Pulmonary Edema
“Acute systolic heart failure” is useful
for hospital billing, but pulmonary
edema is more descriptive.
Pulmonary Edema
Learning Goals
Management of symptomatic pulmonary
edema
 Management of cardiogenic shock


Not in this talk:
Chronic outpatient systolic and diastolic
failure
Case #1
72 W with dilated ischemic
cardiomyopathy, EF=45 %, presents to
the ED after waking up at 2am from
shortness of breath.
 It is now 6 days after Thanksgiving; “I
didn’t eat any salt,” but she admits to
eating canned gravy and canned
cranberry sauce

Case #1, HPI, continued
Notes worsening in ankle swelling and
worsened orthopnea
 Baseline ET 2 blocks, now 20 feet
limited by dyspnea; denies chest pain
 Usually she makes copious urine after
taking furosemide, but had almost no
urine output after yesterday’s dose

Case #1, ROS, continued
Denies lightheadedness and syncope
 Notes a new decrease in appetite; on
further questioning she still feels hungry
and wants to eat, but feels full after only
2-3 bites of food

72 W DICM, ate too much salt

PMH: HTN, DM, CAD, CHF
 PSH: Cath one year ago showed chronic total
occlusion of mid LAD; no other severe lesions
on cath; no intervention performed
 Medications:
Lisinopril 10mg PO daily
Carvedilol 12.5mg PO bid
Furosemide 40mg PO daily
ASA 81, Simvastatin 40, Insulin
72 W DICM, ate too much salt
NKDA
 Social: Quit tobacco one year ago,
drinks 1-2 8oz glasses of wine per
week, denies drug use
Lives next door to her daughter and
grandchildren, weighs herself and
checks her BP at home daily
 Family: Father died age 63 of MI

72 W DICM, ate too much salt
150/90 P82 R28 SpO2=93% 2L T=98.4
 Weight is 62kg; baseline is 57kg
 Jugular venous pressure 12cmH2O
 Crackles to mid lung fields bilaterally
 RRR, II/VI apical holosystolic murmur
 Bilateral pitting ankle edema;
extremities warm

72 W DICM, ate too much salt
CBC normal, coags normal
 Na=129 K=4.9 BUN=18 Cre=1.1
 Albumin=3.6, LFT’s otherwise normal
 EKG shows normal sinus rhythm, left
atrial enlargement, left ventricular
hypertrophy, and poor R-wave
progression, all unchanged from routine
EKG taken three months ago

Chest X-Ray
72 W pulmonary edema
ED Course
 Receives furosemide 40mg IV once,
makes 1.5L urine
 Reports complete resolution of her
shortness of breath; now feels normal
 BP 130/80 P80 R21 SpO2=98% 2L
 JVP=10; ankle edema persists
72 W pulmonary edema
What to do next?
 Emergent cardiac catheterization
 Transfer to CCU, consider inotropes
 Admit to telemetry, rule out MI
 Discharge home with close clinic f/u
Intestinal edema

Early satiety is one of the most sensitive and
specific symptoms of heart failure
exacerbation
Jakob SM. Clinical review: splanchnic ischemia. Crit Care.
2002;6:306–
312.15.
Higgins CB, Vatner SF, Franklin D, et al. Pattern of differential
vasoconstriction in response to acute and chronic low-output
states in the conscious dog. Cardiovasc Res. 1974;8:92–
98.16.
Zelis R, Nellis SH, Longhurst J, et al. Abnormalities in the
regional circulation accompanying congestive heart failure. Prog
Cardiovasc Dis. 1975;18:181–
199.


