Management of Cardiogenic Pulmonary Edema
Protocol
for the Acutely Ill Patient
About
this Document
Most
patients improved despite ineffective treatment. Possible benefits were
sedation and physician reassurance
reducing sympathetic overactivity.
Agents used were:
Oxygen
Semi-Fowlers
position
Morphine
Mercurial
diuretics
Rotating
tourniquets
IV
Digoxin
With
the exception of oxygen, all these interventions have been shown to be
ineffective or harmful.
Most patients
improve quickly with initial treatment. A small minority progress rapidly to
respiratory failure, intubation and death.
Interventions are difficult to study for these reasons, and diagnosis
can be incorrect 50% of the time. Few interventions have been well proven to
reduce risk of intubation and death even with present treatment. We have been slow to abandon
ineffective or harmful treatments.
Left ventricular
contractility can no longer handle pulmonary venous return. This results in increased
preload.
Pulmonary
hydrostatic pressure exceeds alveolar hydrostatic pressure, and fluid leaks from pulmonary vessels into the
alveolar space.
Sympathetic
activation causes vasoconstriction and increased afterload, further increasing heart work load.
Preload,
afterload and contractility are often all disordered by the time of ED
presentation.
The
problem is often one of disordered fluid distribution, with too much fluid in
the lung compartment. There may be
excess body water, but this is not always the case.
Goals
of treatment therefore are to:
If first 2 goals
are met, contractility usually improves.
Assessment of
hemodynamic profile:
The
majority of patients are dyspneic, well perfused and hypertensive.
A
smaller number are dyspneic and less well perfused. Some of these are in cardiogenic shock.
Patients
presenting with hypertension benefit most from clinical interventions.
Patients
with hypotension may require inotropes and invasive monitoring.
Vomiting,
rash and urticaria cause release of catecholamines, increasing afterload.
Myocardial
and respiratory depression at variable doses.
Venodilation
is peripheral, and a histaminic side effect.
Pulmonary
artery cath studies show no reduction in preload.
The
ADHERE Registry shows increased intubation and mortality with morphine.
Independent
predictor of mortality with odds ratio 4.84 when evaluated in retrospective
studies.
Increased
need for ICU admission and intubation with use of morphine in the ED.
Pre-hospital
prospective studies show deterioration in symptoms and hemodynamic parameters
in patients given morphine.
Adverse
pre-hospital outcomes are particularly common in patients with a missed
respiratory diagnosis eg. pneumonia, COPD exacerbation, asthma.
Most of
the benefit probably results from anxiolysis and reduction of catecholamines,
reducing afterload.
Safer
anxiolysis might be achieved with a benzodiazepine.
Summary for
Morphine:
No
studies have ever shown benefit
Reduced symptoms
due to sedation and respiratory depression.
Not
demonstrated to produce venodilation or reduce preload in Swan studies.
Increased
intubation and death rates in large retrospective studies.
Poorer
outcomes for pre-hospital patients, especially those with a missed respiratory
diagnosis.
Benzodiazepines
safer for sedation to reduce sympathetic activation.
Should probably
not be used unless pain is an issue.
Furosemide:
Multiple
pulmonary artery catheter studies from the 1970’s and 1980’s show increased
preload and afterload prior to diuresis.
Preload
reduction does not occur until diuresis, which can be delayed in pulmonary
edema.
Diuresis
may be delayed for 30-120 minutes and may be preceded by clinical improvement,
suggesting that other factors produce the benefit.
Preload
and afterload reduction with NTG and captopril produces immediate diuresis.
There
is initial increase in afterload with reduced stroke volume and cardiac output
following furosemide administration due to increased catecholamines, renin
activity and vasopressin.
Renal
blood flow is reduced to 20% in pulmonary edema due to vasoconstriction. Preadministration of vasodilators mitigates
this process.
40-50% of patients are not volume overloaded. Vigorous use of diuretics in volume depletion results in problems with hypotension on day 2. With prehospital use, 20% of patients required later fluid repletion.
