Heart Failure

Yusra Pintaningrum

Fakultas Kedokteran Universitas Mataram /

RSUP NTB
ABSTRACT

Nearly 1 million new cases of chronic heart failure:

- 5 million people in the U.S.A
- 6.5 million people in Europe
- 2.4 million people in Japan
- Three-quarters of all patients hospitalized for the
first time with heart failure will die within 5 years a
survival rate far worse than for most types of
cancer.
 Definition

• Heart failure can be defined as

an abnormality of cardiac structure or function
leading to failure of the heart to deliver oxygen
at a rate commensurate with the requirements
of the metabolizing tissues, despite normal
filling pressures (or only at the expense of
increased filling pressures)

European Heart Journal (2012) 33, 1787–1847

 Definition

• HF is defined, clinically,
as a syndrome in which patients have typical
symptoms (e.g.breathlessness, ankle swelling,
and fatigue) and signs (e.g. Elevated jugular
venous pressure, pulmonary crackles, and
displaced apex beat) resulting from an
abnormality of cardiac structure or function.

European Heart Journal (2012) 33, 1787–1847

European Heart Journal (2012) 33, 1787–1847
 Causes of heart pump failure

A. MECHANICAL ABNORMALITIES

1. Increased pressure load

– central (aortic stenosis, aortic coarctation.)
– peripheral (systemic hypertension)

2. Increased volume load

– valvular regurgitation
– hypervolemia

3. Obstruction to ventricular filling

– valvular stenosis
– pericardial restriction
 B. MYOCARDIAL DAMAGE

1. Primary
a) cardiomyopathy
b) myocarditis

c) toxicity (e.g. alcohol)

d) metabolic abnormalities (e.g. hyperthyreoidism)

2. Secondary
a) oxygen deprivation (e.g. coronary heart disease)

b) inflammation (e.g. increased metabolic demands)

c) chronic obstructive lung disease

 C. ALTERED CARDIAC RHYTHM

1. ventricular flutter and fibrilation

2. extreme tachycardias

3. extreme bradycardias
 Many etiologies of CHF

• Coronary artery disease

• Hypertension
• Valvular heart disease
• Congenital heart disease
• Toxins
• Peripartum cardiomyopathy
• Many others
McMurray, Pfeffer. JACC 2004;44:2398-405
Pinski. JAMA 2003;289:754-6
Schmitt. Science 2003;299:1410-3
 Symptoms and signs of heart failure

1. forward failure:
symptoms result from inability of the heart to pump enough
blood to the periphery (from left heart), or to the lungs (from
the right heart)

a) forward failure of left heart:- muscle weakness, fatigue,

dyspepsia, oliguria....

 general mechanism: tissue hypoperfusion

b) forward failure of right heart: - hypoperfusion of the

lungs  disorders of gas
exchange
- decreased blood supply
to the left heart
2. backward failure:
– symptoms result from inability of the heart to accept
the blood comming from periphery and from lungs

a. backward failure of left heart:

– increased pulmonary capillary pressure  dyspnoea
and tachypnoea, pulmonary edema (cardiac asthma) 
 arterial hypoxemia and hypercapnia....

b. backward failure of right heart:

– increased pressure in systemic venous system 
 peripheral edemas, hepatomegaly, ascites nocturnal diuresis....
CHF: Systole vs. Diastole

• Diastolic HF (HF- • Systolic HF

PSV) – Dyspnea
– Dyspnea – Congestion (edema)
– Congestion (edema) – ↑BNP
– ↑BNP – ↓LVEF
– Normal LVEF – ↓LV mass
– ↑LV mass – ↑LVEDV
– Normal LVEDV – Usually also have
– Abnormal mitral inflow diastolic
– Abnormal mitral abnormalities
annular velocity
Aurigemma, Gassch. NEJM 2004;351:1097-1105
Brucks. Am J Cardiol 2005;95:603-6
European Heart Journal (2012) 33, 1787–1847
European Heart Journal (2012) 33, 1787–1847
• European Heart Journal (2012) 33, 1787–1847
 Advances in the treatment of heart failure - how
many goals

Neurohormones Abnormalities in: Necrosis

Cytokines Cardiac receptors Fibrosis
iNOS Signalling processes Inappropriate
Ischaemia Calcium homeostasis hypertrophy
Free radicals Contractile protein Cardiac dilation
Apoptosis desensitisation
Endothelial dysfunction

Progressive cardiac dysfunction

Worsening heart failure
Death
Remme, 1998
 Heart rate: a goal for the
treatment of heart failure (1)

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 (2)

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
 Heart rate: a goal for the treatment of heart failure (3)

Drug Action Effect Effect

on heart rate on mortality

Nifedipine Calcium antagonist risk

Amlodipine Calcium antagonist 0 0

Mibefradil T/L-calcium Small risk

channel blocker

Amiodarone Antiarrhythmic risk

Xamoterol b1-adrenoceptor risk

partial agonist in severe HF

Digoxin Positive inotrope 0

HF = heart failure; = increase; = decrease; 0 = no change

Steeds and Channer, 1998
 Neurohormones: a goal for therapeutic intervention in heart failure (1)
Evidence for neurohormonal effect in trials of CHF patients

