ACUTE & CHRONIC

HEART FAILURE
An Overview on Diagnosis and Treatment

Dr. Nurkhalis, SpJP, FIHA.

Cardiology and Vascular Medicine Department of Syiah Kuala University

Dr.Zainoel Abidin Hospital, Banda Aceh
Introduction
EPIDEMIOLOGY
Europe

The prevalence of symptomatic HF range from 0.4-2%.

10 million HF pts in 900 million total population
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560

USA

nearly 5 million HF pts.

± 500,000 pts are D/ HF for the 1st time each year.
Last 10 years  number of hospitalizations has
increased.
Nearly 300,000 patients die of HF each year.
ACC/AHA Guidelines for the
Evaluation and Management of Chronic Heart Failure in the Adult 2001
Definition : Heart Failure
“The situation when the heart is incapable of
maintaining a cardiac output adequate to
accommodate metabolic requirements and the
venous return.“ E. Braunwald

“Pathophysiological state in which an

abnormality of cardiac function is responsible
for the failure of the heart to pump blood at a
rate commensurate with the requirements of
the metabolizing tissues.” Euro Heart J; 2001. 22: 1527-1560
DESCRIPTIVE TERMS in HEART FAILURE

 Acute vs Chronic Heart Failure

 Systolic vs Diastolic Heart Failure
 Right vs Left Heart Failure
 Mild , Moderate, Severe Heart Failure

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1528
 The Donkey Analogy
Ventricular dysfunction limits a patient's
ability to perform the routine activities of
daily living…
New York Heart Association (NYHA)
Classification of Heart Failure
No limitation : ordinary physical exercise does
Class – I not cause undue fatigue, dyspnoea or palpita-
tions.

Slight limitation of physical activity : comfor-

Class – II table at rest but ordinary activity results in
fatigue, dyspnoea, or palpitation.

Marked limitation of physical activity : comfor-

Class - III table at rest but less than ordinary activity
results in symptoms.
Unable to carry out any physical activity with-
out discomfort : symptoms of heart failure are
Class - IV present even at rest with increased discomfort
with any physical activity.
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1531
(Adapted from Williams JF et al., Circulation. 1995; 92 : 2764-2784)
 ACC/AHA – A New Approach To The Classification of HF
Stage Descriptions Examples
A Patient who is at high risk for Hypertension; CAD; DM;
developing HF but has no rheumatic fever.
structural disorder of the heart.

B Patient with a structural disorder LV hypertrophy or fibrosis;

of the heart but who has never LV dilatation; asymptomatic VHD;
developed symptoms of HF. MI.

C Patient with past or current Dyspnea or fatigue ec LV systolic

symptoms of HF associated with dysfunction; asymptomatic
underlying structural heart patients with HF.
disease.

D Patient with end-stage disease Frequently hospitalized pts ; pts

awaiting heart transplantation etc

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
Patophysiology of C H F
 DETERMINANTS OF
VENTRICULAR FUNCTION

CONTRACTILITY

PRELOAD AFTERLOAD

STROKE
VOLUME

- Synergistic LV contraction HEART

- LV wall integrity RATE
- Valvular competence

CARDIAC OUTPUT
 PULMONARY VENOUS
PRESSURE

Input

Filling Emptying
Stroke
ED volume x EF effective = volume
LV Distensibility Contractility x
Relaxation Afterload Heart
Left atrium Preload
Mitral valve rate
Structure
Pericardium
Diastolic function Systolic function

Output

CARDIAC OUTPUT

Block diagram of left ventricular pump performance

(Little, 2001)
Pathophysiological Sequence of
CHF

Heart Failure

Inadequate Cardiac Output

( ) O2 Delivery (rest and/or exercise)

Systemic Vasoconstriction

SNS (NE) RAAS (A-II)

() Flow to Skin, Gut,
and Renal Circulations
 Sympathetic nervous system up-regulation

Increased
Norepinephrine levels

Activation of the Decreased Direct

RAA system Renal blood Myocardial toxicity
flow
Myocyte dysfunction
Increased
Angiotensin II & Increased HR, PVR & Myocyte
Aldosteron arteriolar vasoconstriction necrosis