Significant hypokalemia when given in a prehospital setting. Not recommended for use where accurate evaluation of fluid and electrolyte status is suboptimal.
Summary for
Furosemide:
20%
renal blood flow due to vasoconstriction in pulmonary edema
Initial
increase in afterload and reduced cardiac output.
Preload
initially increases - reduction only through diuresis.
Delayed
adverse effects in volume depletion.
Significant
hypovolemia and electrolyte imbalance with prehospital use.
Beneficial
effect accelerated by vasodilator pretreatment.
Third
line after vasodilators
Pharmacodynamics
Venodilation (Preload Reduction)
Low doses up to 60
ug/min.
Sublingual NTG 0.4
mg every 5 minutes equivalent to 60 ug/min.
Venodilation
maximal at low concentrations with little dose effect. This is probably maximal in 2 hr 1.
Preload reduction
has little hypotensive effect in patients with cardiogenic pulmonary edema
because of parallel decrease in afterload and increase in cardiac output 2.
Effect declines
after 2-3 minutes with single administration 3.
Peripheral arterial vasodilation (Afterload Reduction)
Doses above 60
ug/min
Increasing
arteriolar dilation as administration dose increases 4.
Tolerance develops
over 2-12 hours
Arteriolar dilation
effect is very brief, requiring continuous IV or repeated bolus administration 3.
Afterload
reduction helps to maintain increased stroke volume and cardiac output in the
presence of reduced preload, particularly in the failing myocardium. Patients in heart failure are much less
sensitive to reduction in preload than to reduction in afterload 2.
Evidence
Numerous small
case control studies showing benefit and suggesting safety.
Three better
quality studies 5,6,7 demonstrating improved outcomes with good
safety numbers.
Evidence existing
sufficient for generation of an administration protocol, but the definitive
large RCT has yet to be done.
Rationale for use
of this modality lies in demonstrated clear superiority to “standard”
therapies.
Early and adequate
NTG therapy is a first line
intervention.
Contraindications
Phosphodiesterase
inhibitors (Viagra, etc.)
Severe volume
depletion
Hypotension
Preload dependent
states
Right ventricular
infarction
Aortic stenosis
Mitral
regurgitation
Pulmonary hypertension
Article I.
Adverse Outcomes
Tolerance can
develop between 2 and 12 hours with continuous use.
Reflex tachycardia
usually not an issue, as clinical improvement produces reduction in adrenergic
drive.
Bradycardia occurs
rarely. Treat using ACLS protocols.
Reduced BP
reflects improving clinical status.
Hypotension with hypoperfusion requires discontinuation and volume
support. This is usually effective.
Headache is rarely
severe.
Summary for
Nitroglycerin:
NTG is a first line intervention, shown
to be more effective than CPAP 6 (also a first line intervention)
and diuretics 5.
NTG must be given
early and at high dose to achieve optimal results.
Treatment to
target symptoms and clinical parameters determines optimal dosage.
Tailored therapy
with respect to presenting systolic BP determines acceptable degree of BP
lowering and helps predict whether use of diuretics can be beneficial.
Specific
inhibition of maladaptive feedback loop which activates renin-angiotensin
system
Evidence
exists for IV Enalapril and SL Captopril in cardiogenic pulmonary edema.
Captopril
readily available and easily used as single dose.
Gives
some preload reduction as well as afterload reduction; can be used as single
agent if NTG not tolerated. Confirmed by many Swan studies.
Use of
Captopril:
Oral
tab dipped in water and given SL for more rapid absorption.
Systolic
BP>110 dosage 25 mg.
Systolic
BP<110 dosage 12.5 mg.
Onset of action within 5 minutes.
Can be
used with NTG with additive effect.
Early
use may avoid need for diuretics.
Delay
diuretic administration 30 minutes after vasodilators.
Good
hemodynamic stability and few adverse effects.
Improved
outcomes with fewer ICU days and fewer intubations.
Summary for
Captopril:
Can be
used in place of NTG
Good
hemodynamic stability with few side effects.
Easily
administered in single dose.
Additive
effects when used with NTG.