Cannot
absorb
PO meds
Intestinal
edema
Ate salt
Central venous
pressure
increases;
mesenteric venous
pressure increases
72 W pulmonary edema
What to do next?
 Emergent cardiac catheterization
 Transfer to CCU, consider inotropes
 Admit to telemetry, rule out MI
 Discharge home with close clinic f/u
And increase furosemide dose from 40mg PO
daily to 80mg PO bid for five days; instruct pt.
to return to clinic immediately if weight fails to
return to baseline
72 W pulmonary edema
What to do next?
 Emergent cardiac catheterization
 Transfer to CCU, consider inotropes
 Admit to telemetry, rule out MI
 Discharge home with close clinic f/u
“This is not a heart failure exacerbation,
it’s Lasix deficiency syndrome.”
Case #2

71 W with a one-year history of asthma
treatment from a community physician,
presents to the ED after waking up at
2am with shortness of breath.
Case #2, HPI, continued
Often awakens in the middle of the
night; gets up and takes albuterol,
usually feels good enough to go back to
sleep
 Baseline ET 1 block, now has dyspnea
at rest; denies chest pain
 Sometimes feels lightheadedness and
palpitation after taking albuterol

71 W “asthma”
PMH: HTN, DM, CHOL, asthma (PFT’s never done)
 PSH: None
 Medications:
Amlodipine 10mg PO daily
Aliskiren 300mg PO daily
HCTZ 25mg PO daily
Albuterol PRN; using 6-8 puffs a day now
Advair 500/50 2 puffs PO bid
ASA 81, Pravastatin 10, Insulin

71 W “asthma”
NKDA
 Social: Smokes 1/2 ppd x50 years, no
EtOH, denies drug use
 Family: Father died age 63 of MI

71 W “asthma”






102/64 P118 R32 SpO2=91% 4L T=99.4
Diaphoretic
Jugular venous pressure 12cmH2O
Expiratory wheeze from lung bases to mid
lung fields bilaterally
Rapid rate, regular rhythm, III/VI apical
holosystolic murmur
Bilateral pitting ankle edema; extremities
warm
71 W “asthma”
Labs drawn; results pending
 EKG shows sinus tachycardia, left atrial
enlargement, left ventricular
hypertrophy with ST-T changes that
could be due to hypertrophy or
ischemia, and poor R-wave progression
No prior EKG for comparison

Chest X-Ray
71 W pulmonary edema
ED Course
 “Doctor. Please help me. (Gasp.) I feel
terrible.”
 What do you do?
71 W pulmonary edema
Albuterol?
Xopenex?
Furosemide?
Tirofiban?
ASA?
Plavix?
Metoprolol?
Heparin?
Intubation?
IABP?
Morphine?
Nitroglycerin?
Simvastatin?
BiPAP?
Diltiazem?
Digoxin?
Levophed?
Dopamine?
Dobutamine?
Nesiritide?
Nexium?
Hydralazine?
Lisinopril?
Captopril?
71 W pulmonary edema
Albuterol?
Xopenex?
Furosemide?
Tirofiban?
ASA?
Plavix?
Metoprolol?
Heparin?
Intubation?
IABP?
Morphine?
Nitroglycerin?
Simvastatin?
BiPAP?
Diltiazem?
Digoxin?
Levophed?
Dopamine?
Dobutamine?
Nesiritide?
Nexium?
Hydralazine?
Lisinopril?
Captopril?
Here, have a mnemonic
Lasix IV (high dose if pt. prev. on it)
 Morphine (at least 4mg IV to start)
 Nitroglycerin (SL, paste, or drip)
 Oxygen (100% NRBM, then PAP)
 Positive pressure ventilation
(noninvasive bilevel positive airway
pressure “BiPAP™” or intubation)

Someone comes rushing in.

“The labs came back! The troponin is
elevated. We have our diagnosis: This
is a NSTEMI! Rush the patient to the
cath lab!”
Laboratory Values
CBC normal, coags normal
 Na=126 K=5.1 BUN=28 Cre=1.3
 Albumin=3.4, mildly elevated
transaminases, LFT’s otherwise normal
 Troponin I=0.13, CK=164

Physical examination now

98/62 P96 R26 SpO2=99% on Bilevel PAP
set at IPAP=10, EPAP=5, FiO2=60%
 Diaphoretic
 Bilateral pitting ankle edema; extremities
warm
Yikes! We have troponin!
You shout: “Are you having any chest
discomfort at all?” She shakes her head no.
“How is your breathing?” She indicates
through the mask that she is starting to feel
better.
 Repeat EKG shows normal sinus rhythm,
otherwise unchanged (LVH, LAE, ST-T wave
changes of hypertrophy or ischemia)

