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Welcome

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ACLS
Advanced Cardiac Life Support

Copyright Emergency Care Consultants - 2005


Presented by

Emergency
Care
Consultants
Post Office Box 725
Harvard, Illinois 60033-0725

(800) 322 8844

www.EmergencyCareConsultants.com
Emergency
Care Consultants
Established 1976
Offices in Chicago, Minneapolis & Kansas City

American Heart Association


Multi-Region Training Center for ACLS-PALS-BLS

Emergency Care Institute ACLS Training Center

American Safety & Health Institute


ACLS - PALS Training Center

NurseTesting.com Skills Evaluation Site

Over 25,000 people trained to date


Course Requirements
Instructors are licensed healthcare providers regularly
delivering emergency response, critical care, and ACLS

Please put comments on the evaluation form. We work


hard to improve our programs. Our clients receive copies of
your evaluations. Your suggestions and comments are
carefully reviewed

Without properly completed Course Registration Form you


will not receive your certification

This is a combined ACLS BLS Healthcare Provider course to


minimize the time for ACLS & BLS certification

This course is designed to enhance skill proficiency and


integrate progressive skills in a cost-effective manner
ACLS Required Skills
ECG Lead Placement and Analysis

Basic Life Support (CPR)

Oxygen Administration

AED Operation

Airway Management (ALS & BLS)

Defibrillation & Cardioversion (hands free and paddles)

Transcutaneous External Pacing

ACLS and Cardiac Arrest Drug Administration


ACLS Course Objectives

Properly manage adult cardiac and


respiratory arrest for the first 10 minutes
ACLS Course Objectives
Proficiently operate a cardiac monitor, Automated External
Defibrillator (AED), manual defibrillator, and transcutaneous
external pacemaker

Rapidly identify and initiate proper treatment of potentially


lethal cardiac conditions and rhythms

Provide initial assessment and appropriate management for


the adult AMI and stroke patient
ACLS Course Objectives
Understand know how to apply the components of the
Chain of Survival

Provide both basic and advanced (invasive) airway


management for the adult patient

Provide appropriate Basic Life Support (BLS-CPR) in the


healthcare environment and out- of- hospital setting
Standards vs. Guidelines

Fighting heart disease and stroke

ACLS guidelines are based on scientific research and


a consensus of opinion by international organizations
and experts. Future changes are to be based on peer
reviewed scientific evidence only.
Course Overview
This is a hands on interactive course
Review of the ACLS algorithms

BLS Proficiency

AED Proficiency

No Pulse - Too Fast - Too Slow Algorithms

Airway Management Station

Written and Practical Skill Assessment


Please . . . . . .
Turn your pagers and cells off - or put on vibrate

The alternatives may not be pleasant


Causes of Death

1. Coronary Heart Disease (743,000)


2. Rx Medications (186,000)
3. Cancer (150,000)
4. Stroke (150,000)

Trauma is the leading cause of death


between ages of 1 and 44
Problems
52% of AMI patients drive themselves
to medical care

50% of cardiac arrests occur outside


the hospital

Out of hospital cardiac arrest survival


is less than 5% - even with CPR
A better future ?
30% decline in deaths since 1979
50 84% survival rate for out of hospital
cardiac arrest with AED use within 4 minutes

Over 40 million people trained in CPR

176,000 AEDS sold to date


90 95% of first time AMI patients survive
Dont try and make something
out of nothing

Look at the basics and more importantly


LOOK AT THE PATIENT
EMS System Entry

Call 9-1-1 or your local


emergency number

Notify internal First


Responders

Bring emergency
equipment to the scene
(AED, oxygen, crash carts)
911

Nature of Problem

Address or Location

Hazards

Number of Patients

Call Back Number

Oak Lawn, Illinois


Legal Issues
Consent
Implied consent
Informed consent
Documentation
Advanced Directives
Do Not Resuscitate orders
Personal Protective
Equipment

Disposable gloves
Eye protection
Barrier device, face
shield, or pocket mask
Universal precautions
Disposable electrodes
Cardiovascular
Risk Factors
High Blood Pressure
High Cholesterol
Smoking
Family History
Diabetes
Past Medical History
Age
Sex
Stress
Sedentary life style
In an emergency, first
Determine Patient Status

