Heart Emergency According to

Conscious State
Conscious -> acute coronary
syndrom
Unconscious -> cardiac arrest

Cardiac Arrest
Abrupt cessation of cardiac pump function
which may be reversible by a prompt
intervention but will lead to death in its
absence
Rare spontaneous reversions
Likelihood of successful interventions
relates to mechanism of arrest, clinical
setting, and prompt return of circulation

Epidemiology of Cardiac
Arrest
Between 77,000 and 174,000
patients -> treated for out-of-hospital
cardiac arrest each year in the US
The incidence of VF as the initial
rhythm has declined over time -> 2038% (now)
ROSC -> 9 to 65% -> only 1 to 31% of
patients survive to hospital discharge

Epidemiology of Cardiac
Arrest
Approximately 50% of cardiac arrest
survivors -> comatose and treated
with hypothermia

Common causes of Nontraumatic Cardiac Arrest

General

Specific

Cardiac

Respiratory

Disease/Agent
CAD
Cardiomiopathies
Structural abnormalities
Valve dysfunction

Hypoventilation

CNS dysfunction
Neuromuscular disease
Toxic and metabolic
encephalopathies

Upper airway obstruction

CNS dysfunction
Foreign body
Infection
Trauma
Neoplasm

Pulmonary dysfunction

Asthma,COPD
Pulmonary edema
Pulmonary embolus
Pneumonia

Common causes of Nontraumatic Cardiac Arrest

General

Specific

Disease/Agent

Circulatory

Mechanical obstruction

Tension pneumothorax
Pericardial tamponade
Pulmonary embolus

Hypovolemia

Hemorrhage

Vascular tone

Sepsis
Neurogenic

Metabolic

Electrolyte abnormalities

Hypokalemia or
Hyperkalemia
Hypermagnesemia
Hypomagnesemia
Hypocalcemia

Toxic

Prescription medications

Antidysrhythmics
Digitalis beta-blockers
CCB
Tricyclic antidepressants

Drug of abuse

Cocaine
Heroine

Toxins

CO, Cyanide

Common causes of Nontraumatic Cardiac Arrest

General
Enviroment
al

Specific

Disease/Agent
Lightning
Electrocution
Hypothermia or
hyperthermia
Drowning/near-drowning

Etiology of Cardiac Arrest

Primary respiratory failure -> initial HT and
tachycardia -> followed by hypotension
and bradycardia -> PEA, VF, or asystole
Circulatory obstruction and hypovolemia
-> initial tachycardia and hypotension ->
bradycardia to PEA -> may deteriorate to
VF or Asystole
The Most common metabolic cause :
hyperkalemia

Manifestation of Cardiac
Arrest
Unresponsiveness
Pulselessness
Shallow, gasping respirations may persist
for a few minutes
Occasionally preceded by:
Chest pain
Dyspnea

Manifestation of Cardiac
Arrest
Palpitations
Seizure activity
Immediately prior to arrest:
Shock or hypotension
Impaired mentation

Manifestation of Cardiac
Arrest
Cardiopulmonary arrest -> triad :
1.Unconsciousness
2.Apnea
3.Pulselessness (carotid or femoral artery)

Clinical Characteristics of
Cardiac Arrest
The onset of the clinical transition -> an
acute change in cardiovascular status
preceding cardiac arrest by up to 1 h
ECG -> VF begin with a run of nonsustained or
sustained VT
Progression to biologic death -> depend
on the mechanism of cardiac arrest, the length
of the delay before interventions

Classification of Cardiac
Arrest
Primary cardiac arrest -> occur in
the absence of hemodynamic
instability
Secondary cardiac arrest -> occur
in patients in whom abnormal
hemodynamics dominate the clinical
picture before cardiac arrest

History of Cardiac Arrest

Information surrounding the events
1.Whether the arrest was witnessed
2.The time of arrest
3.What the pasien was doing (e.g., eating,
exercising, trauma)
4.The possibility of drug ingestion, time of
initial CPR
5.Initial ECG rhythm

History of Cardiac Arrest

6. Interventions by EMS providers
Past medical history
1. baseline health and mental status
2. Previous heart, lung, renal, malignant
disease
3. Hemorrhage, Infection
4. Risk factors for CAD and pulmonary
embolism
Current medications and allergies