72 W pulmonary edema
What to do next?
 Emergent cardiac catheterization
 Transfer to CCU, consider inotropes
 Admit to telemetry, continue LMNOP
 Call the cardiology fellow to ask “Should
we give heparin?”
Pt. goes to the CCU: Best case

Pt. continues to feel better with repeat
furosemide dosing. Blood pressure
improves. Stops BiPAP. Echo shows
EF=35%, mod MR. Weight drops 4kg in
two days; edema resolves. Cardiac
catheterization two days later shows
chronic total occlusion of mid LAD. No
other significant lesions noted.
Best case scenario, continued

Pt. sent home on ACE, beta blocker,
diuretic, statin, aspirin, insulin. Quits
smoking. Fires her old internist and
chooses a physician at Jacobi’s internal
medicine continuity clinic. Echo 3
months later shows EF=45%, mild MR.
Doesn’t go to the ED again until shortly
after Thanksgiving of the following year.
The worst outcome
Pulmonary edema is not treated
promptly. Patient has RR=44,
SpO2=89%, then starts to become
lethargic.
 Intubated for hypoxic respiratory failure.
 (After all, intubation is the ultimate form
of positive pressure ventilation.)

Why this is bad
This is not bad because of the patient’s
long-term prognosis--it’s bad because we
physicians failed the patient.
 This patient can still recover and turn out
just as well as in the best-case scenario
long-term (so long as she doesn’t
develop ventilator complications). She
just had to suffer needlessly to get there.

Pt. goes to the CCU:
Intermediate outcome, case #2

Despite LMNOP, the patient continues
to complain of shortness of breath in the
CCU. Extremities become cooler. BP
drops to 92/52, HR=112. Echo shows
EF=30%, mod MR. Pt. cannot lie flat for
cardiac catheterization; she continues to
deny chest pain.
What’s the term for this?
There’s a name for this cluster of findings:
 Hypotension
 Elevated JVP
 Pulmonary edema
 Cool extremities
What to do now?
Albuterol?
Xopenex?
Furosemide
Tirofiban?
ASA
Plavix?
Metoprolol?
Heparin?
Intubation?
IABP?
Morphine
Nitroglycerin
Simvastatin
BiPAP
Diltiazem?
Digoxin?
Levophed?
Dopamine?
Dobutamine?
Nesiritide?
Nexium
Hydralazine?
Lisinopril?
Captopril?
Cardiogenic shock:
Principles of Therapy





Palliate symptomatic pulmonary edema
Confirm diagnosis
Reduce afterload
Remove edema fluid
Increase inotropy
This discussion does not apply to the septic
(“distributive shock”) patient who also has
heart failure
Cardiogenic shock:
Principles of Therapy
First, exclude surgical emergency:
 To cardiac cath lab stat if etiology is acute
coronary syndrome
 If acute structural heart disease is etiology
(e.g. endocarditis, ventricular septal wall
rupture), consider IABP and OR stat

Get EKG and auscultate; check emergent
echo if concerns persist
Cardiogenic shock:
Principles of Therapy
Palliate symptomatic pulmonary edema
 Confirm diagnosis
 Reduce afterload
 Remove edema fluid
 Increase inotropy

Cardiogenic shock:
Principles of Therapy
Palliate symptomatic pulmonary edema
 Confirm diagnosis
 Reduce afterload
 Remove edema fluid
 Increase inotropy

Afterload reduction options
Hydralazine
 ACE/ARB
 Dobutamine/Milrinone
 Nesiritide

Diuresis/Ultrafiltration
 Phlebotomy

Hydralazine (with nitrates)

Hydralazine 10mg PO tid is a reasonable
starting dose
 Titrate upward every day as BP tolerates;
goal systolic BP is usually 95-100
 Maximum dose is 300mg daily
 Drug-induced lupus is dose-dependent

