Rural management of acute cardiogenic pulmonary
edema should be based upon avoidance of adverse outcomes such as in hospital
mortality, need for ICU care, and need for intubation and mechanical
ventilation. Current evidence suggests
that early non-invasive continuous positive airway pressure and early
aggressive preload reduction with IV
nitroglycerin are first line interventions.
Afterload reduction with sublingual captopril with or without
nitroglycerin improves outcomes and is a second line intervention. Furosemide is associated with adverse outcomes
when used alone, and should be given only after vasodilator therapy as a third
line intervention. Inotropes should be
used only with demonstrably poor perfusion, as they do not improve outcomes,
and may indeed be associated with increased mortality. Concurrent vasodilator therapy should be
considered as soon as possible.
Morphine should not be used, as it is associated with adverse outcomes. If sedation is desirable, benzodiazepines
should be considered.
The
possible precipitants of CPE will sometimes mandate alternative therapies which
are beyond the scope of this discussion.
Sometimes, as with hypertension, the treatment may not differ. At other times, as with myocardial
infarction, treatment follows another path.
The “MADHATTER” mnemonic (Box 2) is a useful
memory aid [7].
As
will be discussed, the possible reason for evidence for harm with the use of
some of our time tested therapies is misdiagnosis. In a study of pre-hospital treatment of CPE, Hoffman [12] found a
23% incidence of alternative diagnoses, possibly accounting for adverse
outcomes in patients given morphine if respiratory disease was the actual cause
of symptoms. We will never be exact in
all our diagnoses in the emergency department, so we must think of the
differential (Box 3) and avoid therapies which can
make an alternative condition worse.
Signs and symptoms reflect increased pulmonary
congestion, and, less frequently, poor perfusion (Box 1). Best outcomes result from reduction of
congestion by reducing preload and afterload.
Treatment options are:
1.
Reduce
preload
2.
Reduce
afterload
3.
Improve
contractility
By the time the patient presents, usually impairment
of all three processes is well advanced [4].
There
is now outstanding evidence for benefit of non-invasive airway interventions in
the treatment of CPE. Sound data exists
from multiple meta-analyses [12,13,14] indicating improvement in preload,
afterload and outcomes. This
intervention is now considered to be a non-pharmacologic treatment measure
rather than a supportive measure [12], and a first-line intervention in
treatment of CPE [11].
1.
Most
of the evidence originally existed for nasal continuous positive airway
pressure (CPAP). There is now ample
evidence that bilevel positive airway pressure (BIPAP) is as effective [15,16].
2.
The
most common CPAP setting is 10 cm H2O. BIPAP settings are 10 cm H2O expiratory (EPAP) and 15
cm H2O inspiratory (IPAP) [15].
3.
This
intervention should be instituted early in the course of treatment [4,11],
preferably on arrival in the emergency department.
4.
This
intervention is one of the least likely to produce adverse effects when the
diagnosis is in doubt, as it can be of benefit in respiratory disease as well.
5.
Devices
for administration of positive airway pressure are becoming less expensive and
more available to rural emergency departments.
The 10 cm CPAP setting is easy to set up.
6.
Most
studies show significant reduction in ICU admission, need for intubation, and
mortality in patients given this intervention.
In one pre-hospital study intubation was reduced by an odds ratio of
4.04 and mortality was reduced by an odds ratio of 7.48 [17].
7.
If
it is not possible to maintain SpO2 > 90 with this intervention,
intubation and mechanical ventilation is required. Other intubation indications include Glasgow Coma Scale 8 or
less, PaO2 < 60, and PaCO2 > 5 over baseline despite
non-invasive treatment. Failed
non-invasive ventilation and cardiogenic shock are also indications [4]. If
intubation is necessary CPAP of 10 cm should be maintained.
Although
morphine seems to have improved dyspnoea in patients with CPE reliably over
many years, there are major concerns regarding outcomes in these patients. The assumption that it functions by
venodilation, and, therefore preload reduction is also questioned.
1.