Increased myocardial Intracellular

Na+ & water oxygen demand Ca2+ overload/
retention Energy depletion

Vasoconstriction Cardiac remodeling Apoptosis

Cesario et.al; Reviews in cardiovascular medicine, vol 3, no.1, 2002

 Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone (RAAS)
Angiotensinogen
Renin
Angiotensin I
Angiotensin
Converting
Enzyme Angiotensin II

AT I receptor

Vasoconstriction Vascular remodeling

Oxidative Stress LV remodeling

Cell Growth Proteinuria

Etiology of Heart Failure
What causes heart failure?
The loss of a critical quantity of
functioning myocardial cells after
injury to the heart due to:
Ischemic Heart Disease
Hypertension
Idiopathic Cardiomyopathy
Infections (e.g., viral myocarditis,
Chagas’ disease)
Toxins (e.g., alcohol or cytotoxic drugs)
Valvular Disease
Prolonged Arrhythmias
Diagnosis of C H F
 ECG
 A low Predictive Value
 LAH and LVH May Be Associated wit LV Dysfunction
 Anterior Q-wave and LBBB a good predictors of EF ↓↓
 Detecting Arrhytmias as Causative of HF

CHEST X-RAY

 A Part of Initial Diagnosis of HF

→ Cardiomegaly, Pulmonary Congestion
 Relationship Between Radiological Signs and
Haemodynamic Findings may Depend on the Duration
and Severity HF
HAEMATOLOGY & BIOCHEMISTRY
A Part of Routine Diagnostic
 Hb, Leucocyte, Platelets
 Electrolytes, Creatinine, Glucose, Hepatic Enzyme,
Urinalysis
 TSH, C-RP, Uric Acid

ECHOCARDIOGRAPHY
 The Preferred Methods
 Helpful in Determining the Aetiology
 Follow Up of Patients Heart Failure
 ALGORITHM FOR THE DIAGNOSIS OF THE HF
(ESC, 2001)
Suspected Heart Failure Because
of symptoms and signs

If Normal
Assess Presence of Cardiac Disease by ECG, X-Ray Heart Failure
or NatriureticPeptides (Where Available) Unlikely

Tests Abnormal

Imaging by Echocardiography (Nuclear If Normal

Angiography or MRI Where Available) Heart Failure
Unlikely

Tests Abnormal

Assess Etiology, Degree, Precipitating

Factors and Type of Cardiac Dysfunction
Additional Diagnosis Tests
Where Appropriate (e.g.
Coronary Angiography)
Choose Therapy
Treatment of C H F
 General Measures
Medical Considerations:
Lifestyle
Modifications: Treat HTN,
hyperlipidemia,
Weight reduction diabetes, arrhythmias
Discontinue Coronary
revascularization
smoking
Anticoagulation
Avoid alcohol and
Immunization
other cardiotoxic
substances Sodium restriction
Exercise Daily weights
Close outpatient
monitoring
Stages in the evolution of HF and recommended therapy by stage

Stage A Stage B Stage C Stage D

Pts with : Pts with : Pts with : Pts who have

• Hypertension • Previous MI • Struct. HD marked symptoms
• CAD Struct. • LV systolic Develop Refract. at rest despite
• DM Heart dysfunction Symp.of • Shortness of Symp.of maximal medical
breath and fatigue,
• Cardiotoxins Disease • Asymptomatic HF HF at rest therapy.
reduce exercise
• FHx CM Valvular disease
tolerance

THERAPY THERAPY THERAPY THERAPY

• Treat Hypertension • All measures under • All measures under • All measures under
• Stop smoking stage A stage A stage A,B and C
• Treat lipid disorders • ACE inhibitor • Drugs for routine use: • Mechanical assist
• Encourage regular • Beta-blockers • diuretic device
exercise • ACE inhibitor • Heart transplantation
• Stop alcohol • Beta-blockers • Continuous IV
& drug use • digitalis inotrphic infusions for
• ACE inhibitor palliation

