By: Varla Septrinidya Gharatri

(405090215)

Occurs as a result of a multitude of

cardiovascular, metabolic, infectious,
neurologic, inflammatory, & traumatic
diseases.
Several specific causes: drug toxicity,
myocardial ischemia, hyperkalemia, torsades
de pointes, cardiac tamponade,& tension
pneumothorax.

Activate EMS or the designated code team.

Perform basic life support (CPR).
Evaluate heart rhythm and perform early
defibrillation as indicated.
Deliver advanced life support (e.g.,
intubation, intravenous access, transfer to a
medical center/ intensive care unit).

Conduct a primary ABCD survey

Place

airway device as soon as possible.

Confirm placement, secure device, and confirm
oxygenation and ventilation.
Establish IV access, identify rhythm, and
administer drugs appropriate for rhythm and
condition.
Search for and treat identified reversible causes,
with focus on basic CPR and early defibrillation.

On arrival to an unwitnessed cardiac arrest

or downtime longer than 4 minutes, five
cycles (approximately 2 minutes) of CPR are
to be initiated before evaluation of rhythm.
If

the cardiac arrest is witnessed or downtime is

shorter than 4 minutes, one shock may be
administered immediately if the patient is in
ventricular fibrillation or pulseless ventricular
tachycardia.

If the patient is in ventricular fibrillation or

pulseless ventricular tachycardia, shock the
patient once using 200 J on biphasic (or
equivalent monophasic, 360 J).
Resume CPR immediately after attempted
defibrillation, beginning with chest
compressions.
Rescuers

should not interrupt chest compression

to check circulation (e.g., evaluate rhythm or
pulse) until five cycles or 2 minutes of CPR have
been completed.

If there is persistent or recurrent ventricular

tachycardia or ventricular fibrillation despite
several shocks and cycles of CPR, perform a
secondary ABCD survey with a focus on more
advanced assessments and pharmacologic
therapy.
Pharmacologic

therapy should include

epinephrine (1-mg IV push, repeated every 3 to 5
minutes) or vasopressin (a single dose of 40 U IV,
one time only).

Consider using antiarrhythmics for persistent

or recurrent pulseless ventricular tachycardia
or ventricular fibrillation.
These

include amiodarone, lidocaine, magnesium

(if there is a known hypomagnesemic state), and
procainamide (class indeterminate for persistent
and Class IIb for recurrent).

Resume CPR and attempts to defibrillate.

Assess the patient and conduct a primary

ABCD survey.
Review for the most frequent causes of
pulseless electrical activity, the five Hs and
five Ts:
Hypovolemia,

hypoxia, hydrogen ion (acidosis),

hyperkalemia (or hypokalemia), and hypothermia
and tablets (drug overdose, accidents)
Tamponade (cardiac), tension pneumothorax,
thrombosis (coronary), and thrombosis
(pulmonary embolism).

Administer epinephrine (1-mg IV push

repeated every 3 to 5 minutes) or atropine (1
mg IV if the heart rate is slow, repeated
every 3 to 5 minutes as needed, to a total
dose of 0.04 mg/kg).
Conduct a secondary ABCD survey.

Determine whether the bradycardia is slow

(heart rate less than 60 beats/min) or
relatively slow (heart rate less than expected
relative to underlying condition or cause).
Conduct a primary ABCD survey.
Check for serious signs or symptoms caused
by the bradycardia.
If no serious signs or symptoms are present,
evaluate for a type II second-degree
atrioventricular block or third-degree
atrioventricular block.

If neither of these types of heart block is

present, observe.
If one of these types of heart block is present,
prepare for transvenous pacing.
If

symptoms develop, use a transcutaneous

pacemaker until the transvenous pacer is placed.

If serious signs or symptoms are present, begin

the following intervention sequence:
Atropine,

0.5 up to a total of 3 mg IV
Transcutaneous pacing, if available
Dopamine, 5 to 20 mcg/kg/min
Epinephrine, 2 to 10 mcg/min
Isoproterenol, 2 to 10 mcg/min

Conduct a secondary ABCD survey.

