Pulmonary Edema

“Acute systolic heart failure” is useful for hospital billing, but pulmonary edema is more descriptive.

Pulmonary EdemaLearning 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 dailyCarvedilol 12.5mg PO bidFurosemide 40mg PO dailyASA 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.

Ate salt

Central venous pressure increases; mesenteric venous pressure increasesIntestinal

edema

Cannot absorb PO meds

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

Intubation?IABP?Morphine?Nitroglycerin?Simvastatin?BiPAP?Diltiazem?Digoxin?

Albuterol?Xopenex?Furosemide?Tirofiban?ASA?Plavix?Metoprolol?Heparin?

Levophed?Dopamine?Dobutamine?Nesiritide?Nexium?Hydralazine?Lisinopril?Captopril?

71 W pulmonary edema

Intubation?IABP?Morphine?Nitroglycerin?Simvastatin?BiPAP?Diltiazem?Digoxin?

Albuterol?Xopenex?Furosemide?Tirofiban?ASA?Plavix?Metoprolol?Heparin?

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?

Intubation?IABP?MorphineNitroglycerinSimvastatinBiPAPDiltiazem?Digoxin?

Albuterol?Xopenex?FurosemideTirofiban?ASAPlavix?Metoprolol?Heparin?

Levophed?Dopamine?Dobutamine?Nesiritide?NexiumHydralazine?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 TherapyFirst, 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 dysfunctionWinner: 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 blockerWinner: 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?

Intubation?IABP?MorphineNitroglycerinSimvastatinBiPAPDiltiazem?Digoxin?

Albuterol?Xopenex?FurosemideTirofiban?ASAPlavix?Metoprolol?Heparin?

Levophed?Dopamine?Dobutamine?Nesiritide?NexiumHydralazine?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