Sanders: Mosby`s Paramedic Textbook, Revised 3

Transcription

Sanders: Mosby's Paramedic Textbook, Revised 3rd Edition
PowerPoint Lecture Notes
Chapter 29: Cardiology
Chapter 29
Cardiology
Copyright © 2007, 2006, 2001, 1994 by Mosby, Inc., an affiliate of Elsevier Inc.
Objectives
z
Identify risk factors and prevention strategies for
cardiovascular disease
z
Describe cardiovascular physiology
z
Discuss cardiac electrophysiology
z
Outline the electrical conduction system of the heart
z
Outline cardiovascular assessment
Objectives
z
Describe ECG monitoring techniques
z
Explain how the ECG tracing relates to the heart’
heart’s
electrical activity
z
Describe the steps in ECG interpretation
z
Identify features of normal sinus rhythm
z
Interpret ECG tracings, including rhythm, site, causes,
significance, and prehospital management
Mosby, Inc. items and derived items © 2007, 2006 by Mosby, Inc., an affiliate of Elsevier Inc.
1
Objectives
z
Describe assessment and management of
patients with cardiovascular disorders
z
List relevant information for cardiovascular
pharmacological agents
z
Identify actions to be taken for prehospital
termination of resuscitation
Objectives
z
List indications, contraindications, and prehospital
considerations for:
Basic life support
MonitorMonitor-defibrillators
¾ Implantable cardiovertercardioverter-defibrillators
¾ Synchronized cardioversion
¾ Transcutaneous cardiac pacing
¾
¾
Scenario
An elderly, diabetic female is complaining of
weakness and an “aching”
aching” feeling in her chest. She is
pale, diaphoretic, and has a blood pressure of 100/70
mm Hg, P is 110/min; and blood sugar is 90 mg/dL.
You prepare to perform a 1212-lead ECG as your
partner starts an IV after placing her on oxygen.
Suddenly, her eyes roll back and her head slumps
limply to the side. As you realize she has no carotid
pulse, you note a chaotic rhythm on the monitor and
recognize that she is in ventricular fibrillation.
2
Discussion
z
List this patient’
patient’s risk factors for cardiovascular disease.
z
Describe the steps in initial cardiac care that were
indicated on this call?
z
What changes on the 1212-lead would have confirmed
myocardial infarction?
z
Outline steps that need to be taken now that her
condition has changed.
Cardiovascular Disease
Age
Family history
Diabetes
Hypertension
Hyperlipidemia
High cholesterol
z
z
z
z
z
z
z
z
z
z
Cigarette smoking
Preexisting cardiac
disease
Cocaine use
Carbohydrate intolerance
Heart Anatomy
z
Muscular pump
¾
¾
Two atria
Two ventricles
z
Cone shape
z
Size of closed fist
3
Heart Anatomy
In mediastinum of
thoracic cavity
z
¾
2/3 of heart's mass
lies left of midline of
sternum
Pericardium
z
Fibrous outer layer, thin
inner layer surround
heart
z
Cavity between layers
contains pericardial fluid
¾
Reduces friction
Coronary Vessels
z
Seven large veins carry
blood to the heart
¾
¾
z
Pulmonary veins
Superior and inferior
vena cavae
Coronary sinus
4
Coronary Vessels
z
Aorta
z
Pulmonary trunk
z
Coronary arteries
supply heart muscle
Heart Chambers and Valves
z
Septum separates right
and left chambers
¾
¾
Interatrial septum
Interventricular septum
Atrioventricular Valves
z
Allow blood flow from
atria into ventricles
z
Prevent backflow
z
Tricuspid valve
z
Mitral (bicuspid) valve
5
Semilunar Valves
z
Aortic and pulmonary
semilunar valves
¾
¾
¾
Block blood flow
Blood pushes against
valves, forcing them open
Blood flowing from aorta or
pulmonary trunk causes
valves to close
Peripheral Circulation
z
Flow of blood
Ventricles
Arteries
¾ Arterioles
¾ Capillaries
¾ Venous system
¾
¾
Capillary Network
z
Blood supplied to capillary
network by arterioles
z
Blood flows through
network into venules
¾
z
Regulated precapillary
sphincters
Exchange nutrients and
wastes
6
Arteries and Veins
z
Three layers in all blood vessel walls (except
capillaries and venules)
Tunica intima
• Inner layer
¾ Tunica media
• Middle layer
¾ Tunica adventitia
• Outer layer
¾
Types of Arteries
z
Conducting arteries
¾
z
Distributing arteries
¾
z
Large
Small to medium
Arterioles
¾
Smallest
Venules
z
Similar to capillaries
z
Collect blood from
capillaries and transport
to small veins
z
Nutrient exchange
across walls of venules
7
Veins
z
Walls are layer of
smooth muscle cells
z
MediumMedium-sized and large
veins
¾ Carry blood to venous
trunks and then the
heart
z
Large veins
¾
¾
Valves allow blood flow to
but not from the heart
Prevents backflow of blood
Arteriovenous Anastomoses
(AV Shunts)
z
Allows blood flow from arteries to veins
¾
z
Natural AV shunts
¾
¾
z
Without passing through capillaries
Sole of foot and nail beds
Regulate body temperature
Pathological shunts
¾
Injury or tumors
Coronary Arteries
z
Supply arterial blood to
heart muscle
¾
¾
z
Left coronary artery carries
about 85% of blood supply
to myocardium
Right coronary artery
carries remainder
Originate above aortic
valve
8
Left Coronary Artery
z
Divides into left anterior
descending and
circumflex arteries
¾
Left anterior descending
(LAD) supplies:
• Anterior wall of left
ventricle
¾
• Interventricular septum
Circumflex supplies:
• Lateral and posterior
portions of left ventricle
• Part of right ventricle
Coronary Arteries
z
Right coronary artery and
left anterior descending
artery supply:
¾
¾
z
Most of right atrium and
ventricle
Inferior aspect of left
ventricle
Anastomoses provide
collateral circulation
Coronary Capillaries
z
Exchange nutrients and
metabolic wastes
z
Merge to form coronary
veins
z
Coronary sinus empties
into right atrium
¾
Major vein draining
myocardium
9
Physiology
z
Heart is two pumps in one:
LowLow-pressure pump (right atrium and right
ventricle)
• Supplies pulmonary vasculature
¾ HighHigh-pressure pump (left atrium and left ventricle)
• Supplies systemic vasculature
¾
Blood Flow through the Heart
z
Blood enters right atrium from
systemic circulation by inferior
and superior vena cavae and
from the heart by the coronary
sinus
z
Blood passes into right ventricle
z
Ventricles push blood against
tricuspid and semilunar valves
z
Blood enters pulmonary trunk
Blood Flow through the Heart
z
Pulmonary arteries carry blood
to lungs
¾
¾
Carbon dioxide released
Oxygen picked up
z
Blood enters left atrium
through pulmonary veins
z
Left atrium contracts and fills
ventricles
z
Blood enters aorta and is sent
through body
10
Cardiac Cycle
z
Systole
¾
¾
z
Atrial
Ventricular
Diastole
¾
¾
Atrial
Ventricular
Heart Action during Atrial Systole
Heart Action during Ventricular Systole
11
Cardiac Output
z
Stroke volume
z
Heart rate
z
Contractility
z
Starling's law
Nervous System Control of the Heart
z
Extrinsic control by parasympathetic
and sympathetic nerves influences:
Heart rate
Conductivity
¾ Contractility
¾
¾
Nervous System Control of the Heart
z
Sympathetic and parasympathetic nerve
fibers in atria
z
Ventricles mainly have sympathetic nerves
12
Sympathetic Control
z
Postganglionic sympathetic fibers release
norepinephrine; have effects on myocardium:
Inotropic
Dromotropic
¾ Chronotropic
¾
¾
Sympathetic Control
z
Sympathetic stimulation of the heart
Dilation of coronary blood vessels
Constriction of peripheral vessels
¾ Increased oxygen demands of the heart met by
increase in blood and oxygen supply
¾
¾
Sympathetic Control
z
Norepinephrine release results from
stimulation of alphaalpha- and betabeta-adrenergic
receptors in the heart
z
Sympathetic stimulation increases the heart
rate
13
Parasympathetic Control
z
Parasympathetic innervation of the heart by
vagus nerve
¾
Continuous inhibitory influence on the heart by
decreasing heart rate and contractility
Hormonal Regulation of the Heart
z
Sympathetic impulses are transmitted to
adrenal medulla and blood vessels
¾
Adrenal medulla secretes epinephrine and