Conduct a primary ABCD survey.

Perform transcutaneous pacing immediately
if needed.
Consider

transvenous pacing if transcutaneous

pacing fails to capture.

Administer epinephrine (1-mg IV push,

repeated every 3 to 5 minutes) or atropine (1
mg IV repeated every 3 to 5 minutes, up to a
total of 3 mg).

Conduct a secondary ABCD survey.

If asystole persists, consider withholding or
ceasing resuscitative efforts.

A diagnostic tool that is

routinely used to assess
the electrical and
muscular functions of the
heart.
The electrocardiogram
can measure the rate and
rhythm of the heartbeat.

Raterefers to how fast the heart beats.

Normally, the

SA node generates an electrical

impulse 60-100 times per minute.
Bradycardia describes a heart rate less than 60
beats per minute.
Tachycardia describes a heart rate faster than
100 beats per minute.

Rhythmrefers to the type of heartbeat.

The P wave looks at the atria.

The QRS complex looks at the ventricles
The T wave evaluates the recovery stage of
the ventricles while they are refilling with
blood.
The time it takes for electricity to travel
from the SA node to the AV node is measured
by the PR interval.

The QRS interval measures electrical travel

time through the ventricles
The QT interval measures how long it takes
for the ventricles to recover and prepare to
beat again.

normal sinus rhythm

each

P wave is followed by a QRS

P waves normal for the subject
P wave rate 60 - 100 bpm with <10% variation

rate <60 =sinus bradycardia

rate >100 =sinus tachycardia
variation >10% = sinus arrhythmia

normalQRS axis

normal P waves
height

< 2.5 mm in lead II

width < 0.11 s in lead II

for abnormal P waves seeright atrial hypertrophy,

left atrial hypertrophy,atrial premature beat,
hyperkalaemia

normal PR interval
0.12

to 0.20 s (3 - 5 small squares)

for short PR segment consider

Wolff-Parkinson-White syndromeor
Lown-Ganong-Levine syndrome(other causes Duchenne muscular dystrophy, type II glycogen
storage disease (Pompe's), HOCM)
for long PR interval seefirst degree heart blockand
'trifasicular' block

normal QRS complex

<

0.12 s duration (3 small squares)

for abnormally wide QRS considerrightorleftbundle

branch block, ventricular rhythm,hyperkalaemia, etc.

nopathological Q waves
no evidence ofleftorrightventricular

hypertrophy

normal QT interval
Calculate

the corrected QT interval (QTc) by

dividing the QT interval by the square root of the
preceeding R - R interval. Normal = 0.42 s.
Causes oflong QT interval

myocardial infarction, myocarditis, diffuse myocardial

disease
hypocalcaemia, hypothyrodism
subarachnoid haemorrhage, intracerebral haemorrhage
drugs (e.g. sotalol, amiodarone)
hereditary
Romano Ward syndrome(autosomal dominant)
Jervill + Lange Nielson syndrome (autosomal
recessive) associated with sensorineural deafness

normal ST segment
no

elevation or depression

causes of elevation include acute MI (e.g.anterior,

inferior),left bundle branch block, normal variants
(e.g. athletic heart, Edeiken pattern, high-take off),
acute pericarditis
causes of depression include myocardial ischaemia,
digoxin effect,ventricular hypertrophy,
acute posterior MI,pulmonary embolus,
left bundle branch block

normal T wave

causes of tall T waves includehyperkalaemia,

hyperacute myocardial infarctionand
left bundle branch block
causes of small, flattened or inverted T waves are
numerous and include ischaemia, age, race,
hyperventilation, anxiety, drinking iced water,LVH,
drugs (e.g.digoxin), pericarditis,PE, intraventricular
conduction delay (e.g.RBBB)and electrolyte
disturbance.

normal U wave

Refers to a spectrum of clinical presentations

ranging from those for ST-segment elevation
myocardial infarction (STEMI) to
presentations found in nonST-segment
elevation myocardial infarction (NSTEMI) or
in unstable angina.
In terms of pathology, ACS is almost always
associated with rupture of an atherosclerotic
plaque and partial or complete thrombosis of
the infarct-related artery.

