Sinaia 2 Oct 2014 -Final-Acute Heart Failure

8/9/2019 Sinaia 2 Oct 2014 -Final-Acute Heart Failure

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Acute Heart Failure

Prof univ dr Ion C. intoiuȚ


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Acute HeartFailure

Prof univ dr Ion C. intoiu


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Objectives

• Definitions• Epidemiology• Pathophysiology• Diagnosis

• Management• Summary of Guidelines• Recommended Reading


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• Definitions• Epidemiology• Pathophysiology• Diagnosis• Management• Summary of uidelines• !ecommended !eading


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"he definition of acute heartfailure has not #een firmly

esta#lished $%&.

It is recogni'ed (hen symptoms ofheart failudevelop rapidly (ithin

hours anddays% in patients (ithout prior

evidence of cardiacdecompensation )


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cute !eart "ailure

• !apid onset of symptoms and signsrelated to a#normal cardiac function

• As a result of Systolic Dysfunction*Diastolic Dysfunction* Arrhythmias* orPreload+After load Mismatch


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Acute heart failure

AHF,AHF, "he rapid onset of symptoms and signs secondary to a#normalcardiac function.$reduced C-* tissue hypoperfusion congestion* increase in PC/P&

0. /ith or (ithout previous cardiac disease.1. "he cardiac dysfunction can #e related,

a& to systolic or diastolic dysfunction#& to a#normalities in cardiac rhythmc& to preload and afterload mismatch

2. -ften life threatening and re3uires urgent treatment.

"he "as4 Force on Acute Heart Failure of the European Society of"he "as4 Force on Acute Heart Failure of the European Society ofCardiologyCardiology


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ESC Guidelines, 2005• DEFI5I"I-5# Rapid onset of symptoms and signs secondary to

abnormal cardiac

function$ %t may occur &ith or &ithout previous cardiac disease$ 'he cardiac dysfunction can be related to

systolic or diastolic dysfunction(abnormalities incardiac rhythm or to pre)load and after load• mismatch *


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Acute heart failure is heterogeneousAcute heart failure is heterogeneoussyndromesyndrome

CardiogenicCardiogenicshockshock

PULMONARYPULMONARYEDEMAEDEMA

Right Heart FailureRight Heart Failure

High Output FailureHigh Output FailureH pertensi!e HFH pertensi!e HF

AcuteAcuteDeco"pensatedDeco"pensatedCHFCHF

Filippatos 1667Filippatos 1667


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-vervie(, Acute Heart Failure• Comple8 syndrome caused #y

impaired cardiac function• 1 types,

• left ventricular systolicdysfunction $9:SD&

• Heart failure (ith preservede;ection fraction$HFPEF


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• Definitions• Epidemiology• Pathophysiology

• Diagnosis• Management• Summary of uidelines• !ecommended !eading


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• Definitions• Epidemiology• Pathophysiology

• Diagnosis• Management• Summary of uidelines• !ecommended !eading


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Pathophysiology

-. dysfunction/ccumulation of fluid$

Decrease in 0O !ypoperfusion$

Reciprocal ctivation of 1R S2 3a( &ater retention$

G%% E'4 5 .asopressin$

Refle, activation of S3S/ Epi( 3E$


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A Vicious Circle


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3atural history of congestive heartfailure

#nitial phase#nitial phase Last ear Last ear

Nor"al heartNor"al heart Chronic heart $ailureChronic heart $ailure% "illion in the U&% "illion in the U&'( "illion in Europe'( "illion in Europe

DeathDeath

#nitial#nitial" ocardial" ocardialin)urin)ur

First ADHF episode*First ADHF episode*Pul"onar ede"aPul"onar ede"aER ad"issionER ad"ission

Later ADHF episodes*Later ADHF episodes*Rescue therapRescue therap#CU ad"ission#CU ad"ission

heorghiade M. Am Cardiol. 1667 $suppl A&,0+> .heorghiade M. Am Cardiol. 1667 $suppl A&,0+> .

H e a r t

+ i a , i l i t

H e a r t

+ i a , i l i t


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cute E,acerbations May 0ontribute tothe Progression of the Disease

Gheorghiade M, Fonarow G, Filippatos G et al. Am J Cardiology 2005

Time

V e n

t r i c l a r

! n c

t i o n

Ac te e"ent /ith each event*hemodynamic alterationscontri#ute to progressiveventricular dysfunction.


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Clinical CLASIFICATION

Initial and Serial Evaluation ofthe AHF Patient


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Acute Heart Failure , Classification

Acute de novo $ ne( onset of AHF in a patient(ithout previously 4no(n cardiacdysfunction 2$or Acute decompensation of chronic heartfailure.

"he "as4 Force on Acute Heart Failure of the European Society of Cardiology"he "as4 Force on Acute Heart Failure of the European Society of Cardiology

Can present itself as,Can present itself as,


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illip Classification

Stage I, 3o clinical signs of decompensation$

Stage II /

!eart failure$ Rales( S6( P.!$Stage III,

Severe heart failure$ Pulmonary edema &ith ralesthroughout the lung fields$Stage I:,

0ardiogenic Shoc7/ !ypotension( peripheralvasoconstriction( oliguria( cyanosis and diaphoresis$


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"orrester 0lassification

Su#set I13ormal28arm and Dry

Su#set II10ongestion28arm and 8et

Su#set III1!ypoperfusion20old and Dry

Su#set I:10ongestion andhypoperfusion20old and 8et

4

9

6

:

;

Cardiac Inde8$9


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Acute Heart Failure , G Clinical severity classification

, #ased on o#servation of the peripheral cir+culation and onauscultation of the lungs for congestion

Class I,

dry and (arm* Class II,

(et and cold* Class III,

cold and dry and Class I:,

cold and (et&.

5ohria A et al, ACC 1662 >0,0B B+0 6>.5ohria A et al, ACC 1662 >0,0B B+0 6>.


23/2855ohria A et al, ACC 1662 >0,0B B+0 6>.5ohria A et al, ACC 1662 >0,0B B+0 6>.

drydr y// absence of signs of congestionabsence of signs of congestion (( &et&et// elevated filling pressures(elevated filling pressures(&arm&arm // adeAuate systemic perfusion(adeAuate systemic perfusion( coldcold // inadeAuate systemic perfusioninadeAuate systemic perfusion

GG Clinical severity classificationClinical severi ty classification


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Clinical and pathophysiologicalclassification of acute heart failure

More than -(. o$ patients hospitali/ed 0ith heart $ailure ha!e congestion 10et2and sho0 ele!ated PC3P '45

Re$erences* '6 Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart ail. !"""#!$%&!'%&(. Availa)le at$ htt $**+++.sciencedirect.com*science* ournal*!- " /%. 56 onaro+ 0C. The treatment tar ets in acute decom ensated

Warm 6 7ry

PC3P7nor"al

C#8 nor"al1co"pensated2

Warm 6 Wet

PC3Pele!ated

C# nor"al

Cold 6 7ry

PC3Plo09nor"al

C# decreased

Cold 6 Wet

PC3Pele!ated

C# decreased

Congestion at rest

Lo0 per$usionat rest

+asodilators4diuretics

No

No

Yes

Yes

Nor"al &+R High &+R

H d i # i G h


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Hemodynamic su#sets in Gacute heartfailure #y cardiac inde8

3ormal5ormal

Pulmonaryedema

Cardiacinde89-*'><

reduced #lood pressure

high #lood pressure

Cardiogenicshoc4

Hypovolaemicshoc4

Mor,1.1?Mor,1.1? Mor,06.0?Mor,06.0?

Mor,11.>?Mor,11.>?

Mor,77.7?Mor,77.7?