norepinephrine
Epinephrine
z
Epinephrine increases rate and force of
contraction
z
Epinephrine also:
Constricts blood vessels in skin, kidneys, GI tract,
and other organs
¾ Dilates skeletal and coronary vessels
¾
14
Norepinephrine
z
Causes constriction of peripheral blood
vessels in most areas of the body
z
Stimulates cardiac muscle
Role of Electrolytes
z
Myocardial cells bathed in electrolyte solution
z
Electrolytes that influence cardiac function:
Calcium
Potassium
¾ Sodium
¾ Magnesium
¾
¾
Electrophysiology of the Heart
z
Two cell types in myocardium
Cells of electrical conduction system
• Formation and conduction of electric current
¾ Working myocardial cells
• Contractility
¾
15
Electrical Activity of Cardiac Cells
z
Ions are charged particles that are electrically
positive or negative
¾
¾
Cations
Anions
Electrical Activity of Cardiac Cells
z
Charged particles are like magnets:
Need energy to push apart if opposite electrical
charges
¾ Need energy to join if like electrical charges
¾
Membrane Potentials
z
MagneticMagnetic-like attraction
gives separated particles
of opposite charges
potential energy
¾
¾
Membrane potential
between inside and outside
of cell
Charge between inside and
outside of cells expressed
in millivolts (mV)
16
Resting Membrane Potential
z
Cell in “resting”
resting” state
z
Has electrical charge difference
¾
¾
Resting membrane potential (RMP)
Inside of cell is negative compared to outside of
cell membrane
Resting Membrane Potential
z
RMP due to
difference between
intracellular and
extracellular
potassium ion level
Depolarization
z
Sodium—
Sodium—Positively
charged ion on outside
of cell
¾
¾
Chemical and electrical
gradient
Tends to move
intracellularly
Sodium channels remain closed in resting
cell membrane
17
Depolarization
z
Depolarization (electrical conduction) takes
place when sodium rushes into the cell,
making inside more positive compared with
outside
Depolarization
Depolarization of cell membrane causes sodium channels to open
Diffusion through Ion Channels
z
Cell membrane is:
Relatively permeable to potassium
Less permeable to calcium chloride
¾ Minimally permeable to sodium
¾
¾
18
Diffusion through Ion Channels
z
ProteinProtein-lined channels allow passage of ions
through cell membrane
z
Permeability influenced by:
Electrical charge
Size
¾ Gating proteins
¾
¾
SodiumSodium-Potassium Pump
z
Actively pumps sodium ions out of cell and
potassium ions into cell
z
Transports three sodium ions out for every
two potassium ions taken in
z
Returns cell to its resting state
SodiumSodium-Potassium Exchange Pump
19
Channels in Cardiac Muscle Cells
z
Sodium and calcium ions enter cells
through two separate channel systems in
cell membrane:
¾
¾
Fast channels
Slow channels
Channels
z
Fast channels are sensitive to small changes
in membrane potential
As cell nears threshold level:
• Fast sodium channels open
¾ Sodium ions rush intracellularly
• Rapid depolarization
¾
z
Slow channels are selectively permeable to
calcium and sodium
Cell Excitability
z
Nerve and muscle cells are capable of
producing action potential
z
Threshold potential
20
Propagation of Action Potential
z
Action potential on cell membrane stimulates
adjacent cell membrane
Excitation process is spread along length of cell
and on to the next
¾ AllAll-oror-none principle
¾
Cardiac Action Potential
z
Phase 0 (rapid depolarization phase)
z
Phase 1 (early rapid depolarization phase)
z
Phase 2 (plateau phase)
z
Phase 3 (terminal phase of rapid repolarization)
z
Phase 4 (resting period)
Action Potential of Myocardial Cells
21
Absolute Refractory Period
z
Absolute refractory period
¾
z
Cardiac muscle cell is
completely insensitive to
stimulation
Refractory period of
ventricles is about same
duration as action potential
Relative Refractory Period
z
Muscle cell is more
difficult than normal
to excite but can still
be stimulated
Electrical Conduction System
z
Sinoatrial node (SA node)
z
Atrioventricular (AV) junction
¾
¾
z
AV node
Bundle of His
HisHis-Purkinje system
¾
Bundle branches
• Right
• Left anterior fascicle
• Left posterior fascicle
22
Characteristics of Myocardial Cells
z
Automaticity
z
Excitability
z
Conductivity
z
Contractility
Intrinsic Rates
z
SA node
¾
z
AV junctional tissue
¾
z
6060-100/min
4040-60/min
Ventricles (bundle
branches and Purkinje
fibers)
¾
2020-40/min
Ectopic Electrical Impulse Formation
z
Ectopic beat results when pacemaker
function is assumed by cells other than in SA
node
¾
¾
Premature beats
Early in diastole before SA node is scheduled to
discharge
23
z
Premature beats
Atrial origin—
origin—Premature atrial complexes (PACs)
Junctional origin—
origin—Premature junctional
complexes (PJCs)
¾ Ventricular origin—
origin—Premature ventricular
complexes (PVCs)
¾
¾
z
Two mechanisms for ectopic impulse
generation in the heart:
¾
¾
Enhanced automaticity
Reentry
Enhanced Automaticity
z
Acceleration in depolarization
z
Due to high leakage of sodium ions into cells
¾
¾
z
Cells reach threshold prematurely
Rate of impulse formation in potential pacemakers
increases beyond their inherent rate
Causes dysrhythmias in Purkinje fibers
¾
Other myocardial cells
24
Enhanced Automaticity
Excess catecholamines
Digitalis toxicity
Hypoxia
Hypercapnia
Myocardial ischemia or infarction
Increased venous return (preload)
Hypokalemia or electrolyte abnormalities
Atropine administration
z
z
z
z
z
z
z
z
Reentry
z
Reactivation of myocardial tissue by same
impulse
z
Occurs when electrical impulse is delayed,
blocked in segments of the heart's electrical
conduction system
Reentry
Conduction through normal and severely depressed Purkinje fibers
25
Reentry
z
Reentry dysrhythmias can occur in:
SA node
Atria
¾ AV junction
¾ Bundle branches
¾ Purkinje fibers
¾
¾
Delayed Impulses
z
Causes of delayed or blocked impulses
Myocardial ischemia
Certain drugs
¾ Hyperkalemia
¾
¾
Assessment of Cardiac Patient
z
Chief complaint
z
History of event and significant past medical
history
z
Physical exam
26
Chief Complaint
z
Cardiac disease chief complaints
Chest pain or discomfort
• Shoulder, arm, neck, or jaw pain or discomfort
¾ Dyspnea
¾ Syncope
¾ Abnormal heart beat or palpitations
¾ May vary
¾
Chest Pain or Discomfort
z
Common chief complaint in myocardial
infarction
z
Noncardiac causes of chest pain
Pulmonary embolus
Pleurisy
¾ Reflux esophagitis
¾
¾
z
History of chest pain is important
¾
OPQRST method
Dyspnea
z
May occur with myocardial infarction
z
Symptom of heart failure
z
Dyspnea unrelated to heart disease
Chronic obstructive pulmonary disease
Respiratory infection
¾ Pulmonary embolus
¾ Asthma
¾
¾
27
Dyspnea
z
Factors important to differentiate dyspnea:
Duration
Circumstances of onset
¾ What aggravates or relieves, including medications
¾ Previous episodes
¾ Associated symptoms
¾ Orthopnea
¾ Prior cardiac problems
¾
¾
Syncope
z
Sudden decrease in cerebral perfusion
z
Cardiac causes decrease cardiac output
¾
Dysrhythmias
Syncope
z
Noncardiac causes of syncope
Stroke
Drug or alcohol intoxication
¾ Aortic stenosis
¾ Pulmonary embolism
¾ Hypoglycemia
¾
¾
28
Syncope—
Syncope—History
Aura (nausea, weakness, lightheadedness)
Circumstances
z
z
¾
¾
¾
Position before event
Pain
Stress
Duration of syncopal episode
Symptoms before syncope
Other symptoms
Previous episodes
z
z
z
z
Palpitations
z
Sometimes normal
z
May indicate serious dysrhythmia
Palpitations
z
History and physical exam
Pulse rate (if obtained)
Regular versus irregular rhythm
¾ Circumstances
¾ Duration
¾ Chest pain, diaphoresis, syncope, confusion, dyspnea
¾ Previous episodes
¾ Medications
¾
¾
29
Significant Past Medical History
z
Is the patient taking prescription medications,
particularly cardiac medications?