Acute coronary syndrome (ACS) is caused

primarily by atherosclerosis.
The vulnerable plaque is typified by a large lipid
pool, numerous inflammatory cells, and a thin,
fibrous cap.
Elevated demand can produce ACS in the
presence of a high-grade fixed coronary
obstruction, due to increased myocardial oxygen
and nutrition requirements, such as those
resulting from exertion, emotional stress, or
physiologic stress (eg, from dehydration, blood
loss, hypotension, infection, thyrotoxicosis, or
surgery).

CLASS 1

NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2

SLIGHT LIMITATION OF PHYSICAL ACTIVITY PAIN

OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS

CLASS 3

SEVERE LIMITATION OF DAILY ACTIVITY PAIN

OCCURS ON MINIMAL EXERTION

CLASS 4

UNABLE TO CONDUCT ANY ACTIVITY WITHOUT

PAIN, PAIN AT REST

Pain occurring at rest duration > 20min, within one week

of first visit
New onset angina ~ Class 2 severity, onset with last 2
months
Worsening of chest pain increase by at least 1 class,
increases in frequency, duration
Angina becoming resistance to drugs that previously gave
good control.
NB! ECG normal, ST depression(>0.5mm), T wave changes

ECC/ACC DEFN rise and fall in cardiac enzymes with one

or more of the following:

Ischaemic type chest pain/symptoms

ECG changes ST changes, pathological Q waves
Coronary artery intervention data
Pathological findings of an acute MI

NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES
STEMI = ST ELEVATION ON ECG + SYMPTOMS

Distruption of coronary artery

plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
Severity of coronary vessel
obstruction & extent of
myocardium involved
determines characteristics of
clinical presentation

Identifying those with chest pain suggestive of IHD/ACS.

Thorough history required:
Character of pain
Onset and duration
Location and radiation
Aggravating and relieving factors
Autonomic symptoms
TYPICAL VS ATYPICAL HISTORY
Failure to recognise symptoms other than chest pain ->
approx 2 hr delay in seeking medical attention

CHARACTERISTIC

SUGGESTIVE OF ANGINA

LESS SUGGESTIVE OF
ANGINA

TYPE OF PAIN

DULL
PRESSURE/CRUSHING
PAIN

SHARP/STABBING

DURATION

2-5 MIN, <20 MIN

SECONDSTO
HOURS/CONTINUOUS

ONSET

GRADUAL

RAPID

LOCATION/CHEST WALL
TENDERNESS

SUBSTERNAL, NOT
TENDER TO PALP.

LATERAL CHEST
WALL/TENDER TO PALP.

REPRODUCIBALITY

WITH EXERTION/ACTIVITY WITH

BREATHING/MOVING

AUTONOMIC SYMPTOMS

PRESENT USUALLY

ABSENT

RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:

ATYPICAL SYMPTOMS:

Diabetes, females, non white patients, elderly, dementia, no prior history

of MI
GIT symptoms
Syncope
SOB
Pleuritic/positional pain
Chest wall tenderness
No chest pain/symptoms

NRMI 2 STUDY MI without chest pain -> increased risk of death

(23% vs 9%)
More complications hypotension,heart failure, stroke
Delayed ED presentation, delayed intervention

Palpitations
Pain, which is usually described as pressure,
squeezing, or a burning sensation across the
precordium and may radiate to the neck,
shoulder, jaw, back, upper abdomen, or
either arm
Exertional dyspnea that resolves with pain or
rest
Diaphoresis from sympathetic discharge
Nausea from vagal stimulation
Decreased exercise tolerance

Hypotension - Indicates ventricular dysfunction

due to myocardial ischemia, infarction, or acute
valvular dysfunction
Hypertension - May precipitate angina or reflect
elevated catecholamine levels due to anxiety or
to exogenous sympathomimetic stimulation
Diaphoresis
Pulmonary edema and other signs of left heart
failure
Extracardiac vascular disease
Jugular venous distention
Cool, clammy skin and diaphoresis in patients
with cardiogenic shock

