Download Dyspnea in the elderly

馬偕急診醫學科
主治醫師 龔律至
Differential Diagnosis
 Pulmonary embolism
 Pericarditis
 Asthma
 COPD
 Pneumonia, pneumonitis, lung fibrosis……
 High cardiac output：anemia, thyroid disorder
Heart failure
 A 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 dysfunction
 Diastolic dysfunction
History
 Dyspnea, ankle or abdominal swelling： excess fluid accumulation
 Fatigue, weakness：reduction in cardiac output
 Classic exertional angina usually indicates ischemic heart disease
 Acute HF after an antecedent flu-like illness suggests viral myocarditis
 Long-standing hypertension or alcohol use suggests hypertensive or
alcoholic cardiomyopathy
 Primary valvular dysfunction should be considered in a patient with a
cardiac murmur.
CLINICAL ASSESSMENT
 History
 Physical examination
 Diagnostic tests
INITIAL TESTS
 Electrocardiogram (ECG)
 Chest radiograph
 Echocardiography
 Exercise testing
 Complete blood count (CBC)
 Baseline evaluation of glucose, electrolytes liver function and
BUN/creatine
 Brain 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 oximetry
 Vital signs assessment with attention to hypotension or hypertension
 Continuous cardiac monitoring
 Intravenous access
 Seated posture
 Diuretic therapy
 Vasodilator therapy
 Urine output monitoring (perhaps with urethral catheter placement)
Tailor the therapy to the individual patient
 The 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 oxygen
 If 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 endexpiratory pressure (PEEP)
 Oxygen supplementation can be titrated in order to keep the patient
comfortable and arterial oxygen saturation above 90%
Diuretics
 Patients 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 dosing
 Furosemide(Lasix)– 40 mg intravenously
 Bumetanide(Burinex)– 1 mg intravenously
 Patients 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 administration
 Addition of an aldosterone antagonist (spironolactone) is recommended
in selected patients with systolic HF to improve survival.
Sodium and fluid restriction
 The 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 therapy
 vasodilators such as intravenous： nitroglycerin, nitroprusside
 Nitroglycerin — 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)
Nitroprusside
 Nitroprusside 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 THERAPY
 ACE inhibitors and ARBs
 Inotropic agents
 Vasopressor therapy
 Beta blockers
 Aldosterone antagonist therapy
 Venous thromboembolism prophylaxis
 Morphine 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 agents
 Dobutamine：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：Dopamine
 Low doses of 1 to 3 µg/kg/min：acts primarily on dopamine-1 receptors to
dilate the renal and mesenteric artery beds
 3 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)
Vasopressor
 Used 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.