Digoxin
Furosemide (or other diuretics)
¾ Nitroglycerin
¾ Beta blockers
¾
¾
z
Is the patient being treated for any other
illness?
z
Has the patient ever had:
Myocardial infarction or angina pectoris
Coronary artery bypass procedure or
angioplasty
¾ Implanted pacemaker or ICD
¾ Heart failure
¾ Hypertension
¾ Diabetes
¾ Chronic lung disease
¾
¾
z
Allergies
z
Other risk factors for cardiac event
z
Implanted pacemaker or implantable
cardiovertercardioverter-defibrillator (ICD)
30
Physical Examination
z
Classic presentation of myocardial infarction:
¾
z
Other signs and symptoms
¾
¾
¾
¾
¾
z
Pain or discomfort under sternum for longer than 15 min
Apprehension
Diaphoresis
Dyspnea
Nausea and vomiting
Sense of impending doom
Atypical presentations
Initial Assessment
z
Level of consciousness
z
Respirations
z
Pulse (rate, regularity)
z
Blood pressure
z
Skin
Physical Examination
z
“LookLook-listenlisten-feel”
feel” approach
31
Look
z
Skin color, capillary refill, skin moisture
¾
¾
z
Oxygenation (pulse oximetry)
Cardiac function (peripheral perfusion)
Jugular vein distention (JVD)
¾
¾
Evaluate with head elevated to 45 degrees
Difficult to assess in obese patients
Look
z
Peripheral and presacral edema
BackBack-pressure in venous circulation
Obvious in dependent areas
¾ Nonpitting
• Minimal depression of tissue after removal of finger pressure
¾ Pitting
• Depression of tissue remains after removal of finger
¾
¾
pressure
Look
z
Indicators of cardiac disease
Nitroglycerin patch
Midsternal scar from coronary surgery
¾ Implanted pacemaker or automatic implantable
cardiovertercardioverter-defibrillator (left upper chest;
abdominal wall)
¾ Medic alert information
¾
¾
32
Listen
z
Lung sounds
¾
¾
z
Equality
Adventitious sounds
• May indicate pulmonary congestion or edema
Heart sounds
¾
Gallops
Heart Sounds
z
Auscultate for:
Frequency (pitch)
Intensity (loudness)
¾ Duration
¾ Timing in the cardiac cycle
¾
¾
Auscultating Heart Sounds
33
Point of Maximal Impulse (PMI)
z
Apical impulse
¾
¾
z
Visible and palpable
Produced by contraction of left ventricle
Pulse deficits noted by palpating or
auscultating apical impulse and carotid pulse
simultaneously
Heart Sounds
z
Aortic
¾
z
2nd intercostal space to right of sternum
Pulmonic
¾
2nd intercostal space to left of sternum
Heart Sounds
z
Tricuspid
¾
z
5th left intercostal space close to sternal border
Mitral
5th intercostal space medial to left midclavicular line
Over left ventricle
¾ Apical area or apex
¾
¾
34
S1
z
“Lub”
Lub” sound
¾
¾
z
Mitral and tricuspid valve closure
Beginning of ventricular systole
Diaphragm of stethoscope at apex of heart
¾
5th intercostal space
S2
z
“Dub”
Dub” sound
¾
¾
z
Aortic and pulmonic valve closure
End of ventricular systole
Use diaphragm of stethoscope at 2nd
intercostal space to right and left of the
sternum
¾
Aortic and pulmonic areas
S3
z
Extra heart sound
¾
Rapid ventricular filling
z
Common in children, athletes, and young adults
z
Abnormal in persons >30 y/o
z
Use bell of stethoscope at apex
35
S3
z
Sounds like “KenKen-TuckTuck-Y”
¾
¾
z
Emphasis on “Tuck”
Tuck”
“Ken”
Ken” = S1, “Tuck”
Tuck” = S2, “Y” = S3
Warning sign of congestive heart failure
S4
Last of ventricular filling
Tensing of atrioventricular valves
Atrial contraction
Just before S1
Heard at apex with stethoscope bell
Sounds like “TenTen-nesnes-see”
see”
z
z
z
z
z
z
¾
¾
Emphasis on “Ten”
Ten”
“Ten”
Ten” = S4, “Nes”
Nes” = S1, “See”
See” = S2
Feel
z
Peripheral or presacral edema
z
Pulse
Rate
Regularity
¾ Equality
¾ Pulse deficit
¾ Pulsus paradoxus
¾ Pulsus alternans
¾
¾
36
Feel
z
Skin
Diaphoretic, pale skin
• Peripheral vasoconstriction
• Sympathetic stimulation
¾ Cyanosis
• Poor oxygenation
¾ Fever
• Infection
¾
ECG Monitoring
z
Graphic representation of the heart's
electrical activity
z
Generated by depolarization and
repolarization of atria and ventricles
ECG Monitoring
z
Tool to identify cardiac abnormalities:
Abnormal heart rates and rhythms
Abnormal conduction pathways
¾ Hypertrophy or atrophy of portions of the heart
¾ Location of ischemic or infarcted cardiac muscle
¾
¾
37
ECG Monitoring
z
ECG tracing shows the heart's electrical
activity
z
Does not provide information regarding
mechanical events (e.g., force of contraction
or blood pressure)
ECG Monitoring
z
Sum of action potentials in heart during
cardiac cycle measured on body surface
Obtained by applying electrodes to skin and
connecting them to an ECG machine
¾ Voltage changes fed to machine
• Amplified and displayed on screen
• Printed on ECG paper
¾
Voltage
z
Positive
¾
z
Negative
¾
z
Upward deflection on ECG tracing
Downward deflection on ECG tracing
Isoelectric
¾
¾
Straight baseline on ECG
No current detected
38
ECG Leads
z
Two surface electrodes of opposite polarity
Bipolar lead
• Two electrodes of opposite polarity
¾ Unipolar lead
• Single positive electrode and reference point
¾
Leads
z
Bipolar leads
¾
¾
z
Limb leads
I, II, III
Unipolar leads
¾
Augmented limb leads
¾
Precordial leads
• aVR, aVL, and aVF
• V1 through V6
z
Each lead assesses electrical activity from a different
angle
Lead Comparison
I, II, III
Limb lead Bipolar
aVR, aVL, aVF Limb lead Unipolar
V1-V6
Chest lead Unipolar
39
Leads and Cardiac Surfaces
Lead
Cardiac Surface Viewed
II, III, aVF
Inferior wall
V1, V2
Septum
V3, V4
Anterior wall
V5, V6, I, aVL
Lateral wall
Waveforms
z
Leads produce different ECG tracings:
If depolarization moves toward a positive
electrode, ECG shows an upward deflection
¾ If the wave moves away from a positive electrode,
a negative deflection appears on the ECG
¾
Rule of Electrical Flow
40
Standard Limb Leads
z
Record difference in
electrical potential
between left arm, right
arm, and left leg
electrodes
z
Represent axes
Axis
z
Average direction of
the heart’
heart’s electrical
activity
z
Triaxial reference
system
Axis
z
Lead I is a lateral
(leftward) lead
¾
Assesses electrical
activity from a
viewpoint defined as 0°
0°
on a circle divided into
an upper negative 180°
180°
and a lower positive
180°
180°
41
Axis
Leads II and III are
inferior leads
z
¾
Assess the heart's
electrical activity from
vantage points of +60°
+60°
and +120°
+120°
Bipolar Lead Placement
Limb lead placement
Lead
Positive Electrode
Negative Electrode
I
Left arm
Right arm
II
Left leg
Right arm
III
Left leg
Left arm
Augmented Limb Leads
z
Same electrodes as limb leads
z
Record difference in electrical potential
between extremity lead sites and a reference
point
¾
¾
Zero electrical potential
At center of the heart’
heart’s electrical field
42
Axis of each lead is
formed by line from
electrode site to
center of the heart
z
z
aVR, aVL, and aVF leads intersect at angles
different from those of the standard limb
leads
z
Produce three other intersecting lines of
reference
¾
With standard limb leads, these leads make up a
hexaxial reference system
Lead aVR
z
Distant recording
electrode
z
Looks at heart from right
shoulder
43
Lead aVL
z
Lateral lead
z
Records electrical
activity from left
shoulder
¾
-30°
30°
Lead aVF