Study Drug Neurohormonal Clinical effect

studied effect

V-HeFT II ACE inhibitor plasma mortality

noradrenaline

CONSENSUS ACE inhibitor Presumed Greatest survival in

patients with most
neurohormonal activation

Nifedipine vs ISDN Calcium RAAS Deterioration

vs combination antagonist stimulation

DIMT Digoxin plasma Improved exercise time

DIG Digoxin Blunted mortality trend

US Carvedilol Carvedilol Blunted mortality, hospitalisation

HF study

Pool, 1998
 Neurohormones: a goal for therapeutic
intervention in heart failure (2)
ACE Aldosterone
AIIAs
inhibitors antagonists

Angiotensin I

Aldosterone
secretion
Angiotensin II Responses in:
Brain
Vasculature
Myocardium
Adrenal gland
Cardiac remodelling: a goal for therapeutic intervention in heart failure

Cardiac remodelling in worsening heart failure

Calcium sensitisation and troponin C
Tissue growth
Collagen metabolism

Calcium ACE
sensitising drugs inhibitors

Growth hormone AIIAs

Oxidative stress: a goal for therapeutic
intervention in heart failure
Oxidative stress
Carvedilol
Cardiac ischaemia
and wall stress ACE
inhibitors
Activation of
transcription factors
Beta-blockers
Induction of nitric oxide
Cytokine release
Apoptosis

Worsening heart failure

Vaasodilators
-Afterloaad
Congestive Inotropics
unloaders (ACE
inhibitors) Heart Failure agents
-Preload (digoxin,
unloaders(diuret dobutamine)
ics, nitrates)

- Increase systemic vascular - Decrease cardiac

resistance (afterload) output
- Increase blood volume - Increase LV end
(preloaad) diastolic pressure

Compensatory RAAS  ACE inh

response
Symphathetic 
Beta blocker
 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 *
Pharmacologic Agents
Digitalis
Diuretics
Vasodilators
Inotropes
ß-Adrenoceptor antagonists
Neurohormonal antagonists
 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
 Cardiac glycosides
• William Withering used
foxglove to treat edema in 1785:
An Account of the Foxglove,
and Some of Its Medical Uses
• Inhibits Na-K ATPase, intracellular
Na, Ca through Na-Ca exchange
• Recent studies show digoxin
– Sensitizes cardiac baroreceptors
– Decreases sympathetic nervous outflow
– Decreases renin secretion
• Neurohormonal modulator NEJM 1993;329:1-7
NEJM 2002;347:1403-11
Ann Int Med 2005;142:132-4
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
Diuretics in CHF

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

No direct effect on Cardiac Output, but may

Decrease CO with excessive preload reduction

Improves arterial distensibility

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

• Unsuccessful as monotherapy
• Potential for electrolyte
imbalance
• Less improvement in exercise
capacity
• More frequent reoccurrence
Angiotensin Converting
Enzyme Inhibitors
 b-Blockers in CHF

• Decrease hospital admissions.

• Improve survival.

• Slow onset of the effect

• Low doses
ß-Adrenergic Antagonists
Possible Beneficial Effects
Density of b1 receptors
Inhibit cardiotoxicity of catecholamines
Neurohormonal activation
HR
Antihypertensive and antiangina
Antiarrhythmic
Antioxidant
Antiproliferative
 Positive inotropes:
Conclusions
May increase mortality
Safer in lower doses
Use only in refractory CHF
NOT for use as chronic therapy
 Suspicion of heart failure

History and physical exam

• Considerations:HF history, chest pain, CAD, DCM, HTN, infection, anemia
Congestion Perfusion
Rapid clinical assesment of hemodynamic profiles
Ax : Orthopnea DP : - Narrow BP < 25%
• Congestion: yes or no
DP : - JVP up - Pulse Pressure
• Perfusion decreased: yes or no
- Hepatojugular Refl - Pulsus alternan
- Ascites Helpful diagnostic findings - Sympt Hypotension
- Squarewave BP ( Valsv) • ECG:ischemia or arrhythmias - Cool ext
- S3 (+/-) • CXR:congestion and/or cardiomegaly - Impaired Ment Stat
- Rales 80% NEGATIF SBP-DBP : SBP
- Periph edema ( insensitive) • Establish diagnosis
• Initiate treatment based on clinical assesment of hemodynamic profile

Dry-warm profile Wet-warm profile Wet-cold profile Dry-cold profile

Initial management Initial management Initial management Initial management

 Continue oral heart
failure medications
 Search for other causes
of symptoms including
PE,ACS,depression,
anemia,hypothyroidism
 IV loop diuretics
 IV nesiritide or IV
vasodilator
 Oxygen, if indicated
Admit: Telemetry or
observation unit
 IV loop diuretics  Continue RHC
 Consider RHC if high SVR  Inotrope and/or
 IV nesiritide or IV Pressor
vasodilator if high SVR.  Consider decrease of beta
 Inotrop or pressor if low SVR blocker dose
Admit: ICU or telemetry unit Admit: ICU or telemetry unit

Upon compensation optimize oral heart failure medications ACE inhibitors,

beta blockers, aldosteron antagonist, evaluate/manage comorbidities, assess
sudden death risk, optimize HR patient education, optimize discharge
planning and follow-up care

Discharge
FOR YOUR ATTENTION