Venodilation
in the extremities has been demonstrated, but the volume of blood sequestered
by this mechanism is trivial [18].
2.
Patients
with acute myocardial infarction and pulmonary edema were studied by
measurement of pulmonary artery end diastolic pressure [19], with no benefit
being found following morphine administration.
It was concluded that the action of morphine in relieving dyspnoea (all
patients improved in this regard) was not explained by venous pooling, but that
action on the CNS produced the benefit.
3.
Retrospective
studies have now shown increases in ICU admission and intubation rates in
patients treated with morphine in the emergency department [20,21]. The largest study from the ADHERE heart
failure registry also links morphine use with significantly increased mortality
[21].
4.
Two
small pre-hospital treatment studies have been done. Wuerz observed that of patients treated with nitroglycerin,
furosemide and/or morphine, the ones with final diagnoses of asthma, COPD,
pneumonia or bronchitis had a higher than expected mortality [22]. Hoffman’s pre-hospital study patients
received the same drugs in different combinations. 23% of these patients subsequently were found to have a diagnosis
other than pulmonary edema. Subsequent
adverse effects or worsening of clinical condition was seen significantly more
often in patients treated with morphine [23].
There is clearly major concern with use of morphine when diagnosis is in
doubt, which is often the case in a rural setting.
5.
Morphine
has side effects including myocardial depression, which can reduce perfusion,
and nausea and vomiting, producing catecholamine release and increased
afterload. Even its acknowledged
beneficial effect of sedation is a side effect. Sedation might be more safely achieved with a benzodiazepine
which causes no nausea or hypotension [11].
In
summary, while morphine can produce dramatic reduction in symptoms, it is a
demonstrable risk in patients with a respiratory diagnosis, who are often
thought to have CPE. In addition, the outcomes
of ICU admission, intubation, and death are significantly increased in patients
treated with morphine. Sedation can be
achieved more safely with benzodiazepines if desired. Morphine probably has no place in modern treatment of CPE [11].
Of
the vasodilators capable of reducing pulmonary capillary wedge pressure (PCWP)
and preload, nitroglycerin (NTG) is the drug available in Canada. Nesiritide, available in the USA, is
promoted heavily as being superior to NTG based on the VMAC (Vasodilation in
the Management of Acute CHF) study [24] , which was a randomized trial
involving 489 patients in CPE. This
trial, supported by the manufacturer, compared nesiritide with an inadequate
dose of NTG (42 mcg./min at 3 hours), and, although there was a trend toward
superiority for nesiritide, the difference was not significant. Unfortunately, most drug trials involving
vasodilators are now reported by clinicians with links to the manufacturer of
nesiritide, and it is difficult to find new data on NTG. Because nesiritide is unavailable, associated with a significant risk of renal
dysfunction [10], and shows a trend to increased mortality [25], its use cannot
be recommended, and NTG becomes the vasodilator of choice at one-fortieth of
the cost. It is a first-line
intervention [11].
1.
Early
aggressive vasodilator therapy has been shown to be important [26].
2.
Sublingual
NTG is easy to give early, with a 0.4 mg dose every 5 minutes being
bioequivalent to 60 micrograms/min. IV.
Thereafter, early aggressive advancement of IV dosing to 60-100
micrograms/min is important to achieve optimal effect [11]. At higher doses, some afterload reduction is
achieved [27].
3.
NTG
is shown to have superior outcomes in comparison to furosemide in survival to
hospital discharge [28] and reduction in PCWP [29]. One prospective study shows reduced mortality using NTG in high
dose compared to furosemide in high dose [30].
When it is considered that furosemide is used in 88% of CPE treatment
and that 75% of patients receive no vasodilators [31], we need to review our
priorities with respect to these two types of therapy.
4.
Furosemide
given alone takes 45-120 min. to diuresis due to initial marked
vasoconstriction. Vasodilators given
early to reduce preload help reverse this initial increase in PCWP and promote
early diuresis [27].
5.