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Acute Heart Failure , Classification

cute decompensated heart failure 1de novo or as decompensation of 0!"2 / 8ith mild signs and

symptoms of !" and do not fulfil criteria for cardio)genic shoc7( pulmonary oedema orhypertensive crisis $

!ypertensive acute heart failure / Signs and symptoms of !" 5 high BP 5 preserved -." 5 chestradiograph findings PO$Pulmonary oedema / .erified by chest C)ray( severe respiratory distress( or)thopnoea &ith SaO 9


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Underlying diseases and co!or"idities in acute #eart failure Coronary artery disease

$alvular disease

Prost#etic valve t#ro!"osis

Aortic dissection

AHF and #y%ertension

&enal failure

Pul!onary diseases and "ronc#oconstriction Arr#yt#!ias and AHF

Peri o%erative AHF 'usually due to

!yocardial isc#ae!ia(


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0ommon Precipitating "actorsMedication non)adherence$Dietary indiscretion$%nfection 1pneumonia( K'%( etc$2

Renal failure$0ardioto,icHnephroto,icmedication$Kncontrolled hypertension

0ardiac rrhythmiasMyocardial ishemia.alvular disease

Pulmonary embolus0OPD

nemia

'hyroid disorders 3ondihydropyridine 00BSodium retaining medications


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Clinical )valuation



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0linical Presentation.olume Overload -o& 0ardiac Output

DyspneaH"atigueRalesH8heeJing

L.DH!LRH LR PulmonaryHPitting EdemaReduced o,ygen saturation

S6 or S:Electrolyte disturbance%ncreased serum creatinine

3arro& Pulse Pressureltered Mental Status

Pre)renal aJotemia0ool e,tremitiesDecreased urine output

Refractory to %. diuresis


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"he etiology of acute heart failure can varysignificantlly

8 Pri"ar dilatedcardio" opath

8 Acute coronars ndro"

8 Arterial h pertension4dia,etes "ellitus

8 ?o@ic cardio" opath1cocaine4 alchohol2


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ADHE!E registry, "reatment ofacute heart failure

• ADHE!E 1Acute Decompensated HE art "ailure 3ational!E gistry2

• Data from 4


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Clinical presentation of acute heartfailure in ma;or clinical studies


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Clinical presentations of acute heart failurein EHFS II and A9A!M+HF studies

A9A!M+HFEHFS II

Pulmonary oedema $0 ? vs 2B?& and cardiogenic shoc4

$>? vs 01?& are significantly different #et(een the t(o studies.


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• Diagnosis Epidemiology• Pathophysiology

• Definition• Management• Summary of uidelines• !ecommended !eading


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Diagnosic

• EC• CJ! • AK• 9a#oratory "ests

– A s!all elevationin cardiactro%onin !ay "e

seen in %atients*it# AHF *it#outACS.

• Echo

Di ti h t t


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Diagnostic approach to acuteheart failure 160> AHA


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Diagnosis-o&)%ntermediate clinical suspicion of D!"

B3P 1 2

B3P ;


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Diagnosis, Cardiac Kiomar4ersIn patients (ith symptoms and signs of heartfailure,

Measure serum natriuretic peptides

!efer to have echocardiography and specialistassessment (ithin 1 (ee4s if

+ Previous MI

•K5P L >66 pg66 pg


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0ardiac Biomar7ers

"roponin


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0linical Potential of B3PH3')

proB3P• E,tensively studied

+ #lood test for heart failure N

• Diagnosis)Raised in -.SDH "H-.!H.!DH 0S• Screening for asymptomatic -.SD• Ris7 stratification Prognosis in established !"

• 'herapy monitoring• 'reatment of !"

3ormal B3P ma7es -.SD very unli7ely

5E A"I:E P!EDIC"I:E :A9NE


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• Definitions• Epidemiology• Pathophysiology• Summary of uidelines• Management

• Summary of uidelines• !ecommended !eading


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! H 00 Guideline160> AHA


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EVIDENCE

Applying guidelines in acute

heart failure, Facts or fancy O


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ACCF6 pages

Canadian Cardiovascular Society


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Canadian Cardiovascular SocietyConsensus !ecomendations


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Australia


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?reat"ent o$ acute heart $ailurealancing R#&B& AND ENEF#?&

$or indi!idual patients

AHF


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• Definitions

• Epidemiology• Pathophysiology• Management

$5onpharmacologicaltreatment

.Summary of uidelines• !ecommended !eading


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+arious targets $or therapies used in the"anage"ent o$ acute deco"pensated

heart $ailure6

Allen L A 4 and O Connor C M CMA; 5((


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5oninvasive ventilation $5I:&

4$ Bilevel positive air&ay pressure1KiPAP& or 9$ 0ontinuous positive air&ay

pressure1CPAP 2$


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3oninvasive PP.

Fig. +B


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0P P vs$ %ntubation

CPAP• 5on+invasive• Easily discontinued• Easily ad;usted• Nse #y EM"+K• Minimal complications

• Does not re3uiresedation

• Comforta#le

Intu#ation• Invasive• Intu#ated stays intu#ated• !e3uires highly trained

personnel• Significant complications• Can re3uire sedation or

!SI• Potential for infection


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Kltrafiltration

• !APID+CHF "rial + >6 patients + ADHF and !enal

Insufficiency $Cr L0.7& + Nltrafiltration had

significant increase influid removal after 1>hours

+ > 76 9 vs 1 2 9

• N59-AD "rial + 166 patients + !enal insufficiency (as

not a criteria for inclusion + Standard care vs ultra

filtration + > Hours >. 9 vs 2.29 + 6 Days fe(er

rehospitali'ations .11 vs .> and fe(er unscheduledclinic visits 10 vs >>

:ption in the setting of failed diureticand vasodilator therapy


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Cardiac and :entricular AssistDevices


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9eft :entricular Assist Device

• "he 9:AD assists left ventricular function #y pumping

#lood from left atrium to aorta


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!ight :entricular Assist Device

• "he !:AD assists isolated right ventricular dysfunction #y

pumping #lood from right atrium to pulmonary artery


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E0MO

• ECMO removes carbon dioxide from and adds oxygen o venousblood via an ar ificial membranelung

Severe respiratoryfailure Cardiac ailure+ith ina)ility to +ean off;ypass ;ridge toCardiac Transplant

Acute Hert Failure and -perative


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Acute Hert Failure and -perativeMortality Prediction Score

• !e3uirement for ventilatorsupport Q > points

• Clinical picture of post+

cardiotomy shoc4 Q 1 points

• Nse of temporary 9:AD prior toHeart+Mate insertion Q 1 points

• Central venous pressure L0mmHg Q 0 point

• Prothrom#in time L0 seconds Q0 point

• Scoring + 6+7, 9o( ris4

• Mortality ?

+ 7+B, Intermediate !is4 • Mortality 21? + +06, High !is4

• Mortality > ?


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briefdiscussion ofthe &or7s ofthis thing$$$


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Ruestions


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AFLENAFLEN

Triflusal


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THE END

Thank you for your attentionThank you for your attention


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NNe0e0 &trategies&trategies

$or $or NTIPL TELETTRETMENT

Prof univ dr Ion C."intoiu


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:entricular Assist Device

6


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Acute Heart Failure

5on+pharmachologic treatment• Kalance #et(een myocardial o8ygen demand

and delivery• "emperature control• Mechanical circulatory support

• Intraaortic #alloon pump• Cardiopulmonary interaction role of

mechanical ventilation


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Intraaortic Kalloon Pump

.


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E8tracorporeral Mem#rane -8ygenation

Advantages disadvantages• Possi#ility of providing total cardiopulmonary support

and allo(ing for cardiac and pulmonary healing* #utneeds for higher level of anticoagulation* leads to#leeding* increased #lood loss* #lood productre3uirement* multiple e8ploration* and potentialinfection

Indications• 5eonatal respiratory failure• Pediatric respiratory failure• 5eonatal and pediatric cardiac failure• Adult cardiorespiratory failure


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Mechanical Circulatory Support

"echnical principles• In children* the most common form of :AD involves

use of centrifugal pump• Atrial pressure lines are neccessory to monitor for

ade3uate decompression and 4ept as close to 'ero aspossi#le to ensure ventricular decompression

• All inotropes should #e (ithheld if possi#le during therecovery period

• Serial stress echocardiography should #e performedevery 0+2 days to document progression of recovery

• Decannulation should #e performed #y gradually(eaning :AD support and #e a team approach (ithpreparation of volume catecholamine infusion ready.


