OVERVIEW OF TREATMENT
OF
CONGESTIVE
HEART FAILURE
OVERVIEW

Background and Historical Perspective
 Determinants of Cardiac Output and
Hemodynamic Intervention
 Newer Therapeutics
EVOLUTION IN CONCEPTS

Cardio-renal (pre 1970) : Digoxin, diuretics
 Hemodynamic 1970’s and 1980’s: + Inotropics, VD
 Neurohormonal 1990’s: RAS, SNS
DETERMINANTS OF
CARDIAC PERFORMANCE

HEART RATE
 CONTRACTILITY
 PRELOAD
VASODILATOR THERAPY

AFTERLOAD
RATE
PRELOAD
LV
CONTRACTILITY
AFTERLOAD
CO = SV x HR
EF = CO
HEART RATE

COMPENSATORY RESPONSE

ATROPHINE

ISUPREL

PACER
CONTRACTILITY

Inherent property of the myocardium

Allows the heart to increase its extent and
force of shortening independent of the
Starling mechanism

Not directly measurable
CONTRACTILITY

DIGITALIS
 DOBUTAMINE
 DOPAMINE
 ISUPREL
 EPINEPHRINE
 CALCIUM
 GLUCAGON
 AMIRANOME (Miliron)
STARLING’S LAW
THE MORE A MYOCARDIAL FIBER IS
STRETCHED DURING DIASTOLE, THE
MORE IT WILL SHORTEN IN SYSTOLE
IT WILL ALSO SHORTEN WITH
GREATER FORCE
PRELOAD
The length to which a cell is stretched prior.
To the next contraction
The volume or pressure generated in the
ventricles at end-diastole
Degree to which a cell is stretched in
diastole (preload) force during systole
AFTERLOAD
IMPEDANCE OF BLOOD FROM
THE VENTRICLE
Determined by:
The volume and mass of blood ejected from
the ventricle
The compliance and total cross-sectional
area of the vascular space into which the
blood is ejected.
AFTERLOAD – RESISTANCE
PROXIMAL IMPEDENCE
SYSTEMIC VASCULAR
RESISTANCE
SVR= (MAP-RAP) (80)
CO
MAP= MEAN ARTERIAL PRESSURE
RAP= RIGHT ATRIAL PRESSURE
CO= CARDIAC OUTPUT
BASIC HEMODYNAMIC
PARARMETERS
Preload
=
Afterload =
PCWP
SVR

LVEDP = LA = PVP = PCWP = PAP
1
3
2
4
1
2
3
4
VASODILATOR DRUGS
AGENT
ARTERIAL
VENOUS
(Afterload)
(Preload)
Nitropusside
+++
+++
Nitrates
++
+++
Hydralazine
++++
+
Prazosin
++
++
Nesiritide
(Natrecor)
++
+++
Clinical Profile of Nesiritide

Vasodilation (venous > arterial)
 Rapidly improves symptoms of congestion
 Does not increase heart rate (decreases
myocardial oxygen demand)
 Is not proarrhythimic
 Neurohormonal suppression (decreases
aldosterone, endothelin-1)
 Mild diuresis/natriuresis
Clinical Profile Nesiritide (cont.)

No evidence of tachyphylaxis
 Symptomatic hyptension as low as 4% in
the VMAC study
 Dosing convenience (bolus plus standarddose IV infusion
PATIENT PRESENTATION
P.E.
CXR
EKF
BP
OUTPUT
R.A.
P.A.
PCW
BNP
SOB
CHF
ST
110/70
20cc/hr
15
45/30
30
++
SOB
CHF
ST
210/120
40cc/hr
15
45/30
30
++
SOB
CHF
ST
80/50
20cc/hr
15
45/30
30
++
SOB
CLEAR
ST
80/50
20cc/hr
15
45/30
6
+
LETHARGIC
CLEAR
ST
80/50
0
2
25/4
3
N
SOB
HAZY
ST
110/70
20cc/hr
15
45/20
12
+
UNCONCIOUS
CHF
VT
60/40
0
15
45/30
30
+
ALERT
CLEAR
MSR
240/140
20cc/hr
8
30/18
18
+
ALERT
CLEAR
MSR
80/50
20cc/hr
20
50/20
12
++
LETHARGIC
CLEAR
ST
80/50
20cc/hr
8
30/8
8
N
EVOLUTION IN CONCEPTS

Cardio-renal (pre 1970): Digoxin, diuretics

Hemodynamic 1970’s and 1980’s: +
Inotropics, VD

Neurohormonal 1990’s: RAS, SNS
CLINICAL APPROACH
Control Volume
(Rx Symptoms)
Hemodynamic Stability
Slow Progression
Diuretic
Inotropic Vasodilators
Neurohormonal
NEUROHORMONAL FACTORS
IN HEART FAILURE
PROGRESSION