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
 Pharmacologic Management
ACE Inhibitors
Blocks the conversion of angiotensin I to angiotensin II;
prevents functional deterioration
Recommended for all heart failure patients
Relieves symptoms and improves exercise tolerance
Reduces risk of death and decreases disease progression
Benefits may not be apparent for 1-2 months after initiation
Use as first line therapy
Should be up titrated to the dosages shown in the large
clinical trial, and not titrated based on symptomatic
improvement
Pharmacologic Management
Diuretics
Used to relieve fluid retention
Improve exercise tolerance
Facilitate the use of other drugs indicated for heart
failure
Patients can be taught to adjust their diuretic dose
based on changes in body weight
Electrolyte depletion a frequent complication
Should never be used alone to treat heart failure
Higher doses of diuretics are associated with
increased mortality
 Diuretics, ACE Inhibitors
Reduce the number of sacks on the
wagon
 Pharmacologic Management
Beta-Blockers
Cardioprotective effects due to blockade of
excessive SNS stimulation
In the short-term, beta blocker decreases
myocardial contractility; increase in EF after 1-3
months of use
Long-term, placebo-controlled trials have
shown symptomatic improvement in patients
treated with certain beta-blockers1
When combined with conventional HF therapy,
beta-blockers reduce the combined risk of
morbidity and mortality, or disease progression1
1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of
Chronic Heart Failure in the Adult, 2001 p. 20.
 ß-Blockers
Limit the donkey’s speed, thus saving
energy
Pharmacologic Management
Digoxin
Enhances inotropy of cardiac muscle
Reduces activation of SNS and RAAS
Controlled trials have shown long-term
digoxin therapy:
Reduces symptoms
Increases exercise tolerance
Improves hemodynamics
Decreases risk of HF progression
Reduces hospitalization rates for
decompensated HF
Does not improve survival
 Digitalis Compounds
Like the carrot placed in front of the
donkey
 Pharmacologic Management
Aldosterone Antagonists
Generally well-tolerated
Shown to reduce heart failure-related
morbidity and mortality
Generally reserved for patients with NYHA
Class III-IV HF
Side effects include hyperkalemia and
gynecomastia. Potassium and creatinine
levels should be closely monitored
 Pharmacologic Management
Angiotensin Receptor Blockers (ARBs)
Block AT1 receptors, which bind circulating
angiotensin II
Examples: valsartan, candesartan, losartan
Should not be considered equivalent or
superior to ACE inhibitors
In clinical practice, ARBs should be used to
treat patients who are ACE intolerant due to
intractable cough or who develop
angioedema
Cardiac Resynchronization
Therapy
Increase the donkey’s (heart) efficiency
 Cardiac Resynchronization
Therapy
Patient Indications for CRT device:
Moderate to severe HF (NYHA Class III/IV)
patients
Symptomatic despite optimal, medical therapy
QRS  130 msec
LVEF  35%

CRT plus ICD : Same as above with ICD

indication
Treatment options
Non-pharmacological management
General advice and measures
Exercise and exercise training
Pharmacological therapy
Angiotensin-converting enzyme (ACE) inhibitors
Diuretics
Beta-adrenoceptor antagonists
Aldosterone receptor antagonists
Angiotensin receptor antagonists
Cardiac glycosides
Vasodilator agents (nitrates/hydralazine)
Positive inotropic agents
Anticoagulation
Antiarrhythmic agents
Oxygen
Devices and surgery
Revascularization (catheter interventions and surgery), other forms of
surgery
Pacemakers
Implantable cardioverter defibrillators (ICD)
Heart transplantation, ventricular assist devices, artificial heart
Ultrafiltration, haemodialysis
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
 Acute heart failure
AHF: The rapid onset of symptoms and signs secondary to
abnormal cardiac function.
(reduced CO, tissue hypoperfusion + congestion, increase in
PCWP)

1. With or without previous cardiac disease.

2. The cardiac dysfunction can be related:
a) to systolic or diastolic dysfunction
b) to abnormalities in cardiac rhythm
c) to preload and afterload mismatch
3. Often life threatening and requires urgent treatment.

