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 Change in heart rate

Inotropy Change in contractile
force
Dromotropy 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 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.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 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
Renal sodium failure
Oedema
retention

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

8-17.
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

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

peptides

Reduce Decrease Augment Vasodilate

fluid preload contractilit ; reduce
volume and y fluid
afterload 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
Sign of congestion:
Congestion at rest
Orthopnea,elevated
JVP,edema,pulsatile
No Yes hepatomegaly, ascites,
Low perfusion at rest

rales,louder S3,P2 radiation left

ward, abdomino-jugular reflex,

No A B valsava square wave

Warm & dry Warm & wet

Cold & dry Cold & Wet

Yes L C
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

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

 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
S U D D EN C A R D IA C D EATH
 D efi
nition
Natural death from a cardiac cause
within a short time period (1 hour) from
the onset of symptoms
Commonly result from cardiac arrest
due to a fatal arrhythmia
Epidemiology of VA & SCD
Classification of Ventricular
Arrhythmia
by Electrocardiography
Nonsustained ventricular tachycardia (VT)
Monomorphic
Polymorphic
Sustained VT
Monomorphic
Polymorphic
Bundle-branch re-entrant tachycardia
Bidirectional VT
Torsades de pointes
Ventricular flutter
Ventricular fibrillation
 Epidemiology of VA & SCD
Classification of Ventricular
Arrhythmia
by Disease
Chronic Entity
coronary heart disease
Heart failure
Congenital heart disease
Neurological disorders
Structurally normal hearts
Sudden infant death syndrome
Cardiomyopathies
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular (RV)
cardiomyopathy
Nonsustained Monomorphic VT
Nonsustained LV VT
Sustained Monomorphic VT
72-year-old woman with CHD
Nonsustained Polymorphic VT
Sustained Polym orphic VT
Exercise induced in patientw ith no structuralheartdisease
Bundle Branch Reentrant VT
 Ventricular Flutter
Spontaneous conversion to NSR (12-lead ECG)
VF with Defibrillation (12-lead ECG)
W ide Q RS Irregular Tachycardia:
AtrialFibrillation w ith antidrom ic conduction in patientw ith
accessory pathw ay N otVT
 Mechanisms and
Substrates
Mechanisms of Sudden Cardiac Death
in 157 Ambulatory Patients

Ventricular fibrillation - 62.4%

Bradyarrhythmias (including advanced AV
block and asystole) - 16.5%
Torsades de pointes - 12.7%
Primary VT - 8.3%

Bayes de Luna et al. Am Heart J 1989;117:1519.

 Clinical Presentations of
Patients with VA & SCD
Asymptomatic individuals with or without electrocardiographic
abnormalities
Persons with symptoms potentially attributable to ventricular
arrhythmias
Palpitations
Dyspnea
Chest pain
Syncope and presyncope
VT that is hemodynamically stable
VT that is not hemodynamically stable
Cardiac arrest
Asystolic (sinus arrest, atrioventricular block)
VT
Ventricular fibrillation (VF)
Pulseless electrical activity
Cardiac Arrest

Mechanisms
Ventricular Fibrillation
Pulseless Ventricular Tachycardia
Asystole
Pulseless Electrical Activity (PEA)
A condition; Not an ECG rhythm
 all cases accompanied
with hypoxia
extracardiac

Causes of cardiac
arrest

cardiac
Primary lesion of cardiac muscle leading
to the progressive decline of contractility,
conductivity disorders, mechanical factors
Cardiac Arrest

Most common rhythms

Adults: ventricular fibrillation
Children: Asystole, Bradycardic PEA
Pediatric V-fib suggests:
Drug toxicity
Electrolyte imbalance
Congenital heart disease
 Causes of circulation
arrest
Cardiac Extracardiac
Ischemic heart disease
(myocardial infarction, airway obstruction
stenocardia) acute respiratory failure
Arrhythmias of different shock
origin and character
Electrolytic disorders reflector cardiac arrest
Valvular disease embolisms of different
Cardiac tamponade origin
Pulmonary artery drug overdose
thromboembolism
electrocution
Ruptured aneurysm of
aorta poisoning
 arrest
Blood pressure
measurement