The diagnosis of acute myocardial infarction

can be made if workup reveals the typical
rise and fall of biochemical markers of
myocardial necrosis along with either the
development of pathologic Q waves or the
presence (on ECG or in the setting of a
coronary intervention) of ischemic STsegment changes

Changes that may be seen during anginal

episodes include the following:
Transient

ST-segment elevations
Dynamic T-wave changes - Inversions,
normalizations, or hyperacute changes
ST depressions - May be junctional, downsloping,
or horizontal

IDEAL MARKER:

High concentration in myocardium

Myocardium specific
Released early in injury
Proportionate to injury
Non expensive testing

Troponins
CKMB
Myoglobin
Other markers

Chest radiography helps in assessing

cardiomegaly and pulmonary edema, or it may
reveal complications of ischemia, such as
pulmonary edema.
Echocardiograms may play an important role
in the setting of ACS.
Radionuclide myocardial perfusion imaging
has been shown to have favorable diagnostic
and prognostic value in the emergent setting,
with an excellent early sensitivity in the
detection of acute myocardial infarction not
found in other testing modalities.

Cardiac catheterization helps in defining

coronary anatomy and the extent of a
patients disease.
Computed Tomography Coronary
Angiography and CT Coronary Artery
Calcium Scoring
This

technology allows for noninvasive and early

diagnosis of CAD and thus earlier treatment
before the coronary arteries become more or
completely occluded.

Anxiety
Aortic Stenosis
Asthma
Cardiomyopathy, Dilated
Esophagitis
Gastroenteritis
Hypertensive Emergencies in Emergency
Medicine
Myocardial Infarction
Myocarditis
Pericarditis and Cardiac Tamponade

Initial therapy for acute coronary syndrome

should focus on stabilizing the patient's
condition, relieving ischemic pain, and
providing antithrombotic therapy to reduce
myocardial damage and prevent further
ischemia.
Pharmacologic Anti-ischemic Therapy
Nitrates,

Beta-blockers.

Pharmacologic Antithrombotic Therapy

Aspirin,

Clopidogrel, Prasugrel, Ticagrelor,

Abciximab, Epitifibatide, Tirofiban,

Pharmacologic Anticoagulation Therapy

Unfractionated

heparin, Low molecular weight

heparin, Factor Xa inhibitors.

Thrombolysis
Coronary Interventions
Concomitant therapy

Educate patients about the dangers of

cigarette smoking, a major risk factor for
coronary artery disease (CAD).
Patients should be informed about the
benefits of a low-cholesterol, low-salt diet.
In addition, educate patients about AHA
dietary guidelines regarding a low-fat, lowcholesterol diet.

The following memonic may useful in

educating patients with CAD regarding
treatments and lifestyle changes
necessitated by their condition:
A

= Aspirin and antianginals

B = Beta blockers and blood pressure (BP)
C = Cholesterol and cigarettes
D = Diet and diabetes
E = Exercise and education

Complications of ischemia include pulmonary

edema, while those of myocardial infarction
include rupture of the papillary muscle, left
ventricular free wall, and ventricular
septum.

Six-month mortality rates in the Global

Registry of Acute Coronary Events (GRACE)
were 13% for patients with NSTEMI ACS and
8% for those with unstable angina.
An elevated level of troponin (a type of
regulatory protein found in skeletal and
cardiac muscle) permits risk stratification of
patients with ACS and identifies patients at
high risk for adverse cardiac events (ie,
myocardial infarction, death) up to 6 months
after the index event.

Cardiac arrest is the abrupt loss of heart

function in a person who may or may not
have diagnosedheart disease.
It occurs instantly or shortly after symptoms
appear.

The frequency of sudden cardiac arrest is

related to the frequency of coronary artery
disease.
If public health initiatives work to decrease
risk the factors for heart disease, the risk for
sudden death should decrease as well.