H eart Failure

&
Cardiac Arrest

Rony Yuliwansyah

Cardioloy Sub Division

artment Of Internal Medicine University Of Andalas - Dr M. Djamil - Padang Ind

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
Inotropy
Dromotropy

Change in heart rate

Change in contractile
force
Change in conduction

velocity
Can be positive or negative

PEN G ARUH SYARAF TH D JAN TU N G

Simpatis: bersifat meningkatan
a. frekuensi denyut jantung (kronotropik
+)
b. kuat kontraksi jantung (inotropik +)
c. perambatan impuls (dromotropik +)

Parasimpatis: bersifat mengurangkan

Kronotropik
Inotropik
Dromotropik -

M echanism s ofheart 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

G rading ofH eart Failure

NYHA functional
class
Class I
Class II (s)
Class II (m)

Definition
No limitation: ordinary physical exercise does not cause dyspnoea.
Slight limitation of physical activity: dyspnoea on walking more than 200 yards or
on stairs;
Moderate limitation of physical activity: dyspnoea walking less than 200 yards.

Class III

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

and dressing, or walking from room to room.

Class IV

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

with any level of physical activity.

Coronary heart disease statistics: heart failure supplement., BHF 2002, http://www.heartstats.org, acc
Prevalence data is from a population based study: Davies MK et al. The Lancet 2001; 358: 439-444.

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

Com m on Causes ofH eart 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 com m on causes ofH eart

Failure
Congenital heart disease
Infiltrative cardiomyopathy: amyloid,

sarcoid, restrictive
Familial
Hemachromotosis
Thyroid disease
Pheocromocytoma
Chronic renal disease
Viral and HIV cardiomyopathy

Pathophysiology ofH eart Failure

(due to LVSD )

Coronary artery
disease
Hypertension

Arrhythmia
Left-ventricular
injury

Pathologic
remodelling

Left-ventricular
dysfunction

Cardiomyopathy

Valvular disease

Vasoconstriction
Endothelial
dysfunction
Renal sodium
retention

Death
Pump
failure

Neurohormonal
activation

Symptoms:
Dyspnoea
Fatigue
Oedema

.Adapted from Fonarow GC et al. Rev Cardiovasc Med. 2003; 4(1):

8-17.

Heart
failure

A C U TE H EA R T
FA ILU R E

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 ofAcute H eart 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

Heart J 2005;26:384-416
the single most costly medicalEursyndrome

M ortality ofAH F
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 G oals ofAH F

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):S7S1

O xygenation 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

Pharm acologic option in AH F

Diuretics

Reduce
fluid
volume

Vasodilators Inotropes

Decrease
preload
and
afterload

Augment
contractilit
y

Natriuretic
peptides

Vasodilate
; reduce
fluid
volume;
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

Low perfusion at rest

Congestion at rest

No

No

Yes

Warm & dry

Warm & wet

Cold & dry

Cold & Wet

Yes

Sign of congestion:
Orthopnea,elevated
JVP,edema,pulsatile
hepatomegaly, ascites,
rales,louder S3,P2 radiation left
ward, abdomino-jugular reflex,
valsava square wave

Sign of low perfusion:

Narrow pulse pressure,cool
extremities,sleepy, suspect
from ACEI hypotension, low
Na, renal worsening

European Heart Journal of Heart Failure,2005; 7:323-331

PATIENT TREATMENT SELECTION

Low perfusion at rest

Congestion at rest

No

No

Yes

Warm & dry

Warm & wet

Cold & dry

Cold & Wet

Yes
VOLUME
LOADING

Diuretic
Vasodilator

C
Inotropic drugs :
Dobutamine
Milrinone
Levosimendan
European Heart Journal of Heart Failure,2005; 7:323-331

Therapeutic Goal in AHF

Hemodynamic

Clinical

PCWP < 18 mm
CO and/or SV

Symptoms
(Dyspnea and/or fatigue)
Clinical sign
Body weight
Diuresis
Oxygenation

Laboratory
Serum electrolytes normal
BUN
Plasma BNP
Blood glucose normalization
Tolerability
Low rate of with drawl from therapy
Low incidence of adverse effects

Outcome
Length of stay in ICU
Duration of hospitalization
Time to hospital readmission
Mortality

Eur Heart J 2005;26:384-416

D iuretics
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
Thank You