Physical Examination of Cardiac

Arrest
It is necessarily focused on a few key goals
1.Ensure adequacy of airway maintenance
and ventilation
2.Confirm the diagnosis of cardiac arrest
3.Find evidence of cause
4.Monitor for complications of therapeutic
interventions

Physical Examination Findings Indicating

Potential Cause of Cardiac Arrest and
Complications of Therapy
Physical
Examination

Abnormalities

Potential Causes

General

Pallor
Cold

Hemorrhage
Hypothermia

Airway

Secretions, vomitus, or
blood

Aspiration
Airway obstruction

Resistance to positivepressure ventilation

Tension Pneumothorax
Airway obstruction
Bronchospasm

Jugular venous distention

Tension Pneumothorax
Cardiac tamponade
Pulmonary embolus

Tracheal deviation

Tension Pneumothorax

Median sternotomy scar

Undelying cardiac
disease

Neck

Chest

Physical Examination Findings Indicating

Potential Cause of Cardiac Arrest and
Complications of Therapy
Physical
Examination

Abnormalities

Potential Causes

Lungs

Unilateral breath sounds

Tension Pneumothorax
Right main stem
intubation
Aspiration

Distant or no breath sounds

or no chest expansion

Esophageal intubation
Airway obstruction
Severe bronchospasm

Wheezing

Aspiration
Bronchospasm
Pulmonary edema

Rales

Aspiration
Pulmonary edema
Pneumonia

Audible heart tones

Hypovolemia
Cardiac tamponade

Heart

Physical Examination Findings Indicating

Potential Cause of Cardiac Arrest and
Complications of Therapy
Physical
Examination

Abnormalities

Potential Causes

Abdomen

Distended and dull

Ruptured abdominal
aortic aneurysm or
ruptured ectopic
pregnancy

Distended, tympanitic

Esophageal intubation
Gastric insufflation

Rectal

Blood, melena

GI hemorrhage

Extremities

Asymmetrical pulses

Aortic dissection

AV shunt or fistula

Hyperkalemia

Needle tracks or abscesses

IV drug abuse

Burns

Smoke inhalation
Electrocution

Skin

Supporting Examination of
Cardiac Arrest
Lab
Indicated only when successful ROSC is
achieved:
Electrolytes
Blood urea nitrogen/creatinine
Creatinine kinase with isoenzymes, cardiac
troponin
Arterial blood gas (avoid arterial puncture
in thrombolysis candidates)

Supporting Examination of
Cardiac Arrest
Lab

CBC
Therapeutic drug levels
Toxicological testing
Imaging
ECG:
Establish or rule out acute coronary
syndrome

Supporting Examination of
Cardiac Arrest
Imaging
Chest radiograph:
Endotracheal tube position
Cardiac silhouette
Pneumothorax

ECG:
Pericardial effusion

Supporting Examination of
Cardiac Arrest
Imaging
ECG:
Wall motion abnormality
Valvular dysfunction

Differensial Diagnose of
Cardiac Arrest

Differensial Diagnose of
Cardiac Arrest
Sudden loss of consciousness with a
palpable pulse:
Syncope
Seizure
Acute stroke
Hypoglycemia
Acute airway obstruction
Head trauma, Toxins

Managem
ent of
Cardiac
Arrest

Treatment of Cardiac Arrest

5 stages:
(1)initial evaluation and basic life
support if arrest is confirmed
(2) public access defibrillation (when
available)
(3) advanced life support
(4) postresuscitation care
(5) long-term management

Treatment of Cardiac Arrest

Pre Hospital
Initial Stabilization
ED Treatment
Medication (Drugs)
Follow-Up

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

Pre Hospital
Prompt initiation of standard CPR or
active compression-decompression
CPR (ACD-CPR)
Confirm underlying rhythm
Early defibrillation of ventricular
tachycardia (VT) or ventricular
fibrillation (VF):
Automated external defibrillator
EMT-D or layperson

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

Pre Hospital
Consider CPR before defibrillation in cases of
if arrest >5 minutes.
Secure airway and provide adequate
respirations:
Endotracheal intubation
Laryngeal mask airway
Post-resuscitation care:
Identify cause of arrest
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Pre Hospital
- 12-lead ECG, Monitor vital signs

Transport to the closest facility:

If return of spontaneous circulation,
consider transport to center equipped for
interventional cardiac care.
Pediatric critical care center for children

Termination of resuscitative efforts:

Persistent, confirmed asystole, Prolonged
arrest
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Initial Stabilization
Initiate advanced cardiac life support
(ACLS).
Perform standard CPR as long as no
pulse is palpable.
Consider ACD-CPR:
Stop CPR only briefly to check cardiac
rhythm or intubate.

