CARDIAC ARREST

Causes & prevention of

Cardio respiratory arrest
Definition: A respiratory arrest is when
breathing stops (apnea). A cardiac arrest is
when the heart stops contracting & pumping
blood.
Causes:
1. Airway problems.
2. Breathing problems.
3. Cardiovascular problems.
3

Cardiovascular Emergencies
1. Unconscious
Cardiac Arrest
- Ventricular Fibrillation / Pulseless Ventricular
Tachycardia
- Asystole
- Pulseless Electrical Activity (PEA)

2. Conscious
Acute Coronary Syndrome (ACS)
- Unstable Angina Pectoris (UAP)
- Acute Non ST-Elevation Myocardial infarction
(NSTEMI)
- Acute ST-Elevation Myocardial infarction
(STEMI)

Cardiac Arrest
Cardiac arrest is characterized by
abrupt loss of heart function
Main sign of cardiac arrest :
loss of consiousness + pulseless
Can be resuscitated within few
minutes (4-5m) if CPR is initiated

Why cardiac arrest is

dangerous?
10-15 seconds : Loss of consciousness
30 seconds : ECG become flat, respiration
may arrested
60 seconds : Pupil dilates fully
4-6 minutes : Brain damage
8-10 minutes : Irreversible cerebral
cortical damage

ETIOLOGY
Acute coronary ischemia:
Primary dysrhythmia(Cardiomyophaty and
myocarditis)
Cardiac rupture
Pericardial tamponade
Metabolic abnormalities
Noncardiac etiologies(Tension pneumothorax,
sepsis, etc):
Drugs(Cocaine and Heroin,etc)

Pathophysiology of Cardiac
Arrest
3 basic mechanism :
1.Ventricular Fibrillation / Pulseless
Ventricular Tachycardia
2.Asystole
3.Pulseless Electrical Activity
* Asystole and PEA are not
shockable.

ECG waveform characteristics and their corresponding

positions in heart.

Ventricular Fibrillation
Occur in 30% of in-hospital cardiac arrest
More common in ischemic and infarction heart
disease
More likely to respond to treatment

ECG : bizarre irregular waveform, random in both

frequency and amplitude
Shows disorganized electrical activity in
myocardium
The only effective treatment is early defibrillation

 Clinical Manifestations:

Pulse disappears with onset of VF

Collapse, unconsciousness
Agonal breaths apnea in <5 min
Onset of reversible death

Etiologies:
Acute coronary syndromes leading to ischemic
areas of myocardium
Stable-to-unstable VT, untreated
PVCs with R-on-T phenomenon
Multiple drug, electrolyte, or acid-base
abnormalities

Coarse VF

Fine VF

 Treatment:
Early defibrillation is essential
Agents given to prolong period of reversible
death (oxygen, CPR, intubation,
epinephrine,vasopressin)
Agents given to prevent refibrillation after a
shock causes defibrillation (lidocaine,
amiodarone, procainamide, -blockers)
Agents given to adjust metabolic milieu
(sodium bicarbonate, magnesium)

ALGORITH
M
FOR
VF / VT

14

Harrisons Principle of Internal Medicine 18th E

Pulseless Electrical Activity

(PEA)
Cardiac conduction impulses occur in organized
pattern, but this fails to produce myocardial
contraction (former electromechanical
dissociation); or insufficient ventricular filling
during diastole; or ineffective contractions
Occur 5% of in-hospital cardiac arrest

ECG: Rhythm displays organized electrical activity

(not VF/pulseless VT)
Seldom as organized as normal sinus rhythm
Poor prognosis

 Clinical Manifestations:
Collapse; unconscious
Agonal respirations or apnea
No pulse detectable by arterial palpation

Etiologies
Hypovolemia
Tablets (drug OD, ingestions)
Tamponade, cardiac

 Treatment:
Per PEA algorithm
Primary ABCD (basic CPR)
Secondary
AB (advanced airway and ventilation);
C (IV, epinephrine, atropine if electrical
activity <60 complexes per minute);
D (identify and treat reversible causes)

ASYSTOLE
Occur in 25% of in-hospital cardiac arrest
Occur 10% of out-side hospital cardiac arrest
Characterized by ventricular standstill due
to suppression of the cardiac peacemaker by
myocardial disease, anoxia, electrolyte
imbalance,or drugs

ECG shows flat traces

Often represent massive heart damage
Survival less than 4%

 Clinical Manifestations:
Early may see agonal respirations; unconscious;
unresponsive
No pulse; no blood pressure
Cardiac arrest

Etiologies:
End of life (death)
Ischemia/hypoxia from many causes
Acute respiratory failure (no oxygen; apnea;
asphyxiation)
Massive electrical shock: electrocution; lightning strike
Postdefibrillatory shocks