Stable
or
Unstable
? ? ?
Stable vs. Unstable
Clues that may help

Level of consciousness
Heart rate
Blood pressure
Pulse oximeter
Past medical history
Availability of resources
Consider your location
Emergency Department (ED) Intensive Care Unit (ICU)
Coronary Care Unit (CCU) Urgent Care Center (UCC)
Outpatient Department (OPD) Physicians Office
Physician or Dental Clinic Non-healthcare setting
Cardiovascular Intensive Care Unit (CVICU)
Essentials for ACLS
Monitor/Defibrillator Supplies

The No. 1 reason pacing fails is because the equipment can not be located
Defibrillation Supplies

Pre-Gelled Defib Pads Hands free defibrillation electrode


Treat the patient,
not the monitor
Pulseless Rhythms
Ventricular fibrillation
(V Fib)

Ventricular
tachycardia (V tach)

Pulseless electrical
activity (PEA)

Asystole
Pulseless Rhythms

mmmmmm

Always verify absence of pulse


Verify monitor leads are in place
Increase the gain on monitor
Assess patient and intervene rapidly
Eliminate artifact, if possible
Ventricular Fibrillation

Initiate immediate CPR


Defibrillate as soon as possible
Ventricular Tachycardia

Wide complex Ventricular Tachycardia may


quickly progress to Ventricular Fibrillation
Pulseless Electrical Activity
PEA

Normal appearing rhythm, but no pulse


Asystole *

Adjust gain to increase size of complexes

Always verify asystole in a second ECG lead

Make sure leads are attached to patient


New guidelines: defibrillation
One immediate precordial thump may be
considered in monitored cardiac arrest if
defibrillator is not available
Defibrillation pad/paddle placement anterolateral
(preferred), anterior-posterior, apex-posterior
Biphasic energy is safe and effective (120-150
J); insufficient evidence for specific energy level.
Use 360 J for monophasic defibrillation
One shock vs three stacked. One shock
minimizes interruption in CPR. Three stacked
shocks can be optimized if minimal interruption
in CPR
Oropharyngeal - Nasopharyngeal
Airways

Devices to facilitate maintaining an open airway


Bag Valve - Mask
Self-inflating, oxygen not
required

Use supplemental oxygen


source, if available

Concentrations vary
greatly amongst brands
(35 85% with 12 lpm)
NEVER ventilate at
more than 8-12 per minute

Use supplemental oxygen source @ 10 12 liters per minute


Invasive Airway Management
Laryngeal Mask Airway
Combitube

Endotracheal
tube
The Gold Standard
Endotracheal
intubation
Invasive Airway Management
New guidelines: Medication
administration
IV access is preferred.
Give medications via tracheal route if no
IV access.
No benefits from endobronchial injections
vs. directly into ETT. Dilute with water
instead of 0.9% saline shows better
absorption
Vasopressin or Epinephrine

1 mg every 3 5 minutes
40 International Units Look at the concentration
Half life of 10 20 minutes (1:1000 and 1:10,000)
Epinephrine has been the standard; insufficient evidence to support or refute use of
Vasopressin either alone or in conjunction with epinephrine in cardiac arrest
Amiodarone or Lidocaine
Amiodarone is the preferred medication!!!

Cardiac arrest only dose:


300 mg IVP followed by 1 1.5 mg/kg
150 mg IVP Maximum of 3 mg/kg
Procainamide (Pronestyl)
20 mg/minute IV

May give up to 50
mg/minute in urgent
situations

Maximum dose is 17
mg/kg

Seldom used in cardiac


arrest due to time factor
Magnesium Sulfate

Dose is 1 2 grams IV
Only for hypomagnesemia and torsades de pointes,
not cardiac arrest
VF or VT Progressing to Return of
Spontaneous Circulation

Post Resuscitation Care


Maintain and protect airway; stabilize airway devices with
commercially available device or tape (new guidelines
mention tape)
Monitor ventilation (ETCO2) and oxygenation (O2)
Do not ventilate at respiratory rates that exceed 8-12 per
minute
Monitor and give appropriate meds. If defibrillation is
successful after anti-arrhythmic drug, continue
maintenance infusion of same.
Do not give prophylactic antiarrhythmics to patients who
survive arrest situation
New guidelines: Asystole
Transcutaneous pacing is no longer
recommended for asystole!!!