Secure the airway

The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Initial Stabilization
Obtain IV access
Cardiac monitor
Therapy based on the underlying
rhythm according to ACLS protocols

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

ED Treatment
Pulseless VT or VF
Immediate defibrillation with up to
three countershocks:
200 J
200 - 300 J
360 J

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

ED Treatment
If defibrillation is unsuccessful:
Epinephrine
Vasopressin

If refractory to defibrillation and

epinephrine:
Amiodarone
Lidocaine
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

ED Treatment
- Procainamide
Magnesium for Torsades de Pointes

Asystole
Dismal prognosis if this is the
presenting rhythm
Confirm in two or more leads
Epinephrine
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

ED Treatment
Atropine
Consider transcutaneous pacing for
severe brady-asystolic rhythm.
Pulseless Electrical Activity
Epinephrine
Atropine

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

ED Treatment
Treat for reversible cause of pulseless
electrical activity
Pneumothorax
Cardiac tamponade
Hypoxia
Pulmonary embolus
Hypovolemia (hemorrhage)
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

ED Treatment
Post-Resuscitation
Treat the underlying cause of the arrest.
ECG to establish presence of acute
coronary syndrome:
Immediate catheterization or thrombolysis
for ACS

Ventilatory support
Continue antidysrhythmic therapy.
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

ED Treatment
Post-Resuscitation
Correct electrolyte abnormalities.
Initiate volume resuscitation and
provide inotropic support as needed.

The 5-Minute Emergency Medicine

Consult (Rosen and Barkin-_s) 3ed

Medication (Drugs)
Amiodarone: 300 mg (peds: 5 mg/kg) IVP
Atropine: 1 mg (peds: 0.02 mg/kg) IV tiap
15min up to 0.04 mg/kg
Epinephrine: 1 mg (peds: 0.01 mg/kg) IVP
tiap 15min
Lidocaine: 100 mg (peds 1 mg/kg) IVP,
then 2x4 mg/min IV continuous infusion
Magnesium: 1x2 g slow IV
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Medication (Drugs)
Procainamide: 20 mg/min slow IV to a
total of 1 g or until arrhythmia is
suppressed; maintenance infusion 1x4
mg/min (peds: 15 mg/kg over 30 min
IV)
Sodium bicarbonate: 1 mEq/kg slow IV
Vasopressin: 40 U IVP (adults with
VT/VF only)
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Follow-Up
Disposition
Admission Criteria
Return of spontaneous circulation:
1.Coronary care unit or intensive care
unit
2.Postresuscitation care
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed

Indicators of Inadequate Blood Flow During

Cardiopulmonary Resuscitation
Monitoring Technique

Indicator

Carotid or femoral pulse Not palpable

CPP

<15 mmHg

ETCO2

<10 mmHg (before

vasopressor)

ScvO2

<40%

CPR

Tintinalli's Emergency Medicine 7th

Step 3: opening the air way

Head TiltChin Lift Maneuver -> gently
extend the patient's neck, by placing one
hand under the patient's neck and the
other on the forehead and extending the
head in relation to the neck. This
maneuver should place the patient's head
in the sniffing position, with the nose
pointing up.

Tintinalli's Emergency Medicine 7th

Step 3: opening the air way

Jaw Thrust Maneuver
the safest method for opening the airway.
This maneuver helps to maintain the
cervical spine in a neutral position. The
rescuer, who is positioned at the head of
the patient, places the hands at the sides
of the victim's face, grasps the mandible
at its angle, and lifts the mandible forward.