Reduces
ICU use and need for intubation.
Second-line
intervention after CPAP and NTG.
Preload and Afterload Reduction:
High
dose Nitroglycerin
Sublingual
Captopril
Non-invasive Positive
Pressure Ventilation
(a)
Nesiritide:
Recombinant
form of BNP available in the
Defining
data come from the VMAC study, which compared it to an inadequate dose of
nitroglycerin, and showed a trend toward superiority.
Pooled
analyses of trials show increased incidence of renal dysfunction and a trend
toward increased mortality.
Not
currently recommended.
Non-invasive Positive Pressure Ventilation
Includes
CPAP and BiPAP. CPAP much simpler to
administer and equally effective.
CPAP
of 10 cm. water used in most studies.
Effective
in both preload and afterload reduction.
Early implementation gives the best results.
3
meta-analyses show reduced mortality and intubation rates. By early 2008, it was believed to be
unethical to do trials without including this modality:
Since then a large prospective study of over 1000 patients has concluded (N Engl J Med 2008;359:142-51
In
patients with acute cardiogenic pulmonary edema, noninvasive ventilation
induces a more rapid improvement in respiratory distress and metabolic
disturbance than does standard oxygen therapy but has no effect on short-term
mortality.
Possible
reasons for differing findings:
–
Different
populations. This study was ER only.
–
Only 8
patients intubated in this study (3%) vs. 20% in many series.
–
Treatment
crossover was 15% with most failures going to CPAP or BiPAP. Analysis by intention to treat, therefore
noninvasive venilation may have influenced outcomes in the control arm.
–
Crossover
probably done because authors believed NIPPV could avoid intubation.
–
Time
to treatment institution is critical.
This was not recorded.
–
Intervention
could be as brief as 2 hours in this study.
Indications
The following are conditions possibly
benefiting from early CPAP, listed in order of level of evidence:
Acute
COPD exacerbation.
Acute
cardiogenic pulmonary edema.
Pneumonia.
Benefit is only shown in patients with infection associated with COPD and in
immunocompromised patients, such as those with pneumocystis or those who have
had transplant surgery, for whom intubation should be avoided.
Do-not-intubate
status. Reversal of deterioration or improvement in acute dyspnoea may occur in
patients with COPD or pulmonary edema without much risk from the intervention.
The wishes of the patient and the course of the disease process must be
completely understood by physician and patient.
Extubation
failure. This might occur after a brief course of intubation for COPD or
pulmonary edema in a rural practice. CPAP might ease this transition, but there
must always be a fallback plan for reintubation.
Asthma
- CPAP is not currently recommended.
Other
causes of respiratory failure (acute respiratory distress syndrome, trauma).
Little consistent benefit has been reported.
Some of the criteria for respiratory
failure should be met, including symptoms, signs and physiologic parameters:
respiratory distress
tachypnoea
use of accessory muscles or abdominal
paradoxical movement
pH less than 7.35
partial pressure of carbon dioxide greater
than 5.9 kPa (45 mm Hg)
partial pressure of oxygen less than 12 kPa
(90 mm Hg) on maximal concentration fraction of inspired oxygen
chest radiography may be useful in
diagnosis, but is not sensitive enough to aid in decision-making.
Contraindications
medical instability with immediate need for
intubation
respiratory or cardiac arrest
pneumothorax must always be excluded unless
a chest tube is in place
patient is unable to protect the airway
vomiting or excessive secretions.
agitated or uncooperative patient
unable to achieve mask seal because of
facial contour
recent upper airway or upper abdominal
surgery
hypovolemia
hypotension with systolic pressure less
than 90 mm Hg
conditions that are preload dependent, such
as right ventricular infarction. Like nitroglycerin, CPAP will impair right
ventricular filling
intracranial hemorrhage or increased
intracranial pressure
respiratory muscle fatigue
patient is younger than 12 years
Complications
pain or ulcer over the nasal bridge
mucosal dryness
patient fear that the device is limiting
the patient's ability to breathe
eye irritation if the mask seal is not
complete
aspiration or gastric insufflation (rare)
Conclusions for
CPAP:
CPAP
equally effective to BiPAP and easier to use.