The Task Force on Acute Heart Failure of the European Society of Cardiology
 “BACKWARD
FAILURE”
:
Increased pulmonary
venous pressure,
pulmonary edema

“FORWARD FAILURE” (Low Cardiac Output):

Decreased perfusion of the brain (confusion).
kidneys (impaired renal function),
skin (cyanosis) etc.
Goals of treatment of the patient with
acute heart failure

Outcome
 length of stay in the intensive care unit
 duration of hospitalization
 time to hospital re-admission
 mortality

Tolerability
Low withdrawal rate
Low incidence of adverse effects

The Task Force on Acute Heart Failure of the European Society of Cardiology
 “ Clinical severity classification”

dry: absence of signs of congestion, wet: elevated filling pressures,

warm: adequate systemic perfusion, cold: inadequate systemic perfusion
Nohria A et al: JACC 2003;41:1797-1804.
 Acute Heart Failure : Classification
The patient with AHF may present with one of several distinct
clinical conditions:

 Acute decompensated heart failure (de novo or as decompensation of

CHF) : With mild signs and symptoms of AHF and do not fulfil criteria
for cardio-genic shock, pulmonary oedema or hypertensive crisis.
 Hypertensive acute heart failure: Signs and symptoms of HF + high BP +
preserved LVF + chest radiograph findings APO.
 Pulmonary oedema: Verified by chest X-ray, severe respiratory distress,
or-thopnoea with SaO2 <90%.
 Cardiogenic shock: Reduced BP (SBP<90mmHg or drop of mean AP
>30mmHg) and/or low urine output (<0.5 ml/kg/h), with pulse rate >60
bpm with or without evidence of organ congestion.
 High output failure: High CO + HR, pulmonary congestion, sometimes
low BP (arrhythmias, thyrotoxicosis, anaemia, Paget’ disease, iatrogenic
etc)
 Right heart failure: Low CO + increased jugular venous pressure +
increased liver size + hypotension.

The Task Force on Acute Heart Failure of the European Society of Cardiology
Underlying diseases and co-morbidities in
acute heart failure

 Coronary artery disease

 Valvular disease

 Prosthetic valve thrombosis

 Aortic dissection

 AHF and hypertension

 Renal failure

 Pulmonary diseases and bronchoconstriction

 Arrhythmias and AHF

 Peri-operative AHF (usually due to myocardial ischaemia)

 Goals of treatment of the patient with
acute heart failure

Clinical
 symptoms (dyspnea and/or fatigue)
 clinical signs
 body weight
 diuresis
 oxygenation
Laboratory examinations
 BUN and/or creatinine
 serum electrolyte normalisation
 plasma BNP
blood glucose normalisation
Haemodynamic
 pulmonary wedge pressure to < 18 mm Hg
 cardiac output and/or stroke volume

The Task Force on Acute Heart Failure of the European Society of Cardiology
Patient with AHF: immediate treatment goals

The Task Force on Acute Heart Failure of the European Society of Cardiology
 Medical Treatment

 Morphine and its analogues (early stage, dyspnoea, restlessness, 3 mg IV)

 Anticoagulation (less evidence,no clinical improvement,less venous thrombosis)

 ACE inhibitors (are not indicated in the early stabilisation, role in pt with AMI)

 Diuretics

 Vasodilators

 b-blocking agents

 Inotropic agents
 Rationale for inotropic drugs

The Task Force on Acute Heart Failure of the European Society of Cardiology
Surgical treatment in acute
heart failure
Conclusion

Management of HF must be starting

from the earlier stage (AHA/ACC stage
A). Treatment at each stage can reduce
morbidity and mortality.