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:AD for Pediatric Patients

9imitations of development4 Si'e constraints

9 Differences in pathophysiology of failure 0& !ight ventricular failure

1& Kiventricular failure

2& Pulmonary failure


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9eft :entricular Assist Device

• "he 9:AD assists left ventricular function #y pumping

#lood from left atrium to aorta


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!ight :entricular Assist Device

• "he !:AD assists isolated right ventricular dysfunction #y pumping #lood from right atrium to pulmonary artery


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Kerlin Heart :AD

• Kerlin Heart :AD is a paracorporeal air+driven pulsatile :AD


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arvi4 1666 System

• avi4 1666 is an intraventricular a8ial flo( impeller pump re3uiring

percutaneous electric po(er of possi#le implanted #attery po(er


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Kiventricular Assist Device

• "horatec. KI:AD


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E8tracorporeral Mem#rane -8ygenation


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Cardiopulmonary Support System

Initial and Serial Evaluation of


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Clinical )valuation




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,iagnostic Tests




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Noninvasive CardiacI!aging



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-ec#anical CirculatorySu%%ort

Guideline for HF


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Surgical PercutaneousTranscat#eterInterventional

Treat!ents of AHF

Guideline for HF

Conclusions


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• Evidence)based guideline directed diagnosis( evaluation and

therapy should be the mainstay for all patients &ith !"$• Effective implementation of guideline)directed best Auality

care reduces mortality( improves O- and preserves healthcare resources$

• Ongoing research is needed to ans&er the remaining Auestionsincluding/ prevention( nonpharmacological therapy of !"including dietary adjustments( treatment of !" ! E"(management of hospitaliJed !"( effective reduction in !"readmissions( more precise use of device)based therapy(smaller M0S platforms and cell)based regenerative therapy$

Conclusions


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Overvie&/ cute !eart "ailure

• 5e( ESC guidelines• Diagnosis

+ Serum natriuretic peptides• 5on+invasive ventilation• Inotropes• 5esiritide• Cardiac Devices


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Objectives

Revie& the pathophysiology of D!"$Describe the clinical presentation of D!"$

pply effective therapeutic strategies using consensusguidelines from the 1!"S 2 and the 1ES02$E,amine the clinical evidence of milrinone and

niseritide in the treatment of D!"$Evaluate the appropriateness of treatment$


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D!"

Rapid onset of signs and symptoms secondary to abnormal cardiacfunction due to systolic( diastolic dysfunction( abnormalities incardiac rhythm or to pre)load and after)load mismatch$

De novo or acute decompensation of 0!"$Q;


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Acute heart failure


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Acute heart failure


0. /ith or (ithout previous cardiac disease.

1. "he cardiac dysfunction can #e related,a& to systolic or diastolic dysfunction#& to a#normalities in cardiac rhythmc& to preload and afterload mismatch



Hemodynamic su#sets in Gacute heartfailure


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failure

3ormal5ormal

Pulmonary

edema

C

ardiacinde89-*'><

reduced #lood pressure

high #lood pressure

Cardiogenic

shoc4

Hypovolaemicshoc4

Mor,1.1?Mor,1.1? Mor,06.0?Mor,06.0?

Mor,11.>?Mor,11.>?

Mor,77.7?Mor,77.7?

Acute Heart Failure ,


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-ther Classifications%n !" after M%( best applied to acute denovo heart failure/%n !" after M%( best applied to acute denovo heart failure/

'he illip classification / based on clinical signs and chest C)ray findings 1Stage %/ 3o heart failure( Stage %%/ !eartfailure( Stage %%%/ Severe heart failure and Stage %./ 0ardiogenic shoc72$'he "orrester classification/ based on clinical signs and haemodynamic cha)racteristics$

%n a cardiomyopathy service( best applied to chronic decompensated heart failure/%n a cardiomyopathy service( best applied to chronic decompensated heart failure/ 0linical severity classificationN /

based on observation of the peripheral cir)culation and on auscultation of the lungs for

congestion10lass %/ dry and &arm( 0lass %%/ &et and cold( 0lass %%%/ cold and dry and 0lass %./ cold and&et2$

3ohria et al/ L 00 9)4=


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cute decompensated heart failure 1de novo or as decompensation of 0!"2 / 8ithmild signs and symptoms of !" and do not fulfil criteria for cardio)genic shoc7(

pulmonary oedema or hypertensive crisis $!ypertensive acute heart failure / Signs and symptoms of !" 5 high BP 5 preserved-." 5 chest radiograph findings PO$Pulmonary oedema / .erified by chest C)ray( severe respiratory distress( or)thopnoea

&ith SaO 9


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H! SKP CI P08P 0ongestionillipH

"orrester

Diuresis !ypo) perfusion

End organhypo)

perfusion

%. Acutedecompensatedcongestive heartfailureU


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!or idities in acute #eart failure Coronary artery disease

$alvular disease

Prost#etic valve t#ro!"osis

Aortic dissection


&enal failure

Pul!onary diseases and "ronc#oconstriction

Arr#yt#!ias and AHF

Peri o%erative AHF 'usually due to!yocardial isc#ae!ia(

4oals of treat!ent of t#e %atient*it# ac te #eart fail re


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Clinical↓ sy!%to!s 'dys%nea and or fatigue( clinical signs

"ody *eig#t diuresis

o/ygenationLa"oratory e/a!inations +UN and or creatinine seru! electrolyte nor!alisation↓ %las!a +NP

"lood glucose nor!alisationHae!odyna!ic%ul!onary *edge %ressure to 0 12 !! Hg

cardiac out%ut and or stro3e volu!e

*it# acute #eart failure


4oals of treat!ent of t#e %atient


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*it# acute #eart failure

Outco!e length of stay in the intensive care unit duration of hospitali'ation

time to hospital re+admission mortality Tolera"ility9o( (ithdra(al rate

9o( incidence of adverse effects



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cute E,acerbations May 0ontribute tothe Progression of the Disease

Gheorghiade M, Fonarow G, Filippatos G et al. Am J Cardiology 2005

Time

V e n

t r i c l a r ! n c t

i o n

Ac te e"ent /ith each event*hemodynamic alterationscontri#ute to progressiveventricular dysfunction.


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illip 0lassification

Stage %/ 3o clinical signs of decompensation$Stage %%/ !eart failure$ Rales( S6( P.!$

Stage %%%/ Severe heart failure$ Pulmonary edema &ithrales throughout the lung fields$Stage %./ 0ardiogenic Shoc7/ !ypotension( peripheralvasoconstriction( oliguria( cyanosis and diaphoresis$



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orrester 0lassification

Su#set I13ormal2

8arm and Dry

Su#set II10ongestion2

8arm and 8et

Su#set III

1!ypoperfusion20old and Dry

Su#set I:

10ongestion andhypoperfusion20old and 8et

4

9

6

:

;

Cardiac Inde8$9


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0ommon Precipitating "actorsMedication non)adherence$Dietary indiscretion$%nfection 1pneumonia( K'%( etc$2Renal failure$0ardioto,icHnephroto,icmedication$Kncontrolled hypertension0ardiac rrhythmiasMyocardial ishemia.alvular disease

Pulmonary embolus0OPD

nemia'hyroid disorders

3ondihydropyridine 00BSodium retaining medications


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L.DH!LRH LR PulmonaryHPitting EdemaReduced o,ygen saturationS6 or S:Electrolyte disturbance%ncreased serum creatinine