Must
be applied early. Few contraindications.
Strong
evidence for early improvement in symptoms and physiologic parameters.
Patients
treated initially with NIV do better than those with standard therapy even if
intubation eventually needed.
Still
uncertain whether intubation or death are reduced.
Any
further large prospective studies need to avoid crossover of treatments. Doubtful if this will clear ethics.
This
is a first-line intervention along with nitroglycerin
Indicated
only in situations of hypotension with poor perfusion
All
agents improve numbers, but are associated with increased mortality
Effects
of some agents blunted by chronic beta blockade
Alpha
acting agents increase myocardial oxygen demand, arrhythmias and ischemia
These
patients probably require pulmonary artery catheterization if no prompt and
enduring response.
Follow
ACLS protocols.
Agents
–
Digoxin
– no role
–
Dobutamine
– primarily beta 1 activity
–
Milrinone
– unaffected by beta blockade
–
Norepinephrine
– primarily alpha activity
–
Dopamine
– alpha and beta 1 activity
Levosimendan – sensitizes myocardium to calcium
Primary
treatment concepts:
There
is a spectrum of findings in pulmonary edema.
Only
about half of patients have impaired systolic function.
40% of
patients are not volume depleted
Systolic
BP gives the best prediction of morbidity and mortality.
Early
goal-directed therapy with CPAP and vasodilators may improve outcomes.
When
diagnosis is in doubt, use of CPAP, nitroglycerin and beta-agonists can be beneficial and does
no harm.
Systolic BP can
be a reliable guide for choice of therapy:
Conclusions for Rural Management:
Early
administration of CPAP 10 mm Hg
Early
high dose nitroglycerin sublingual and IV
Early
consideration of captopril SL in specific
settings
Delayed
furosemide administration of in volume
overload
Avoidance
of morphine
Consider
trial of volume replacement for hypotension
If inotropes or vasoconstrictors are needed,
consider early referral
When
diagnosis is in doubt, use of CPAP, nitroglycerin and salbutamol do not seem to
impart increased risk
1.
2.
Selected
References:
1.
Elkayam U, et al.
Comparison of effects on left ventricular filling pressure of intravenous
nesiritide and high-dose nitroglycerin in patients with decompensated heart
failure. Am J Cardiol 2004; 93: 237-240.
2.
Haber HL, et al.
Bolus intravenous nitroglycerin predominantly decreases afterload in patients
with excessive arterial elastance. JACC 1993; 22(1): 251-257.
3.
Muikku O, et
al. Venodilator properties of
nitroglycerin and isosorbide dinitrate during cardiopulmonary bypass. British
Journal of Anaesthesia 1992; 68(4): 376-380.
4.
Imhof PR, et al.
Difference in nitroglycerine dose-response in the venous and arterial beds. Eur
J Clin Pharmacol 1980; 18: 455-460.
5.
Cotter G, Metzkor E, Kaluski E, et
al. Randomized trial of high-dose isosorbide dinitrate in severe
pulmonary oedema. Lancet 1998; 351:
389-393.
6.
Sharon A, et
al. High-dose intravenous
isosorbide-dinitrate is safer and better than bi-pap ventilation combined with
conventional treatment for severe pulmonary edema. J Am Coll Cardiol 2000;
36(3): 832-837.
7.
Levy P, et
al. Treatment of severe decompensated
heart failure with high-dose intravenous nitroglycerin: a feasibility and
outcome analysis. Ann Emerg Med 2007; 50(2): 144-152.
8.
Mattu A, Martinez
JP, Kelly BS. Modern management of
cardiogenic pulmonary edema. Emergency Medicine Clinics of North America 2005;
23: 1105-1125.
9.
Chatti R, et al.
Algorithm for therapeutic management of acute heart failure syndromes. Heart
Fail Rev 2007; 12: 113-117.
10.
11.