Before initiating therapy :

Established the correct diagnose.
Consider management outline.
Conclusion

Heart failure is a chronic, progressive disease that is

generally not curable, but treatable

Most recent guidelines promote lifestyle

modifications and medical management with ACE
inhibitors, beta blockers, digoxin, and diuretics

It is estimated 15% of all heart failure patients may

be candidates for cardiac resynchronization therapy
(see later section for details)

Close follow-up of the heart failure patient is

essential, with necessary adjustments in medical
management
Thank YoU
 Nitrates in acute heart failure
a. Titration to the highest haemodynamically tolerable dose
of nitrates with low dose furosemide is superior to high
dose diuretic treatment alone.

(Class I, LOE-B)

b. Be cautious in aortic stenosis, SBP < 90 – 100 mmHg,

 MAP 10mmHg

c. In acute heart failure caused by acute coronary syndro-

mes, are favoured over nitroprusside (may cause corona-
ry steal syndrome)

The Task Force on Acute Heart Failure of the European Society of Cardiology
 Beta – blocking agents

1. “Pts on b-blockers admitted to hospital due to worsening

heart failure should be continued on this therapy unless
inotropic support is needed (reduce dose)”.

2. Pts with acute myocardial infraction who stabilize after

acute heart failure, b-blockers should be initiated early.

(Class IIa, LOE-B).

The Task Force on Acute Heart Failure of the European Society of Cardiology
Medical Treatment - Vasodilators

The Task Force on Acute Heart Failure of the European Society of Cardiology
 Beta – blocking agents
3. Pts with overt acute heart failure and more than basal
pulmonary rales, b-blockers should be used cautiously. If
ongoing ischaemia and tachycardia consider I.V. meto-
prolol

(Class IIb, LOE-C)

4. Pts with congestive heart failure, b-blockers should be

initiated when the patient has stabilized after the acute
episode (usually after 4 days)

(Class I, LOE-A)

The Task Force on Acute Heart Failure of the European Society of Cardiology
 If clinical situation does not improve with
vasodilators and diuretics?

AHF

Vasodilators
Diuretics

Levosimendan
Inotropes
Dopamine/adrenaline
if shock with low BP

Assist devices Surgery

Surgical
treatment in
AHF:
mechanical
assist devices
and heart
transplantatio
n (algorithm)
 Acute Heart Failure : Classification
HR SBP CI PCWP Congestion Diuresis Hypo- End organ
Killip/ perfusion hypo-
Forrester perfusion

I. Acute +/- Low Low Mild K II / F II + +/- -

decompensated Normal normal / elevation

/ High
congestive heart High
failure*

II Acute heart Usually High +/- >18 K II- IV/ FII-III +/- +/- +, with CNS
failure with increased symptoms
hypertension/
hypertensive crisis

III Acute heart + Low Low Eleva KIII/ FII + +/- -

failure with normal ted

pulmonary oedema

Cardiogenic + Low Low, <2.2 >16 K III-IV / low + +

shock*: normal F I-III

IVa. Low output
syndrome

IVb Cardiogenic >90 <90 <1.8 >18 K IV/ F IV Very low ++ +

shock

V. High output + +/- + +/- KII/FI-II + - -

failure

VI. Right sided Usually Low Low Low FI +/- +/-, acute +/-
acute heart failure low onset
ACE INHIBITORS USED TO TREAT HEART FAILURE

DOSE RANGE TARGET DOSE FOR

DRUG (mg)FREQUENCY SURVIVAL BENEFIT*

Captopril 6.25 – 150 Three times daily 50 mg three times daily

Enalapril 2.5 – 20 Twice daily 10 mg twice daily
Lisinopril 2.5 – 40 Daily -
Ramipril2.5 – 10 Once or twice daily 5 mg twice daily
Quinapril 5 – 20 Twice daily -
Zofenopril† - - 30 mg twice daily
Trandolapril† - - 4 mg daily
Imidapril HCl 5 – 10 Once daily 10 mg daily

* Target doses are those associated with increased survival in clinical trials
† This drug is not approved in the United States
 Benefits of “Add-on” β-Blocker
Short-term :
1. Improvement of symptoms (LVEF ↑)
2. Improvement of NYHA class
3. Improvement of daily activities
4. Reduction of hospitalization rate & length of
hospital stay (financial & psychological burden)
Long-term :
1. Slowing the progression of CHF
2. Increase of survival rate
 Chronic heart failure — choice of
A
pharmacological therapy