Tintinalli's Emergency Medicine 7t

Step 4 dan 5

Tintinalli's Emergency Medicine 7t

Ventilation Technique

Tintinalli's Emergency Medicine 7th

Step 6 dan 7

Prognose of Cardiac Arrest

Depend on initial interventions
-> if delayed (>4 or >6 minutes),
it can be progressive biologic
death because of progressive
brain cell death

Complication of Cardiac
Arrest
Sudden cardiac death
Multi organ failure

Acute Coronary Syndrome: MI

Imbalance in myocardial blood supply + O2
requirement
Acute cardiac ischemia encompasses a
spectrum of disease processes:
Unstable angina pectoris
Acute myocardial infarction (AMI)
ST elevation myocardial infarction (STEMI)
Non-STEMI

Etiology of MI
Atherosclerotic narrowing of coronary
vessels
Vasospasm although this is usually at rest
and considered unstable if new onset
Microvascular angina or abnormal
relaxation of vessels with diffuse vascular
disease
Plaque disruption
Thrombosis

Etiology of MI
Arteritis:
Lupus
Takayasu disease
Kawasaki disease
Rheumatoid arthritis

Prolonged hypotension
Anemia -> Hemoglobin <8 g/dL

Etiology of MI
Hyperbarism or elevations in
carboxyhemoglobin
Coronary artery gas embolus
Thyroid storm
Structural abnormalities of coronary
arteries:
Radiation fibrosis
Aneurysms
Ectasia

Etiology of MI
Cocaine- or amphetamine-induced
vasospasm
Cardiac risk factors include:
Hypercholesterolemia
Diabetes mellitus
Hypertension
Smoking
Family history in a first-degree relative
<55 years old

Etiology of MI
Cardiac risk factors include:
Men, age >55 years
Postmenopausal women

Signs and Symptoms of MI

Chest pain:
Most common presentation of MI
Substernal pressure
Heaviness
Squeezing
Burning sensation
Tightness

Signs and Symptoms of MI

Anginal equivalents (MI without chest pain):
Abdominal pain
Syncope
Diaphoresis
Nausea or vomiting
Weakness

Signs and Symptoms of MI

May localize or radiate to arms, shoulders,
back, neck, or jaw
Associated symptoms:
Dyspnea
Syncope
Fatigue
Diaphoresis

Signs and Symptoms of MI

Nausea
Vomiting
Symptoms are usually reproduced by
exertion, eating, exposure to cold, or
emotional stress.
Symptoms commonly last 30 minutes or
more.
Symptoms may occur with rest or during
exertion.

Signs and Symptoms of MI

Often preceded by crescendo angina
May be improved or relieved with rest or
nitroglycerin
Symptoms generally unchanged with position
or inspiration
Positive Levine sign or clenched fist over
chest is suggestive of angina.
Blood pressure (BP) is usually elevated during
symptoms

Physical Exam of MI
Physical exam is usually unrevealing.
Occasional physical findings include:
S3 or S4 due to left ventricular systolic
or diastolic symptoms
Papillary muscle dysfunction resulting in
mitral regurgitation
Diminished peripheral pulses

Supporting Exams of MI
ECG
Lab
1.CK-MB and troponin I or T
2.Hematocrit
3.Coagulation profile
4.Creatinine

Differential Diagnosis of MI

Anxiety
Aortic dissection
Biliary colic
Costochondritis
Esophageal reflux
Esophageal spasm
Herpes zoster

Differential Diagnosis of MI

Hiatal hernia
Mitral valve prolapse
Myocardial infarction
Panic disorder
Peptic ulcer disease
Pneumonia
Psychogenic

Differential Diagnosis of MI
Pulmonary embolus
Unstable angina

Treatment of MI
Pre Hospital
IV access
Aspirin, Oxygen
Cardiac monitoring
Sublingual nitroglycerin for symptom relief
12-lead ECG, if possible, with transmission
or results relayed to receiving hospital

Treatment of MI
Alert
All chest pain should be treated and
transported as a possible life-threatening
emergency.
Do not administer thrombolytics or heparin
if aortic dissection is suspected.
Initial Stabilization
IV access

Treatment of MI

Oxygen
Cardiac monitoring
Oxygen saturation
Continuous BP monitoring and pulse
oximetry

ED Treatment
STEMI requires reperfusion therapy as
soon as possible:

Treatment of MI
Thrombolytics should be used if
percutaneous coronary intervention is not
readily available within a 90-minute time
frame (see Reperfusion Therapy, Cardiac).
Patients with non-STEMI, if started on
glycoprotein IIb/IIIa inhibitors and if they
subsequently receive a stent, benefit from a
PCI within a 48-hour time frame.