Because
most patients in CPE present with well preserved perfusion along with
congestion, NTG is usually well tolerated.
It should be used with caution, or along with inotropic support if
systolic BP is below 100 [1]. It should
be avoided in mitral regurgitation, aortic stenosis, pulmonary hypertension,
right ventricular infarction and in patients using agents for erectile
dysfunction. Tolerance can develop
after 12 hours of use [11].
Furosemide
is a time-tested intervention in CPE, often used alone as therapy [31] with the
assumption that it is a vasodilator, and that, along with diuresis, it will
reduce preload. As will be shown, best
evidence does not entirely support this, and there is evidence for harm which
must be taken into account if we are to make best use of this medication. It is probably a third-line intervention [27].
1.
The
SOLVD database indicates that non-potassium sparing diuretic use is associated
with increase in fatal arrhythmias in patients with systolic LV dysfunction
[32].
2.
40-50%
of CPE patients have euvolemia or hypovolemia [11,33,34]. These are the patients who develop
hypotension the day following initial treatment with diuretics. The problem is one of fluid maldistribution
rather than fluid overload [11].
3.
Administration
of furosemide produces diuresis after 45-120 minutes. The immediate effect is vasoconstriction with increased
afterload, increased PCWP and much reduced renal perfusion [27,35]. PCWP only falls over time, and after
diuresis. This delay in effect may be
significant in gravely ill patients.
4.
A
prospective study by Krause [27] demonstrated that these adverse effects of
furosemide were mediated by the neurohumoral axis, and that immediate diuresis
could be achieved by venous or arterial vasodilators given prior to
diuretics. Several authors now
recommend prior use of high-dose NTG, sublingual captopril, or both, prior to
diuretic administration [4,27,35,36].
There
are numerous heterogenous prospective studies to show benefit for both
sublingual captopril and IV enalapril in reducing afterload and improving
outcomes in CPE. Captopril is cheap and
easily administered in a small emergency department, while availability of IV
enalapril is problematic. While there
is accumulating evidence, there is no definitive meta-analysis, and given the
generic nature of the medications, funding for such studies is more difficult
to obtain. With appropriate caveats,
however, sublingual captopril can be presented as a second-line intervention
[11]. Available evidence, outlined
below, suggests it is safe and effective - certainly much more so in terms of
outcomes than morphine and diuretics, which were the previous mainstays of
therapy.
1.
ACE
inhibition can often be given as a single dose in the emergency department, and
need not be repeated until a decision for chronic dosing is made [4,37].
2.
Sublingual
captopril has been compared with sublingual nifedipine in acute hypertension and
found to be effective, with less flushing, headache and tachycardia. Onset of action was within 5 minutes [38].
3.
A
sublingual captopril tablet is dipped in water for more rapid absorption. For systolic pressures <110, the dose is
12.5 mg. For pressures > 110, the
dose is 25 mg. It can be used in
combination with nitroglycerin if systolic pressure remains high or side
effects of NTG limit adequate dosing.
Combination with NTG exceeds the benefits of either used alone
[11,27,39]. It produces benefit later
in onset than NTG, but improvement is more pronounced and prolonged [40].
4.
Early
use of captopril will often produce diuresis without furosemide [41]. There is a reduction of preload and
afterload after 10 minutes [40,41,42,43,44], and it is recommended that
diuretics be delayed for 30 min. after vasodilators are given to allow for
increase in renal blood flow [11,27,35].
5.
ACE
inhibitors have been administered in acute decompensated heart failure in
numerous trials with good hemodynamic stability and few adverse effects
[41,42,45,46,47].
6.
Improved
outcomes include fewer ICU days [20,47] and reduced rates of intubation with
mechanical ventilation [20,41,48].
This
probably has no place in emergency treatment of CPE. Some sources still suggest it as an alternative for reducing
ventricular response if rapid atrial fibrillation is present, however
amiodarone is now more often used for this indication [1].
