Acute Heart Failure

Heart Failure is heart’s inability to eject blood (systolic dysfunction) or fill with blood (diastolic dysfunction), causing circulatory congestion, dyspnea, fatigue and weakness. Acute HF is a sudden reduction in cardiac performance, resulting in acute pulmonary edema and hypotension with or without peripheral edema. 
Classification: ACC/AHA)  task force divided CHF into the following stages:
  1. Stage A – At high risk for HF but without structural heart disease or symptoms of HF
  2. Stage B – Structural heart disease but without signs or symptoms of HF
  3. Stage C – Structural heart disease with prior or current symptoms of HF
  4. Stage D – Refractory HF requiring specialized interventions
  • Infections: Coxsachie virus
  • Ischemia: leading to impaired contraction or relaxation.
  • Mechanical complications of ischemia including VSD, papillary muscle rupture, rupture of chordae tendinae or mitral valve prolapse.
  • Acute valvular regurgitation due to endocarditis, prosthetic valve dehiscence.
  • Arrhythmias: Tachyarrhythmias can reduce time available for ventricular filling. there is also a loss of atrial kick in supraventricular tachyarrhythmias (e.g., atrial fibrillation).
  • Myocarditis
  • Cardiac tamponade
  • Sepsis induced cardiomyopathy
  • Takotsubo cardiomyopathy
  • Tachycardia induced cardiomyopathy
  • Pulmonary embolism
  • Anemia leading to high output cardiac failure
  • Thyrotoxicosis and pregnancy
  • Uncontrolled hypertension 
  • Wet beriberi
Symptoms & Signs
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Cardiac asthma: nocturnal dyspnea, wheezing, and cough due to bronchospasm
  • Acute pulmonary edema
  • Cerebral symptoms including altered mental status due to reduced cerebral perfusion
Physical findings
  • Systolic hypotension (in severe acute HF)
  • Jugular venous distention
  • Third and fourth heart sounds: often present, but not specific for HF
  • Pulsus alternans
  • Pulmonary rales with or without expiratory wheeze
  • Hydrothorax (pleural effusion)
  • Jaundice, congestive hepatomegaly
Differential Diagnosis
  • Acute renal failure with fluid overload
  • ARDS
  • Diffuse parenchymal lung disease
  • Pulmonary venous occlusive disease
  • Atypical pneumonia
Laboratory Tests
  • Cardiac biomarkers to rule out MI
  • BNP and N-terminal pro-BNP: Levels increase with age, renal impairment, are more elevated in women, sepsis and can be elevated in right HF from any cause.  Levels could be normal in obese people. Normal concentration of natriuretic peptides in an untreated patient is extremely useful for excluding the diagnosis of HF.
  • Urinalysis : Albuminuria, high specific gravity, low sodium level
  • Renal function: Prerenal azotemia
  • Dilutional hyponatremia in late HF
  • Liver function testing: Hepatic enzymes are frequently elevated, Elevated direct and indirect bilirubin level (late finding)
  • ECHO
  • Chest radiography
  • Cardiac MRI
Diagnostic Procedures
  • ECG
  • ECHO
  • Coronary angiogram
Pharmacologic management of acute HF (Dilators, diuretics and digoxin)
  • Loop diuretics like Furosemide, Bumetanide (1mg iv bumex is equal to 40mg iv lasix or 20mg of Torsemide).  
  • In acute heart failure, the initial intravenous diuretic dose should be equal to or greater than (eg, 2.5 times) their maintenance oral dose. For example, if pt. is taking 40mg oral lasix BID, start with 40-60mg lasix IV BID (equal to 80-120 of oral lasix). Peak diuresis typically occurs 30 minutes after administration.
  • Patients who fail to respond to diuretics, especially who have underlying renal insufficiency, may benefit from ultrafiltration to remove excess fluid.
  • There is no significant difference in the end points between continuous vs intermittent diuretics. However, continuous infusions are better hemodynamically tolerated. N Engl J Med. 2011 Mar 3;364(9):797-805 , Cochrane Database Syst Rev. 2005 Jul 20;(3):CD003178
  • Lasix/bumex drip should always be preceded by a bolus to establish the drug levels quickly.
  • In patients with decompensated heart failure and worsened renal function, a stepped up therapy with diuretics was superior to a strategy of ultrafiltration for the preservation of renal function at 96 hours. Hence, don't opt for ultrafiltration just because creatinine is high. In diuretic responsive patients, diuretics should always be the first choice therapy. CARRESS-UF study
  • After diuretics, vasodilators are the most useful medications for management of acute HF. These are contraindicated in CHF from aortic stenosis.