z
Inferior lead
z
Records electrical
activity from left lower
extremity
¾
+90°
+90°
Limb Leads
z
Leads II, III, aVF
¾
z
Inferior leads
I, aVL
¾
Lateral leads
44
Modified Lead Recording
z
Limb lead placement altered to mimic
precordial leads (V1 through V6)
¾
¾
z
Modified chest leads
MCL1 to MCL6
May help:
Distinguish between supraventricular tachycardia
with aberration and ventricular tachycardia
¾ Diagnose bundle branch blocks
¾
MCL1
z
Positive electrode in
V1 position
¾
z
4th intercostal space,
right of sternum
Negative electrode
placed anteriorly
¾
Below lateral end of
left clavicle
MCL6
z
Positive electrode on left
midaxillary line at 5th
intercostal space
¾
z
As for lead V6
Negative electrode
placed anteriorly, below
left shoulder
45
Routine ECG Monitoring
z
Usually lead II or MCL1
¾
¾
Best leads to visualize P waves
Monitor for dysrhythmias
SingleSingle-Lead ECG Monitoring
z
Information gathered
Heart rate
Regularity
¾ Length of conduction in areas of the heart
¾
¾
z
Limitations
¾
May fail to reveal abnormalities
• Particularly ST segment changes that signal myocardial
injury or infarction
1212-Lead ECG Monitoring
z
10 electrodes
Four limb leads (right arm, right leg, left arm, left
leg)
• Leads I, II, and III, and aVF, aVL, and aVR
¾ Six chest leads
• V1 through V6
¾
46
z
Leads view left ventricle
from position of its
positive electrode
Identifies ST segment and TT-wave changes
z
¾
Myocardial ischemia, injury, and infarction
z
Identifies VT in widewide-complex tachycardia
z
Determines electrical axis
¾
Presence of fascicular blocks
Determines presence and location of bundle branch
blocks
z
Precordial Leads
z
Six precordial leads are projected through
anterior chest wall toward back
z
Positive leads are placed on chest in
reference to thoracic landmarks
¾
Record electrical activity in transverse or
horizontal plane
47
Precordial Leads
z
V1 and V2: Septal leads
z
V3 and V4: Anterior leads
z
V4 through V6: Lateral
leads
Application of Monitoring Electrodes
z
Electrodes are applied to chest wall
z
When applying electrodes:
¾
¾
Cleanse area to remove moisture and dirt
Use inner surfaces of arms and legs
Application of Monitoring Electrodes
z
When applying electrodes:
Trim excess body hair (if needed)
Attach ECG cables to electrodes
¾ Attach electrodes
¾ Turn on ECG monitor
¾ Obtain baseline tracing
¾ Record tracing at significant events
¾
¾
48
Monitoring Electrodes
z
If poor signal, recheck cable connections and
electrode contact
z
Other causes of poor signal
Excessive body hair
Dried conductive gel
¾ Poor electrode placement
¾ Diaphoresis
¾
¾
1212-Lead Electrode Application
Locate the jugular notch
Palpate for the angle of Louis
...
Follow the angle of Louis to patient’s
right until it articulates with 2nd rib
Locate the 2nd IC space
(immediately below 2nd rib)
49
From the 2nd IC space, the 3rd and
4th IC spaces can be found
V1 is positioned in the 4th IC
space just right of the sternum
From V1, find the corresponding
IC space on the left side of the sternum
Place V2 electrode in the 4th IC
space just left of sternum
From V2 position, locate 5th IC space,
follow to the midclavicular line
Position V4 electrode in 5th IC space in
midclavicular line
50
Position V3 halfway between V2 & V4
V5 is positioned in
anterior axillary line, level with V4
Position V6 in the midaxillary line, level with V4
Video Clip: Placement of 12-lead ECG
51
9-Lead from a 33-Lead
z
Obtain 99-lead reading from 33-lead monitor
z
Enable diagnostic setting (if available)
z
Run leads I, II, and III
¾
Obtain a strip of each lead and label
9-Lead from a 33-Lead
z
Leave monitor in lead III
¾
Negative electrode at left shoulder
z
Move left leg cable to each of MCL positions
(from V1 to V6) to obtain a readout
z
Label each strip
9-Lead ECG Readout
52
ECG Graph Paper
z
Standardized to allow ECG analysis
z
Squares 1 mm in height and width
Darker lines every fifth square, vertically and
horizontally
¾ Large square is 5 mm high and 5 mm wide
¾
ECG Graph Paper
z
As paper moves past stylus of ECG machine, it
measures time and amplitude
z
Time measured on horizontal plane
¾
z
Side to side
ECG recorded at standard speed of 25 mm/sec:
¾
¾
Each small square equals 1 mm (0.04 second)
Each large square equals 5 mm (0.20 second)
ECG Graph Paper
z
Amplitude measured on vertical axis (top to
bottom) of graph paper
z
Each small square of graph paper = 0.1 mV
z
Each large square (five small squares) = 0.5 mV
53
ECG Graph Paper
Calibration
z
Sensitivity of 1212-lead ECG machine is
standardized
z
When calibrated, a 1 mV electrical signal
produces a 10 mm deflection (2 large squares)
on ECG tracing
Time Interval Markings
z
Denoted by short vertical lines on ECG graph
paper
z
At standard speed, the distance between
each short vertical line is 75 mm (3 sec)
54
Relationship of ECG to Electrical Activity
z
z
Each waveform represents conduction of an electrical impulse
through a specific part of the heart
Waveforms begin and end at isoelectric line
¾
Isoelectric line shows absence of electrical activity in cardiac tissue
z
Deflections above baseline—
baseline—positive
z
Deflections below baseline—
baseline—negative
¾
¾
Electrical flow toward positive electrode
Electrical flow away from positive electrode
z
Normal ECG consists of a P
wave, a QRS complex, and a T
wave
z
Also evaluate:
¾
¾
¾
z
PR interval
ST segment
QT interval
Combination of these waves
represents a single heartbeat
¾
One complete cardiac cycle
55
P Wave
z
First positive (upward)
deflection on ECG
z
Atrial depolarization
z
Rounded and precedes QRS
complex
¾
¾
Begins with first positive
deflection from baseline
Ends when wave returns to
baseline
P Wave
z
z
z
Duration normally <0.10 sec
Amplitude normally 0.50.5-2.5 mm
Followed by QRS complex unless conduction disturbances
PR Interval
z
Time it takes for
electrical impulse to be
conducted through atria
and AV node up to
ventricular
depolarization
¾
¾
Measured from beginning
of P wave to beginning of
next deflection on
baseline
0.120.12-0.20 sec
56
PR Interval
Normal PR interval
indicates electrical
impulse conducted
through atria and AV
node, normally and
without delay
z
QRS Complex
z
Three individual waves
¾
¾
¾
Q
R
S
z
Begins where first wave of
complex deviates from
baseline
z
Ends where last wave of
complex begins to flatten at,
above, or below baseline
QRS Complex
z
Direction of QRS
complex may be:
Predominantly positive
• Upright
¾ Predominantly
negative
• Inverted
¾ Biphasic
• Partly positive, partly
¾
negative
57
QRS Complex
z
Normal QRS complex is
narrow and sharply
pointed
z
Duration
¾
z
<0.080.08-0.10 sec
Amplitude
¾
<5 mm to >15 mm
Q Wave
z
First negative
(downward) deflection
of QRS complex on
ECG
¾
z
May not be present in all
leads
Depolarization of
interventricular septum
R Wave
z
First positive deflection after the P wave
¾
Subsequent positive deflections in the QRS complex that
extend above the baseline and that are taller than the first R
wave are called R prime (R’
), etc.
