C A R D IO G EN IC S H O C K

(LK 3B )

M eaning
Cardiogenic shock is
characterized by a decreased
pumping ability of the heart
that causes a shock like state
(i.e., global hypo perfusion)

Incidence
Cardiogenic shock occurs in

8.6% of patients with STEMI

MI with 29% of those
presenting to the hospital
already in shock.
It occurs only in 2% of
NSTEMI

M ortality/M orbidity
Leading cause of death in AMI
The overall in-hospital mortality rate

is 57%.
Persons older than 75 years, the
mortality rate is 64.1%.
Younger than 75 years, the
mortality rate is 39.5%.
Overall mortality when
revascularization occurs is 38%. If
not attempted, mortality rates
approach 70%.

R isk factors

Pre existing myocardial

damage
Diseases like diabetes
Advanced age
Previous AMI
AMI (Q-wave, large or anterior
wall AMIs) dysrhythmia

Etiology
Acute myocardial ischemia
Others: Beta-blocker
overdose, calcium channel
blocker overdose, myocardial
contusion, respiratory
acidosis, hypocalcaemia,
hypophosphatemia, and
cardio toxic drugs (e.g.,
doxorubicin [Adriamycin])

Ventricular hypertrophy and

restrictive Cardiomyopathy
After load - Aortic stenosis,
hypertrophic Cardiomyopathy,
dynamic outflow obstruction,
aortic coarctation, and
malignant hypertension
Valvular/structural - Mitral
stenosis, endocarditis, mitral or
aortic regurgitation, atrial
myxoma or thrombus, and
tamponade

Pathophysiology
AMI

Dead myocardium does not

contract

Marked decrease in
contractility reduces the
ejection fraction and
cardiac output

Increased ventricular filling

pressures, cardiac chamber
dilatation

Univentricular or biventricular
failure

Systemic hypotension and/or

pulmonary edema

Myocardial ischemia

Decrease in contractile function

Left ventricular dysfunction and

decreased arterial pressure

Exacerbate the myocardial ischemia

Severe cardiovascular decompensation.

Other pathophysiological
mechanisms
papillary muscle rupture

leading to acute mitral

regurgitation (4.4%)
ventricular septal defect
(1.5%)
wall rupture (4.1%) as a
consequence of AMI

 Right ventricular (RV) infarct,

may lead to hypotension and

shock because of reduced
preload to the left ventricle.
Cardiac tamponade may result

as a consequence of
Pericarditis, uremic pericardial
effusion, or in rare cases
systemic lupus erythematosus.

M edications

Calcium channel blockers may cause

profound hypotension with a normal or
elevated heart rate.
Beta-blocking agents may also cause
hypotension with or without bradycardia,
or AV node block.
Nitroglycerin, Angiotensinconverting enzyme inhibitors,
opiate, and barbiturates can all cause
a shock state and may be difficult to
distinguish from cardiogenic shock.

C linical m anifestations
The physical examination

findings are consistent with

shock.
Patients are in frank distress
Profoundly diaphoretic
Visibly dyspneic

 A- Airway usually is patent initially

B- Breathing may be labored, with

audible coarse crackles or wheezing

C-Circulation is markedly impaired.

Tachycardia, delayed capillary refill,

hypotension, diaphoresis, and poor
peripheral pulses are frequent
findings
Signs of end-organ dysfunction (eg,
decreased mental function, urinary
output) may be present

D iagnostic m easures
History collection
General physical examination
Initial vital sign assessment
Neck examination may reveal

jugular venous distention

LV dysfunction, characterized by
pulmonary edema, can be
auscultated as crackles with or
without wheezing.

Lab Studies
No one test is completely

sensitive, laboratory studies are

directed at the potential
underlying cause.
Following are assessed in cases of
suspected cardiac ischemia:
Cardiac enzymes (eg, creatine kinase,

troponin, myoglobin)
CBC
Electrolytes
Coagulation profile (eg, prothrombin
time, activated partial thromboplastin
time)

 An ABG may be useful to evaluate

acid-base balance because acidosis

Elevated serum lactate level is an

indicator of shock.
Brain natriuretic peptide (BNP)

may be useful as an indicator of

congestive heart failure and as an
independent prognostic indicator
of survival.

Im aging Studies
Portable chest radiograph
Overall impression of the
cardiac size
Pulmonary vascularity
Coexistent pulmonary
pathology
A rough estimate of
Mediastinal and aortic

O ther Tests
ECG

Helpful if it reveals an acute

injury pattern consistent with an
AMI
Echocardiogram
*To reveal akinetic or
dyskinetic areas of ventricular wall
motion.

*To reveal surgically

correctable causes, such as
valvular dysfunction and

D if e
frential D iagnosis

Acute coronary syndrome

Aortic Regurgitation
Cardiomyopathy
Congestive cardiac failure
Mitral regurgitation
Hypovolemic or septic shock

M A N A G EM EN T

Prehospital Care:
Aim: minimize any further ischemia and
shock.
All patients require intravenous access,
high-flow oxygen administered by mask,
and cardiac monitoring.
Twelve-lead electrocardiography, The ED
physician, can thus be alerted, and may
mobilize the appropriate resources.

