3_12_Mattu_Cardiogenic Pulm Edema.pdf

8/14/2019 3_12_Mattu_Cardiogenic Pulm Edema.pdf

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Winning at Failure

Modern Management of

Cardiogenic Pulmonary Edema

Amal Mattu, MD, FAAEM, FACEP

Professor and Vice Chair

Department of Emergency Medicine

University of Maryland School of Medicine

Baltimore, Maryland

Case

! 65 yo. man presents with dyspnea Developed over the past 6 hours History of hypertension, tobacco use Diaphoretic, normal mental statusAfebrile, HR 110, BP 180/110, RR 26,

pox 88%

Lungs crackles, JVD

Case

Kerley B Lines

Cephalization

Case

! 100% NRB pulse ox 93%! Monitor, IV, ECG

Sinus tachycardia, no acute ST/T-waveabnormalities


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Case

What is the optimal treatment in the first5-10 minutes??

a) morphineb) furosemidec) morphine + furosemided) nitroglycerin + (morphine + furosemide)e)

nesiritide + (morphine + furosemide)f) none of the above

OUTLINE

! Definition! Pathophysiology! Pharmacological management

Preload reductionAfterload reduction Inotropic support

! Noninvasive Positive Pressure Ventilation! Prehospital Issues! Summary

CARDIOGENIC

PULMONARY EDEMA

! Definition: Leakage of fluid from the pulmonary

capillaries and venules into the alveolarspace as a result of increased hydrostaticpressure

Inability of the LV to effectively handle itspulmonary venous return

ANATOMY

lungs

Normal


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PATHOLOGY

Pulmonaryedema!!

lungs

PHYSIOLOGY

preload

afterload

LV function

lungs

PATHOPHYSIOLOGY

preload

afterload

LV functionPulmonary edema!!

lungs

PATHOPHYSIOLOGY

preload

lungs


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PATHOPHYSIOLOGY

1. increasedpreload

Pulmonary edema!!

lungs

PATHOPHYSIOLOGY

afterload

lungs

PATHOPHYSIOLOGY

2. increased

afterload

Pulmonary edema!!

lungs

PATHOPHYSIOLOGY

LV function

lungs


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PATHOPHYSIOLOGY

3. decreasedLV function

Pulmonary edema!!

lungs

PATHOPHYSIOLOGY

2. increasedafterload

3. decreasedLV function

Pulmonary edema!!

lungs

1. increasedpreload

GOALS OF TREATMENT

1. decreasepreload

2. decreaseafterload

3. improveLV function

lungs

GOALS OF TREATMENT

lungs

body

Pulmonary edemaTotal body hypovolemia or euvolemia


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CARDIOGENIC

PULMONARY EDEMA

! Note:more than 50% of patientswith cardiogenic pulmonary edemaare euvolemic!!

! Treatment should be based notnecessarily on fluid removal, but onfluid redistribution.

body

GOALS OF TREATMENT

Pulmonary edema

lungs

body

GOALS OF TREATMENT

lungs

body

CARDIOGENIC

PULMONARY EDEMA

! Causes Excessive venous return (preload) Excessive SVR (afterload) LV dysfunction

" disorders of contractility" disorders of rate and rhythm


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GOALS OF TREATMENT

1. decreasepreload

lungs

PRELOAD REDUCTION

! Traditional treatment Morphine Furosemide Nitrates

MORPHINE

!Advantages Histamine effect causes decrease in

preload

Anxiolysis may decrease catecholamines" decrease afterload

MORPHINE

! Disadvantages Side-effects may increasecatecholamines

" rash/urticaria from histamine release" nausea/vomiting

Respiratory depression with high doses Concerns if patient has low blood pressure

" myocardial depressant Limited evidence (none?)to support direct

hemodynamic benefits


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MORPHINE

!Vismara, et al (Circulation, 1976) Effect of morphine on venous tone in

patients with acute pulmonary edema

Evaluated venous pressure in the hand andforearm vessels

" venous pressure in the hand decreased, venousvolume in the forearm increased

Does this correlate with decreasedpreload?