(R’), R double prime (R’’
(R’’),
58
S Wave
z
Negative deflection after
R wave
¾
¾
Subsequent negative
deflections are called S
prime (S’
(S’), S double prime
(S”
(S”)
R and S waves are
electrical forces from
depolarization of right and
left ventricles
QRS Complex
z
Follows P wave
z
Approximate beginning of mechanical systole of
ventricles
¾
z
Continues through onset of T wave
Ventricular depolarization
¾
Conduction of electrical impulse from AV node through
bundle of His, Purkinje fibers, and right and left bundle
branches
QRS Complex
59
ST Segment
z
Early phase of
repolarization of
ventricles
z
Follows QRS complex
z
Ends with onset of T
wave
ST Segment
z
ST segment “takes off”
off”
from the QRS complex
at J point
ST Segment
z
Position of ST segment is commonly judged using
baseline of PR or TP interval for reference
¾
¾
ST segment elevation
ST segment depression
60
ST Segment
z
Abnormal ST segments
Infarction
Ischemia
¾ Pericarditis
¾ After digitalis administration
¾ Other disease states
¾
¾
T Wave
z
Repolarization of ventricular
cells
z
Last part of ventricular
systole
z
Above or below isoelectric
line
z
Usually rounded and slightly
asymmetrical
T Wave
z
Deep, symmetrically inverted T waves may
suggest cardiac ischemia
z
T wave elevated more than half the height of
the QRS complex may indicate:
¾
¾
Onset of myocardial ischemia
Hyperkalemia
61
QT Interval
Onset of the QRS
complex until end of T
wave
z
Artifact
z
Deflections on ECG produced by factors
other than the heart's electrical activity
z
Causes
Improper grounding of ECG machine
Patient movement
¾ Loss of electrode contact with skin
¾ Patient shivering or tremors
¾ External chest compressions
¾
¾
Artifact—
Artifact—Muscle Tremors
62
Artifact—
Artifact—Loose Electrode
Artifact—
Artifact—Biotelemetry
Rhythm Analysis
z
To determine if potential for lifelife-threatening
rhythm disturbances, ask:
Is the patient sick?
What is the heart rate?
¾ Are there normalnormal-looking QRS complexes?
¾ Are there normalnormal-looking P waves?
¾ What is the relationship between P waves and
QRS complexes?
¾
¾
63
Step 1: Analyze the QRS Complex
z
z
Analyze for regularity and width
Supraventricular QRS complexes are <0.10 sec wide
Normal QRS Complexes
Step 1: Analyze the QRS Complex
z
Complexes >0.12 sec wide indicate:
¾
¾
Conduction abnormality in ventricles
Focus that originates in ventricles and is abnormal
64
Analyzing the QRS Complex
z
To evaluate abnormal QRS width, identify
lead with widest QRS complex
¾
Part of QRS complex may be blended with
baseline in some leads
Abnormal QRS Complexes
65
Step 2: Analyze the P Waves
z
Present?
z
Regular?
z
One P wave for each QRS complex, and a QRS
complex follows each P wave?
z
Upright or inverted?
z
All alike?
Normal P Waves
66
Step 3: Analyze the Rate
z
Rate <60 = Bradycardia
z
Rate >100 = Tachycardia
Heart Rate Rulers
z
Various manufacturers
z
Accurate if rhythm is regular
¾
May not be readily available
Heart Rate Calculator Ruler
67
Triplicate Method
z
Memorize two sets of numbers: 300300-150150-100 and 75756060-50
¾
Accurate only if rhythm is regular and >50 bpm
R-R Method 1
z
z
Measure distance in seconds between peaks of two
consecutive R waves
Divide this into 60 to obtain heart rate
R-R Method 2
z
z
Count large squares between peaks of two
consecutive R waves
Divide into 300 to obtain heart rate
68
R-R Method 3
z
z
Count small squares between peaks of two
consecutive R waves
Divide into 1500 to obtain heart rate
6-Second Method
z
Least accurate method
z
Count number of QRS complexes in 66-sec interval
and multiply number by 10
¾
Quickly obtain rate in regular and irregular rhythms
Step 4: Analyze the Rhythm
z
To analyze rhythm, compare RR-R intervals from left to
right,
z
If distances between R waves are equal or vary by
<0.16 sec, rhythm is regular
z
If shortest and longest RR-R intervals vary by >0.16 sec,
rhythm is irregular
69
Determining the Rhythm
Regular Rhythm
z
Regularly irregular rhythm
¾
Patterned irregularity or group beating
70
Occasionally irregular
z
¾
Only one or two RR-R intervals are unequal to the others
Irregularly irregular
z
¾
Totally irregular; no relationship between RR-R intervals
Step 5: Analyze the PR Interval
z
Time it takes for electrical impulse to be
conducted through atria and AV node
z
Should be constant across ECG tracing
71
Step 5: Analyze the PR Interval
z
Prolonged PR interval
Delay in impulse conduction through AV node or
bundle of His
¾ AV block
¾
z
Short PR interval
¾
Impulse progressed from atria to ventricles
through pathways other than AV node
Normal PR Intervals
Normal PR Intervals
72
Abnormal PR Intervals
Abnormal PR Intervals
Causes of Cardiac Dysrhythmias
z
z
z
z
Myocardial ischemia
Autonomic nervous
system imbalance
Distention of heart
chambers
AcidAcid-base
abnormalities
z
z
z
z
z
z
Hypoxemia
Electrolyte imbalance
Drug effects or toxicity
Electrical injury
Hypothermia
CNS injury
73
Classification of Dysrhythmias
z
Based on a number of factors
Changes in automaticity versus disturbances in
conduction
¾ Cardiac arrest (lethal) rhythms and noncardiac
arrest (nonlethal) rhythms
¾ Site of origin
¾
Dysrhythmias Originating in the SA Node
z
Sinus bradycardia
z
Sinus tachycardia
z
Sinus dysrhythmia
z
Sinus arrest
Dysrhythmias Originating in the Atria
z
Wandering pacemaker
z
Premature atrial complex (PAC)
z
Paroxysmal supraventricular tachycardia (PSVT)
z
Atrial flutter
z
Atrial fibrillation
74
Dysrhythmias Originating in the AV Node
z
Premature junctional complex (PJC)
z
Junctional escape complexes or rhythms
z
Accelerated junctional rhythm
Dysrhythmias Originating in the Ventricles
z
z
z
z
z
z
Ventricular escape complexes or rhythm
Premature ventricular complex (PVC)
Ventricular tachycardia (VT)
Ventricular fibrillation (VF)
Asystole
Artificial pacemaker rhythm
Disorders of Conduction
z
AV blocks
¾
¾
¾
¾
FirstFirst-degree AV block
SecondSecond-degree AV block type I
SecondSecond-degree AV block type II
ThirdThird-degree AV block
z
Disturbances of ventricular conduction
z
Pulseless electrical activity (PEA)
z
Preexcitation syndrome: WolffWolff-ParkinsonParkinson-White (WPW)
syndrome
75
Treatment Guidelines
z
Treat patient, not monitor
z
Algorithms presume condition persists,
¾
z
In cardiac arrest CPR is always performed
Apply different interventions if indications exist
z
Airway, ventilation, oxygenation, chest
compression, and defibrillation
z
Take precedence over initiating an IV line or
administering drugs
z
Some medications can be administered via
endotracheal tube
¾
z
Use endotracheal dose 22-2½ times IV dose for adults
In arrest, with few exceptions IV meds are
administered rapidly by bolus method
¾
Follow with a 2020-30 mL bolus of IV fluid and