  • Nitroglycerin: Predominantly a venodilator, used to reduce preload in acute pulmonary edema and vasodilation of coronary vasculature. It reduces after load only at high doses. Tachyphylaxis can occur within hours with administration of high doses of nitroglycerin and the strategy of nitrate-free interval used to reduce tolerance during chronic therapy could result in adverse hemodynamic effects.
  • Nitroprusside: It causes both venous and arterial dilation. Used predominantly in hypertensive emergencies with fluid overload. Also, a useful adjuvant in acute aortic regurgitation and mitral regurgitation. Because of high potential to lower blood pressure rapidly, it needs an arterial catheter placement. Major limitation of nitroprusside is cyanide toxicity (predominantly as GI and central nervous system manifestations including nausea, vomiting, confusion, hyperreflexia and new or worsening lactic acidosis). However, it is more likely at higher doses (> 1mcg/kg/min) rather than with longer duration.
  • Nesiritide, a recombinant form of BNP, is both a vasodilator and also increases urine output by natriuresis. Nesiritide increased rates of hypotension, did not alter rates of death or re hospitalization at 30 days, and showed a borderline significant trend toward reducing dyspnea. ASCEND-HF trial.  
  • Vasodilation with hypotension and tachyarrythmias are the most common side effect of all 3 vasodilating agents.
Inotropic agents
  • Dobutamine:  Most commonly used combination of inotropic and vasodilator agent. Dosing at an infusion rate of 5–20 μg/kg/min. It has both β-1 and β-2 adrenergic agonist properties which help improve myocardial contractility (β-1) and peripheral vasodilation (β-2) .  Little added benefit to increasing the dose above 10 μg/kg per min. Patients maintained on chronic infusions for >72 h generally develop tachyphylaxis and require increasing doses. In rare cases, dobutamine can cause eosiniphilia with fever, renal failure and myocarditis. 
  • Milrinone: It is inotropic as well as systemic/ pulmonary vasodilator. Dosing is typically 0.125 -0.75mcg/kg/min. Milrinone is renally cleared and dose adjustments should be made in patients with low GFR. Because of long half life of 2 hours, it takes about 6 hours before peak effect is seen. It is a PDE inhibitor and hence preferable in advanced heart failure patients who are on β blockers. Oral eplerenone is sometimes used for long term management but evidence has been very weak. PROMISE Trial
  • Dopamine :  Dosing at an infusion rate of 5–20 μg/kg per min. At doses less than 10 μg/kg/min, it has primarily inotropic and chronotropic effects on the heart but also produces an undesirable elevation in pulmonary capillary wedge pressure (PCWP). At doses between 10 to 20 μg/kg/min, alpha-receptor mediated vasoconstriction dominates, increasing the afterload, which is unfavorable in the treatment of patients with severe left ventricular dysfunction. Dopamine is more prone to cause tachyarrhythmias and ischemic events than pure vasodilators. 
  • Levosimendan — Levosimendan is a positive inotropic drug with vasodilator effects. It is a calcium sensitizing agent and it improves myocardial efficiency without either increasing myocardial oxygen demand or impairing ventricular relaxation.. However, outcomes are not any better than dobutamine or milrinone. SURVIVE Trial , J Cardiothorac Vasc Anesth. 2016 Jun;30(3):639-46 , J Clin Diagn Res. 2016 Dec; 10(12): UC05–UC08 
  • Norepinephrine: It has both β1 and α actions leading to inotropic and vasopressor effect. It is more preferred to epinephrine in cardiogenic shock, as epinephrine can promote thrombosis in the coronary vasculature.
  • Epinephrine: An alternative to norepipnephrine and dobutamine combination but no additonal benefit. Crit Care Med. 2011 Mar;39(3):450-5.  It also increases myocardial oxygen demand and hence, not a good choice in cardiogenic shock due to cardiac ischemia. Epinephrine does have α action at higher doses and can cause vasoconstriction and mesenteric ischemia. 
  • Used to support systemic blood pressure in patients with HF
  • Dopamine , norepinephrine, Epinephrine , Phenylephrine , Vasopressin.   
Other therapy
  • Digoxin : Useful in LV dysfunction with atrial fibrillation or flutter associated with rapid ventricular rate. The goal is to keep levels between 0.5 to 1. 