Pre)renal aJotemia0ool e,tremitiesDecreased urine outputRefractory to %. diuresis


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Differential Diagnosis

PneumoniaReactive air&ay disease

Pulmonary embolus


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Diagnosis

Diagnosis of D!" should be primarily based on signs and symptoms$ 102


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B3P 1 2

B3P ;


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Predictors of Mortality

BK3 :6 mgHdl

SBP 44; mm!gs0r 9$>; mgHdl

"onaro& G0 et al$ JAMA" 9


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Diagnosis, Cardiac Kiomar4ersIn patients (ith symptoms and signs of heartfailure,

Measure serum natriuretic peptides

!efer to have echocardiography and specialist

assessment (ithin 1 (ee4s if

+ Previous MI

•K5P L >66 pg66 pg


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0ardiac Biomar7ers

"roponin


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) yp9U

Acute M#

? pe ' ? pe 5 ? pe > ? pe

? pe a

? pe %

? pe ,

Secondary tospasm,

embolism, anaemia,arrhythmia, BP

changes

Tro%oninitis

0linical Potential of B3PH3')


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0linical Potential of B3PH3 ) proB3P

• E,tensively studied + #lood test for heart failure N

• Diagnosis)Raised in -.SDH "H-.!H.!DH 0S• Screening for asymptomatic -.SD• Ris7 stratification Prognosis in established !"• 'herapy monitoring• 'reatment of !"

3ormal B3P ma7es -.SD very unli7ely5E A"I:E P!EDIC"I:E :A9NE


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• 3e& ES0 guidelines• Diagnosis

+ serum natriuretic peptides• 5on+invasive ventilation• %notropes

• 3esiritide• 0ardiac Devices

cute 0ardiogenic Pulmonary Oedema


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• 0ommon + 4;)9


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%nitial 'reatment

• The evidence infavour of morphineuse for AHF islimited

• Multiple agents are usedto manage !"( butthere is a pa city o!clinical trials data andtheir se is largelyempiric $

• Most agents improvehaemodynamics but noagent has #een shownto red ce mortality $

3on)invasive .entilation %n cute 0ardiogenicPulmonary Oedema


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Pulmonary Oedema

!"hen the household vacuum cleaner is employed,the machine should be run for some minutes #rst of

all to get rid of dust$

Poulton %P, &'on ()* +eft sided heart failure -ithpulmonary oedema* .ts treatment -ith the /pulmonary

plus pressure machine / Lancet 0123456731*281 283

Physiological %mprovement &ith 0P P in Patients&ith 0PO


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9ell et al Eur Heart 7::7

&ith 0PO


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Mortality reducedfrom 99F to 44F

RR


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Kac4groundims

• 0linical effectiveness of non)invasive ventilation

• 0omparative effectiveness of0P P and 3%PP.• Safety of non)invasive ventilation

!ypothesis/

• 3on)invasive ventilation reducesmortality

Intervention• Randomised 14/4/42

+ Standard o,ygentherapy 1by facial mas72 + 0P P 1; cm! 9O up

titrated to a ma,imumof 4; cm! 9O2 + 3%PP. 1=H: cm! 9O up

titrated to a ma,imumof 9


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Mor ali y

Standard"herapy

5on+Invasive

:entilation

-dds !atio 7?Confidence

Intervals

P :alue

B+Day . ? .7? 6. B 6. 2 to 0.> 6.

26+Day 0 .B? 07.>? 6. 2 6. 7 to 0.21 6. 7

Active Trial 1:42 patients @ 3=: per armBaseline ?haracteristics matchedBaseline )edications matched

Outcome/ !ospital stay3?P&


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Standard CPAP 5IPP: P+value

Admitted to intensiveCare

. ? .0? . ? 6.>00

Admitted to high+dependency Care

B.B? 06.2? 06. ? 6.260

Admitted to coronaryCare

2 .0? >2.B? >6. ? 6.22B

Median length of hospitalstay in days $ IR!&

$7+02& $7+0 & $7+0 & 6.202

o si ni#cant di erences PC: :=

0O30 KS%O3S3?P&


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0O30-KS%O3S

• In patients (ith acute cardiogenic pulmonaryoedema non+invasive ventilation $06 patients&

Produces more rapid resolution of meta#olic a#normalitiesand respiratory distress

Has no ma;or effect on B+day or 26+day mortality

Is #eneficial irrespective of the mode $CPAP or 5IPP:& ofdelivery

O i &/ ! " il


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+ serum natriuretic peptides• 3on)invasive ventilation• %notropes


' l d BP


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'reatment related to BP

!espiratory support* Furosemide $infusion&I: Do#utamine plus lo( dose I: "5

V IAKP

Oth t t t ti


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Other treatment options

• .asopressin antagonists + Knproven

• -evosimendan is a calciumsensitiser that improvescardiac contractility

• E,erts significantvasodilatation mediatedthrough 'P)sensitive

potassium channels

• -evosimendan infusionincreases cardiac outputand stro7e volume andreduces pulmonary &edge

pressure( systemic vascularresistance( and pulmonaryvascular resistance$

• .asopressors

1norepinephrine2 are notrecommended as first)lineagents

O i &/ t ! t " il


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+ serum natriuretic peptides• 3on)invasive ventilation• %notropes


0auses of death in heart failure


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0auses of death in heart failure

Pump failurePump failure

Other Other

Sudden deathSudden death

49F49F

9:F9:F@:F@:F

3V! %% 3V! %%

9@F9@F

4;F4;F; F; F

3V! %%% 3V! %%%

;@F;@F

44F44F

66F66F

3V! %. 3V! %.

. o +imitation

.. S&B on severee'ertion... S&B on mild

e'ertion

Pre)implant counselling!o& do you &ant to dieU


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!o& do you &ant to dieUHeart failure death Sudden death

Device C Rays


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y

ICD 9ead Ki: 9: 9ead position

%0D Myths


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%0D Myths

• Myths + %0Ds prevent syncope + 0ontacts can be electrocuted by

%0D discharge

+ 3ot safe to use mobile phone(mirco&ave( playstation etc$ + 8ill stop you dying from ."

• Diathermy 7ills patients devicesN

+ PPM + may inhibit 1pulseo,imetry2

+ %0D + &ill detect as ."1reprogram2

0onseAuences of tachycardia therapy


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:" Storm Inappropriate shoc4s

End of life issues/ 3E0 3


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End of life issues/ 3E0.3

.entricular arrhythmias andHor poor -. function W is an %0D indicated U'emporarily disabled &ith a ring magnet

'he "utureU


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he utureU

.ntrathoracic .mpedance* ?oncept

'he Reality


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(rierlungsmeanstheintrathor

"etterlungsmeanstheintrathor

+essFluid

)oreFluid

he Reality

Epidemiology


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Mortality is appro,$ ;


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Objectives

Revie& the pathophysiology of D!"$Describe the clinical presentation of D!"$

pply effective therapeutic strategies using consensusguidelines from the 1!"S 2 and the 1ES02$E,amine the clinical evidence of milrinone andniseritide in the treatment of D!"$Evaluate the appropriateness of treatment$

D!"


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D!

Rapid onset of signs and symptoms secondary to abnormal cardiacfunction due to systolic( diastolic dysfunction( abnormalities incardiac rhythm or to pre)load and after)load mismatch$ De novo or acute decompensation of 0!"$Q;


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-. dysfunction/ccumulation of fluid$

Decrease in 0O !ypoperfusion$

Reciprocal ctivation of 1R S2 3a( &ater retention$

G%% E'4 5 .asopressin$

Refle, activation of S3S/ Epi( 3E$



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Stage %/ 3o clinical signs of decompensation$Stage %%/ !eart failure$ Rales( S6( P.!$Stage %%%/ Severe heart failure$ Pulmonary edema &ithrales throughout the lung fields$Stage %./ 0ardiogenic Shoc7/ !ypotension( peripheralvasoconstriction( oliguria( cyanosis and diaphoresis$



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Subset %13ormal2

8arm and Dry

Subset %%10ongestion2

8arm and 8et

Subset %%%

1!ypoperfusion20old and Dry

Subset %.