Hypoxia Tablets (OD)


Hypothermia Tamponade
Hypovolemia Tension
Hyper/hypokalemia pneumothorax
H+ ions Thrombosis, coronary
Thrombosis,
pulmonary
Atropine
Usually 0.1 mg/mL
Large quantities being stock
piled in powder form for
chemical weapons
(organophosphate) exposure
treatment
Dosage: 0.5-1.0 mg IV every
3-5 minutes to a total of 3
mg (0.04 mg/kg)
Vasopressor Agents

Continuous infusions of Dopamine, Epinephrine or


Isoproterenol to support blood pressure
Indications for Transcutaneous
Pacing
Hemodynamically unstable
bradycardia
Patients with sinus node dysfunction,
Type II 2nd degree block & 3rd-degree
heart block
Bradycardia with symptomatic
ventricular escape beats
Transcutaneous Pacing
Capture vs No Capture
Bradycardia
With no pacing

Pacer Spikes
Pacing below
threshold:
no capture

Capture:
Spike + broad QRS
QRS: opposite polarity

Pacing above threshold:


with capture
Reasons TCP Fails

Patient cant
tolerate pain

Providers cant
operate equipment

Providers cant find


equipment TCP Pacing Cable

Most pacing failures are inexcusable


Medicate Patient Before
Application of TCP

Midazolam (Versed)

Benzodiazepines for sedation


Morphine for analgesia
Morphine sulfate
Flumazenil (Romazicon)
0.2-0.5 mg IV over 30 seconds May repeat to 4.0 mg

Temporary reversal for sedative and respiratory


depression caused by benzodiazepines
Naloxone (Narcan)
Reversal agent for opiate overdose

Standard dose is 0.4-2.0 mg IV/SC q2-3 min


Tachycardia
Narrow complex stable
Vagal maneuvers
Adenosine
6 mg IVP, rapid flush with saline
12 mg IVP, rapid flush with saline
12 mg IVP, rapid flush with saline
Amiodarone
150 mg over 10 minutes IV
1 mg/min continuous infusion x 6 hrs
0.5 mg/min continuous infusion x 18 hrs
ECG during adenosine
administration

Adenosine given: Sinus pause


Tachycardia
Wide complex stable
Amiodarone
150 mg over 10 minutes IV
1 mg/min continuous infusion x 6 hrs
0.5 mg/min continuous infusion x 18 hrs
Procainamide
20 mg/min until QRS widens > 50%, max of 1.5
gms infused, hypotension develops, arrhythmia
resolved
Maintenance infusion: 1-4 mg/min
Atrial Fibrillation

Amiodarone 150 mg over 10 min; then 1


mg/min infusion x 6 hrs, 0.5 mg/min x 18 hours
Magnesium 1-4 gms IV
Diltiazem 0.25 mg/kg IV; then 5-15 mg/hr
continuous infusion
Electrical Cardioversion
Immediate cardioversion is indicated for
unstable patients with serious signs and
symptoms related to tachycardia
Electrical Cardioversion
Premedicate with sedating, analgesic agent
Place cardiac monitor place defibrillator in
the synchronized mode
Hands free electrodes are best technique
If using paddles hold them steady for
several seconds
Patient must be on cardiac monitor during
synchronized cardioversion to determine
underlying rhythm
If first shock is not successful, need to set
the defibrillator to synchronized mode
again
Elective Cardioversion

Remove oxygen before cardioversion.


Be prepared to resuscitate the patient.
Synchronized Cardioversion

Energy selection for cardioversion


50 - 100 J, 200 J, 300 J, 360 J
(Monophasic)
Polymorphic VT with pulse
200 J, 200 to 300 J, 360 J
(Monophasic)
Cardioversion
Acute Myocardial Infarction
The Chest Pain Patient
Requires rapid
assessment

Maintain high degree


of suspicion

30 minute door to
drug time

90 minute door to
catheter time
Time is Muscle
Time to treatment is
critical determinant of
outcome

Maximal benefit from


fibrinolytic therapy
achieved within 1-2
hours of symptom onset

Few AMI patients


receive treatment
within one hour of
symptom onset
The Four Ds
Door
Data
Decision
Drug or Needle
The National Heart Attack Alert Program Recommendations

Door to Needle 30 minutes


Door to PCI 90 minutes
Immediate Assessment
( < 10 minutes )

Check vital signs with automatic or standard


BP cuff (manual if below 90 mm Hg); determine oxygen
saturation

Obtain IV access (large bore normal saline) & 12-lead


ECG

Obtain a brief, targeted history & perform


physical examination; use checklist (yes-no);
focus on eligibility for fibrinolytic therapy

Obtain blood sample for initial cardiac


marker levels; glucose levels; electrolyte;
and coagulation studies
Pain Scale
Have patient rank pain on
scale of one to ten -- ten
being the worst pain they
can imagine.