Hydralazine + nitrates saves lives compared
to placebo; please don’t ask about BiDil
ACE/ARB

Compared to hydralazine and nitrates, ACE
or ARB therapy extends life still more
 This effect is not dose-dependent (low-dose
ACE/ARB as life-extending as high dose)
 In severely low output states, can cause renal
hypoperfusion and injury (evidence poor)
 No evidence that adding ACE to ARB or vice
versa has any benefit
Dobutamine/Milrinone

These are inotropes, not pressors
 They are both arterial vasodilators
 A good combination, physiologically, for relief
of cardiogenic shock
Dobutamine/Milrinone
adverse reactions

Can cause tachyarrhythmia (AF, Afl, VT, VF)
 Decrease dose in case of relentless
tachycardia or frequent nonsustained
ventricular tachycardia
If inotrope deemed necessary and unable to
control tachyarrhythmia with reduced dose:
 Consider amiodarone
 Consider digoxin (keep K>4, Mg>2)
Dobutamine v. Milrinone
Renal insufficiency:
Milrinone accumulates, causing worsened ability to monitor; still okay
for short-term (1-2) day use in renal dysfunction
Winner: Dobutamine

Beta blockers wanted:
Dobutamine cannot be used with a beta blocker (dobutamine is a
beta agonist); however a patient can be on milrinone with a beta
blocker
Winner: Milrinone


Dopamine or Norepinephrine is in the room:
Increases afterload--usually a bad idea in heart failure, but may
seem necessary in septic shock
Loser: Dopamine and Norepinephrine
Dobutamine/Milrinone
adverse reactions

In patients with acute coronary syndrome, can worsen
infarct (increased oxygen demand)

Never shown to reduce mortality; several
studies show increase in mortality
Nesiritide





Controversial
Reduces afterload
Potentially effective in diastolic heart failure
Potentially protects kidneys
Potentially shortens life
Diuresis/Ultrafiltration

Reduce afterload by decreasing effective
circulating volume
 Removes the edema

Phlebotomy used to be performed for this
until we learned that anemia worsens heart
failure
Diuresis/Ultrafiltration

Monitor urine output and daily weight
 Make sure kidneys are perfused (reduce
afterload and increase inotropy as needed)
 Escalate furosemide dose until brisk diuresis
is achieved; add metolazone as needed
 If unable to diurese, begin ultrafiltration
What to do now?
Albuterol?
Xopenex?
Furosemide
Tirofiban?
ASA
Plavix?
Metoprolol?
Heparin?
Intubation?
IABP?
Morphine
Nitroglycerin
Simvastatin
BiPAP
Diltiazem?
Digoxin?
Levophed?
Dopamine?
Dobutamine?
Nesiritide?
Nexium
Hydralazine?
Lisinopril?
Captopril?
Intermediate outcome, cont.
Pt. is started on dobutamine
5mcg/kg/min. Furosemide changed to
continuous IV drip (10mg/hr), and
nitroglycerin changed to IV drip
(10mcg/min).
 Once pulmonary edema resolves, drips
titrated off. Pt. starts beta-blocker, ACE,
diuretics; follows with cardiology.

A word about Beta Blockers in
Pulmonary Edema

Long-term heart failure management:
Yes.
Beta-blockers prolong life.

Management of patient in pulmonary
edema on the verge of intubation:
Avoid.
(It’s a negative inotrope.)
Special situations: Beta Blockers
in Pulmonary Edema

Pulmonary edema due to hypertensive
emergency:
Esmolol is as good as any other hypertensive
emergency drug. (Nitroglycerin is not.)

Patient on dobutamine: Avoid.

Patient with HOCM, tachycardia, and
pulmonary edema: Use beta blockers
Choose your own adventure.
What would you like to discuss now?
 Furosemide pharmacokinetics
 DDx of elevated troponin
 Heparin/LMWH in UA/NSTEMI
 Why is this patient hyponatremic?
 HOCM/ASH/IHSS/LVOT obstruction

Something completely different