Aldosterone
LV systolic dysfunction ACE inhibitor Diuretic Beta-blocker
Antagonist

Asymptomatic LV
Indicated Not indicated Post MI Not indicated
dysfunction

Indicated if
Symptomatic HF (NYHA II) Indicated Indicated Not indicated
Fluid retention

Indicated Indicated
Worsening HF (NYHA III-IV) Indicated Indicated
comb. diuretic

Indicated Indicated
End-stage HF (NYHA IV) Indicated Indicated
comb. diuretic

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
 Chronic heart failure — choice of
B
pharmacological therapy
Angiotensin Vasodilator
(hydralazine/ Potassium -sparing
LV systolic dysfunction II receptor Cardiac glycosides
isosorbide diuretic
antagonists dinitrate)
Asymptomatic LV
Not indicated With AF Not indicated Not indicated
dysfunction
(a) when AF If ACE inhibitors
If ACE inhibitors If persisting
and angiotensin
are not tolerated (b) when improved hypokalaemia
Symptomatic HF (NYHA II) from more severe II antagonists
and not on beta-
HF in sinus are not
blockade
rhythm tolerated
If ACE inhibitors
If ACE inhibitors If persisting
and angiotensin
are not tolerated hypokalaemia
Worsening HF (NYHA III-IV) indicated II antagonists
and not on beta-
are not
blockade
tolerated
If ACE inhibitors
If ACE inhibitors If persisting
End-stage HF (NYHA IV) and angiotensin
are not tolerated hypokalaemia
indicated II antagonists
and not on beta-
are not
blockade
tolerated

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560
DEFINITION OF HEART FAILURE.
Criteria 1 and 2 should be fulfilled in all cases

1. Symptoms of heart failure

(at rest or during exercise)
And
2. Objective evidence of cardiac dysfunction
(at rest)
And
(in cases where the diagnosis is in doubt)
3. Response to treatment directed towards heart
failure
Task Force Report. Guidelines for the diagnosis and treatment of chronic heart failure.
European Society of Cardiology.2001
 Left Ventricular Dysfunction
Systolic: Impaired contractility/ejection
Approximately two-thirds of heart failure
patients have systolic dysfunction1
Diastolic: Impaired filling/relaxation

30%
(EF > 40 %)
(EF < 40%)

70%

Diastolic Dysfunction
Systolic Dysfunction
1 Lilly, L. Pathophysiology of Heart Disease. Second Edition p 200
 Left Ventricular Dysfunction
Volume Pressure Loss of Impaired
Overload Overload Myocardium Contractility

LV Dysfunction
EF < 40%

 End Systolic Volume

 Cardiac
Output
 End Diastolic Volume

Hypoperfusion Pulmonary Congestion

Hemodynamic Basis for
Heart Failure Symptoms
Hemodynamic Basis for
Heart Failure Symptoms
LVEDP 

Left Atrial Pressure 

Pulmonary Capillary Pressure 

Pulmonary Congestion
Left Ventricular Dysfunction
Systolic and Diastolic
Physical Signs
Symptoms
Basilar Rales
Dyspnea on
Exertion Pulmonary Edema
Paroxysmal S3 Gallop
Nocturnal Dyspnea
Pleural Effusion
Tachycardia
Cheyne-Stokes
Cough Respiration
Hemoptysis
Right Ventricular Failure
Systolic and Diastolic
Physical Signs
Symptoms
Peripheral Edema
Abdominal Pain
Jugular Venous
Anorexia
Distention
Nausea
Abdominal-Jugular
Bloating Reflux
Swelling Hepatomegaly
Compensatory Mechanisms
Frank-Starling Mechanism

