Decompensated Clinical case - … Heart Failure Clinical case Abdelfatah Elasfar MD, FACP Consultant...

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Transcript of Decompensated Clinical case - … Heart Failure Clinical case Abdelfatah Elasfar MD, FACP Consultant...

Decompensated Heart FailureDecompensated Heart FailureClinical caseClinical case

Abdelfatah Elasfar MD, FACP Consultant Cardiologist & Heart Failure/Transplant 

SpecialistSpecialistPrince Salman Heart Center, King Fahad Medical 

City, Riyadh,S di A biSaudi Arabia

Acute MI or Acute Decompensated HF?S f h blScope of the problem

((GheorghiadeGheorghiade M, et al. Circulation 2005;112:3958M, et al. Circulation 2005;112:3958--68)68)

Chronic Congestive Heart Failurel f l lEvolution of Clinical Stages

NORMAL

Asymptomatic LV Dysfunction

Compensated

No symptomsNormal exerciseNormal LV fxn

No symptoms CompensatedCHF

Decompensated

No symptomsNormal exerciseAbnormal LV fxn

No symptoms pCHFExercise

Abnormal LV fxnSymptoms

ExerciseRefractoryCHFAbnormal LV fxn CHF

Symptoms not controlled with treatment

Summary of the case presentedSummary of the case presented

• 69 year old male.69 year old male.• ADHF.• 6 years history of DCM6 years history of DCM.• EF 23 %.• Non compliant• Non‐compliant.• BP 105/70, HR around 100, Spo2 91 %• Severe pulmonary and peripheral congestion• Severe pulmonary and peripheral congestion• Creatinine  139, K 3.9, Na 138

Clinical CaseClinical Case 

What are the therapeutic options ?What are the therapeutic options ?

Clinical caseClinical case

• A Salt restrictionA Salt restriction

• B  IV Loop Diuretics

• C  Resume previous treatments

• D  Add new medications

• E Consider other procedures

Models For ADHFCongestion

Models For ADHF

NoNo YesYes

NoNo Warm and DryWarm and Dry Warm and WetWarm and Wet

fusi

on

YesYes Cold and DryCold and Dry Cold and WetCold and WetHyp

oper

f

YesYes Cold and DryCold and Dry Cold and WetCold and Wet

Predictors of Mortality Based on Analysis of ADHERE Database

Classification and Regression Tree (CART) analysis ofClassification and Regression Tree (CART) analysis of ADHERE data shows:

Three variables are the strongest predictors of mortality inThree variables are the strongest predictors of mortality in hospitalized ADHF patients:

BUN > 43 mg/dL

Systolic blood pressure < 115 mmHg

BUN > 43 mg/dL

Systolic blood pressure < 115 mmHg

Serum creatinine > 2.75 mg/dLSerum creatinine > 2.75 mg/dL

Fonarow GC et al. JAMA 2005;293:572-80.

HFSA 2010 Practice GuidelineAcute HF— IV diuretics are main stay therapy

• It is recommended that patients admitted with ADHF and evidence of fluid overload be treated initially with loop diuretics—usually given intravenously rather than orally.g y y

Strength of Evidence = B

Th C di l S d f HFThe Cardiorenal Syndrome of HF

Increased Morbidityand Mortality

Diuretic Therapy

Developmentof Diuretic and

NeurohormonalActivation

NatriureticResistance Diminished

Blood Flow

Impaired RenalFunction Decreased Renal

PerfusionPerfusion

HFSA 2010 Practice GuidelineAcute HF—Diuretic Alternatives

–Restricting sodium and fluid C ti i f i f l di ti–Continuous infusion of a loop diuretic

–Addition of a second type of diuretic orally (Metolazone or spironolactone)orally (Metolazone or spironolactone)

– Ultrafiltration

Strength of Evidence = C

HFSA 2010 Practice GuidelineAcute HF—IV Vasodilators

• Intravenous vasodilators (intravenous nitroglycerin , nitroprusside or Nesiritide) and diuretics are recommended for rapid symptom relief in patients with acute pulmonary edema or severe hypertensionpulmonary edema or severe hypertension.

Strength of Evidence = C

HFSA 2010 Practice GuidelineAcute HF—IV Inotropes

• Intravenous inotropes (milrinone or d b t i ) b id ddobutamine) may be considered :– LV dilation 

d d–Reduced LVEF  –And diminished peripheral perfusion or end organ dysfunction (low outputend‐organ dysfunction (low output syndrome) 

Strength of Evidence = C

• The combination of low‐dose f id d l dfurosemide and low‐dose dopamine, although no different in producing an effective diuresisin producing an effective diuresis and symptom relief, is safer than high‐dose furosemide, because it g ,reduces the risk of WRF and is potassium sparing. 

New TherapiesNew Therapies

l fil i• Ultrafiltration• Vasopressin Receptor Antagonists ( Vaptans)• Adenosine‐1 receptor antagonists• Novel  natriuretic peptides (Carperitide)• Myosin activator• Low dose DopamineLow dose Dopamine

Long term therapiesg p

ACC/AHA 2009 Recommendations

• ACE inhibitors ARBs and BB therapy it isACE inhibitors , ARBs and BB therapy, it is recommended that these therapies be continued in most patients in the absence ofcontinued in most patients in the absence of hemodynamic instability or contraindications. 

(Class I Level of Evidence: C)(Class I ,Level of Evidence: C)

ACC/AHA 2009 Recommendations

• In patients not treated with ACE inhibitors or

ACC/AHA 2009 Recommendations

In patients not treated with ACE inhibitors or ARBs and BB therapy, initiation of these therapies is recommended in stable patientstherapies is recommended in stable patients prior to hospital discharge.

(Class I Level of Evidence: B)(Class I Level of Evidence: B)

Thank youThank you