10ongestion andhypoperfusion20old and 8et

4

9

6

:

;

0ardiac %nde,

1-HminHm92

9$9-HminHm9

3ohria et al$ JAMA$9


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0linical Presentation


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L.DH!LRH LR PulmonaryHPitting EdemaReduced o,ygen saturationS6 or S:Electrolyte disturbance%ncreased serum creatinine


Pre)renal aJotemia0ool e,tremitiesDecreased urine outputRefractory to %. diuresis


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Diagnosis


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Diagnosis

Diagnosis of D!" should be primarily based on signs and symptoms$ 102

Diagnosis


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B3P 1 2

B3P ;


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Predictors of Mortality

BK3 :6 mgHdl

SBP 44; mm!gs0r 9$>; mgHdl

"onaro& G0 et al$ JAMA" 9


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Goals of herapy

%mprove symptoms and signs of congestion andHorhypoperfusion$Reverse hemodynamic abnormalities$

%dentify the etiology$MinimiJe side effects$OptimiJe therapy$ -ength of stay( mortality( time to hospital

readmission$Educate patients on medications and self assessmentof !"$

'reatment Strategy


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Establish a DiagnosisO,ygen and .entilatory ssistanceSymptom Relief

nticoagulation!emodynamic Support/

DiuresisH"luids

.asodilators%notropes

.asopressors

ssess Patient Responsenti)infectives

Glucose 0ontrol

'he Principle


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he Principle

Diuretics

%notropes

.asodilators

Reduce "luid OverloadReduced Preload/ 1E)D.f2( P08P

%ncrease 0ontractility%ncrease 0O( E"( Perfusion

Reduce PreloadReduce fterload

ssess SignsHSymptomsHDetermine!emodynamic Status

E0 %nterventions/


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E0 %nterventions/0ardiac panel/ 10B0 &Hdiff platelets( SM )>

0 )MB( Glucose2( 'S!(Po,( E0G( B3P( C)ray

0onsideralternative diagnosis

Does Patient presents &ithDistress or pain U

0P P

3%PP

3ormal

O,ygen 0

bnormal

Evaluate cardiac function by 9DE

0haracteriJe type and severity

Metoprolol ; mg % %%b0

%s patient hypo,icUVes

3o but difficult breathing

Morphine 6 mg %.PB %%bByes

Does patient present &ith ischemic chest pain resistant to opiates or tachycardiaU

.olume Overloaded$A&M d l O l d


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%. Diuretics"urosmide 9


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I: Diuretics


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SBP =;)4;ugH7g%.PB over4


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'ransient use of .asopressor therapy

Epinephrine


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O,ygen Saturation0B0BPE0GB3PSigns/

Edema( Rales( scites( !epatomegaly( L.DSymptoms/

Orthopnea( P3D( Dyspnea( "atigue( 0ough 3egativeHpositive balance

ElectrolytesKrinalysisBK3HScr

BG

1OP'%ME)0!"2


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1OP %ME)0! 2Outcomes of a Prospective 'rial of%ntravenous Milrinone for E,acerbations of

0hronic !eart "ailure

JAMA, March 9> 9

Objective/ 'o prospectively test &hether a strategy that includes short+term

use of milrinone in addition to standard therapy can improve clinical outcomesof patients hospitaliJed &ith an e,acerbation of chronic heart failure$

Study Design


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Study DesignProspective randomiJed double)blind placebo)controlled trial$%'' $

Similar baseline characteristics$RandomiJation to a := hour infusion of eithermilrinone 1n Z :>>2 or placebo 1 :>92$Milrinone treatment arm/ Started &ith an initialinfusion of


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Primary Efficacy Outcome/'he total number of days hospitaliJed for cardiovascular causes ordays decreased &ithin the @< days after randomiJation$

Secondary endpoints/"ailed therapy because of adverse events$"ailed therapy because of &orsening heart failure$ Proportion of patients achieving target doses of 0E)% therapy$

'ime to achieve target 0E)% dose$Symptom improvement in !" score$

Patient Selection


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at e t Se ect o%nclusion 0riteria E,clusion 0riteria

4= yoaDemonstrated -.E" :


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'reatment &ith milrinone did not reduce the primaryendpoint of days hospitaliJed for cardiovascular causes&ithin @< days compared &ith placebo$

Results 1contI2


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'reatment failure cause at := hours/dverse event

Events during hospitaliJation/M%

3e& atrial fibrillationHflutter .entricular tachycardiaHfibrillationSustained hypotension

Placebo1nZ:>92

Milrinone1n Z :>>2 P value

9$4F 49$@F


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Study did not directly address patients &ithacutely decompensated chronic heart failure for&hom inotropic therapy is essential$

3on)formal therapeutic protocol$0onfounding variables$

0onclusions


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Results do not support the routine use ofmilrinone in patients hospitaliJed &ith ane,acerbation of chronic heart failure$


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Study Design


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y g

RandomiJed double)blind( double dummy trial$Patients &ere stratified to catheteriJed 1nZ9:@2 andnon)catheteriJed 1nZ 9:62Patients &ere then randomiJed to fi,ed dose nesiritide(adjustable dose niseritide( nitroglycerin or placbo forthe first 6 hours$

fter 6 hours patients &ere in the double dummydesign of nesiritide and nitroglycerin treatment arms$

Outcome Measures


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Primary Endpoint/ 0hange in P08P and patientIsself)evaluation of dyspnea from baseline at 6hours$

Secondary Endpoints/Onset of effect on P08PEffect on P08P 9: hrs after the start of study drugSelf)assessed dyspnea and global clinical statusOverall safety profile$

%nclusion


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%nclusion 0riteria E,clusion 0riteria

Dyspnea at rest0ardiac etiology of dyspnea

SBP <.olume depletion0% to %. vasodilatorsMechanical ventillationSurvival less than 6; days

Results


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Reduction in P08P &as greater in thenesiritide group &ith the first measurement$Beyond 9:hr the difference in P08P bet&een

nesiritide and nitroglycerin &as insignificant$%mprovement in dyspnea and global clinicalstatus scores in the nesiritide and nitroglycerin

&ere not significantly different at any time$! &as more common in the 3itroglyceringroup$

-imitations


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!eterogenous patient population'herapeutic protocol$

ssessment of mortalityHmorbidity


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CC, 8ea7ness and Shortness of Breath $


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>


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Medications at Home, tenolol 9; mg Ad( pantopraJole :; mg Ad(

acetaminophen ;


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PhysicianWs assessment


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0. Congestive Heart Failure, Patient &ill receive %.diuretics and monitor for electrolytes$

1. N"I, 0ontinue 0ipro until the completion of the course$

2. A#normal cardiac en'ymes, Represent myocardialinjury$ 0ardiology consulted$>. Acute !enal insufficiency, Monitor creatinine( diuresis

and BP$


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! H 00 Guideline160> AHA


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Nishi"ura R A et al6 Circulation6 5(' ='5-*e%5' e >

Copyright 9 American Heart Association< =nc. All rights reserved.

Diagnosis and ?reat"ent o$ #E6 7Earl surger de$ined as during initial hospitali/ation ,e$oreco"pletion o$ a $ull therapeutic course o$ anti,iotics6


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Nishi"ura R A et al6 Circulation6 5(' ='5-*e%5' e >

Copyright 9 American Heart Association< =nc. All rights reserved.

"he definition of acute heartfailure has not #een firmly

esta#lished $%&.