Continually reassess and document


pain levels after medications
No. 1 Symptom of AMI
Im too
young

I just had
a physical

I take an
Aspirin daily
DENIAL
ECG Analysis
To diagnose patients with atypical
presentations

To aid in risk stratification

To establish treatment regimen criteria

Need to develop stringent criteria


ST segment elevation >0.1 mV in two or
more contiguous leads
Serum Markers
Acute Myocardial Infarction
CK-MB (Total CK, CK Index)
Myocardial cells have 85%
MM and 15% MB (very little BB)
Rise within 4 - 6 hours; peak
at 10 - 18 hours; baseline in
48 - 72 hours

Myoglobin
Rise within 1 - 4 hours

Troponin-I
Rise within 4 - 6 hours

LDH, LDH isoenzymes, SGOT


Myocardial Infarction
Diagnosis

History

Risk Factors

12 lead ECG

Serum markers
Myocardial Infarction
Treatment

M
O
N
A Mona
Oxygen

Increases oxygenation of ischemic tissue


Always administer when AMI is suspected
Start with nasal cannula at 4 Liters/minute
Aspirin
Standard therapy for all patients with pain
suggestive of AMI

Give immediately - Dose: 160 to 325 mg


Precautions
Relatively contraindicated in active peptic ulcer
disease
Contraindicated in patients with known aspirin
hypersensitivity; bleeding disorders
Aspirin
Dose: 160 325 mg by mouth

Chewable is more palatable

If the patient says they took an aspirin,


make sure it was an aspirin
Nitroglycerin
Treatment for patients with ST-segment
elevation or depression in first 24 48
hours including:
LV failure (acute pulmonary edema or CHF)
Elevated BP (especially with signs of LV failure)
Large anterior infarction
Persistent ischemia
Suspected ischemic chest pain
Unstable angina (change in angina pattern)
Acute pulmonary edema (Systolic BP > 90 mmHg)
Nitroglycerin
Sublingual: 0.3 to 0.4 mg; repeat
every 5 minutes
Spray inhaler: Metered dose every 5
minutes
IV infusion: 12.5 to 25 g bolus, then
10 to 20 mcg/min infusion, titrated
up to 200 mcg/min
Morphine Sulfate
ACTIONS:
Reduces pain of ischemia
Reduces anxiety
Reduces extension of ischemia by
reducing oxygen demand

INDICATIONS:
Continuing pain
Evidence of vascular congestion
(acute pulmonary edema)
Systolic blood pressure >90 mm Hg
No hypovolemia
Morphine Sulfate
Dose
2 to 10 mg titrated to effect
0.05 mg/kg
Goal is to eliminate pain

Watch for drop in BP with:


