DJOKO

SOEMANTRI
I was born

July 25th 1949

Semarang, Central Java, Indonesia
I am basically

A Cardiologist
I am also

A Researcher

A Professor
Studied in

Faculty of Medicine, Airlangga University

Surabaya, East Java, Indonesia
..

IRM Fellow in Cardiology

Philippine Heart Center for Asia, Manila

PhD in Health Science

Airlangga University, Surabaya
 Resident of Cardiology and Vascular Medicine, Faculty of Medicine, Airlangga
University, Surabaya, Indonesia
(1976 1980)

Head of Cardiology & Vascular Medicine Outpatient Clinic, Dr. Soetomo General
Hospital - Airlangga University, Surabaya, Indonesia
(1981 present)

Head of Exercise Stress Test Division of Dr. Soetomo General Hospital - Airlangga
University, Surabaya, Indonesia
(1983 present)

Staff of Cardiology & Vascular Medicine Department, Faculty of Medicine,

Airlangga University, Surabaya, Indonesia
(1976 present)

Members of Surabaya Heart Center, Dr. Soetomo General Hospital Airlangga

University, Surabaya, Indonesia
(1979 present)
Member of

Indonesian Medical Association

The Indonesian Society of Internal Medicine

Indonesian Heart Association

Asia Pacific Society of Cardiology

Asean Federation of Cardiology

Scientific Publication & Research

Writer
145 Papers

Co-Writer
100 Papers
Nice to meet you ..
Lets begin ..
 HOW TO MANAGE HEART
FAILURE IN PRIMARY HEALTH
CARE

Department of Cardiology
Faculty of Medicine, Airlangga University / Dr. Soetomo General Hospital
Surabaya, Indonesia
 ABSTRACT

Nearly 1 million new cases of chronic heart failure (CHF) are

diagnosed annually worldwide, making it the most rapidly
growing cardiovascular disorder. Approximately 12% of the
adult population in developed countries has HF.
HF is a clinical syndrome, no single test can establish its presence
or absence. The diagnosis of HF is usually based on history,
physical examination, Chest X-Ray and if available LV function
assessment.
Chronic heart failure (CHF) is a large medical problem, but in
recent years significant progress has been made in its treatment.
 Acute Heart Failure (AHF), which is defined as rapid onset
of symptoms and signs due to acute deterioration of cardiac
function. Patients with AHF may present de novo or as an
acute decompensation of chronic heart failure which present as
cardiogenic pulmonary edema and need prompt treatment.
The goal of pharmacological treatment in patients with heart
failure is to improve symptoms and signs, decrease hospital
admission (particularly for patients with established heart failure)
and improve longevity. The initial aim of pharmacological
treatment is to relieve symptoms.
Currently, primary care physicians are responsible for delivering a
large amount of the care that these patients require.
 PATHOPHYSIOLOGY

Cardiovascular Function

Diastolic Function Systolic Function

(Ventricles) (Ventricles)

Blood

Preload System Afterload System

(Veins etc.) (Arteries etc.)
Preload, Afterload & Contractility

Preload Contractility Afterload

 INITIAL EVENT
(myocardial Infarction , inflammation, or afterload/chronotropy, lusitropy, inotropy-mismatch)

MYOCARDIAL
ISCHEMIA
STRETCH

WALL STRESS

NEUROENDOCRINE
ACTIVATION
RAAS
BARORECEPTOR/METABORECEPTOR DYSFUNCTION
SYMPATHETIC
ACTIVATION
TNFa

FORWARD FAILURE BACKWARD FAILURE

REDUCE ORGAN FUNCTION OEDEMA

CHRONIC HF MANAGEMENT IN
PRIMARY CARE
The goal of treatment is to improve symptoms and signs
and avoid or reduce hospital admissions.
Survival
Morbidity
Exercise capacity
Quality of life
Neurohormonal changes
Progression of CHF symptoms
TREATMENT

Diuretic is used first-line to reduce fluid

overload.
An ACE inhibitor and beta-blocker are then
added, followed by spironolactone if the
patient is still symptomatic.
An angiotensin-II receptor blocker, digoxin
and anticoagulants can be added as
appropriate.
Surgical interventions may be considered for
some patients.
 Treating CHF

Reverse the cause of the CHF

Reduce myocardial workload
Control fluid retention
Enhance myocardial contractility
Reduce afterload and/or preload *
Reverse the neuroendocrine components
of CHF *
DIURETICS IN CHF

Almost always
necessary
 Diuretic Effects
Volume and preload
- Improve symptoms of congestion

No direct effect on CO, but may decrease CO

with excessive preload reduction

Improves arterial distensibility

Neurohormonal activation :
Levels of NA, Ang II and PRA
Exception: with spironolactone
 Diuretics

A loop diuretic such as furosemide is recommended as

these are usually more effective than thiazide diuretics.
A reasonable starting dose of oral furosemide for a
patient in a community setting is 20 40 mg, once daily

Unsuccessful as monotherapy
Potential for electrolyte imbalance
Less improvement in exercise capacity
More frequent reoccurrence
Angiotensin Converting
Enzyme Inhibitors
 ACEI
Mechanism of Action
VASOCONSTRICTION VASODILATATION
ALDOSTERONE PROSTAGLANDINS
VASOPRESSIN Kininogen tPA
SYMPATHETIC Kallikrein
Angiotensinogen
RENIN
Angiotensin I
BRADYKININ

A.C.E. Inhibitor Kininase II

ANGIOTENSIN II Inactive Fragments

 Initiation of an ACE inhibitor may result in an increase in
potassium and creatinine.