MORPHINE

! Lappas DG, et al (Anesthesiology, 1975) Filling pressures of the heart and

pulmonary circulation in patients with CADafter intravenous morphine

" 2 mg/kgIV morphine (5mg/min)" left and right heart filling pressures increased" CI decreased

MORPHINE

! Timmis, et al, (Br Med J, 1980) 0.2 mg/kg IV morphine in AMI patients

with severe LVF

15 and 45 minutes after injection, BP, HR,andCI decreased

No decrease in preload

MORPHINE

! Hoffman, et al (Chest, 1987) 57 patients with presumed prehospital

diagnosis of pulmonary edema

38% subjective deterioration 46% objective deterioration No patients receiving NTG without

morphine had deterioration


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MORPHINE

! Sacchetti, et al (Am J Emerg Med,1999)

Odds ratios for intubation and ICUadmission for pulmonary edema patients

Morphine 5 : 1

MORPHINE

! Peacock WF, et al (Emerg Med J, 2008) Morphine vs. no morphine for acute

decompensated heart failure

" independent predictor of mortality (OR 4.84)" increased need for mechanical ventilation, ICU

admission, prolonged hospitalization

MORPHINE

!Anxiolysis Decrease in catecholamines, afterload Why not use a benzodiazepine???

" no concerns with rash/urticaria" no concerns with nausea/vomiting" no concerns with respiratory depression"

no concerns with hypotension

SUMMARY MORPHINE

! Preload reduction Nitrates are superior

!Anxiolysis Side-effect profile favors benzodiazepines


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CONCLUSION MORPHINE

Morphine has no rolein thetreatment of cardiogenicpulmonary edema!

FUROSEMIDE

Wheres the debate??

FUROSEMIDE

! Preload reduction Diuresis

" increased afterload causes decreased RBF" delayed effect: 30 120 minutes

Direct vasoactivity" venodilation little evidence"

does this correlate with decreasedpreload?

FUROSEMIDE

! Pickkers P, et al (Circulation, 1997) Direct vascular effects of furosemide on

the human forearm vascular bed anddorsal hand vein

" local administration of furosemide resultedin dose-dependent venodilaton

Does this correlate with decreasedpreload?


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FUROSEMIDE

! Kiely, et al (Circulation, 1973) Post-AMI CHF Furosemide administered to 15 patients Significant reductions in filling pressures

only in patients that had diuresis

FUROSEMIDE

! Ikram, et al (Clin Sci, 1980) IV furosemide administration in acute CHF Significant reductions (17%) in CO during

first 90 minutes

CO gradually returned to baseline withdiuresis

FUROSEMIDE

! Nelson, et al (Eur Heart J, 1983) IV furosemide (1 mg/kg) administration inAMI patients with LV failure

Initial adverse hemodynamic effects" decreases in CO and SV during initial 90 minutes

Parameters returned to baseline over next60 90 minutes

FUROSEMIDE

! Francis, et al (Ann Intern Med, 1985) Class III or IV CHF patients given IV furosemide Early adverse hemodynamic effects

" 20 minutes after administration!significant increase in HR, SVR (afterload)!significant decrease in SV

Gradual return to baseline with diuresis


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FUROSEMIDE

! Kraus, et al (Chest,1990) Effects of IV furosemide on PCWP over 1 hour

in patients receiving nitrates and/or captopril

Furosemide alone or furosemide plus nitrates" increase in PCWP over initial 15 minutes" then decrease PCWP with diuresis

If premedicatedwith nitrates plus captopril" immediate and sustained decrease PCWP

SUMMARY FUROSEMIDE

! Decreases preload through diuresis Delayed effect

! No consistent data regarding immediatedirect preload reducing effect

! Initial adverse hemodynamic effects Increased SVR Decreased SV, CO

CONCLUSION

FUROSEMIDE

Furosemide should be considereda third-line medicationin thetreatment of cardiogenicpulmonary edema!