Taking the pulse on
peripheral arteries
Loss of time !!!
Auscultation of cardiac
Symptoms
tones of cardiac
arrest
Absence of pulse on carotid arteries a
pathognomonic symptom
Respiration arrest may be in 30 seconds after
cardiac arrest
Enlargement of pupils may be in 90 seconds
after cardiac arrest
Cardiac Arrest
ABCs come first!
Circulation - no pulse in 5 sec chest
compressions
Airway - unobstructed? manually open
Breathing - no or inadequate ventilate

Do NOT wait on equipment

Assure effective BLS before going to
ALS
Rise and fall of chest
Air movement in lung fields
Pulse with compressions
BLS Prim ary Survey

Circulation : is the pulse present?

check carotid pulse at least 5 sec.
Perform CPR
Airway : is the airway open? head
tilt-chin lift or jaw thrust
Breathing : is the patient breathing and
are respiration adequate? look, listen
and feel. Give 2 rescue breath
Defibrillation : if no pulse, check for a
shockable rhythm (manual/AED) DC
shock - CPR
ACLS Secondary Survey

Circulation : what initial and current

cardiac rhythm, access for drug and fluid?
obtain IV access, ECG monitor, give
drug to manage rhythm
Airway : is the airway patent? Is an
advanced airway indicated? maintain
airway patency by OPA or NPA, LMA,
Combitube, ETT
Breathing : are oxygenation and
ventilation adequate? give supplement
oxygen
Differential diagnosis : why arrest?
Cardiac Arrest

Vascular access
Antecubital space
Arm, EJ, Foot (last resort)
IO in peds < 6 y/o
14 or 16 gauge
LR or NS
30 sec - 60 sec of CPR to circulate drug
Cardiac Arrest

Intubation as time allows

Less emphasis today as compared to
past
Epi, atropine, lidocaine may be
administered down tube
2x IV dose
IV is preferred
Analyze the Rhythm
Ventricular Fibrillation (VF)

Characteristics
Chaotic, irregular, ventricular rhythm
Wide, variable, bizarre complexes
Fast rate of activity
Multiple ventricular foci
No cardiac output
Terminal rhythm if not corrected quickly
Most common rhythm causing sudden
cardiac death in adults
Ventricular Fibrillation (VF)
Treatm ent
ABCs
Witnessed arrest: Precordial thump
Little demonstrated value but worth a try
CPR until defibrillator available
Quick Look for VF or pulseless VT
Treat pulseless VT as if it were VF
Defibrillate
200 J, 300 J, 360 J
Quickly and in rapid succession
Identify cause if possible
Ventricular Fibrillation
Treatm ent
If still in VF/VT arrest, continue CPR for 1
minute
Establish IV access and Intubate
If sufficient personnel, attempt both simultaneously
If not, quick attempt at IV access then attempt ETT
Vasopressor Medication
Epinephrine
1 mg 1:10,000 IVP
Repeat every 3-5 mins as long as arrest persists
Vasopressin (alternative to Epinephrine)
40 units IVP one time only
Ventricular Fibrillation
Treatm ent
Shock @ 360 J after each medication given as
long as VF/VT arrest persists
Alternate epi-shock & antidysrhythmic-shock sequence
Antidysrhythmic Medication
amiodarone 300 mg IVP single dose
lidocaine 1-1.5 mg/kg IVP, q 5 min, max 3mg/kg total
procainamide 100 mg IV, q 5 min, max 17 mg/kg total
magnesium 10% 1-2 g IV
if hypomagnesemic or prolonged QT
Ventricular Fibrillation
Treatm ent
Consider NaHCO3 if prolonged
Only after effective ventilations
In many EMS systems, consider terminating
resuscitation efforts in consult with med control
Ventricular Fibrillation

The ultimate unstable tachycardia

Shock early-Shock often
Sequence is drug-shock-drug-shock
Sequence of drugs is epi-antiarrhythmic-
epi-antiarrhythmic
Analyze the Rhythm
Asystole
Characteristics
The ultimate unstable bradycardia
A terminal rhythm
poor prognosis for resuscitation
best hope if ID & treat cause
No significant positive or negative
deflections
Asystole
Possible Causes
Hypoxia: ventilate
Preexisting metabolic acidosis:
Bicarbonate 1 mEq/kg
Hyperkalemia: Bicarbonate 1 mEq/kg,
Calcium 1 g IV
Hypokalemia: 10mEq KCl over 30
minutes
Hypothermia: rewarm body core
Asystole