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It is recogni'ed (hen symptoms ofheart failudevelop rapidly (ithin

hours anddays% in patients (ithout prior

evidence of cardiacdecompensation )

Drug NsualDose

⍺ [4 [9 .asodilati

on

.asoconstri,n

%notro pic

0hronotropic

H! MAP PAP P/P C:P S:! S: C-

Epinephrine1 drenaline2


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\gH7gHmin14):

\gHmin2

555 55 55 ) 555 55 55

3orepinephrine1-evophed2


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ne1Dobutre

,2

\gH7gHmin ] ]

Milrinone1Primacor

2

-D ;< \gH7gover 4< min$(then ;)

;\gH7gHmin

) ) ) 555

) 555 5 OH]

^ ^ ^ OH^

^ ] ]

Gilman G( Rall '8$( et al$ Goodman and GilmanIs 'he Pharmacological Basis of 'herapeutics$ = th ed$ 4 6$Marino P$ 'he %0K Boo7$ 9 nd ed$ 4 =$ Voung -$( oda) imble M$ pplied 'herapeutics$ @ th ed$ 4 ;$ irby R$( 'aylor R$( et$ al$ !andboo7 of 0ritical 0are$ 9 nd ed$ 4 >$Darovic G$( "ran7lin 0$ !andboo7 of !emodynamic Monitoring$ 4 $

5uove prospettive nel trattamentodello scompenso acuto


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Michele Emdin*Fonda'ione a#riele Monasterio* Pisa

Congresso regionale A$MC% Toscana,Viareggio, & %TT%'() 20**

Acute Heart Failure Syndrome$s&

• A t h t f il $AHF& i d fi d id t


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• Acute heart failure $AHF& is defined as a rapid onset

or change in the signs and symptoms of HF* resultingin the need for urgent therapy.

• Symptoms are primarily the result of severepulmonary congestion due to elevated left ventricular$9:& filling pressures $(ith or (ithout lo( cardiac

output&.

• AHFS can occur in patients (ith preserved or reducede;ection fraction $EF&.

• Conc rrent cardio"asc lar conditions s ch as coronaryheart disease +C - , hypertension, "al" lar heartdisease, atrial arrhythmias, and/or noncardiacconditions +incl ding renal dys! nction, dia#etes, anemia are o!ten present and may precipitate orcontri# te to the pathophysiology o! this syndrome

AHFS, 5-" :E!IFIED %


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EKM in AHFSO• "he first randomi'ed place#o+controlled AHFS trials

(ere pu#lished as late as 1661


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(ere pu#lished as late as 1661.Cuffe MS* et al. f or the -utcomes of a Prospective "rial of Intravenous Milrinone for E8acer#ations of Chronic Heart Failure $-P"IME+CHF&

Investigators. Effects of short+term* intravenous milrinone on acute e8acer#ation of chronic heart failure, a randomi'ed controlled trial. JAMA. 1661

1 B, 07>0=07>B.

Pu#lication Committee for the :MAC Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure, a

randomi'ed controlled trial. JAMA. 1661 1 B, 0720=07>6

• 5one of the place#o+controlled AHFS studies conductedto date has sho(n either a consistent improvement of in+hospital or postdischarge survival or a decrease inreadmissions.

AHFS = oals of treatment• X Emergency treatment phase


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g y p• Improve symptoms• !estore o8ygenation• Improve organ perfusion and haemodynamics• 9imit cardiac


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of therapy O• "raditionally* reduction in pulmonary capillary

(edge pressure $PC/P& and


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• "he emergency

treatment phase

Patient Selection and 'reatmentCongestion at !est


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YesNo

3ar" J Dr>CW> normal

C= normal 4compensated5

Cold J 3et>CW> elevatedC= decreased

Cold J Dr>CW> lo+*normal

C= decreased

Vasodilators?itroprusside?itroglycerin

#notropic DrugsDo,uta"ine

MilrinoneCalciu" &ensiti/ers

?ormal SV1

HighSV1

9o(Perfusion

at !est

No

Yes

3ar" J 3et>CW> elevated

C= normal

?atriuretic>eptide?esiritide or

Stevenson LW. Eur J Heart Fail. 1999;1:251 .

&eco!!ended a%%roac# to t#e use of inotro%ic su%%ort in%atients #os%itali=ed *it# acute HF e/acer"ation


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?opyright E7:1: American Heart Association

4old#a"er5 6. I. et al. Circulation 78189171:1;


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Intravenous loop diuretics may improve symptoms and fluid loss initially #ut also

may contri#ute to renal function decline. "his may #e related not only tointravascular volume depletion #ut also to further neurohormonal activationresulting in a vasomotor nephropathy.

• Intravenous loop diuretics may #e associated (ith (orse outcomes in AHFS patients.

• 3notropic Therapy

Intravenous inotropes increase myocardial o8ygen consumption* causing myocardialdamage in the setting of hi#ernating myocardium. Nse of inotropes has consistently#een associated (ith increased mortality.

• VasodilatorsE8cessive vasodilatation in AHFS may lead to #lood pressure decrease* potentiallye8acer#ating myocardial ischemia and renal hypoperfusion.

AHFS, (hich appropriate targetsof therapy O


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Perspectives• Managing fluids*

• Preserving renal function

AHFS, (hich appropriate targetsof therapy O


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o t e apy O

• Contractility

• Diastole

AHFS, 5on farmachologicaltherapy


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py

• :asomotion


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AHFS (here are (eO /here are (e goingO

• AHFS is a comple8 condition (ith su#stantial mor#idity and mortality andenormous utili'ation of health resources and cost.


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• "here are numerous challenges in caring for this population.• Nniform AHFS classification is currently lac4ing* and management

strategies vary mar4edly.

• "here is a general consensus that to reduce mortality* mor#idity* and theeconomic #urden of AHFS* systematic research efforts on clinical applicationand translation of promising #asic science results are needed.

• Pathophysiologically #ased interventions $eg* cardiorenal syndrome& may #eparticularly appealing.

• A special focus should #e on choice of appropriate management strategies*including minimi'ing the use of drugs (ith adverse effects and developmentand validation of 4no(n prognostic mar4ers to guide AHFS interventions .


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C-5C9NSI-5...of note* every large pu#lished clinical trialconducted in patients (ith AHFs has #een negativein terms of efficacy* safety* or #oth.

%Ho(ever* most international multicenter clinical

trials completed to date (ere conducted on fairlyundifferentiated populations of patients (ith AHFs.

%.homogeneous pathophysiological disease states(ithin the heterogeneity of aHFs is of paramount

importance to clinical trial design and aHFs therapy.

% Future trials conducted in aHFs must a#andonthe Yone+si'efits+ allW approach in favor of anapproach that ta4es into account the varied anddistinct pathophysiologies of aHFs.

o@ 56


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208/285

Fig6 '* Appro@i"ation o$ cardiac s stolic $unction and cardiac $illing pressures in !ariousacute illnesses6>(6


209/285



210/285



211/285



212/285


0. /ith or (ithout previous cardiac disease.1. "he cardiac dysfunction can #e related,

a& to systolic or diastolic dysfunction#& to a#normalities in cardiac rhythmc& to preload and afterload mismatch



Acute Heart Failure ,-ther Classifications

%n !" after M%( best applied to acute denovo heart failure/%n !" after M%( best applied to acute denovo heart failure/


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'he illip classification / based on clinical signs and chest C)ray findings 1Stage %/ 3o heart failure( Stage %%/ !eartfailure( Stage %%%/ Severe heart failure and Stage %./ 0ardiogenic shoc72$'he "orrester classification/ based on clinical signs and haemodynamic cha)racteristics$

%n a cardiomyopathy service( best applied to chronic decompensated heart failure/%n a cardiomyopathy service( best applied to chronic decompensated heart failure/ 0linical severity classificationN /

based on observation of the peripheral cir)culation and on auscultation of the lungs forcongestion

10lass %/ dry and &arm( 0lass %%/ &et and cold( 0lass %%%/ cold and dry and 0lass %./ cold and&et2$