  • Oxygen therapy
  • Positive pressure ventilation (PPV) if oxygenation is inadequate despite supplemental O2
  • Preload reduction with leg elevation and nitrates. (Can use nitro patch).  
  • Morphine to decrease stress, catecholamine levels, tachycardia, and ventricular overload. Morphine in acute pulmonary edema causes venodilation and decrease pulmonary congestion. 
  • ACE inhibitors/ARB's to reduce afterload and preload. 
  • BIDIL, a combination of hydralazine (reduce after laod) and nitrates (reduce pre load), can be used in patients allergic to ACEi and ARB's. 
  • Entresto is recently approved by FDA to use instead of ACEi or ARB's. It is a combination of valsartan , an angiotensin receptor blocker (ARB), and sacubitril which is a neprilysin inhibitor. It has been shown to have better outcomes than enalapril. PARADIGM-HF trial
Role of PA catheter in acute heart failure:
PA catheters has been traditionally used in decompensated heart failure to titrate inotropes, vasopressors and diuretics. However, studies showed that use of PA catheter has been shown to offer no benefit or even increase mortality. ( SUPPORT Trial , PAC-Man Trial  , ESCAPE Trial ), Crit Care. 2006; 10(Suppl 3): S8 . My opinion on this is that PA catheter itself is not any more harmful than any central line. However, PA catheters have been proven to be more harmful because of the way PA wave forms and PA pressures are misinterpreted. Lot of times, the PA catheter is not even properly wedged or not in proper cardiac axis. The readings in those situations are highly erroneous and may lead to inadverent fluids or diuretics. Also, some physicians are more obsessed in normalizing cardic output/index and PCWP at the cost of ignoring the patient variables. My take home message is that unless somebody absolutely knows how to use PA catheter, we should not be using them. Putting a PA catheter in place and just relying on non invasive cardiac monitors like Vigilance to look at the numbers is even more dangerous. 
Monitoring , if PA catheter is placed
 Therapeutic goals
  • PCWP of 15–18 mmHg
  • Right atrial pressure of 5–8 mmHg
  • Cardiac index > 2.2 L/min per m2
  • Systemic vascular resistance of 800–1200 dyne • s/cm5
Refractory cardiac shock:
Use of advanced modalities like IABP, Impella, LVAD, RVAD and VA ECMO can be considered.
  • IABP: inflation during early diastole increases coronary artery perfusion pressure and increases diastolic BP by 15-30% and increases SBP as well. It helps with diastolic augmentation of blood pressure. When on IABP, always take BP readings from pump. Pump can be tuned to 1:1, 1:2, 1:3 augmentation.  The primary goal of IABP treatment is to improve the ventricular performance of the failing heart by facilitating an increase in myocardial oxygen supply and a decrease in myocardial oxygen demand. It is indicated in acute MI, acute heart failure, Acute MR and post cardiac transplant. When patients are on IABP, they need to be on full dose anticoagulation, especially when they are on 1:2 or 1:3.
  • Impella: A step up therapy from LVAD and provides for more cardiac output. For simplification, If LVAD was to be considered a 50hp motor, impella can be considered as a 100hp motor. It can provide cardiac output upto 3 liters/min. However, it needs ongoing anticoagulation and major side effects incluse mechanical hemolysis. 
  • Tandem Heart: It is a device that withdraws oxygenated blood from an inflow cannula that is placed via the femoral vein in the left atrium through a transseptal puncture. Oxygenated blood returns to a pump, which sits outside the patient and is then returned via a cannula placed within the femoral artery. The TandemHeart device is capable of providing 4 to 5 L of flow. 
  • LVAD: There is no wide variation between systolic and diastolic BP readings and the only reading we see on LVAD is a MAP. An excellent article to help with basic understanding of  LVAD can be found here.
Cardiogenic shock:
The goal of therapy is do maintain adequate perfusion pressure and adequate blood flow to the tissues. Please remember not to chase the numbers (CO, CI, and PCWP) blindly. The main drugs used are –
  • Inotropes: Milrinone and dobutamine predominantly cause increase in stroke volume and cardiac output, and modest decrease in systemic vascular resistance and pulmonary capillary wedge pressure. 
  • Vasopressors: used to maintain perfusion pressure, even though they have a theoretical risk of increasing afterload and thereby dropping cardiac output.