Neurohormonal Activation

Ventricular Remodeling
 Compensatory Mechanisms
Frank-Starling Mechanism
a. At rest, no HF
b. HF due to LV systolic
dysfunction
c. Advanced HF
 Compensatory Mechanisms
Neurohormonal Activation
Many different hormone systems are
involved in maintaining normal
cardiovascular homeostasis, including:
Sympathetic nervous system (SNS)
Renin-angiotensin-aldosterone
system (RAAS)
Vasopressin (a.k.a. antidiuretic
Compensatory Mechanisms:
Sympathetic
DecreasedNervous
MAP System

Sympathetic Nervous System

 Contractility Tachycardia Vasoconstriction

MAP = (SV x HR) x TPR

 Sympathetic Activation in
Heart Failure
 CNS sympathetic outflow

 Cardiac sympathetic  Sympathetic

activity activity to kidneys
+ peripheral vasculature

1- 2- 1- Activation

1- 1-
receptors receptors receptors of RAS

Myocardial toxicity Vasoconstriction

Increased arrhythmias Sodium retention

Disease progression
Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
 Compensatory Mechanisms:
Renin-Angiotensin-
Aldosterone (RAAS)
Renin-Angiotensin-Aldosterone
( renal perfusion)

Salt-water retention Sympathetic

Vasoconstriction
Thirst augmentation

MAP = (SV x HR) x TPR

 Compensatory Mechanisms:
Neurohormonal Activation –
Vasopressin Decreased systemic blood pressure

Central baroreceptors
-

Increased systemic blood pressure Stimulation of hypothalamus, which produces

vasopressin for release by pituitary gland

Vasoconstriction Release of vasopressin by pituitary gland

Compensatory Neurohormonal
Stimulation: Summary
Decreased Cardiac Output

Sympathetic Renin-angiotensin Antidiuretic hormone

nervous system system (vasopressin)

Contractility Heart Vasoconstriction Circulating volume

rate
Anteriolar Venous

Maintain
blood
pressure Venous return
to heart
( preload)
Cardiac
+ output - Peripheral edema
and pulmonary
+ congestion
Stroke
volume
Neurohormonal Activation

Activation of
RAS and ANS

Hurst. The Heart. Diagnosis and Management of Heart Failure.10th ed. 688
 Compensatory
Ventricular Remodeling
Mechanisms
Alterations in the heart’s size, shape, structure, and function
brought about by the chronic hemodynamic stresses
experienced by the failing heart.

Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction
delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2.
 Other Neurohormones
Natriuretic Peptides: Three known
types
Atrial Natriuretic Peptide (ANP)
Predominantly found in the atria
Diuretic and vasodilatory properties
Brain Natriuretic Peptide (hBNP)
Predominantly found in the cardiac ventricles
Diuretic and vasodilatory properties
C-type Natriuretic Peptide (CNP)
Predominantly found in the central nervous
system
 Pharmacological Actions of
hBNP Hemodynamic
(balanced vasodilation)
• veins
M
K
D
R I SS
S
S
• arteries
G

• coronary arteries
R L
G G H
F R
C R
C S S K V L
S P K M V
Q G S
G
Neurohormonal
aldosterone
norepinephrine
Renal
diuresis & natriuresis

Abraham WT and Schrier RW, 1994

 Endothelium-Derived
Vasoactive Substances
Produced by a thin lining of cells within the
arteries and veins called the endothelium
Endothelium-derived relaxing factors (EDRF) –
Vasodilators:
Nitric Oxide (NO)
Bradykinin
Prostacyclin
Endothelium-derived constricting factors
(EDCF) – Vasoconstrictors:
Endothelin I
 Mediators of Heart Failure
Cytokines
Small protein molecules produced by a
variety of tissues and cells
Negative inotropes
Elevated levels associated with worse
clinical outcomes
Examples:
Tumor necrosis factor (TNF)-alpha
Interleukin 1-alpha
Interleukin-2
 Vicious Cycle of Heart Failure
LV Dysfunction

Decreased cardiac output

Increased cardiac workload and
(increased preload and afterload) Decreased blood pressure