immediately elevate extremity
76
Sinus dysrhythmias
z
¾
Often from increases or decreases in vagal tone
SA node gets inhibitory parasympathetic impulses
from vagus nerve to keep rate below discharge rate
of pacemaker cells
z
¾
¾
If vagal discharge increases, heart rate becomes
bradycardic
If vagal discharge decreases, sympathetic stimulation results
in sinus tachycardia
z
SA node dysrhythmias
Normal duration of QRS complex
• If no bundle branch block
¾ Upright P waves in lead II
¾ P waves similar
¾ Normal duration of PR interval
• If no AV block
¾
Sinus Rhythm
77
Sinus Bradycardia
z
Slowing of pacemaker rate of SA node
z
Causes
¾
¾
¾
¾
¾
¾
¾
Adult HR <60 bpm
Sinus node disease
Increased vagal tone
Hypoxia
Hypothermia
Drugs
AMI
Can decrease cardiac output and cause:
z
¾
¾
¾
Hypotension
Syncope
Angina
Sinus Bradycardia
Sinus Bradycardia—
Bradycardia—Management
z
Observe, if patient clinically stable
z
If unstable, treatment may include:
Oxygen
Atropine
¾ Dopamine infusion
¾ Epinephrine infusion
¾ Transcutaneous pacing
¾
¾
78
Sinus Tachycardia
z
Increase in rate of sinus
node discharge
¾
Adult HR >100 bpm
z
Causes
¾
¾
¾
z
Treat underlying cause
¾
¾
¾
¾
Exercise
Fever
Ingestion of drugs
Smoking
Hypovolemia
Anemia
Congestive heart failure
Sinus Tachycardia
Sinus Dysrhythmia
z
Difference between the longest and shortest
R-R intervals is >0.16 sec
z
Often normal
z
Occurs in heart disease, drug treatment
z
No clinical management needed
79
Sinus Dysrhythmia
Sinus Arrest
z
Marked depression in
SA node automaticity
z
Causes
¾
¾
z
Sinus node fails,
causes periods of
cardiac standstill until:
¾
¾
Other pacemakers
discharge
Sinus node resumes
normal function
¾
¾
¾
¾
Hypoxia
Ischemia
Excess digitalis or
propranolol
Hyperkalemia
Damaged SA node
Sinus Arrest
z
z
z
z
z
May cause decreased cardiac output
Syncope
Asystole possible
Observe
If symptomatic:
¾
¾
Atropine
TCP
80
Sinus Arrest
z
Originate in tissues of atria or internodal
pathways
z
Causes of atrial dysrhythmias
Ischemia
Hypoxia
¾ Atrial dilation caused by:
• Congestive heart failure
• Mitral valve abnormalities
• Increased pulmonary artery pressures
¾
¾
z
ECG features common to atrial dysrhythmias
(if no ventricular conduction disturbance):
Normal QRS complexes
P waves (if present) that differ in appearance from
sinus P waves
¾ Abnormal, shortened, or prolonged PR intervals
¾
¾
81
Wandering Atrial Pacemaker
z
Transfer of pacemaker sites from sinus node to other
pacemaker in atria or AV junction
z
Shift in site is usually transient
z
May be normal
z
Can result from digitalis toxicity
z
Not often clinically significant
Wandering Atrial Pacemaker
Multifocal Atrial Tachycardia
z
Variant of wandering atrial pacemaker
¾
Rates in the 120 to 150 per minute range
z
Common in severe COPD
z
Treat underlying disorder
z
ECG characteristics
z
Clinical significance
z
Management
82
Premature Atrial Complex
z
Single impulse originating in atria
¾
Outside sinus node
z
Single ectopic pacemaker site or multiple sites in
atria
z
Enhanced automaticity or reentry mechanism
z
Isolated PACs not significant
z
Multiple PACs may predispose to SVT
Premature Atrial Complex
z
Causes
¾
¾
¾
¾
¾
¾
z
Increased sympathetic
tone
Stimulant use
Drugs
Hypoxia
Cardiac disease
Treatment
¾
¾
Observation
If not conducted:
• May need bradycardia
treatment
PACs
83
SVT and PSVT
z
Supraventricular tachycardias (SVTs)
Paroxysmal supraventricular tachycardia (PSVT)
Nonparoxysmal atrial tachycardia
¾ Multifocal atrial tachycardia
¾ Junctional tachycardia
¾ Atrial flutter
¾ Atrial fibrillation
¾
¾
SVT and PSVT
z
PSVT
¾
z
Atrial origin
¾
z
Paroxysmal atrial tachycardia (PAT)
AV junction
¾
z
Supraventricular tachycardia that begins abruptly
Paroxysmal junctional tachycardia (PJT)
Rapid atrial or junctional depolarization overrides SA
node
SVT and PSVT
z
Often reentry mechanism
z
Stress, overexertion, tobacco, caffeine
z
WolffWolff-ParkinsonParkinson-White syndrome
z
May be tolerated briefly if healthy
z
Can cause:
¾
¾
¾
Compromised cardiac output
Hypotension syncope
CHF
84
SVT and PSVT—
PSVT—Treatment
z
Stable
z
Unstable
¾
Vagal maneuvers
¾ Adenosine
¾ Calcium Channel
Blockers or
¾ Beta blockers
¾
Synchronized cardioversion
• 50 J (PSVT or Atrial Flutter)
• 100 J
• 200 J
• 300 J
• 360 J
h
Or equivalent biphasic
PSVT
Atrial Flutter
z
Usually rapid atrial
reentry focus
z
Associated with:
¾
¾
z
Conduction variable
z
Sawtooth or picketpicketfence appearance
¾
¾
¾
z
Loss of atrial kick
z
May decrease perfusion
¾
¾
Cardiomyopathy
Cardiac hypertrophy
Digitalis toxicity
Hypoxia
CHF
Pericarditis
Myocarditis
85
Atrial Flutter
Atrial Fibrillation
z
Multiple areas of reentry in atria or ectopic
atrial pacemakers
z
Chaotic impulses too numerous to be
conducted by AV node through ventricles
AV conduction is random
Ventricular response irregular
¾ Usually rapid unless patient is on medication to
slow ventricular rate
¾
¾
Atrial Fibrillation
z
P waves absent
z
F waves
z
Causes
¾
¾
¾
¾
z
Atrial kick lost
z
More unstable with rapid
ventricular response
z
Cardiac decompensation
¾
“Holiday heart”
heart” syndrome
Rheumatic heart disease
CHF
Cardiac disease
Chest trauma
86
Atrial Fibrillation
A-Fib & AA-Flutter Management
Management based on:
z
¾
¾
¾
Time of rhythm onset
Signs and symptoms
Heart function
Rate control with:
z
¾
¾
¾
Diltiazem
Beta blockers
Magnesium
z
Unstable
¾
Synchronized
cardioversion
• 50 J (Atrial Flutter)
• 100 J
• 200 J
• 300 J
• 360 J
h
Or equivalent
biphasic
Atrial Fibrillation and WolffWolffParkinson White Syndrome
z
Do not administer:
Adenosine
Diltiazem or verapamil
¾ Beta blockers
¾ Digoxin
¾
¾
87
Dysrhythmias of the AV Junction
z
If SA node and atria don’
don’t generate electrical
impulses, AV node or area surrounding it may
assume role of secondary pacemaker
Dysrhythmias of the AV Junction
z
May occur because of:
Hypoxia
Ischemia
¾ Myocardial infarction
¾ Drug toxicity
¾
¾
z
Usually benign arrhythmia
z
Assess to determine patient's response to
rhythm
Premature Junctional Complex
z
Single electrical impulse
z
Originates in AV junction
z
Occurs before next expected sinus impulse
z
P waves occur before, during, or after QRS
z
Abnormal P wave
z
PRI <0.12 sec
88
Premature Junctional Complex
z
Usually no clinical
significance
z
Causes
¾
¾
z
No treatment needed
¾
¾
¾
Medications
Hypoxia
AV junction damaged
PJCs
Junctional Escape Complex or Rhythm
z
Isolated impulse or rhythm
z
Rate of primary pacemaker falls below AV junction
or with SA or AV block
z
P waves may be absent
z
If present before, during, or after QRS
z
PRI <0.16 sec
z
Rate: 4040-60/min
89
z
Decreased cardiac
output
¾
z
Causes
¾
¾
¾
Slowed SA discharge
AV block
Stable
¾
z
Usually rates below
50/min
