cardiac remodeling. Typically continued in the perioperative period.
      3. SGLT-2i: Some proposed mechanisms of its beneficial effect include optimization of cardiac energy metabolism, inhibition of adverse cardiac remodeling, diuresis and blood pressure lowering. It is a glycosuric that can increase the risk for UTIs. May also trigger euglycemic diabetic ketoacidosis particularly if patients are NPO. Hold this agent if patient NPO or unable to take adequate nutrition, and approximately 72 hours prior to surgery.
      4. In general, holding GDMT during acute HF is associated with higher risks of hospital mortality, short-term mortality, and rehospitalization (meta-analysis for β blockers and registry data for ACEI/ARB). Guidelines suggest to not hold GDMT for mild aberrations in blood pressure or renal function; however, shock may preclude use of β blockers and vasodilators. Titration and reinitiation of GDMT agents typically conducted once the patient has left the ICU and is on the inpatient unit.