 Treatment:
Always check for status
Primary ABCD survey (basic CPR)
Secondary ABCD survey

ALGORYTH
M
FOR
BRADYCAR
DIA OR
ASYSTOLE

21

Harrisons Principle of Internal Medicine 18th E

ACUTE CORONARY
SYNDROME

Initial Assessment

Acute myocardial
infarction(STEMI)
MI when arterial blood flow to the
myocardium is suddenly decreased /
interrupted.
Its usually due to atherosclerotic occlusion
by thrombus / emboli.
Complete occlusion (ST segment
elevation) 80-90% because of the
thrombus

Patophysiology

Unstable plaque
Plaque rupture
Unstable angina
Microemboli
Occlusive thrombus

Clinical finding
Chest discomfort typically
substernal radiate to the neck /
left arm
Pain classically oppresive or
squeezing
May associated with SOB(shortness of
breathing),dizziness,
syncope/presyncope, , nausea,
vomitting, dyspnea, and diaphoresis

ECG

Hyperacute T waves
Flipped T waves
Elevated ST segment
Abnormal Q waves
Normal ECG does not rule out the
possibility
of MI / ACS.

Laboratory findings
CK-MB less sensitive than Troponin
Troponin cTnt & cTni the most
cardiac specific biochemical marker.
Mioglobin marker for injured
cardiac sensitive early marker

Differential Diagnosis

Aortic dissection
Aneurysm
Pericarditis
GI bleeding

Killip Classification

Unstable Angina Pectoris

(UAP)& NSTEMI
UA is defined as angina pectoris or
equivalent ischemic discomfort with at
least one of three features
it occurs at rest usually lasting >10
minutes
it is severe and of new onset (i.e.,
within the prior 46 weeks); or
it occurs with a crescendo pattern

 NSTEMI is a result of an acute

imbalance between myocardial
oxygen demand and supply, most
commonly due to a reduction in
myocardial perfusion.
Most often it is caused by a nonocclusive thrombus that develops
in a disrupted atherosclerotic
plaque.

 UA and nSTEMI the thrombus

partially occludes blood flow
down a coronary artery, starving the
heart muscle of oxygen and
nutrients.
This can result in symptoms with or
without ECG changes and cardiac
enzyme release.

History and Physical

Examination
The clinical hallmark of UA/NSTEMI is
chest pain
typically located in the substernal region
or sometimes in the epigastrium, that
radiates to the neck, left shoulder, and/or
the left arm
Anginal "equivalents" such as dyspnea
and epigastric discomfort may also occur,
and these appear to be more frequent in
women

History and Physical

Examination
The physical examination
Diaphoresis
Pale
Cool skin
Sinus tachycardia
Hypotension

Cardiac Biomarkers
Patients with NSTEMI who have
elevated biomarkers of necrosis, such
as CK-MB and troponin, are at
increased risk for death or recurrent
MI
Patients with UA who havent
elevated biomarkers of
necrosiscardiac biomarkers not
increased

Drugs Commonly Used in Intensive Medical Management

of Patients with Unstable Angina and Non-ST Segment
Elevation MI
Drug
Category

Clinical Condition

Dosage

Nitrates

Administer sublingually, and, if

symptoms persist,
intravenously

Topical, oral, or buccal

510 mikrogram/min

Beta
blockers

Unstable angina

Metoprolol 2550 mg
by mouth every 6 h

Calcium
channel
blockers

Patients whose symptoms

are not relieved by
adequate doses of nitrates
and beta blockers, or in
patients unable to tolerate
adequate doses of one or both
of these agents, or in patients
with variant angina

Dependent on specific
agent

Morphine
sulfate

Patients whose symptoms

are not relieved after three

25 mg IV dose May
be repeated every 5

Acute Coronary Syndrome

Acute Coronary Syndrome

CARDIOGENIC SHOCK

Description
Inadequate tissue perfusion due to
cardiac dysfunction
Underlying mechanisms in acute
myocardial infarction (AMI):
Pump failure:
left ventricle (LV) infarct
Infarct in pre-existing LV dysfunction
Reinfarction

Description
Mechanical complications:

Acute mitral regurgitation

Ventricular septal defect
LV rupture
Pericardial tamponade

Right ventricular (RV) infarction

Etiology

AMI
Sepsis
Myocarditis
Cardiomyopathy
Drug toxicity:
Beta-blocker
Calcium channel blocker
Adriamycin

etc

Signs and Symptoms

General:
Cyanosis
Pallor
Diaphoresis
Dulled sensorium
Decrease in body temperature
Urine flow of less than 20 mL/h

Signs and Symptoms

Cardiac:
Ischemic chest pain
Systolic apical blowing murmur
Gallop rhythm:
S3 reflects severe myocardial dysfunction
S4 is present in 80% patients in sinus
rhythm with AMI