Mebazza
A, et al. Practical recommendations for prehospital and early in-hospital
management of patients presenting with acute heart failure syndromes. Crit Care
Med 2008; 36(1): S129-S139.
12.
Lappas
DG et al. Filling pressures of the heart
and pulmonary circulation of the patient with coronary artery disease after
large intravenous doses of morphine. Anesthesiology 1975; 42(2): 153-159.
13.
Timmis
AD et al. Haemodynamic effects of intravenous morphine in patients with acute
myocardial infarction complicated by severe left ventricular failure. BMJ 1980;
280(6219): 980-982.
14.
Peacock
WF et al. Morphine and outcomes in acute decompensated heart failure: an ADHERE
analysis. Emergency Med J 2008; 25: 205-209.
15.
Sacchetti
et al. Effect of ED management on ICU use in acute cardiogenic pulmonary
edema. Am J Emerg Med 1991; 17(6):
571573.
16.
Hoffman
JR, et al. Comparison of nitroglycerin, morphine and furosemide in treatment of
presumed pre-hospital pulmonary edema. Chest 1987; 92: 586-593.
Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990; 98: 124-128.
18.
Francis
GS, et al. Acute vasoconstrictor response to intravenous furosemide in patients
with chronic congestive heart failure. Activation of the neurohumoral axis. Ann
Int Med. 1985; 103(1): 1-6.
19.
Figueras
J, Weil MH. Blood volume prior to and
following treatment of acute cardiogenic pulmonary edema. Circulation 1978; 57(2): 349-355.
20.
Ceyhan
B, et al. Comparison of sublingual captopril and sublingual nifedipine in
hypertensive emergencies. Jpn J Pharmacol 1990; 52: 189-193.
21.
Emerman
CL. Treatment of the acute decompensation of heart failure: efficacy and
pharmacoeconomics of early initiation of therapy in the emergency department.
Rev Cardiovasc Med 2003; 4(Suppl7): S13-20.
22.
Tallman TA, Peacock FW, Emerman CL, Lopatin M, Blicker JZ, et al. Noninvasive Ventilation Outcomes in 2,430 Acute Decompensated Heart Failure Patients: An ADHERE Registry Analysis. Acad Emerg Med 2008; 15(4): 355-362.
Protocol for the Acutely Ill Patient:
Immediate Titration of High-Dose NTG
Optional Use of Sublingual Captopril
Delayed/Elective IV Furosemide
Simplified
CPAP Application: First-line immediate intervention
The Single-Use Boussignac
CPAP System: An easily
applied method for non-invasive ventilation.
Equipment
The components of the system are as
follows:
sized mask, valve (the hard plastic device)
and tubing for connection to oxygen source
oxygen port capable of 25 L/min with flow
regulator
optional pressure manometer (Fig3)
optional nebulizer
port for optional (recommended) end-tidal
carbon dioxide monitor
A 20-mL syringe is needed to inflate the
cuff around the mask for optimal fit.
Procedure
1.
Select
the mask size.
–
child
- #3
–
female
adult - #4–5
–
male
adult - #5–6
2.
Inflate
the air cuff around the mask using 20– 40 mL air. Have a 20-mL syringe
available to subsequently facilitate an airtight seal to the patient's face.
3.
Connect
green tubing to oxygen source.
4.
Connect
white end of the valve to the face mask.
5.
With
the patient in the sitting position, hold the mask to the patient's face and
begin oxygen at 15 L/min (CPAP of 5 cm H2O).
Take time to explain the procedure to the patient.
6.
Secure
the harness around the head with straps above and below the ears. Check for
leaks around the mask and adjust the air seal as necessary.
7.
Gradually
increase oxygen flow to 25 L/min (CPAP of 10 cm H2O) as tolerated.
8.
Suction
through the large end port of the mask as necessary.
9.
If the
manometer is used, place it in-line between the valve and the mask (Fig3).
10. If a nebulizer is used, place it in-line
between the valve and the mask. Set the
valve oxygen source at 15 L/min and the nebulizer source at 6 L/min.