Volume depletion
RV infarction

Side Effects:
Depression of ventilation
Nausea and vomiting
Itching
New Guidelines: Heparins
Non ST Elevation MI (NSTEMI)
In ED, give low molecular weight heparin (LMWH)
instead of unfractionionated heparin (UFH), in
addition to aspirin (considered helpful)
Insufficient data to recommend the time of
administration of LMWH to onset of symptoms
Use UFH if intervention is planned within 24-36 hours
Do not change from one form of heparin to another
during an acute event
ST Elevation MI
Can use LMWH as alternative to UFH in patients < 75
years and receiving fibrinolytic therapy
New Guidelines: Medications and
MI
Give Clopidogrel (Plavix) 300 mg in
addition to ASA to patients with ACS
within 4-6 hours of contact if they have
the following:
Rise in serum biomarkers or EKG consistent
with ischemia when PCI is planned in absence
of ST segment elevation
STEMI patients up to 75 years receiving
fibrinolytics, ASA and heparin
New Guidelines: Medications and
MI
GP IIb/IIIa inhibitors
If revascularization is planned (PCI or
surgery) it is safe to give GP IIb/IIIa in
addition to ASA and heparin in patients with
NSTEMI in ED
If revascularization is not planned
Tirofiban (Aggrastat) and Eptifibatide (Integrilin)
may be administered in patients with NSTEMI in
addition to ASA and heparin
Abciximab (Reopro) may be harmful to patients
with NSTEMI if PCI is not planned. Abciximab is
not recommended for receiving fibrinolytics for
STEMI
New Guidelines: Medications and
MI
Beta-blockers
In the ED, treat patients with ACS with Beta-blockers
(oral or IV), irrespective of the need for
revascularization
Contraindications to Beta-blockers include hypotension,
bradycardia, heart block and reactive airway disease
All patients must be evaluated for fibrinolytics or
PCI if they present within 12 hours with STEMI
All patients should be started on an ACE inhibitor,
unless contraindicated (hypotension), with 24
hours of symptom onset
It is considered safe to start patients on statin
therapy within 24 hours of symptom onset
Stroke
Stroke risk factors

Risk factors are the same


for coronary artery disease

Risks triple after age 55

The goal is to save lives


and reduce disability

Time is brain
Ischemic vs. hemorrhagic

70% of all brain attacks are ischemic events


Rapid Assessment and Intervention
are the keys to success

Goal: 60 minute door to drug treatment decision


Brain Attack Treatment

Consider use of fibrinolytic


drugs (tPA) for acute ischemic
stroke within three hours of
symptom onset
Other fibrinolytics are still
being investigated
Significant benefits of EMS
transporting patients directly
to a Stroke Center hospital
Assessment of the Patient
Basic neurological exam
Review of medical history
Blood sugar
Fibrinolytic screening (use form)
Non Contrast CT Scan
Neurological consult
Radiological consult
Decision to treat Do Not Delay
FAST Test (Face, Arm, Speech test)
Healthy Nutrition Break
Please return in 10 minutes
Always start with the basics
Basic Life Support (CPR)
Basic life support
Old guidelines New guidelines
Adults (Age 8+ ) Adults: 100
100 compressions a compressions/min
minute (15 : 2) (30:2 compression:
Child (Age 1 8 ) ventilation ratio if one
100 compressions a rescuer)
minute (5 : 1) Child: as above
Infant ( < 1 year ) Infant: (at least 100
At least 100 compressions/min) as
compressions a minute above
(5 : 1) Two rescuer CPR ratio
is 15:2
Maintain airway open

Head tilt Chin lift method


Maintain airway during pulse check
Maintain airway during 2 person CPR
Position and depth

Compress lower
one-half of sternum

Compress one-third depth of chest


AED
Automated External Defibrillators

AEDs only defibrillate shockable


rhythms.
AEDs recognize and defibrillate
Ventricular Fibrillation and Ventricular
Tachycardia.
Only apply AED on patients who are
pulseless and apnea (no signs of life
or not moving)
Basic A B C D s
Airway

Breathing

Circulation

Defibrillation
Defibrillation and Time

Less than 50% survival after 4 minutes


Survival reduced 7% to 10% per minute (even with CPR)
Rapid defibrillation is key to success
Proper Equipment

Disposable blanket or plastic sheet and spare electrodes


Special Situations
considerations before defibrillation

Remove all metallic objects from chest


Shave excessive hair
AED Use Requirements
Remove metal from chest
Non-metallic surface for
victim
Dry surface use plastic
No medication patches
remove and wipe dry
Shave hair, if necessary
Dry skin, if necessary Medication
patches
Pediatric Defibrillation

Pediatric electrode = $90

Patient age considerations *


Brand of AED
Electrode placement issues
Identify cause of cardiac arrest
* AHA does not recommend AED use on infants (< 1 year of age)
Provide Primary ABCs

FIRST THINGS FIRST


Assess for unresponsiveness
Open airway and check for breathing
Deliver two-five full, slow breaths
Check for circulation (10 second pulse check)
Initiate CPR until arrival of defibrillator or AED
AED Operation
4 Universal Steps