Systolic click:
Suggests rupture of the chordae tendinae

Signs and Symptoms

Neck:
Jugular venous distention

Abdominal:
Epigastric pain
Nausea and vomiting

Neurologic:
Obtundation

Test
Electrocardiogram
Normal ECG does not rule out AMI.
Findings of AMI (ST-elevations in two
or more contiguous leads)
May occur in non-ST-elevation acute
coronary syndrome
Dysrhythmias
LV hypertrophy

Test
Chest Radiography
Pulmonary congestion
Pleural effusion
Cardiomegaly
Pneumonia
Pneumothorax
Pericardial effusion

Test
Emergent Echocardiography
Transthoracic echocardiography (TTE) with color
Doppler
LV contractility looking for hypokinesis, akinesis
or dyskinesis
Acute mitral regurgitation or septal defects
RV dilatation, tricuspid insufficiency, high
pulmonary artery and RV pressures suggest
pulmonary embolism
RV hypokinesis or akinesis, RV dilatation, normal
pulmonary pressures suggest RV infarction
Pericardial effusion, right atrium or RV diastolic
collapse suggest cardiac tamponade

Lab
B-type natriuretic peptide (BNP):
Diagnostic and prognostic value

Creatine kinase (CK), CK-Mb, troponin

Electrolytes and renal function
Acute renal failure is a strong predictor
of mortality

CBC:
Identify anemia or elevated WBC

Drug levels (e.g., digoxin)

Differential Diagnosis
Obstructive shock
Distributive shock
Hypovolemic shock

Treatment
Pre Hospital
ABCs, IV access, O2, monitor
Consider fluid bolus if no crackles.
Aspirin
Nitroglycerin or morphine sulfate for
chest pain in absence of hypotension
Transport AMI patients to facility with 24hour cardiac revascularization capability.

Treatment
Initial Stabilization
ABCs
Two large bore peripheral IV lines
Cardiac monitor
Endotracheal intubation for airway
compromise:
Consider etomidate for induction (minimal
effect on blood pressure)

Fluid challenge (100250 mL normal

saline) in absence of pulmonary congestion
Foley catheter to monitor urine output

Treatment
Medication (Drugs)
Dobutamine
Dopamine
Furosemide
Milrinone
Nitroglycerin
Nitroprusside
Norepinephrine

CPR

Definition
CPR is an organized, sequential response
to cardiac arrest, including
Recognition of absent breathing and circulation
Basic life support with chest compression and
rescue breathing
Advanced cardiac life support (ACLS) with
definitive airway and rhythm control
Postresuscitative care

Prompt initiation of chest

compression and early defibrillation
(when indicates) are the key of
success.

When to start CPR

Anyone who initiate resuscitation knowledge and
skills to initiate CPR when dealing with cases of
cardiac arrest.
A.Incidence of cardiac arrest who witnessed
If we are witnessing the cardiac arrest, was
should
immediately started CPR. However, there
are
circumstances like this some
underlying
unnecessary
CPR started:
There is evidence of demand for family
CPR efforts will harm people who helped
Possible CPR can restore spontaneous circulation is
very small
Cardiac arrest happened on terminal illness who have
been treated to the maximum

B. Incidence of cardiac arrest was not witnessed

Helper ill cardiac know how long it's been
going on. For something like this we do not
need to start doing CPR if the state finds as
follows:
There is a sign that death does not change like
rigor mortis / bruised corpse
It's getting no signs of decay
Patients experiencing trauma that can not be
saved, such as charred, decapitation

When to stop CPR

There are several compelling reasons for rescuers to
stop CPR among other things:
Helpers are doing basic and advanced life support
optimal included:
CPR, defibrillation in patients with VF / VT without a
pulse, vasopressin / epinephrine IV, open the airway,
ventilation and oxygenation using airway aid and all
levels lanut rhythm after treatment performed.

Helpers are considering whether there is a

hypothermia patient. Helpers has established the
presence / absence of hypothermia by measuring
body temperature.

 Helpers have considered whether patients

exposed to toxic materials or an overdose
that inhibits CNS.
Helper was recorded through a monitor
systolic settled for 10 minutes or more.
The time interval pd cardiac resuscitation
efforts
were
unsuccessful
witnessed
restore spontaneous circulation was 25-30
minutes.

General Technique of CPR

continued
If alone, alternate 30 chest compressions
and 2 ventilations for any age patient
In two-rescuer CPR for infant/child,
alternate 15 compressions and 2
ventilations
Chest-encircling method in infant
Give each ventilation over 1 second
Follow local protocol regarding oxygen

Put hand(s) in correct position for

chest compressions

Give 30 chest compressions at rate

of 100 per minute
Then give 2 ventilations