11. Commonly used end-tidal CO2
transducers are designed to connect to an endotracheal tube. They can be inserted in-line only when used
with the manometer, which is also inserted in-line. The order of connection would be
valve>manometer>CO2 transducer>mask. The resulting column would need support, and
would only be suitable for intermittent sampling. A different transducer could be inserted into
the small clear port on the valve or slipped under the seal of the mask.
Subsequent Steps;
1.
Do not
remove CPAP without a backup plan in case of deterioration — either resumption
of CPAP or intubation.
2.
If
CPAP is helpful in stabilizing the patient for transport, it is very important
not to discontinue the intervention suddenly.
3.
Establish
a source of supplied oxygen capable of long-term delivery of 25L/min. An E cylinder will last only 23 min, and even
the
4.
Watch
for gastric distention.
5.
If
nitroglycerine is required, use sublingual tabs rather than spray.
6.
Be
aware that the available fraction of inspired oxygen falls with rises in
respiratory rate and tidal volume – that is, the more air the patient
exchanges, the lower the fraction of inspired oxygen. This tendency is compensated for by maximizing
the level of CPAP.
7.
Look
for results that indicate that the intervention is working:
–
reduced
heart rate
–
reduced
respiratory rate
–
reduced
dyspnoea
–
blood
pressure returning to normal (usually tends to be high in cardiogenic pulmonary
edema)
–
increasing
oxygen saturation
–
decreasing
end-tidal carbon dioxide
–
improving
mental status
8.
If
there is no improvement:
–
troubleshoot
the equipment
–
check
for pneumothorax
–
check
for conditions that might reduce preload (hypovolemia, dehydration, nitroglycerine)
–
consider
pulmonary embolism. One patient in 4 with a COPD exacerbation severe enough to
warrant admission to hospital may have pulmonary embolism
–
consider
proceeding to intubation
High-Dose Nitroglycerin Protocol: First-line immediate
intervention.
Sublingual NTG 0.4
mg. every 5 minutes for 4 doses if needed (equivalent to IV 60 ug/min)8.
–
BP before each
subsequent dose
–
Treat hypotension
with bolus of 500 ml. normal saline.
–
Most physicians
are comfortable with sublingual administration.
They can perhaps become more comfortable with high-dose IV if they
understand that they are already giving 60 ug/min.
–
This frees up 20
min. for preparation of NTG drip.
–
Use premix 400
ug/ml solution or prepare solution of 100 mg. in 250 ml. D5W.
–
Glass bottle
preferred for solution stability.
Remember glass not permitted if air transport required.
–
1.5 ml/hr infusion
administers 10 ug/min.
Begin IV infusion
NTG at 7.5 ml/hr = 50 ug/min (this dose already given sublingually).
Increase infusion
by 1.5 ml/hr = 10 ug/min every 5-10 min. if appropriate/ (see Table 1).
–
BP before each
subsequent increase
–
Treat hypotension
with bolus of 500 ml. normal saline.
–
This allows
adequate high dose administration within the first hour.
Table 1
Section 1.02 IV Rate
|
Dosage Given |
Minutes after First SL Dose |
|
7.5 ml/hr |
50 ug/min |
25 |
|
9 ml/hr |
60ug/min |
30 |
|
10.5 ml/hr |
70 ug/min |
35 |
|
12ml/hr |
80 ug/min |
40 |
|
13.5 ml/hr |
90 ug/min |
45 |
|
15 ml/hr |
100 ug/min |
50 |
|
16.5 ml/hr |
110 ug/min |
55 |
|
18 ml/hr |
120 ug/min |
60 |
–
The upper limit in
rate of administration is not yet well defined.
75-125 ug/min was effective in 2 well-done trials 5,6. The third feasibility trial went as high as 660
ug/min with only 1 episode of hypotension 7, but these doses cannot
yet be recommended for general use.
–
Adverse effects
will be short-lived with IV administration because of the very short duration
of effect of NTG. Hypotension, if seen,
would likely occur early in the phase of venodilation or preload reduction, and
should respond to a saline bolus.
–
The upper limit
of dose administration is determined by
targeted patient response: one must Treat to Target.
