馬偕急診醫學科主治醫師 龔律至

Differential DiagnosisPulmonary embolismPericarditis AsthmaCOPD Pneumonia, pneumonitis, lung fibrosis……High cardiac output ： anemia, thyroid disorder

Heart failureA complex clinical syndrome that can result from any

structural or functional cardiovascular disorder causing systemic perfusion inadequate to meet the body’s metabolic demands

There are many ways to assess cardiac function. However, there is no diagnostic test for HF, since it is largely a clinical diagnosis that is based upon a careful history and physical examination.

Heart failure Systolic dysfunctionDiastolic dysfunction 

HistoryDyspnea, ankle or abdominal swelling ： excess fluid accumulationFatigue, weakness ： reduction in cardiac output Classic exertional angina usually indicates ischemic heart diseaseAcute HF after an antecedent flu-like illness suggests viral

myocarditisLong-standing hypertension or alcohol use suggests hypertensive

or alcoholic cardiomyopathyPrimary valvular dysfunction should be considered in a patient

with a cardiac murmur.

CLINICAL ASSESSMENT HistoryPhysical examinationDiagnostic tests

INITIAL TESTSElectrocardiogram (ECG)Chest radiograph EchocardiographyExercise testingComplete blood count (CBC)Baseline evaluation of glucose, electrolytes liver function and

BUN/creatineBrain natriuretic peptide (BNP) and N-terminal pro-brain

natriuretic peptide (NT-pro-BNP)

Initial stabilization Airway assessment to assure adequate oxygenation and ventilation,

including continuous pulse oximetryVital signs assessment with attention to hypotension or

hypertensionContinuous cardiac monitoringIntravenous accessSeated postureDiuretic therapyVasodilator therapyUrine output monitoring (perhaps with urethral catheter placement)

Tailor the therapy to the individual patientThe mainstay of therapy for these abnormalities in the acute

setting is vasodilator and diuretic therapy. Flash pulmonary edema (due to hypertension) ： require

aggressive vasodilatory therapy. Normotension and volume overload ： best respond to a

combination of diuretic therapy and vasodilators. Hypotension and intravascular overload ： may respond

either to diuretics alone or in combination with inotropes.

Supplemental oxygen and assisted ventilation Non-rebreather facemask delivering high-flow percent oxygenIf respiratory distress, respiratory acidosis, or hypoxia persist ：

noninvasive positive pressure ventilation (NPPV) as the preferred initial modality of assisted ventilation

Intubated for conventional mechanical ventilation with positive end-expiratory pressure (PEEP)

Oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90%

DiureticsPatients with ADHF are usually volume overloaded. Even in the less common situation in which cardiogenic

pulmonary edema develops without significant volume overload (eg, with hypertensive emergency, acute aortic or mitral valvular insufficiency), fluid removal with intravenous diuretics can relieve symptoms and improve oxygenation

Patients with aortic stenosis with volume overload should be diuresed with caution.

Diuretic dosingFurosemide(Lasix)– 40 mg intravenouslyBumetanide(Burinex)– 1 mg intravenouslyPatients who are treated with loop diuretics chronically may need

a higher dose in the acute setting; the intravenous dose should be equal to or greater than (eg, 2.5 times) their maintenance oral dose and then adjusted depending upon the response

Peak diuresis typically occurs 30 minutes after administrationAddition of an aldosterone antagonist (spironolactone) is

recommended in selected patients with systolic HF to improve survival.

Sodium and fluid restrictionThe 2013 ACC/AHA guidelines suggest some degree (eg,

<3g/d) of sodium restriction in patients with symptomatic HF.The 2013 ACC/AHA guidelines suggest fluid restriction (eg,

1.5 to 2 L/d) in patients with refractory HF, particularly in patients with hyponatremia.

Vasodilator therapyvasodilators such as intravenous ： nitroglycerin,

nitroprussideNitroglycerin — reduces left ventricular filling pressure

primarily via venodilation. At higher doses, the drug variably lowers systemic afterload and increases stroke volume and cardiac output.

Longer half-life of isosorbide dinitrate compared to intravenous nitroglycerin (four hours versus three to five minutes)

NitroprussideNitroprusside is a potent vasodilator with balanced venous

and arteriolar effects producing rapid reduction in pulmonary capillary wedge pressure and increase in cardiac output.