NITROGLYCERIN

! Nitroglycerin vs. furosemide for preloadreduction

Cotter, et al (Lancet, 1998) Beltrame, et al (J Card Fail, 1998) Kraus, et al (Chest, 1990) Hoffman, et al (Chest, 1987) Nelson, et al (Lancet, 1983)


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NITROGLYCERIN

!Advantages Rapid, reliable preload reduction Moderate/high doses reduce SVR (afterload)

" maintains or improves SV and CO Multiple forms of administration topical, SL,

IV (be aggressive!)

Short half-life; especially important ifprehospital misdiagnosis

NITROGLYCERIN

! Caution in the presence of HypotensionAcute mitral regurgitationAortic stenosis Pulmonary hypertension Patients taking.

SUMMARY

NITROGLYCERIN

! Better than morphine or furosemide forpreload reduction

! Safer than morphine or furosemide inprehospital setting

! SL nitroglycerin provides rapid andeffective initiation of treatment

Followed by topical NTG if moderate CPE Followed by IV NTG if severe CPE

CONCLUSION

NITROGLYCERIN

Nitroglycerin should be first-lineprehospital and emergencydepartment treatment formoderate CHF and pulmonaryedema.


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GOAL OF TREATMENT

2. decrease

afterloadlungs

AFTERLOAD REDUCTION

! Results in increased CO, restores renalblood flow

Nitroglycerin" SL and moderate/high dose IV" excellent single agent for simultaneous preload

and afterload reduction

Nitroprusside" acute mitral regurgitation, severe hypertension

HydralazineACE-inhibitorsfor acute CPE??

ACE-INHIBITORS

! Barnett, et al (Curr Ther Res, 1991) 25 mg SL captopril if BP > 110 12.5 mg SL captopril if BP < 110 Decreased PCWP (preload) noted by

10 minutes

No change in HR, MAP

ACE-INHIBITORS

! Barnett, et al (Curr Ther Res, 1991) 12 additional patients with florid pulmonary

edema had significant improvement/completeresolution of dyspnea by 15 minutes

" 8/12 patients abrupt increase in diuresiswithout the use of a diuretic!(due to improvedrenal blood flow)


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ACE-INHIBITORS

! Langes, et al (Curr Ther Res, 1993) IV captopril infusion in moderate CHF or

pulmonary edema patients

Onset of action by 6 minutes Decreased PCWP (preload) Increased CO No adverse effects

ACE-INHIBITORS

!Varriale, et al (Clin Cardiol, 1993) Hemodynamic response to 1.25 mg IV

enalaprilat in patients with severe CHF andsevere MR

Increased CO and SV Decreased MAP and SVR (afterload) Decreased PCWP (preload) Decreased the magnitude of MR

ACE-INHIBITORS

! Sacchetti, et al (Am J Emerg Med,1999)

Odds ratios for intubation and ICUadmission for pulmonary edema patients

SL captopril 0.28 : 1

ACE-INHIBITORS

! SL captopril Hamilton, et al (Acad Emerg Med, 1996) Haude, et al (Int J Cardiol, 1990)

! IV enalaprilat Tohmo H, et al (Eur Heart J, 1994)Annane, et al (Circulation, 1996)

! Dialysis patients with pulmonary edema Sacchetti A, et al (Am J Emerg Med, 1993)

! SL and IV forms: hemodynamic and subjectiveimprovement can be seen in 6 12 minutes!!


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ACE-INHIBITORS

! Southall JC, et al (Acad Emerg Med, 2004) Safety of ED use of SL captopril in NYHA

Class IV patients

" no increased incidence of hypotension or need forvasopressors

" decreased ICU length of stay (29 hrs vs. 78 hrs.)

