Heart Failure

Rony Yuliwansyah
Cardioloy Sub Division
Department Of Internal Medicine University Of Andalas - Dr M. Djamil - Padang Indonesia
Internal chambers and valves of the heart
The Cardiac Cycle

Systole :
Period of ventricular contraction
Blood ejected from heart

Diastole :
Period of ventricular relaxation
Blood filling
 Stroke Volume
The amount of blood ejected from the heart in
one beat
Average is 60 - 100 ml
Depends on preload, contractile force and
afterload

Cardiac Output
The amount of blood ejected from the heart in
one minute
Cardiac output = heart rate x stroke volume
 Definitions

Chronotropy Change in heart rate

Inotropy Change in contractile
force
Dromotropy Change in conduction
velocity

Can be positive or negative

 PENGARUH SYARAF THD JANTUNG

Simpatis: bersifat meningkatan

a. frekuensi denyut jantung (kronotropik +)

b. kuat kontraksi jantung (inotropik +)
c. perambatan impuls (dromotropik +)
Parasimpatis: bersifat mengurangkan

Kronotropik
Inotropik
Dromotropik -
 Mechanisms of heart failure

LV systolic dysfunction many causes

Valvular heart disease
Restrictive cardiomyopathy
Pericardial constriction
LV diastolic dysfunction
Cardiac arrhythmias
 Heart Failure

Definition
It is the pathophysiological process in which
the heart as a pump is unable to meet
the metabolic requirements of the tissue for
oxygen and substrates despite the venous
return to heart is either normal or increased
 Grading of Heart Failure

NYHA functional
class
Definition
Class I No limitation: ordinary physical exercise does not cause dyspnoea.

Class II (s) Slight limitation of physical activity: dyspnoea on walking more than 200 yards or
on stairs;
Class II (m) Moderate limitation of physical activity: dyspnoea walking less than 200 yards.

Marked limitation of physical activity: comfortable at rest but dyspnoea washing

Class III
and dressing, or walking from room to room.

Severe limitation of physical activity: dyspnoea at rest, with increased symptoms

Class IV
with any level of physical activity.

Coronary heart disease statistics: heart failure supplement., BHF 2002, http://www.heartst
Prevalence data is from a population based study: Davies MK et al. The Lancet 2001; 358
 General pathomechanisms involved in heart
failure development

Cardiac mechanical dysfunction can develop

as a consequence in preload, contractility and
afterload disorders

Disorders of preload
preload length of sarcomere is more than
optimal strength of contraction

preload length of sarcomere is well below the

optimal strength of contraction
Characteristic features of systolic dysfunction
(systolic failure)

ventricular dilatation

reducing ventricular contractility (either generalized

or localized)
diminished ejection fraction (i.e., that fraction of
end-diastolic blood volume ejected from the
ventricle during each systolic contraction)

in failing hearts, the LV end-diastolic volume

(or pressure) may increse as the stroke volume
(or CO) decrease
Characteristic features of diastolic dysfunctions
(diastolic failure)

ventricular cavity size is normal or small

myocardial contractility is normal or hyperdynamic

ejection fraction is normal (>50%) or supranormal

ventricle is usually hypertrophied

ventricle is filling slowly in early diastole (during the

period of passive filling)
 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 (alcohol)
d) metabolic abnormalities (hyperthyreoidism)

2. Secondary

a) oxygen deprivation (coronary heart disease)

b) inflammation (increased metabolic demands)

c) chronic obstructive lung disease

 C. ALTERED CARDIAC RHYTHM

1. ventricular flutter and fibrilation

2. extreme tachycardias

3. extreme bradycardias
Common Causes of Heart Failure

CAD, with myocardial ischemia the potentially most

reversible cause of HF
HTN
Idiopathic dilated cardiomyopathy
Valvular heart disease
Drugs: alcohol, cocaine, methamphetamine
Postpartum
Less common causes of Heart
Failure
Congenital heart disease
Infiltrative cardiomyopathy: amyloid, sarcoid,
restrictive
Familial
Hemachromotosis
Thyroid disease
Pheocromocytoma
Chronic renal disease
Viral and HIV cardiomyopathy
Pathophysiology of Heart Failure
(due to LVSD)
Coronary artery disease
Arrhythmia

Left-ventricular Pathologic Left-ventricular

Hypertension Death
injury remodelling dysfunction
Cardiomyopathy Pump
failure

Valvular disease Neurohormonal

activation

Vasoconstriction
Symptoms:
Endothelial
Dyspnoea Heart
dysfunction
Fatigue failure
Renal sodium
Oedema
retention

.Adapted from Fonarow GC et al. Rev Cardiovasc Med. 2003; 4(1): 8-17.
ACUTE HEART FAILURE
Definition of Acute Heart Failure

AHF is defined as the rapid onset of

symptoms and signs, secondary to abnormal
cardiac function

Cardiac dysfunction can be related to

systolic or diastolic, to abnormalities in
cardiac rhythm or to preload and afterload
mismatch

It is often life threatening and requires

urgent treatment
ESC guideline for Acute Heart Failure, 2005
 Cause of Acute Heart Failure

Acute coronary syndrome, hypertensive crisis and

other cardiac or non cardiac also precipitate an AHF.