Increased cardiac output (via increased Frank-Starling Mechanism

contractility and heart rate) Remodeling
Increased blood pressure (via vasoconstriction Neurohormonal activation
and increased blood volume)
 Neurohormonal Responses to
Impaired
Initially Adaptive, Deleterious if Sustained
Cardiac Short-Term Performance Long-Term
Response Effects Effects
Salt and Water Retention Augments Preload Pulmonary Congestion,
Anasarca

Vasoconstriction Maintains BP for Exacerbates pump

perfusion of vital organs dysfunction (excessive
afterload), increases
cardiac energy
expenditure
Sympathetic Stimulation Increases HR and Increases energy
ejection expenditure

Jaski, B, MD: Basics of Heart Failure: A Problem Solving Approach

The Vicious Cycle of
Heart Failure Management
Chronic HF
SOB
Diurese &
Home  Weight

Hospitalization MD’s Office

IV Lasix
or Admit PO Lasix

Emergency
Room
Angiotensin II Receptors

AT1 receptor AT2 receptor

• Vasoconstriction • Vasodilation
• Growth Promotion • Growth inhibition
• Anti-apoptotic • Pro-apoptotic
• Pro-fibrotic • ? Fibrosis
• Pro-thrombotic • ? Thrombosis
• Pro-oxidant • ? redox
Resynchronization System
(InSync 8040 Generator / InSync ICD 7272 / Attain Models 2187, 2188,
4193 Leads / 9790/2090 Programmer )
Indications
- The Medtronic InSync device is indicated for the reduction of the symptoms of moderate to severe heart failure (NYHA
Functional Class III or IV) in those patients who remain symptomatic despite stable, optimal medical therapy, and have a left
ventricular ejection fraction less than or equal to 35% and a QRS duration greater than or equal to 130ms. The InSync ICD system
is, also, intended to provide ventricular antitachycardia pacing and ventricular defibrillation for automated treatment of life
threatening ventricular arrhythmia.
- The Medtronic Models 9790 and 2090 Programmers are portable, microprocessor-based instruments used to
program Medtronic implantable devices.
- The Attain Left heart leads have application as part of a Medtronic biventricular pacing system.

Contraindications
- Asynchronous pacing is contraindicated in the presence (or likelihood) of competitive or intrinsic rhythms.
- Unipolar pacing is contraindicated in patients with an implanted defibrillator or cardioverter-defibrillator (ICD)
because it may cause unwanted delivery or inhibition of defibrillator or ICD therapy.
· The InSync ICD is contraindicated in patients whose ventricular tachyarrhythmias may have transient or
reversible causes, or for patients with incessant VT or VF.
· The Attain Models 2187, 2188, and 4193 leads are contraindicated for patients with coronary venous vasculature
that is inadequate for lead placement, as indicated by venogram.
- Do not use steroid eluting leads in patients for whom a single dose of 1.0 mg dexamethasone sodium phosphate may be
contraindicated.

Warnings and Precautions

- Patients should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation,
electrosurgical cautery, external defibrillation, lithotripsy, and radiofrequency ablation. These may result in
underdetection of VT/VF, inappropriate therapy delivery, and/or electrical reset of the device.
- Certain programming and device operations may not provide cardiac resynchronization.
- The InSync Elective Replacement Indicator (ERI) results in the device switching to VVI pacing at 65 ppm. For
this reason, the device should be replaced prior to ERI being set.
- An implantable defibrillator may be implanted concomitantly with an InSync system, provided implant protocols
are followed.
- Leads, stylets and guide wires should be handled with great care, their use may cause trauma to the heart.
When using a Model 4193 lead, only use compatible stylets (stylets with downsized knobs and are 3 cm shorter than
the lead length).
Definition : Heart Failure
“The situation when the heart is incapable of
maintaining a cardiac output adequate to
accommodate metabolic requirements and the
venous return.“ E. Braunwald
“Pathophysiological state in which an
abnormality of cardiac function is responsible
for the failure of the heart to pump blood at a
rate commensurate with the requirements of
the metabolizing tissues.” Euro Heart J; 2001. 22: 1527-1560