Initial dose 5 to 10 mcg/min, dose titrated up to every five minutes, dose range 5 to 400 mcg/min

Hypertensive emergency, acute aortic regurgitation, acute mitral regurgitation, or acute ventricular septal rupture.

The dose is generally titrated to maintain a systolic blood pressure >90 mmHg or mean arterial pressure > 65 mmHg.

ADDITIONAL THERAPYACE inhibitors and ARBs Inotropic agents Vasopressor therapy Beta blockers Aldosterone antagonist therapy Venous thromboembolism prophylaxisMorphine sulfate

ADDITIONAL CONSIDERATIONS Mechanical cardiac assistance Ultrafiltration

Additional therapy Among patients with ADHF, the role of angiotensin inhibition

depends upon whether the patient is already receiving such therapy.

Continued therapy —  maintenance oral therapy can be cautiously continued during an episode of ADHF in the absence of hemodynamic instability or contraindications.

Initiation of therapy — Do not recommend this approach. (the first 12 to 24 hours)

Inotropic agents Dobutamine or milrinone may be helpful in selected patients

with severe left ventricular systolic dysfunction and low output syndrome.

The 2013 American College of Cardiology Foundation/American Heart Association guideline on HF recommended short-term continuous intravenous inotropic support to maintain systemic perfusion and preserve end-organ performance until definitive therapy (eg, coronary revascularization, mechanical circulatory support, or heart transplantation) is instituted or resolution of the acute precipitating problem has occurred.

Specific agents Milrinone ： a phosphodiesterase inhibitor that increases

myocardial inotropy by inhibiting degradation of cyclic adenosine monophosphate. Other direct effects ： reducing systemic and pulmonary vascular resistance (via inhibition of peripheral phosphodiesterase) and improving left ventricular diastolic compliance

Specific agentsDobutamine ： primarily on beta-1 adrenergic receptors, with

minimal effects on beta-2 and alpha-1 receptors. The hemodynamic effects of dobutamine include increase in stroke volume and cardiac output, and modest decreases in systemic vascular resistance and pulmonary capillary wedge pressure

It should be started at 2.5 mcg/kg/min and, if tolerated and needed, can be gradually increased to 20 mcg/kg/min

Specific agents ： DopamineLow doses of 1 to 3 µg/kg/min ： acts primarily on dopamine-1

receptors to dilate the renal and mesenteric artery beds3 to 10 µg/kg/min ： also stimulates beta-1 adrenergic

receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate.

Medium-to-high doses ： dopamine also stimulates alpha-adrenergic receptors (although a small study suggested that renal arterial vasodilation and improvement in cardiac output may persist as the dopamine dose is titrated up to 10 µg/kg/min)

VasopressorUsed as a temporizing measure to preserve systemic blood

pressure and end-organ perfusion. Vasopressor use should be limited to patients with persistent

hypotension with symptoms or evidence of consequent end-organ hypoperfusion despite optimization of filling pressures and consideration of the use of inotropic agents.

In this setting, invasive monitoring can be helpful to assess filling pressures and systemic vascular resistance.

Beta blockers Must be used cautiously in patients with decompensated HF

with systolic dysfunction because of the potential to worsen acute HF due to systolic dysfunction

For patients on chronic beta blocker therapy, if the degree of decompensation is mild without hypotension or evidence of hypoperfusion, continuation of beta blocker as tolerated is recommended.

For more severely ill patients, halving of the dose of beta blockers or discontinuation may be necessary.

Do not initiate a beta blocker in the early management of acute HF

Aldosterone antagonist therapy Patients who have New York Heart Association (NYHA)

functional class II HF and an LVEF ≤30 percent; or NYHA functional class III to IV HF and an LVEF ≤35 percent; and patients post-ST elevation myocardial infarction who are already receiving therapeutic doses of ACE inhibitor, have an LVEF ≤40 percent, and have either symptomatic HF or diabetes mellitus. The serum potassium should be <5.0 meq/L and estimated glomerular filtration rate should be ≥30 mL/min per 1.73 m2

Venous thromboembolism prophylaxis Prophylaxis against venous thromboembolism (deep vein

thrombosis and pulmonary embolism) with low-dose unfractionated heparin or low molecular weight heparin.

ADHF who have a contraindication to anticoagulation, venous thromboembolism prophylaxis with a mechanical device (eg, intermittent pneumatic compression device) is suggested.