Possible Causes
Drug overdose
Tricyclics: Bicarbonate
Digitalis: Digibind (Digitalis antibodies)
Beta-blockers: Glucagon
Ca-channel blockers: Calcium
Asystole & PEA D iff
erentials (The
5H s & 5Ts)
Hypovolemia
Hypoxia Tablets (Drug OD)
Hydrogen ions Tamponade
(Acidosis)
Tension
Hyper/hypo-
Pneumothorax
kalemia
Thrombosis,
Hypothermia
Coronary
Thrombosis,
Pulmonary
Asystole Treatm ent
Primary ABCD
Confirm Asystole in two leads
Reasons to NOT continue?
Secondary ABCD
ECG monitor/ET/IV
Differential Diagnosis (5Hs & 5Ts)
TCP (if early)
Epinephrine 1:10,000 1 mg IV q 3-5 min.
Atropine 1 mg IV q 3-5 min, max 0.04 mg/kg
Consider Termination
Analyze the Rhythm

What are you going to do for this patient?

PEA
Possibilities
Massive pulmonary embolus
Massive myocardial infarction
Overdose:
Tricyclics - Bicarbonate
Digitalis - Digibind
Beta-blockers - Glucagon
Ca-channel blockers - Calcium
PEA
Identify, correct underlying cause if
possible
Possibilities:
Hypovolemia: volume
Hypoxia: ventilate
Tension pneumo: decompress
Tamponade: pericardiocentesis
Acute MI: vasopressor
Hyperkalemia: Bicarbonate 1mEq/kg
Preexisting metabolic acidosis: Bicarbonate
1mEq/kg
Hypothermia: rewarm core
PEA Treatm ent
ABCDs
ETT/IV/ECG monitor
Differential Diagnosis
Find the cause and treat if possible
Epinephrine 1:10,000 1 mg q 3-5 min.
If bradycardic,
Atropine 1 mg IV q 3-5 min, Max 0.04 mg/kg
TCP

In many systems, consider termination

of efforts
M A N A G IN G C A R D IA C
A R R ES T
Check pulse after any treatment or
rhythm change
Post-resuscitation Care

If pulse present:
Assess breathing
Present?
Air moving adequately?
Equal breath sounds?
Possible flail chest?
Post-resuscitation Care

If pulse present:
Protect airway
Position to prevent aspiration
Consider intubation
100% Oxygen via BVM or NRB
Vascular access
Post-resuscitation Care

Assess perfusion
Evaluate
Pulses
Skin color
Skin temperature
Capillary refill
BP
Key is perfusion, not pressure
Post-resuscitation Care

Management of Decreased Perfusion

Fluid challenge
Catecholamine infusion
Dopamine, or
Norepinephrine
Titrate to BP ~ 90 to 100 systolic
Post-resuscitation Care

Suppression of ventricular irritability

If VT or VF converted before lidocaine
given, lidocaine bolus and drip
If lidocaine or bretylium worked, begin
infusion
Suppress irritability before giving
vasopressors
Sequence of operations
Check responsiveness
Call for help
Correctly place the victim and
ensure the open airway
Check the presence of spontaneous
respiration
Check pulse
Start external cardiac massage and
artificial ventilation
unconsciousness it is
necessary to estimate
quickly

the open
airway
respiration

hemodynamics
 A (Airway)
ensure open
airway
Open the airway using a
head tilt lifting of chin. Do
not tilt the head too far
back

Check the pulse on

carotid artery using
fingers of the other
hand
B (Breathing)

Tilt the head
back and listen
for. If not
breathing
normally, pinch
nose and cover
the mouth with
yours and blow
until you see
the chest rise.
Restore the circulation,
that is start external
cardiac massage
Cardiac pump during the
cardiac massage

Blood pumping is
assured by the
compression of heart
between sternum
and spine

Between
compressions
thoracic cage is
expanding and
heart is filled with
Thoracic pump at the cardiac massage
Blood circulation is
restored due to the
change in intra
thoracic pressure and
jugular and subclavian
vein valves
During the chest
compression blood is
directed from the
pulmonary circulation
to the systemic
circulation. Cardiac
valves function as in
normal cardiac cycle.
 Drugs used in CPR
Atropine can be injected bolus, max 3 mg to
block vagal tone, which plays significant role in
some cases of cardiac arrest
Adrenaline large doses have been
withdrawn from the algorithm. The
recommended dose is 1 mg in each 3-5 min.
Vasopresine in some cases 40 U can
replace adrenaline
Amiodarone - should be included in algorithm
Lidocaine should be used only in ventricular
fibrillation