The
catecholamine inotropes and milrinone, a phosphodiesterase inhibitor, are
capable of improving blood pressure and cardiac output in the poorly perfused
patient. Although numbers are improved,
outcomes are of concern, with evidence of longer length of stay and increased
in-hospital mortality for patients on inotropes as compared to vasodilators
[49,50]. These agents are best reserved
for patients with impaired LV function and hypotension, and should not be used
if perfusion is adequate.
1.
Dobutamine
is potentially the most beneficial of the catecholamine inotropes because it is
capable of slightly reducing preload and afterload. Activity is blocked, however, in patients on chronic beta
blockade, and higher doses may have to be used. In the event of increasing hypotension, the alpha adrenergic
activity of dopamine or norepinephrine may be required. These agents improve blood pressure, but
also increase myocardial oxygen demand, dysrhythmias and ischemia. Vasodilators should be added as soon as
possible to further reduce preload and afterload, and to improve congestion
[4].
2.
Milrinone
is an “inodilator”, and is unaffected by chronic beta blockade. It is superior to dobutamine in measured
cardiac output, PCWP and systemic vascular resistance. Despite this it has not been shown to
improve hospital length of stay or mortality [4].
3.
Dobutamine
is generally available in small emergency departments. Milrinone, at seven times the cost, is
likely to be difficult to stock in departments which are not associated with an
ICU.
1.
Recognize
alternate diagnoses and precipitating factors early.
2.
Early
institution of CPAP at 10 cm. H2O is a first line intervention.
3.
Early
sublingual nitroglycerine followed by IV administration in high doses (60-100
mcg./min) is a first line intervention.
4.
Sublingual
captopril is a second line intervention and should be considered at 12.5
mg. if BP<110 or 25 mg. if BP>110 in the following situations:
·
Nitroglycerine
is contraindicated.
·
Nitroglycerine
does not produce improvement and the patient remains hypertensive.
·
Congestion
is resistant to the other usual therapies and perfusion is adequate.
·
The
patient presents with intense sympathetic overactivity (the most common
presentation), with hypertension, vasoconstriction and poor urinary output
(given along with nitroglycerine).
·
If
a dialysis patient presents out of hours with volume overload, hypertension and
pulmonary edema (given along with nitroglycerine) [11].
5.
Furosemide
should be given 30 minutes after institution of vasodilator therapy if there is
no initial diuresis in non-urgent situations.
Subsequently, it will sometimes not need to be given at all, or can be
used in lower doses. This is a third
line intervention.
6.
Dobutamine
can be given in cases of poor LV function and hypotension. Vasodilators should be initiated or
continued if there is a good response.
This intervention will not improve mortality.
7.
Morphine
should not be used, as it produces poorer outcomes. If sedation is needed, consider a benzodiazepine.
8.
Critically
scrutinize new studies promoting use of new and expensive drugs, as
methodologies may skew results in favor of newer products. The lack of large studies on outcomes from
older therapies usually reflects lack of funding by industry.
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Box
1: Signs and symptoms of acute cardiogenic pulmonary edema Congestion
(Volume Overload) Dyspnoea
on exertion Orthopnoea Paroxysmal
nocturnal dyspnoea Satiety,
nausea, vomiting Edema Increased
jugular venous pressure Hepatojugular
reflux Ascites Hepatosplenomegaly S3
gallop Rales
Fatigue Altered
mentation Narrow
pulse pressure Hypotension Cool
Extremities Worsening
renal function
Hypoperfusion
Box
2: Precipitating causes of
acute cardiogenic pulmonary edema. MADHATTER
mnemonic: Myocardial infarction Anemia Drugs, Diet (salt) Hypertension Arrhythmia Thyroid disease Toxic (infection) Embolism (pulmonary),
Endocarditis Renal failure
Box
3: Differential diagnosis of
acute cardiogenic pulmonary edema Bronchospasm
or asthma COPD
exacerbation Pneumonia Pulmonary
embolism Adult
respiratory distress syndrome Myocardial
ischemia or infarction Pulmonary
fibrosis Other
cause pulmonary edema (altitude,etc)