If the potassium is < 5.5 mmol/L and the increase in

creatinine is no more than 50% above baseline acceptable
 -Blockers in CHF

Decrease hospital admissions.

Improve survival.

Slow onset of the effect

Low doses
-Adrenergic Antagonists
Possible Beneficial Effects
Density of 1 receptors; decrease ARK
Inhibit cardiotoxicity of catecholamines
Neurohormonal activation
HR
Antihypertensive and antianginal
Antiarrhythmic
Antioxidant
Antiproliferative
 Heart rate: a goal for the
treatment of heart failure

Disease
progression
Intervention
Failing heart
causes increased Effect of intervention on
sympathetic drive heart rate and outcome

Compensatory
mechanisms heart heart
rate rate
heart rate

contractility Good Poor

outcome? outcome?

Steeds and Channer, 1998

 Heart rate: a goal for the
treatment of heart failure

b1 or b1/b2
Selective or
Failing heart
non-selective
beta-blocker
causes increased
sympathetic drive
Carvedilol
b1/b2/a1

Parasympathetic
drive Indirect effect

ACE
inhibitors
 Mineralocorticoid/
aldosterone receptor
antagonists
Spironolactone block receptors that bind
aldosterone and, with different degrees of
affinity, other steroid hormone (e.g.
corticosteroids, androgens) receptors.
Spironolactone or eplerenone are
recommended in all symptomatic patients
(despite treatment with an ACEI and a beta-
blocker) with HFrEF and LVEF 35%
 Digoxin
Neurohormonal Actions
Sympathetic nervous system activity
Plasma Norepinephrine
RAAS activity
Vagal tone
Normalizes arterial baroreceptors
Na-K ATPase Na-Ca Exchange
K+ Na+ Ca++

Myofilaments Ca++
Na+

CONTRACTILITY
 Digitalis as an Antiarrhythmic
Purpose: protect the ventricle
from rapid atrial rates
Types of arrhythmias
Atrial tachyarrhythmias
Paroxysmal supraventricular
tachycardia
Atrial tachycardia

Atrial flutter
Atrial fibrillation
Digoxin

Slow the ventricular rate and therefore

improve symptoms in patients who have
symptomatic heart failure and atrial
fibrillation.
Evidence :
improve symptoms
reduce the rate of hospitalisation
does not improve mortality
Major etiologies of cardiogenic
pulmonary edema

Exacerbation of chronic left ventricular failure

Acute myocardial ischemia/infarction
Severe systemic hypertension
Left-sided valvular disorders
Acute tachydysrhythmias and
bradydysrhythmias
Other etiologies of cardiogenic
pulmonary edema
Sepsis
Severe Anemia
Thyrotoxicosis
Myocarditis
Myocardial toxins
Initial Evaluation of Patients with Suspected
Cardiovascular Pulmonary Edema

Immediate Work-Up
History of heart failure or regular intake of loop diuretics,
previous myocardial infarction, or known significant
valvular disease
Physical examination: check blood pressure, temperature,
signs of peripheral edema, and cardiac and pulmonary
physical findings

Primary health care

setting
Refer to hospital
Hospital setting
Immediate Work-Up
Pulse Oximetry
12-Lead electrocardiogram
Chest radiograph
Arrhythmia monitoring

Advanced Work-up
Complete blood gas analysis
Laboratory evaluation (complete blood cell count,
electrolytes, urea/creatinine, creatine kinase, troponin)
Brain natriuretic peptide measurement (if available)
Echocardiographic evaluation
heart cathetherization
 Treatment (combine with diuretics)

Vasodilator Indication Dosing

Nitroglycerine Pulmonary Start 10-20 g/min,
congestion/oedema increase up to 200 g/min
BP >90 mmHg
Isosorbide Pulmonary Start with 1 mg/h, increase
dinitrate congestion/oedema up to 10 mg/h
BP >90 mmHg
Nitroprusside Hypertensive HF Start with 0.3 g/kg/min
congestion/oedema and increase up to 5
BP >90 mmHg g/kg/min
Nesiritide* Pulmonary Bolus 2 g/kg + infusion
congestion/oedema 0.015 -0.03 g/kg/min
BP >90 mmHg
Inotropic Bolus Infusion rate

Dobutamine No 2 -20 g/kg/min (+)

Dopamine No <3 g/kg/min: renal effect (+)

3 5 g/kg/min: inotropic (+)
>5 g/kg/min: (+), vasopressor
(+)

Milrinone 25 - 75 g/kg over 10-20 min 0.375-0.75 g/kg/min

Enoximone 0.25 - 0.75 mg/kg 1.25 -7.5 g/kg/min

Levosimendan* 12 g/kg over 10 min 0.1 g/kg/min which can be
(optional)** decreased to 0.05 or increased to
0.2 g/kg/min

Norepinephrine No 0.2 - 1.0 g/kg/min

Epinephrine Bolus: 1 mg can be given i.v. 0.05 - 0.5 g/kg/min

during resuscitation, repeated
every 3 5 min
Post Hospital Care
Encourage patients to:
Be aware of their symptoms and how to manage them
if their condition deteriorates

Weigh themselves daily. It is useful to establish a dry

weight so that changes in the patients condition are
detected and managed early.

Participate in regular exercise

Avoid an excessive intake of salt and alcohol

Monitor their fluid intake

Regular review to the doctor

"The very essence of cardiovascular practice is the recognition of
early heart failure.-

SIR THOMAS LEWIS, 1933

FOR YOUR ATTENTION