3ohria et al/ L 00 9)4=


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mild signs and symptoms of !" and do not fulfil criteria for cardio)genic shoc7( pulmonary oedema or hypertensive crisis $!ypertensive acute heart failure / Signs and symptoms of !" 5 high BP 5 preserved-." 5 chest radiograph findings PO$Pulmonary oedema / .erified by chest C)ray( severe respiratory distress( or)thopnoea&ith SaO 9


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decompensated

congestive heartfailure

H!igh

!igh

%% cute heartfailure &ithhypertensionHhypertensive crisis

Ksuallyincreased

!igh 5H) 4= %%) %.H "%%)%%%


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$alvular disease Prost#etic valve t#ro!"osis

Aortic dissection


&enal failure

Pul!onary diseases and "ronc#oconstriction

Arr#yt#!ias and AHF

Peri o%erative AHF 'usually due to!yocardial isc#ae!ia(

Clinical

4oals of treat!ent of t#e %atient*it# acute #eart failure


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Clinical↓ sy!%to!s 'dys%nea and or fatigue( clinical signs

"ody *eig#t diuresis o/ygenation

La"oratory e/a!inations +UN and or creatinine seru! electrolyte nor!alisation↓ %las!a +NP "lood glucose nor!alisationHae!odyna!ic

%ul!onary *edge %ressure to 0 12 !! Hg cardiac out%ut and or stro3e volu!e


Patient (ith AHF, immediate treatment goals


218/285



219/285

O/ygen in acute #eart failure Target Sa& 7 02= – 28 5 Class I5 LO) C

&7 administration in hypo'aemic patients -ith acute heart


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7 yp p

failure

Class IIa5 LO) C

o &7

0or ↑ Fi&75 in patients -ithout evidence of

hypo'aemia

Hypero'ia causes harm*

coronary "lood >o*5

cardiac out%ut

"lood %ressure"he "as4 Force on Acute Heart Failure of the European Society of Cardiology"he "as4 Force on Acute Heart Failure of the European Society of Cardiology

Non ? invasive ventilation 'NI$(and intu"ation 'TI( in acute #eart

failureGse of CPAP and NIPP$ in acute cardiogenic


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pulmonary oedema is associated -ith a signi#cantreduction in the need for endotracheal intubation 0T.5

and mechanical ventilation )D, 'Class IIa5 LO) A( I

T.I. '-$( use* To reverse induced respiratory muscle

fa tigue 0lo- respiratory rate, hypercapnia, confusion5*

a5 .ntervention

b5 &nly if acute respiratory failure does notrespond to vasodilators, & 7 andJor ?PAP or

.PPD"he "as4 Force on Acute Heart Failure of the European Society of Cardiology"he "as4 Force on Acute Heart Failure of the European Society of Cardiology

4uidelines for %ul!onary artery cat#eter'PAC( use in acute #eart failure

• Insertion of PAC for the diagnosis of acute heart failure


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is usually unnecessary

• PAC can #e used to distinguish #et(een a cardiogenic

and a not cardiogenic mechanism in comple8 patients

(ith concurrent cardiac and pulmonary disease.• PAC is fre3uently used to estimate hemodynamic

varia#les and guide therapy in the presence of severe

diffuse pulmo+nary pathology or ongoing

haemodynamic compromise not resolved #y initial

therapy


$Class II#* 9-E+C&


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3on)pharmacologic Management


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Surgical treat!ent inacute #eart failure


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0hronic !")End Stage D!" Collabora ive Managemen

• 5onpharmacologic therapies 1contId2


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+ %ntraaortic balloon pump 1% BP2 therapy• Ksed for cardiogenic shoc7 • llo&s heart to rest

+ .entricular assist devices 1. Ds2• 'a7es over pumping for the ventricles• Ksed as a bridge to transplant

+ Destination therapy)permanent ( implantable . D + 0ardiomyoplasty ) &rap latissimus dorsi around heart + .entricular reduction )ventricular &all resected + 'ransplantH rtificial !eart +

%ntraaortic Balloon Pump 1% BP2

• Provides temporary circulatory assistance + ^ fterload


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+ ugments aortic diastolic pressure• Outcomes

+ %mproved coronary blood flo& + %mproved perfusion of vital organs

=ntraaortic )alloon pump

% BP Machine

http://yourtotalhealth.ivillage.com/intraaortic-balloon-pump.htmlhttp://yourtotalhealth.ivillage.com/intraaortic-balloon-pump.html


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Enhanced E,ternal0ounterpulsation)EE0P


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Pumps during diastole)increasing O9 supply tocoronary arteries$ -i7e % BP

but not invasive$

'he 0ardiology Group( P$$

.entricular ssist Devices 1. Ds2

:entricular Assist Devices$:ADs&

•• Indications for :AD therapyIndications for :AD therapy

http://www.heartcenter.md/eecp.htmlhttp://www.heartcenter.md/eecp.htmlhttp://www.heartcenter.md/eecp.htmlhttp://www.heartcenter.md/eecp.html


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Copyright 9 %33(< %33/< %333< 2os)y< =nc.< an affiliate of Elsevier =nc. All 1ights 1eserved.

•• E8tension of cardiopulmonary #ypassE8tension of cardiopulmonary #ypass•• Failure to (eanFailure to (ean•• Postcardiotomy cardiogenic shoc4Postcardiotomy cardiogenic shoc4

•• Kridge to recovery or cardiacKridge to recovery or cardiac

transplantationtransplantation

8Patients &ith 3e& Vor7 !eart ssociation 0lassification %. &hohave failed medical therapy

>atient Teaching'Cleveland Clinic for Heart ailure LVA7 devices

http://my.clevelandclinic.org/heart/disorders/heartfailure/lvad_devices.aspxhttp://my.clevelandclinic.org/heart/disorders/heartfailure/lvad_devices.aspxhttp://images.google.com/imgres?imgurl=http://www.texmedctr.tmc.edu/NR/rdonlyres/BF21A5C0-2D3F-4FC4-9A56-C94F18540362/389/DeBakeyYeltsin.jpg&imgrefurl=http://www.texmedctr.tmc.edu/root/en/TMCServices/News/2007/10-01/DeBakey+Gold+Medal.htm&h=201&w=300&sz=35&hl=en&start=5&um=1&usg=__kfnCWB8jKqHsftAk-j-ECVZyUko=&tbnid=MTDyDpxm9yapfM:&tbnh=78&tbnw=116&prev=/images?q=patient+teaching+ventricular+assist+devices&um=1&hl=en&safe=active&rls=GGLJ,GGLJ:2006-36,GGLJ:en&sa=Ghttp://my.clevelandclinic.org/heart/disorders/heartfailure/lvad_devices.aspxhttp://my.clevelandclinic.org/heart/disorders/heartfailure/lvad_devices.aspx


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Schematic Diagram of -eft . D

Left ventricular assist device

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Heart2ate ==


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The Heart2ate == 'one of several ne+ LVA7 devices' designed to last longer +ith simplicityof only one moving part# also much lighter and @uieter than its predecessors# ma,or

differences is rotary action +hich creates a constant flo+ of )lood< not pumping actionB.


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Cardiomyo!las y techniAue/ left latissimus dorsi muscle

1-DM2 transposed into chest through a &indo& created byresecting the anterior segment of 9nd rib 1; cm2$ -DM isthen &rapped around both ventricles$ Sensing and pacingelectrodes are connected to an implantable cardiomyostimulator


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ClicD here for Tu)e

Artificial Heart animinationF

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Surgicaltreatment in


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AHF,mechanical

assistdevices and

hearttransplantat

ion

$algorithm&


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Biventricular system devices


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9eft ventricular assist device


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Paracorporeal ventricular assist device


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cute Decompensated !eart "ailure1 D!"2) %npatient Management


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Lennifer umar

"ebruary 9


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• -earn to identify the signs and symptoms ofD!"

• -earn to interpret pertinent laboratory dataand imaging

• -earn the inpatient management of D!"