  • IABP: Predominantly indicated for MI with cardiogenic shock, not responding to medical therapy. However, it was not found to be any superior to early revascularization therapy. IABP-SHOCK II
  • Impella: In IMPRESS Study, Intra-Aortic Balloon vs. Impella Shows Similar Mortality Rates in MI complicated by Cardiogenic Shock.
  • VA ECMO: When everything else fails.
Major studies:
  1. CARESS-HF study: While ultra-filtration was an effective method for fluid volume removal, which provided similar amounts of weight loss to stepped pharmacologic therapy, it was inferior to stepped pharmacologic therapy for preservation of renal function at 96 hours and was associated with a higher rate of adverse events.  Hence, Ultra filtration is reserved for patients who do not achieve an adequate response to an aggressive diuretic regimen. 
  2. Dopamine vs Levophed: Dopamine, as compared with norepinephrine, was associated with an increased rate of death at 28 days among patients with cardiogenic shock. SOAP II study
  3. Levophed + Dobutamine vs Epinephrine: When considering global hemodynamic effects, epinephrine is as effective as norepinephrine-dobutamine. Nevertheless, epinephrine is associated with a transient lactic acidosis, higher heart rate and arrhythmia, and inadequate gastric mucosa perfusion. Thus, the combination norepinephrine-dobutamine appears to be a more reliable and safer strategy. Crit Care Med. 2011 Mar;39(3):450-5
  • Acute decompensation of HF with occult cause may be due to MI, valve lesions or thrombosis of prosthetic valve. Also, rule out dietary noncompliance.
  • Do not give vasodilators in CHF from severe aortic stenosis
  • A normal CxR doesn’t always exclude heart failure.
  • Hepatojugular reflux: Manual compression of the right upper quadrant to increase venous return may elevate jugular venous pressure above the transient 1 to 3 cm elevations seen in normal individuals. 
  • Pulsus alternans: It is virtually pathognomonic of severe left ventricular failure. This phenomenon is characterized by evenly spaced alternating strong and weak peripheral pulses.
  • There was no significant difference in efficacy or safety end points for bolus versus continuous infusion. 
  • During diuresis, some patients experience symptomatic hypotension with decreasing cardiac output and systemic blood pressure due to a lag in re-equilibration of intravascular volume via movement of fluid from the interstitial space.  However, it doesn’t mean to stop diuretics. Instead, can be switched to a continuous infusions which are much more hemodynamically tolerant. Or cut the dose into half and continue with diuresis if hypervolemic.
  • If the BUN rises and the serum creatinine is stable or increases minimally, it reflects a stable GFR. If the patient is still fluid overloaded, the diuretics should be continued.
  • Worsening renal parameters by themselves are not the sole criterion for stopping diuretics. In the presence of elevated central venous pressure and hypervolemia, renal function may improve with diuresis.
  • If patient is hypervolemic but serum creatinine is increased with diuretics, it may reflect intravascular volume depletion and adjunctive inotropic therapy may be required.
  • For patients in whom the diuretic response is inadequate, iv chlorthiazide or oral metolazone or spironolactone are reasonable choices as a second diuretic. Chlorothiazide is the only thiazide diuretic that can be given intravenously (500 to 1000 mg/day).
  • Cardiac resynchronization therapy (CRT) with biventricular pacing can improve symptoms and survival in selected patients who are in sinus rhythm and have a reduced left ventricular ejection fraction with a prolonged QRS duration.
  • In CHF, digoxin appears to be safe at optimal serum concentrations of 0.5 to 0.8. However, in A.fib, levels need to be maintained around 1.5-1.8.
  • Equivalent doses of diuretics are 40mg of oral lasix = 20 mg of oral torsemide = 1mg of oral bumex. For both bumex and torsemide, oral bioavailability is 80-100%. For lasix, oral bioavailability is only 50%.
  • Treatment of CHF from severe mitral regurgitation involves diuretics, decreasing afterload with nitrates and IABP.
  • ACC/AHA recommends dopamine for cardiogenic shock due to STEMI. Norepinephrine can be used for refractory hypotension.
  • Lactic acidosis from cardiogenic shock needs bicarb therapy only for Ph<7.10. Vasopressor responsiveness is not affected for Ph> 7.10.
  • In patients with EF less than 30%, an AICD is indicated. Atleast, they should be discharged on life vest. 
  • In patients with EF less than 35% and QRS>120ms, cardiac resynchronization therapy (CRT) can be considered. 
  • Sepsis can cause both systolic and diastolic dysfunction. 

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