Heart Failure

&
Cardiac Arrest

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):S7–S12.

 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):S7–S12.

 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):S7–S12.

 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
SUDDEN CARDIAC DEATH
 Definition
 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 Entity
•Chronic 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 Polymorphic VT
Exercise induced in patient with no structural heart
disease
Bundle Branch Reentrant VT
 Ventricular Flutter
Spontaneous conversion to NSR (12-lead ECG)
VF with Defibrillation (12-lead ECG)
Wide QRS Irregular Tachycardia:
Atrial Fibrillation with antidromic conduction in
patient with accessory pathway – Not VT
 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;117:151–9.

 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  airway obstruction
(myocardial infarction,
stenocardia)  acute respiratory failure
 Arrhythmias of different  shock
origin and character
 reflector cardiac arrest
 Electrolytic disorders
 Valvular disease  embolisms of different origin
 Cardiac tamponade  drug overdose
 Pulmonary artery  electrocution
thromboembolism
 Ruptured aneurysm of aorta  poisoning
Diagnosis of cardiac arrest
Blood pressure measurement

Taking the pulse on peripheral
arteries

Auscultation of cardiac tones
Loss of time !!!

Symptoms 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 Primary 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? Reversible cause?
 search for reversible cause
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) Treatment
 ABC’s
 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
Treatment
 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
Treatment
 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
Treatment
 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 Differentials
(The 5Hs & 5Ts)
 Hypovolemia  Tablets (Drug OD)
 Hypoxia  Tamponade
 Hydrogen ions  Tension Pneumothorax
(Acidosis)  Thrombosis, Coronary
 Hyper/hypo-kalemia  Thrombosis,
 Hypothermia Pulmonary
Asystole Treatment
 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 Treatment
 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

MANAGING CARDIAC ARREST

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
In case of 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.
 C. Circulation
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 blood
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