z
Observe
Unstable
¾
Treat as bradycardia
Accelerated Junctional Rhythm
z
Increased AV junction automaticity
z
Discharges faster than intrinsic rate
¾
4040-60 bpm
z
Overrides SA node
z
Rate: 6060-99 bpm
z
Usually stable
z
Observe
90
Accelerated Junctional Rhythm
z
Ventricular rhythms often life threatening
z
Failure of atria, AV junction
z
Enhanced automaticity
z
Reentry
z
Associated with myocardial ischemia or infarction
z
Least efficient pacemaker
z
QRS complexes >0.12 sec, bizarre appearance
z
P waves hidden or superimposed on QRS
z
ST deviated from baseline
91
Ventricular Escape Complexes or Rhythms
z
Isolated impulse or rhythm
z
Idioventricular rhythm
z
Impulses from higher pacemakers
¾
¾
¾
z
Fail
Don’
Don’t reach ventricles
Or rate of discharge of higher pacemakers is less than that
of ventricles
Compensatory mechanism
¾
Prevents cardiac standstill
Ventricular Escape Complexes or Rhythms
z
z
Hypotension
Decreased
¾
¾
z
z
z
z
z
Cardiac output
Perfusion to brain
z
Management
¾
¾
¾
Oxygen
TCP
Dopamine
Syncope
Shock
Absent P waves
Rate 2020-40 bpm
Wide QRS
Ventricular Escape Rhythm
92
“Dying Heart”
Heart” or Agonal Rhythm
Premature Ventricular Complexes
z
Single ectopic impulse
z
From irritable focus in ventricle
z
Earlier than expected sinus beat
z
Common
z
Occurs with any cardiac rhythm
z
Enhanced automaticity or a reentry mechanism
PVCs
93
Compensatory Pause
z
Measure interval between R wave before
PVC and R wave after PVC
z
If compensatory, distance equals twice RR-R
interval of underlying rhythm
z
Interpolated PVC
¾
¾
PVC falls between two sinus beats
Doesn’
Doesn’t interrupt rhythm
Interpolated PVC
Unifocal and Multifocal PVCs
z
Unifocal PVCs
¾
¾
z
Originate from single site within ventricles
Look alike
Multifocal PVCs
¾
¾
Originate from different ventricular sites
Varying shapes and sizes
94
Unifocal and Multifocal PVCs
Fusion Beats
z
PVCs occur at same time as ventricular
activation by underlying rhythm
¾
z
Can cause ventricular depolarization
simultaneously in two directions
Fusion beat QRS complex has characteristics
of PVC and QRS complex of underlying
rhythm
Fusion Beat with PVC
95
Grouped Beating
z
PVCs in patterns of grouped beating
Bigeminy
• Every other complex is PVC
¾ Trigeminy
• Every 3rd complex is PVC
¾ Quadrigeminy
• Every 4th complex is PVC
¾
Ventricular Bigeminy and Trigeminy
PVCs
z
PVCs not separated by complex of underlying rhythm
z
Couplets
¾
z
Run of VT
¾
¾
z
Two PVCs in a row
>3 sequential PVCs
Rate: >100 bpm
R-onon-T phenomenon
96
R-onon-T Phenomenon
PVCs—
PVCs—Causes
Healthy individuals
z
¾
Usually no significance
Pathological PVCs
z
¾
¾
¾
¾
¾
¾
¾
Myocardial ischemia
Hypoxia
Increased sympathetic tone
Stimulants
Drugs
PVCs
z
QRS >0.12 sec
z
P waves present or absent
¾
z
No relationship to QRS
Significant if:
Frequent
Multifocal
¾ R-onon-T
¾ Grouped beats
¾
¾
97
PVCs
z
Management, if clinically significant:
Oxygen
Antiarrhythmic drugs
¾ Check potassium at hospital
• Treat hypokalemia if present
¾
¾
Ventricular Tachycardia
z
>3 consecutive ventricular complexes
z
Rate: >100 bpm
z
Overrides primary pacemaker
z
Starts suddenly, triggered by a PVC
z
Atria and ventricles are asynchronous
z
If sustained, may lead to unconsciousness and loss of
pulse
Monomorphic Ventricular
Tachycardia
z
z
z
z
z
z
z
Cardiac disease
Electrolyte imbalances
CHF
Increased catecholamines
Stimulants
Drugs
Long QT interval
z
Stable but symptomatic:
¾
¾
¾
Oxygen
Amiodarone
Procainamide
z
Unstable
z
Pulseless
¾
¾
Cardioversion
Treat as ventricular
fibrillation
98
Monomorphic VT
Torsades de Pointes
z
Prolonged QT interval
¾
z
Treatment varies:
¾
May or may not be
present
¾
¾
z
Idiopathic
z
Drug induced
z
Polymorphic VT
¾
¾
z
DC drugs that prolong QT
Magnesium sulfate
Lidocaine
Isoproterenol
Overdrive pacing
If Unstable:
¾
Unsynchronized
cardioversion
Torsades de Pointes
99
1212-Lead Strategies for
WideWide-Complex Tachycardias
z
Determine axis deviation:
¾
¾
Leads I, II, III, MCL1 (V1), MCL6 (V6)
QRS complex negative in leads I, II, and III
(extreme right axis deviation, or “no man’
man’s
land”
land”) and positive in MCL1 (V1) indicates VT
• If not, proceed to step 2
Criteria for VT
z
If extreme right axis deviation is not
present, assess QRS deflection in MCL1
(V1) and MCL6 (V6):
Negative QS complex
Negative RS complex
¾ Wide Q wave in MCL6 (V6) indicates VT
¾
¾
z
Regardless of the QRS deflection in leads
I, II, and III
100
z
VT if positive QRS deflections with either:
Single peak
Taller left “rabbit ear”
ear”
¾ RS complex with a fat R wave
¾ Slurred S wave in MCL1 (V1)
¾
¾
Note “Rabbit Ear”
Ear”
z
The presence of right axis deviation
(negative QRS complex in lead I; positive
QRS complex in leads II and III) and a
negative QRS complex in MCL1 (V1) indicates
VT
101
Right Axis Deviation and a
Downward MCL1 Indicates VT
z
VT if:
¾
All precordial leads (V leads) are either positive or
negative
• Precordial concordance
VTVT-Concordance
102
z
RS interval >0.10 sec in any V lead indicates
VT
z
Increased ventricular activation time
VT (RS interval is 0.16 sec)
Ventricular Fibrillation
z
Chaotic ventricular rhythm
z
Quivering ventricular movements
z
No pulse
z
Multiple reentry foci in ventricles
103
Ventricular Fibrillation—
Fibrillation—Causes
z
Myocardial ischemia
z
Acidosis
z
AMI
z
z
ThirdThird-degree AV block
z
Electrical injury
z
Cardiomyopathy
z
Drug toxicity
z
Digitalis toxicity
z
Hypoxia
Ventricular Fibrillation—
Fibrillation—Treatment
z
If unwitnessed
¾
z
z
CPR first then:
Epinephrine
¾
May substitute vasopressin
for first or second dose
Defibrillation
z
z
Intubation
z
Vascular access
Amiodarone
¾
z
Lidocaine as alternative
Effective CPR
Ventricular Fibrillation
104
Coarse and Fine VF
Ventricular Asystole
z
Absence of ventricular activity
z
Confirm in two leads
z
Primary event or follows other dysrhythmias
z
No cardiac output
z
Terminal rhythm
Ventricular Asystole—
Asystole—Treatment
z
Effective CPR
z
Intubation/IV
z
Epinephrine
z
Atropine
z
Consider and treat other causes
¾
Sodium bicarbonate possible
105
Ventricular Asystole
Artificial Pacemaker Rhythms
z
Generate rhythm by electrical stimulation
through electrode in the heart
Fixed rate or asynchronous
Demand pacemakers
¾ Atrial synchronous ventricular pacemakers
¾ AV sequential pacemakers
¾ RateRate-responsive pacemakers
¾
¾
Artificial Pacemaker Rhythms
106
Causes of Pacemaker Malfunction
z
Battery failure
z
Runaway pacemaker
z
Failure of sensing device in demand pacemaker
z
Failure to capture
Management of Pacemaker Failure
z
z
z
z
True emergency
Immediate recognition
Rapid transport
Principles to follow:
Look for battery packs under skin/medical ID tag
Follow appropriate algorithm
¾ Manage ventricular irritability