1. Power ON the AED


2. Attach electrodes
3. Analyze rhythm
4. Deliver Shock

ON
Hands Free
Defibrillation Electrode Placement

1. Upper right chest, top of electrode at clavicle


2. Left lateral chest, 4 5 cm below axilla
Proper Electrode Use
1

Some brands of electrodes require


they be placed as indicated on the
package
Pacemakers Catheters
Use alternative electrode placement
The Heart Sandwich
Anterior Posterior Position
AED Safety
With every analysis and shock :

DO NOT TOUCH PATIENT or AED

Look & warn bystanders


Im clear
Youre clear
Everybodys clear
The oxygen is clear

Visually verify all clear before


delivering shock
* AEDs have motion detectors to eliminate artifact.
Safety Requirement
Im clear

Youre clear

Were all clear

The oxygen is clear


Not providing this warning and visual verification of clear
is automatic fail point in cardiac arrest & AED stations.
Break for BLS
PLEASE Just 8 minutes to reassemble

BLS practical skills are next


Update on Treatments for
Myocardial Infarction
Myocardial Infarction
Death and necrosis of a portion of the
myocardium caused by prolonged
ischemia
Etiology: Significant imbalance between
supply and demand
Supply Demand
Patency of coronary arteries Heart rate
Diastolic time Preload
Vascular resistance of Afterload
coronary vessels MVO2 Contractility
In patients with
hypercholesterolemia,
excess LDL infiltrates
the artery and is
retained in the intima.
Oxidative and
enzymatic
modifications lead to
the release of
inflammatory lipids
that induce endothelial
cells to express
leukocyte adhesion
molecules. These
molecules enhance the
cycle of retaining LDL
and attracting
platelets leading to
clot formation in the
intima of the artery.
Monocytes recruited
through the
activated
endothelium
differentiate into
macrophages.
Several endogenous
and microbial
molecules can,
induce activation
and leading to the
release of
inflammatory
cytokines,
chemokines and
other inflammatory
molecules and,
ultimately, to
inflammation and
tissue damage.
Activated immune cells
in the plaque produce
inflammatory cytokines
(interferon- ,
interleukin-1, and
tumor necrosis factor
[TNF]), which induce
the production of
substantial amounts of
interleukin-6. These
cytokines are also
produced in various
tissues in response to
infection and in the
adipose tissue of
patients with the
metabolic syndrome.
Interleukin-6, in turn,
stimulates the
production of large
amounts of acute-phase
reactants, including C-
reactive protein (CRP),
serum amyloid A, and
fibrinogen, especially in
the liver.
Myocardial Infarction
Presentation
Subjective: Pain (>75% of cases) lasting for greater
than 30 minutes, gender differences, dyspnea,
palpitation, N/V, diaphoresis, atypical (elderly and
diabetic patients)
Objective: Tachycardia and hypertensive (anterior
wall), bradycardia and hypotensive (inferior wall),
tachypnea, JVD (inferior wall), diminished heart
sounds (decreased contractility), murmur (papillary
muscle rupture), crackles (LV failure)
Immediate Assessment
Oxygen at 4L/min via Check vital signs
nasal cannula; Determine oxygen saturation
maintain the SaO2 >
90% Obtain IV access
Nitroglycerine 12-lead ECG
Aspirin (160-325 mg) Obtain a targeted history &
Morphine 2-4 mg or perform physical
0.05 mg/kg examination; use checklist
(yes-no); focus on eligibility
for fibrinolytic therapy or PCI
Obtain blood sample for
glucose levels, electrolytes,
coagulation studies and
cardiac damage
Enzyme and protein characteristics
after AMI
Myoglobin CK-MB Cardiac
(intracellular heme (enzyme found in Troponin or
protein) cardiac muscle)
Normal < 75 mcg/L Normal < 4%
Tn I
(mediate the action of
actin & myosin; more
specific than TnT)
Normal < 10 ng/ml

Increase 2-4 hrs 3-6 hrs 4-8 hrs

Peak 9-12 hrs 12-24 hrs 12-16 hrs

Normalize 24-36 hrs 24-72 hrs 5-9 days


ECG changes and myocardial
damage
Leads Artery Area of Complications
damage
II, III, aVF RCA Inferior wall Hypotension,
(V4R) of LV (RV) SA, AV blocks
I, aVL, V5, V6 LCA - Lateral wall LV dysfunction
circumflex of LV
V1, V2 LCA - LAD Septum, Infra nodal and
septal branch Bundle of His BBB
V3, V4 LCA - LAD Anterior wall BBB, complete
diagonal of LV heart block
Myocardial Infarction
Diagnostic tests