–
The lower acceptable
limit for systolic BP depends on presenting systolic function, most easily
estimated by systolic blood pressure.
This limit, and the need for use of diuretics are best estimated using
broad guidelines for Tailored
Therapy, based on presenting systolic BP.
Most studies aim
for an oxygen saturation of 96% with whatever respiratory adjunct is in use, be
it oxygen or CPAP 5,6. CPAP
at 10 cm is recommended.
Other parameters
should show improvement if treatment is effective. Changes should be dramatic, as most critical
patients present in respiratory failure.
–
Reduced
respiratory rate
–
Reduced pulse rate
–
Reduced blood
pressure
–
Improvement in
mental status
–
Reduced subjective
dyspnoea
–
Normalization of
pCO2
It is argued that
a drop in BP is a target in most patients, who present with hypertension and
preserved systolic function. There is a
pressure, however, which should prompt slowing or discontinuation of the drip.
–
Patients
presenting with BP above 160 systolic may tolerate a treatment systolic
pressure below 110. One study
discontinued medication at a systolic of 90 with few adverse effects 7.
–
Patients
presenting with BP of 110-160 systolic should have the drip slowed or
discontinued at a BP of 110/70.
–
Patients
presenting with a BP of 100 – 110 systolic probably have impairment of systolic
function, and may be very preload dependent.
The initial sublingual dose of NTG may produce hypotension, thus a bolus
of 500 ml normal saline should be prepared and ready. If there is improvement with initial
sublingual dosing, the IV protocol can be cautiously initiated, but systolic
pressure should not fall below 100.
–
Patients
presenting with a BP <100 are volume depleted or in cardiogenic shock. A bolus of normal saline should always be
given first. If there is no response,
inotropes must be initiated.
Systolic
pressure over 140 (>50%)
–
Preserved systolic
function
–
These patients
commonly shown to have diastolic dysfunction 10, and are commonly
older, female, and with a history of hypertension.
–
Not commonly fluid
overloaded.
–
Furosemide should
be given only if there is clinical fluid overload. Any administration should be delayed 30 – 120
min. to allow for adequate renal vasodilation by NTG.
–
High dose NTG
protocol can be used aggressively
–
These patients
usually tolerate lower systolic pressures, but often improve before low
pressures occur.
Systolic
pressure 100 – 140 (>40%)
–
Likely some impairment
of systolic function
–
Some are fluid
overloaded.
–
Furosemide more
usually needed, but administration should be delayed at least 30 min. to allow
for adequate vasodilation by NTG.
–
High dose NTG
protocol can be used. There may be more
risk of hypotension in these patients.
–
Systolic pressure
should not fall below 100.
Systolic
pressure <100 (<10%)
–
Volume depletion
or cardiogenic shock
–
Bolus 500 ml.
normal saline.
–
If no response, go
to ACLS protocol and use of inotropes.
Use of Sublingual Captopril: Second-line optional intervention.
Modest preload and potent afterload capabilities.
Can be used if NTG contraindicated or for added
vasodilation with nitrates.
Oral tablet dipped in water and administered
sublingually for absorption within 5 minutes.
Dosage 25 mg. if systolic BP>110, 12.5 mg. if
systolic BP<110.
Given as a single dose.
Use of Furosemide: Third-line delayed/optional intervention.
Renal blood flow in pulmonary edema is 20% of
normal. Use vasodilators for at least 30
min. prior to administration of furosemide.
Confirm clinical volume overload. 40-50% of patients with dyspnoea are not
volume depleted. Some have a primary respiratory diagnosis. They will get worse with furosemide.
Patients with systolic BP<140 are most likely to
benefit from diuretics. Those with
higher pressures often diurese with vasodilators alone.
Use the minimum dose of furosemide to optimize
diuresis. Vasodilators alone may often
be adequate, and clinical improvement may occur before diuresis.
Remember that early administration of furosemide
increases afterload and reduces cardiac output.
Preload reduction does not occur until diuresis. Timely afterload reduction cannot occur
without vasodilators.