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.