SUMMARY

ACE-INHIBITORS

! Rapid reduction in afterload and preload! Rapid reduction in level of distress! Decreased need for intubation, ICU use

Bed availability, hospital costs! Combination with NTG exceeds benefit of

either drug alone

!Acceptable alternative to IV NTG

CONCLUSION

ACE-INHIBITORS

ACE-inhibitors should beconsidered second-line agentsfor moderate CHF or pulmonaryedema; first-line in patientsunable to tolerate nitrates.

PRELOAD AND

AFTERLOAD REDUCTION

! Tei, et al (Circulation, 1995) Studied the effects of thermal vasodilation

in 34 CHF patients (mean EF 25%)

Exposure to sauna for 15 minutes" significant decreases in PCWP (preload)" significant decreases in SVR (afterload)" significant decreases in MR" significant increases in CI, SV, and EF


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GOAL OF TREATMENT

3. improveLV function

lungs

INOTROPIC SUPPORT

! Choices Catecholamines

" dopamine" dobutamine

Phosphodiesterase inhibitors (milrinone) IABP (bridging device before PTCA/CABG)

CATECHOLAMINES

! Drawbacks Tachycardia/arrhythmias Increased MO2consumption, ischemia Myocardial beta-receptors up-regulated in

severe CHF, tolerance develops

!standard doses are less effective!higher doses needed, more adverse effects

Chronic beta-blocker use decreases efficacy

PHOSPHODIESTERASE

INHIBITORS (MILRINONE)

! Work independent of adrenoreceptor activityand plasma CA levels

Work well even in patients on beta-blockers! Induce inotropic support as well asdecreased

preload and afterload

! No development of tolerance!

Butno mortality benefit vs. dobutamine


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CONCLUSION

INOTROPIC SUPPORT

Use what you are comfortablewith.

Consider use of milrinone forpulmonary edema patientsunresponsive to DA/DBT.

NONINVASIVE POSITIVE

PRESSURE VENTILATION

! Maintains positive airway pressure duringentire respiratory cycle

Maintains patency of stiff fluid-filled alveoli,prevents collapse during exhalation

Increases intrathoracic pressure" decreases preload and afterload (and increases CO)

SUMMARY NPPV

! Noninvasive positive pressureventilation is associated with:

Decreased work of breathing Improved O2and CO2exchange Improved preload, afterload, and CO Reduced need for intubation, ICU LOS Reduced hospital costs Reduced mortality (?)

CONCLUSION NPPV

NPPV is an effective method ofproviding airway support andaverting intubation in somepatients (but it must be usedearly!!)


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SUMMARY

! Nitroglycerin first-line agent IV nitroglycerin is excellent single-agent

!ACE-inhibitors second-line agent In addition to or instead of nitroglycerin

! Furosemide third-line agentAfter preload and afterload reduction

SUMMARY

! Morphine just say no! Preload reduction NTG more effectiveAnxiolysis BZDs have fewer side effects

! Nesiritide May prove useful for patients not

responding to optimal treatmentpending more studies

SUMMARY

! Inotropic support No data favors any specific agent Use what you are comfortable with!

! NPPV consider earlyuse Decreased intubations, ICU length of stay,

and hospital costs

Case

! 65 yo. man presents with dyspnea Developed over the past 6 hours History of hypertension, tobacco use Diaphoretic, normal mental statusAfebrile, HR 110, BP 180/110, RR 26,

pox 88%

Lungscrackles, JVD


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Case

! 100% NRBpulse ox 93%! Monitor, IV, ECG

Sinus tachycardia, no acute ST/T-waveabnls.

Case

What is the optimal treatment in the first5-10 minutes??

1. noninvasive ventilation2. SL NTG q5 min (x 3-4 doses)3. 1.25 mg IV enalapril or 25 mg SL captopril

(OR rapid titration of high dose IV NTG)

4. furosemide AFTER above given

REMEMBER!

!More than 50% of patients withcardiogenic pulmonary edemaare euvolemic!!

!Treatment should be based notnecessarily on fluid removal,but on fluid redistribution.

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3_12_Mattu_Cardiogenic Pulm Edema.pdf