CAD contributes to 60-70 % in elderly

Cardiomyopathy, HHD, Arrhythmia, Myocarditis

and Valve diseases found in young

AHF therefore has significantly become the single

most costly medical syndrome in emergency.

Eur Heart J 2005;26:384-416

 Mortality of AHF

In Hospital mortality ( 60 days) : 9.6%

Rehospitalization and mortality : 32,5%
1 year mortality : 30%.

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

 Therapeutic Goals of AHF

Improve hemodynamic status to relief symptoms and

stabilize organ function

Reduce fluid volume

Reduced filling pressures of the heart
Reduce systemic vascular resistance (SVR)
Increase cardiac output (CO)
Reduce neurohormones activity

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

 Oxygenation and ventilatory assist.
The first priority in AHF treatment is adequate
cellular oxygenation to prevent organ target
dysfunction. Oxygen saturation is maintained 95-
98% by

Keep airway Patency

Oksigen supply ; Nasal or Mask or CPAP or non-
invasive positive pressure ventilation (NIPPV).
Ventilator support in case of respiratory failure

ESC guideline for Acute Heart Failure, 2005

 Pharmacologic option in AHF

Diuretics Vasodilators Inotropes Natriuretic

peptides

Reduce Decrease Augment Vasodilate;

fluid preload contractility reduce fluid
volume and volume;
afterload counteract
RAAS/SNS

RAAS = renin-angiotensin-aldosterone system; SNS = sympathetic nervous system

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

 Assessment of Haemodynamic Profile

Congestion at rest Sign of congestion:

Orthopnea,elevated JVP,edema,
pulsatile hepatomegaly, ascites,
No Yes rales,louder S3,P2 radiation left
Low perfusion at rest

ward, abdomino-jugular reflex,

valsava square wave

No A B
Warm & dry Warm & wet

Cold & dry Cold & Wet

Yes L C
Sign of low perfusion:
Narrow pulse pressure,cool ex
tremities,sleepy, suspect from
ACEI hypotension, low Na, renal
worsening European Heart Journal of Heart Failure,2005; 7:323-331
 PATIENT TREATMENT SELECTION

Congestion at rest
No Yes Diuretic
Low perfusion at rest

Vasodilator

No A B
Warm & dry Warm & wet
Cold & dry Cold & Wet

Yes L C
Inotropic drugs :
Dobutamine
Milrinone
VOLUME Levosimendan
LOADING European Heart Journal of Heart Failure,2005; 7:323-331
 Therapeutic Goal in AHF

Hemodynamic Clinical
PCWP < 18 mm Symptoms
CO and/or SV (Dyspnea and/or fatigue)
Clinical sign
Laboratory Body weight
Serum electrolytes normal Diuresis
BUN Oxygenation
Plasma BNP
Blood glucose normalization Outcome
Length of stay in ICU
Tolerability Duration of hospitalization
Low rate of with drawl from therapy Time to hospital readmission
Low incidence of adverse effects Mortality

Eur Heart J 2005;26:384-416

 Diuretics

For achieving optimal volume status eliminate or

minimize congestion
High doses of iv diuretics 2-3 times daily
More effective with continous iv. 5-20 mg/h
Diuretics resistance is a common problem
In case of resistance:
Restrict Na/water intake and follow electrolytes
Volume repletion in hypovolaemia
Increase the dose and/or Combination diuretics

Eur Heart J 2005;26:384-416

 Vasodilators

Nitroprusside, Nitroglycerin, Nitrate family

Work by cGMP mediated smooth muscle
relaxation -> vasodilatation
Decrease myocardial work by afterload and
preload reduction
May cause hypotension
May cause headache

ESC guideline for Acute Heart Failure, 2005

Nitrates
Not evaluated by large scale studies
Many studies shown their favorable effect
Limitation
Side effect
Nitrate Resistance
Nitrate Tolerance
Prevention
Intermittent dosing : 12 hour nitrate free interval
Escalating dose
Concomitant use of hydralazine

Elkayam, The American Journal of Cardiology, 2005

 Inotropes:

Dopamine, Dobutamine, Milrinone

Improve cardiac output by directly
increasing cardiac contractility
Significant proarrhythmic effects
May precipitate ischemia
Not recommended for routine use in AHF,
but clearly have a role in specific patients

ESC guideline for Acute Heart Failure, 2005

Inotropic Doses

>

ESC guideline for Acute Heart Failure, 2005

Rapid assessment and prompt
treatment would result in an
excellent outcome for AHF
patients