%maging/ 0hest ,)ray• Enlarged cardiac silhouette


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• Pulmonary edema

• Pulmonary congestion + 0ephaliJation + erley B lines + Peri)bronchial cuffing

• Pleural effusions( typically bilateral

'ransition to Outpatient


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Summary• %dentify clinical signs and symptoms of D!"


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• Pertinent labs + Sodium( creatinine( troponin( B3P

• Relevant imaging + E G( 0CR( echocardiography

• 'reatment + Diuresis( BB( 0E%H RB( Spironolactone( Digo,in(

%sosorbide dinitrateH!ydralaJine

• 'ransition to outpatient + Strict instructions( close)follo&)up


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briefdiscussion of

the &or7s ofthis thing$$$

"'ERloadPREload 0ontractility


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0urrent 'reatment of cute !eart "ailure

!igh

P l d

!igh

f l d

Poor

0 ili


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DiureticsDiuretics- S%C- S%C

ReduceReducefluidfluid

volumevolume

.asodilate.asodilate

%notropes%notropes)reduce)reduceafterload)afterload)

.asodilators.asodilators 3 3itroglycerinitroglycerin

Preload fterload 0ontractility

ugmentugment 0ontrac)0ontrac) tilitytility

Current "reatment of Acute Heart FailureCurrent "reatment of Acute Heart Failure

.asodilators


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Diuretics

Reducefluidvolume

DecreasePreload

ndfterload

.asodilate

ugment0ontract)ility

-asi, 0E inhibitor 3itroglycerin

-asi, 3tg/ sl( top( ivMSO:

0Ei

BiP P or 0P PUU

M l i l ll f 3 i i


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• Multiple small case reports of 3oninvasive.entilatory Support 13.S2 in patients &ithvarying diagnoses of respiratory failure$

• 3o assessment of hemodynamic findings ina controlled fashion$• 3o assessment of neurohormonal effects of

3.S$


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Effects of 3esiritide+enous4 arterial4 coronar+A&OD#LA?#ON

HEMODYNAM#C NA?R#URE&

D#URE&

RENAL


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rhBNP

D

R I

M

K

R

G

SS

S

SG

L

GF

CC

S S

GSGQV

M

K V LR

RH

KPS

CARD#AC#NDEK

PreloadA$terloadPC3PD spnea

CARD#AC

No increase in HRNot proarrh th"ic

Aldosterone

EndothelinNorepinephrine

&YMPA?HE?#C ANDNEUROHORMONAL &Y&?EM&

Fluid !olu"ePreloadDiureticusage

D#URE&


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Clinical )valuation

"e#nition of Heart FailureClassification E;ection

FractionDescription

%$ !eart "ailure &ithReduced Ejection "raction

1!" rE"2

`:


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1! r E 2 that efficacious therapies have been demonstrated to date$%%$ !eart "ailure &ithPreserved Ejection"raction 1!" ! E"2

;


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sy pto s o ! $0 Structural heart disease &ith prior or

current symptoms of !"$% 3o limitation of physical activity$

Ordinary physical activity does not causesymptoms of !"$

%% Slight limitation of physical activity$0omfortable at rest( but ordinary physicalactivity results in symptoms of !"$

%%% Mar7ed limitation of physical activity$0omfortable at rest( but less than ordinaryactivity causes symptoms of !"$

%. Knable to carry on any physical activity&ithout symptoms of !"( or symptoms of

!" at rest$

D Refractory !" reAuiring specialiJed

interventions$

Initial and Serial Evaluation ofthe HF Patient


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,iagnostic Tests

"ia nostic $ests%nitial laboratory evaluation of patients presenting &ith !"

should include complete blood count( urinalysis( seruml l l d l d ( bl d

I IIaII#III


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should include complete blood count( urinalysis( serumelectrolytes 1including calcium and magnesium2( blood ureanitrogen( serum creatinine( glucose( fasting lipid profile( liverfunction tests( and thyroid)stimulating hormone$

Serial monitoring( &hen indicated( should include serumelectrolytes and renal function$

I IIaII#III

"ia nostic $ests %cont&' 49)lead E0G should be performed initially on all patients

presenting &ith !"$

I IIaII#III


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presenting &ith ! $

Screening for hemochromatosis or !%. is reasonable inselected patients &ho present &ith !"$

Diagnostic tests for rheumatologic diseases( amyloidosis( or pheochromocytoma are reasonable in patients presenting &ith

!" in &hom there is a clinical suspicion of these diseases$

I IIaII#III

I IIaII#III



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+io!ar3ers

A!"ulatory Out%atient

A!(ulator)/*ut+atient

•%n ambulatory patients &ith dyspnea( measurement of B3P orI IIaII#III


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%n ambulatory patients &ith dyspnea( measurement of B3P or 3)terminal pro)B)type natriuretic peptide 13')proB3P2 isuseful to support clinical decision ma7ing regarding thediagnosis of !"( especially in the setting of clinical uncertainty$

•Measurement of B3P or 3')proB3P is useful for establishing prognosis or disease severity in chronic !"$

I IIaII#III

I IIaII#III

A!(ulator)/*ut+atient%cont&'

B3P) or 3')proB3P guided !" therapy can be useful toachieve optimal dosing of GDM' in select clinically euvolemic

I IIaII#III


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achieve optimal dosing of GDM in select clinically euvolemic patients follo&ed in a &ell)structured !" disease management program$

'he usefulness of serial measurement of B3P or 3')proB3P toreduce hospitaliJation or mortality in patients &ith !" is not&ell established$

Measurement of other clinically available tests such as

biomar7ers of myocardial injury or fibrosis may be consideredfor additive ris7 stratification in patients &ith chronic !"$

I IIaII#III

I IIaII#III



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+io!ar3ers

Hos%itali=ed Acute

Hos+itali,ed/Acute

Measurement of B3P or 3')proB3P is useful to supportI IIaII#III


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Measurement of B3P or 3 )proB3P is useful to supportclinical judgment for the diagnosis of acutely decompensated!"( especially in the setting of uncertainty for the diagnosis$

Measurement of B3P or 3')proB3P andHor cardiac troponin isuseful for establishing prognosis or disease severity in acutelydecompensated !"$

I IIaII#III

I IIaII#III

Hos+itali,ed/Acute%cont&'

'he usefulness of B3P) or 3')proB3P guided therapy forI IIaII#III


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e use u ess o B3 ) o 3 )p oB3 gu ded t e apy oacutely decompensated !" is not &ell)established$

Measurement of other clinically available tests such as biomar7ers of myocardial injury or fibrosis may be consideredfor additive ris7 stratification in patients &ith acutelydecompensated !"$

I IIaII#III

I IIaII#III


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CAK in Patients /ith S"EMI


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Krgent 0 BG is indicated in patients &ith S'EM%and coronary anatomy not amenable to P0% &ho haveongoing or recurrent ischemia( cardiogenic shoc7(severe !"( or other high)ris7 features$

0 BG is recommended in patients &ith S'EM% attime of operative repair of mechanical defects$

I IIaII#III

I IIaII#III

CAK in Patients /ith S"EMI

I II II#III


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'he use of mechanical circulatory support isreasonable in patients &ith S'EM% &ho arehemodynamically unstable and reAuire urgent 0 BG$

Emergency 0 BG &ithin @ hours of symptom onsetmay be considered in patients &ith S'EM% &ho donot have cardiogenic shoc7 and are not candidates forP0% or fibrinolytic therapy$

I IIaII#III

I IIaII#III

$ear failure syndromes

"or&ardN !"


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or&ardN ! + 8ea7ness( confusion( lo& BP + .asodilation( fluid replacement( inotropic

support

^ -. intropy( ^S.( ^ 0O( ^P OP

$ear failure syndromes left ventricular dysfunction

-eft)bac7&ardN !"

Documents

Sinaia 2 Oct 2014 -Final-Acute Heart Failure