Treatment of MI
Aspirin should be administered first to all
patients with suspected MI unless the patient
has a known allergy.
If BP is >90-100 mm Hg systolic, administer
sublingual nitroglycerin, nitropaste, or IV
nitroglycerin assuming no ECG criteria of
right ventricular infarct:
Symptoms that persist after three
sublingual nitroglycerin tablets are strongly
suggestive of AMI or noncardiac etiology

 Beta-blockers should be administered if no

contraindications (e.g., bradyarrhythmias,
heart rate <60, congestive heart failure,
hypotension, or obstructive pulmonary
disease) are present.
Morphine may be given to relieve pain and
increase oxygen carrying capacity.
Enoxaparin or heparin is generally
appropriate as the next line of therapy.

 Angiotensin-converting enzyme inhibitors may

effect a small decrease in mortality when
given acutely.
If non-STEMI is clearly the clinical diagnoses, a
glycoprotein IIb/IIIa inhibitor should be started.
Clopidogrel may be of benefit acutely when
added to standard therapy by reducing the
odds of AMI patients having another occluded
artery, or a second heart attack or death by
36% after 1 week of

 Statin therapy reduces clinical events in

patients with stable coronary artery
disease., this may also extend to patients
experiencing an acute ischemic coronary
event.
If patient is in cardiogenic shock, patient
should be transported to a cardiac
catheterization laboratory for angioplasty
and intra-aortic balloon pump as soon as
possible (see Congestive Heart Failure).

 Ventricular dysrhythmias:
See Ventricular Tachycardia
Bradydysrhythmia associated with
hypotension should be treated with
atropine or external pacing:
Conduction disturbances:
First-degree aortic valve (AV) block and
Mobitz I (Wenckebach) are often selflimited and do not require treatment.

 Mobitz II, complete heart block, new

right bundle branch block (RBBB) in
anterior MI, RBBB plus left anterior
branch block or left posterior fascicular
block, left bundle branch block plus firstdegree AV block may require a
temporary transvenous pacemaker.

Medications for MI
Amiodarone: 150 mg IV over 5 minutes
then 0.5 mg/min
Aspirin: 160-325 mg PO
Clopidogrel (Plavix): 300 mg PO load, 75
mg PO per day
Enoxaparin (Lovenox): 1 mg/kg SC q12h
Glycoprotein IIb/IIIa inhibitors:

Medications for MI
Eptifibatide (Integrilin) 180 g/kg IV over
1-2 minutes, followed by continuous
infusion of 2 g/kg/min up to 72 hours
Irofiban (Aggrastat) 0.4 g/kg/min for 30
minutes, then 0.1 g/kg/min for 48-108
hours
Abciximab (ReoPro) for use prior to PCI
only: 0.25 mg/kg IV bolus

Medications for MI
Heparin 80 units/kg IV bolus, then 18
units/kg/h
Lidocaine: 1.5 mg/kg IV bolus,
infusion of 2-4 mg/kg/min
Magnesium: 2 g bolus IV
Metoprolol: 5 mg IV q5min-15min
followed by 25-50 mg PO starting
dose as tolerated

Medications for MI
(note: beta-blockers contraindicated
in cocaine chest pain)
Morphine: 2 mg IV, may titrate
upward in 2-mg increments for relief
of pain assuming no respiratory
deterioration and SBP >90 mm Hg
Nitroglycerin: 0.4 mg sublingual
Nitroglycerin: IV drip at 5-10 g/min

Medications for MI
Nitropaste: 1-2 inches transdermal
Thrombolytics: see Reperfusion
Therapy, Cardiac, for dosing

Follow-Up
Disposition
Admission Criteria
Patients with an AMI require hospital
admission.
If the diagnosis is unclear, admission to
the hospital or an ED observation unit may
be useful for serial cardiac enzymes, ECGs,
and exercise stress testing and/or cardiac
catheterization.

Follow-Up
Discharge Criteria
No patient with an AMI should be
discharged from the ED.
Issues for Referral
If PCI is unavailable in the treating
institution, and particularly if the patient is
in cardiogenic shock, patients should be
transported to another hospital if PCI can
be underway in less than 90 minutes.

References
Harrisons Principles of Internal
Medicine. 18ed
Tintinalli's Emergency Medicine 7th
ed
The 5-Minute Emergency Medicine
Consult (Rosen and Barkin-_s) 3ed
Oxford Handbook of Accident and
Emergency Medicine-2nd Edition