Chest x-ray: may show signs of LV failure


Echocardiogram
Normal
Reduced wall motion (indicative of acute
occlusion)
May show mechanical complications (papillary
muscle rupture, VSD)
Cardiac catherization (coronary artery
occlusion)
Right Ventricular (RV) Infarction
Occurs in the setting of inferior wall MI; approximately
50% of patients with IWMI experience RV infarction
Clinical presentation: hypotension, clear lung fields,
jugular venous distension (~15% of patients)
Pathophysiology
Occlusion of RCA
Elevated RV end diastolic pressure and decreased pulmonary
blood flow due to decreased RV performance
Intra-ventricular septum bows from the RV to the LV, leading to
a decreased cardiac output
Pulmonary vasoconstriction
Treatment
Fluids: saline or LR
Avoid vaso-dilators (nitrates, beta-blockers, diuretics, ACE)
Inhaled nitric oxide
This patient has right-sided heart sounds and an inversion of the electrical
waves in leads I, II, aVR, V4, V5, and V6. Right-sided electrocardiography
demonstrated a normal pattern. What is this called?
ST segment elevation MI (STEMI)
STEMI patients have complete occlusion of
coronary vessel
Mainstay of treatment is reperfusion therapy
(fibrinolytics or PCI);
Door to needle time is 30 minutes
Door to balloon time is 90 minutes
Do not wait for results of cardiac markers; depending
on onset of MI, markers may not be elevated
Waiting for special consultation leads to increased
mortality
Within 24 hours start ACE inhibitors and statin
(atorvastatin/Lipitor, simvastatin/Zocor) therapy,
beta-blockers, clopidogrel (Plavix)
Guidelines: Heparins
Non ST Elevation MI (NSTEMI)
In ED, give low molecular weight heparin (LMWH)
(Enoxaparin/Lovenox) instead of unfractionionated
heparin (UFH), in addition to aspirin (considered
helpful)
Insufficient data to recommend the time of
administration of LMWH to onset of symptoms
Use UFH if intervention is planned within 24-36 hours
Do not change from one form of heparin to another
during an acute event
STEMI
Can use LMWH as alternative to UFH in patients < 75
years and receiving fibrinolytic therapy
Guidelines: Medications and MI
Give Clopidogrel (Plavix) 300 mg in
addition to ASA to patients with ACS
within 4-6 hours of contact if they have
the following:
Rise in serum biomarkers or EKG consistent
with ischemia when PCI is planned in absence
of ST segment elevation
STEMI patients up to 75 years receiving
fibrinolytics, ASA and heparin
Guidelines: Medications and MI
GP IIb/IIIa inhibitors
If revascularization is planned (PCI or
surgery) it is safe to give GP IIb/IIIa in
addition to ASA and heparin in patients with
NSTEMI in ED
If revascularization is not planned
Tirofiban (Aggrastat) and Eptifibatide (Integrilin)
may be administered in patients with NSTEMI in
addition to ASA and heparin
Abciximab (Reopro) may be harmful to patients
with NSTEMI if PCI is not planned. Abciximab is
not recommended for receiving fibrinolytics for
STEMI
Guidelines: Medications and MI
Beta-blockers
In the ED, treat patients with ACS with Beta-blockers
(oral or IV), irrespective of the need for
revascularization
Contraindications to Beta-blockers include hypotension,
bradycardia, heart block and reactive airway disease
All patients must be evaluated for fibrinolytics or
PCI if they present within 12 hours with STEMI
All patients should be started on an ACE inhibitor,
unless contraindicated (hypotension), with 24
hours of symptom onset
It is considered safe to start patients on statin
therapy within 24 hours of symptom onset
A. Normal
anatomy and
cardiac
conduction
system
B. Normal
ventricular
depolarization
C. Left bundle
branch block
D. Bi-ventricular
pacing wires;
leading to
simultaneous
contraction of
right and left
ventricles
Atrial and
biventricular
pacing.
The right atrial and
right ventricular
pacing leads are
inserted in the
standard fashion. The
left ventricular pacing
lead is inserted into
the coronary sinus
and advanced into a
cardiac vein on the
lateral wall of the left
ventricle.