 Emergency Department Care:

Aim: making the diagnosis,

preventing further ischemia, and
treating the underlying cause.
coronary artery bypass is the
treatments of choice within 90 minutes
of presentation; however, it remains
helpful, as an acute intervention, within
12 hours of presentation.
If not immediately available,
thrombolytics should be considered
which is the second best.

Treatment begins with assessment and

management of the ABCs.
Airway should be assessed for patency.
Breathing evaluated for effectiveness
and increased work of breathing.
Endotracheal intubation and
mechanical ventilation is considered in
patients with excessive work of breathing.
Positive pressure ventilation may improve
oxygenation but may also compromise
venous return, preload, to the heart. In any
event, the patient should be treated with
high-flow oxygen.

supporting myocardial perfusion and

maximizing cardiac output.
Intravenous fluids should be provided
to maintain adequate preload, guided
by central venous pressure or
pulmonary capillary wedge pressure
monitoring .

P harm acotherapy
Aim: To reduce morbidity and to
prevent complications
Intravenous vasopressors provide
inotropic support increasing
perfusion of the ischemic
myocardium and all body tissues.
Extreme heart rates should be
avoided because they may increase
myocardial oxygen consumption

1. Dopamine

Provide vasopressor support.

With higher doses, it has the
disadvantage of increasing the
heart rate and myocardial
oxygen consumption
Dose:5-20 mcg/kg/min IV
continuous infusion

Increase by 1-4 mcg/kg/min q1030min to optimal response

(>50% of patients have

2.Dobutamine, inamrinone
(formerly amrinone), or
milrinone
Provide inotropic support. In
addition to their positive
inotropic effects, inamrinone
and milrinone have a beneficial
vasodilator effect, which
reduces preload and after load.
Dose: 5-20 mcg/kg/min IV
continuous infusion

3. Phosphodiestrase enzyme
inhibitors -improve cardiac output
in refractory hypotension and
shock. Milrinone and inamrinone
(formerly amrinone) may be used.
Loading dose: 50 mcg/kg IV over

10 min
Continuous infusion: 0.375-0.75

mcg/kg/min IV

4.Natrecor (nesiritide)
Should be used with caution in
the setting of cardiogenic shock
because it has been shown to
cause hypotension.

5.Vasodilators
Smooth-muscle relaxants and
vasodilators that can reduce
systemic vascular resistance,
allowing more forward flow and
improving cardiac output.

6. Analgesics
Pain control is essential to quality
patient care. It ensures patient
comfort and promotes pulmonary
toilet.
7. Natriuretic peptide
Nitrates and/or morphine
excessive use of either of these
agents can produce profound
hypotension. Neither of these
options has been shown to
improve outcomes in cardiogenic

8.Diuretics
cause diuresis to decrease plasma
volume and edema and thereby
decrease cardiac output BP.
The initial decrease in cardiac output
causes a compensatory increase in
peripheral vascular resistance. With
continuing diuretic therapy,
extracellular fluid and plasma volumes
almost return to pretreatment levels.

Furosemid: 40-80 mg/d IV/IM

Intra-aortic balloon pump

(IABP)
recommended for cardiogenic
shock not quickly reversed with
pharmacologic therapy.
It is also recommended as a
stabilizing measure combined
with thrombolytic therapy when
angiography and
revascularization are not
readily available.

 IABP reduces LV after load and

improves coronary artery blood

flow.
Although complications may occur

in up to 30% of patients, extensive

retrospective data support its use.

C om plications

Cardiopulmonary arrest
Dysrhythmia
Renal failure
Multisystem organ failure
Ventricular aneurysm
Thromboembolic sequelae
Stroke
Death

P rognosis
The prognosis is

universally poor.
The mortality rate is more
than 55% in patients
treated medically.
At best, the rate is 38% in
whom surgical reperfusion
is achieved.

Heart Failure
&
Cardiac Arrest

Rony Yuliwansyah

Cardioloy Sub Division

rnal Medicine University Of Andalas - Dr M. Djamil -

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

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
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

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
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

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
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 9598% 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

Reduce
fluid
volume

Vasodilators Inotropes

Decrease
preload
and
afterload

Augment
contractility

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

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
Thank You

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;117:1519.

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
Ischemic heart disease
(myocardial infarction,
stenocardia)
Arrhythmias of different
origin and character
Electrolytic disorders
Valvular disease
Cardiac tamponade
Pulmonary artery
thromboembolism
Ruptured aneurysm of
aorta

Extracardiac
airway obstruction
acute respiratory failure
shock
reflector cardiac arrest
embolisms of different
origin
drug overdose
electrocution
poisoning

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 tiltchin 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
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
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-antiarrhythmicepi-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
Hypoxia
Hydrogen ions
(Acidosis)
Hyper/hypokalemia
Hypothermia

Tablets (Drug OD)

Tamponade
Tension
Pneumothorax
Thrombosis,
Coronary
Thrombosis,
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