Circulating (RAS, SNS)
Abnormality in regional blood flow, renal sodium
retention
 Endothelin (ET-1, ET-2, ET-3)
Vasoconstrictors
 Natriuretic Peptide, (ANP)
Vasodilators, suppresses RAS
 Cytokines (TNF  , Interleukin)
Depresses contractility, anorexia and cachexia
Neurohormonal Intervention in
Heart Failure
Heart Failure
Reninangiotensin
system
ACE inhibition
Sympathetic
nervous system
Beta Blockade
ACE INHIBITORs (ANGIOTENSIN CONVERTING ENZYMES INHIBITORS)
GENERIC
BRAND NAME
BENAZEPRIL
LOTENSIN
CAPTOPRIL
CAPOTEN
ENALAPRIL
VASOTEC
FOSINOPRIL
MONOPRIL
LISINOPRIL
ZESTRIL, PRINIVIL
MOESIPRIL
UNIVASC
PERINDOPRIL
ACEON
QUINAPRIL
ACCUPRIL
RAMIPRIL
ALTACE
TRANDOLAPRIL
MAVIK
ARBs (ANGIOTENSION RECEPTOR BLOCKERS)
GENERIC
BRAND NAME
CADESARTAN
ATACAND
EPROSARTAN
TEVETEN
IRBESARTAN
AVAPRO
LOSARTAN
COZAAR
OLMESARTAN
BENICAR
TELMISARTAN
MICARDIS
VALSARTAN
DIOVAN
BETA BLOCKERs
GENERIC
BRAND NAME
ACEBUTOLOL
SECTRAL
ATENOLOL
TENORMIN
BETAXOLOL
KERLONE
BISPROLOL
ZEBETA
CARTEOLOL
CARTROL
ESMOLOL
BREVIBLOC
METOPROLOL
LOPRESSOR, TOPROL
NADOLOL
CARGARD
PENUTOLOL
LEVATOL
PINDOLOL
VISKEN
PROPRANOLOL
INDERAL
SOTALOL
BETAPACE
TIMOLOL
BLOCADREN
ALPHA AND BETA BLOCKERs
GENERI9C
BRAND
CARVEDILOL
COREG
LABETALOL
NORMADINE, TRANDATE
Changes LVEF (EF units)
Effect of Carvedilol on Left Ventricular
Ejection Fraction
10
9
8
7
6
5
4
3
2
1
0
Placebo
6.25mg bid
12.5mg bid
25mg bid
Carvedilol
Patients receiving diuretics, ACE inhibitors, digoxin; follow-up 6 months; placebo (n=84), carvedilol (n=261).
Mulitcenter Oral Carvedilol Heart Failure Assessment
Adapted from Bristow et al. Circulation. 1996;94:2807-2816.
P<.05 vs placebo.
DRY
WET
WARM
COLD
CLINICAL ASSESSMENT
Warm vs. Cold (Perfusion)- Pulse Pressure
Dry vs. Wet (Congestion)- Jugular Venus Pressure
Rapid Assessment of Hemodynamic Status
Congestion at Rest
NO
Low
Perfusion
At Rest
NO
YES
A
Warm & Dry
(Low Profile)
L
Cold & Dry
YES
B
Warm & Wet
(Complex)
C
Cold & Wet
Possible Evidence of Low Perfusion:
Narrow pulse pressure
Sleepy/obtunded
Low Serum sodium
Cool extremities
Hypotension with ACE inhibitor
Renal Dysfunction (one cause)
Signs/symptoms
of Congestion:
Orthopnea/
PND
JV Distension
Hepatomegaly
Edema
Rates (rare in
chronic heart
failure)
Elevated est.
PA systolic
Valsalva
square wave
Profiles and Therapies of
Advanced Heart Failure
Congestion at Rest
NO
NO
Low
Perfusion
YES
At Rest
Inotropic Drugs
Dobuamine
Milrinone
Calcium Sensitizers
YES
Warm & Dry
PCW and CI
Normal
Warm & Wet
PCW elevated
CI normal
Cold and Dry
PCW low/normal
CI decreased
Cold & Wet
PCW elevated
CI decreased
NI SVR High SVR
Vasodilators
Nitroprusside
Nitroglycerine
Nesiritied
WARM UP THEN DRY OUT
DRY
WARM
WET
1.
2.
COLD
1.
2.
Vasodilators
Positive Inotropics
1.
2.
3.
Diuretics
Vasodilators
Positive Inotropics
Vasodilators
Diuretics
NEWER THERAPEUTICS
I.
Biventricular Pacing
I.
EECP
I.
Measurement of BNP levels