¾ Defibrillate if needed; do not discharge energy
directly over battery pack
¾ Use TCP if indicated
¾
¾
Heart Blocks
z
Delays or complete interruptions in cardiac
electrical conduction
z
Occur in atria, between SA node and AV node,
or in ventricles between AV node and Purkinje
fibers
z
Caused by:
¾
¾
Pathology in conduction system
Physiological block
107
Heart Blocks—
Blocks—Causes
z
AV junctional ischemia
z
AV junctional necrosis
z
Degenerative disease of conduction system
z
Electrolyte imbalances
z
Drug toxicity
¾
Often digitalis
Heart Blocks—
Blocks—Classification
z
Classified by:
Site of block
• (e.g., left bundle branch block)
¾ Degree of block
• (e.g., secondsecond-degree AV block)
¾ Category of AV conduction disturbances
• (e.g., Type I)
¾
FirstFirst-Degree AV Block
z
Not true block
z
Delay in conduction
¾
Usually at AV node
z
Superimposed on another rhythm
z
Identify underlying rhythm
108
z
PRI >0.20 sec
z
Usually transient
z
Often asymptomatic
z
May progress to other block
z
Observe
SecondSecond-Degree AV Block Type I
(Wenckebach)
z
z
z
Intermittent
AV node
Conduction delay increases from beat to beat until
conduction to ventricle is blocked
¾
¾
z
z
PR intervals get progressively longer until a P wave occurs
that is not followed by QRS complex
Pattern
May be symptoms if rate is very slow
Treat for bradycardia if symptomatic
109
SecondSecond-Degree AV Block Type I
SecondSecond-Degree AV Block Type II
z
Intermittent block
z
Atrial impulses are not conducted to ventricles
z
P waves conducted with a constant PR interval
before a dropped beat
z
Usually a regular sequence with conduction
ratios (P waves to QRS complexes)
¾
2:1, 3:2, and 4:3
110
3:2 AV Block and 4:3 AV Block
z
Below bundle of His
z
Two consecutive impulses (atrial P waves)
fail to be conducted to ventricles
z
HighHigh-grade AV block
111
3:1 HighHigh-Grade AV Block
z
HighHigh-grade AV blocks have underlying atrial
and ventricular rates
z
Slow rates and hypoperfusion
z
May advance to complete heart block
z
Treat symptomatic patients with TCP
ThirdThird-Degree Heart Block
z
Complete electrical block at or below the AV node
¾
Infranodal
z
SA node paces atria, and an ectopic focus paces
ventricles
z
P waves and QRS complexes occur rhythmically, but
the rhythms are unrelated to each other
¾
AV dissociation
112
ThirdThird-Degree AV Block
z
Causes
¾
¾
¾
¾
¾
z
Septal necrosis
Myocarditis
Drug toxicity
Significance
¾
¾
¾
Bradycardia may be severe
Cardiac output decreased
Wide complex is ominous sign
ThirdThird-Degree AV Block—
Block—Treatment
z
Transvenous pacer is needed
z
Initial prehospital care if symptomatic:
TCP
Dopamine
¾ Epinephrine
¾
¾
ThirdThird-Degree AV Block
113
Ventricular Conduction Disturbances
z
Bundle branch blocks or hemiblocks
z
Delay electrical transmission below bundle of
His
Bundle Branch Blocks and Hemiblocks
z
Common causes of bundle branch block
Ischemic heart disease
Acute heart failure
¾ Acute myocardial infarction
¾ Hyperkalemia
¾ Trauma
¾ Cardiomyopathy
¾ Aortic stenosis
¾ Infection
¾
¾
Bundle Branch Anatomy
z
Bundle of His divides:
Left and right bundle branches
Right bundle branch continues toward apex and
spreads through right ventricle
¾ Left bundle branch subdivides into anterior and
posterior fascicles and spreads through left ventricle
¾
¾
z
Electrical impulse conduction through Purkinje
fibers stimulates ventricular contraction
114
z
Normal conduction
Left side of septum is stimulated first
Electrical impulse traverses septum to stimulate
other side
¾ Left and right ventricles are then simultaneously
stimulated
¾
¾
Normal Ventricular Activation
115
Bundle Branch Block—
Block—ECG
z
One ventricle depolarizes and contracts
before the other
z
Ventricular activation is not simultaneous,
therefore QRS complex widens
¾
z
Slurred or notched appearance
• “Rabbit ears”
ears”
QRS complex is >0.12 sec
Bundle Branch Block
z
Criteria for bundle branch block
¾
¾
QRS complex >0.12 sec
QRS complexes produced by supraventricular
activity
Bundle Branch Block
z
Leads V1 and V6
¾
¾
z
MCL1 and MCL6
Permit differentiation of right and left bundle
branch blocks
Normal conduction
¾
¾
V1 (MCL1) is predominantly negative
QRS complex is 0.080.08-0.10 sec
116
Right Bundle Branch Block
z
Left bundle branch performs normally
z
Activates left side of heart before right
z
ECG characteristics
Initial negative deflection (S wave)
RSRRSR-prime pattern
¾ QRS (or in this case, RSR) duration >0.12 sec
¾
¾
Right Bundle Branch Block
Left Bundle Branch Block
z
Fibers that fire interventricular septum are
blocked:
¾
¾
z
Alters normal septal activation
Sends it in opposite direction
ECG characteristics
Initial Q wave in V1 (MCL1)
R wave in V1 (MCL1)
¾ Deep, wide S wave (QS pattern)
¾ QRS duration >0.12 sec
¾
¾
117
Left Bundle Branch Block
Left vs. Right BBB
z
Find J point
z
Draw line back into
QRS complex
z
Fill in triangle created
z
Note direction triangle
points
Anterior Hemiblock
z
More common than posterior hemiblock
z
Anterior fascicle of left bundle branch is a longer
and thinner structure
z
Blood supply primarily from left anterior
descending (LAD) coronary artery
z
Anterior hemiblock characterized by left axis
deviation in patient with supraventricular rhythm
118
Anterior Hemiblock
z
Other ECG findings in anterior hemiblock:
Normal QRS complex (<0.12 sec) or a right
bundle branch block
¾ Small Q wave followed by tall R wave in lead I
¾ Small R wave followed by deep S wave in lead III
¾
z
High risk to develop complete heart block
Anterior Hemiblock
Showing 1 Block of 3 Fascicles
Posterior Hemiblock
z
Right axis deviation with normal QRS
complex or right bundle branch block
z
Other ECG findings
¾
¾
Small R wave followed by deep S wave in lead I
Small Q wave followed by tall R wave in lead III
119
Posterior Hemiblock
Showing 2 of 3 Fascicles Blocked
Bifascicular Block
z
2 of 3 pathways for ventricular conduction
blocked
Right bundle branch block with anterior or posterior
hemiblock
¾ Left bundle branch block
¾
z
Compromises myocardial contractility and
cardiac output
z
May develop complete heart block suddenly
Multilead Determination of Axis and
Hemiblocks
z
Identifying axis can be useful in
determining the presence of hemiblocks
z
Best evaluated by looking at the QRS
complexes in leads I, II, and III
120
Hemiblocks
z
Axis is:
Normal if QRS deflection is positive in bipolar leads
Physiological left (normal in some patients) when QRS
deflection is:
• Positive in leads I and II
• Negative (inverted) in lead III
¾ Pathological left when QRS deflection is:
• Positive in lead I
• Negative in leads II and III (indicating an anterior hemiblock)
¾
¾
Hemiblocks
z
Right axis when QRS deflection is:
¾
¾
¾
z
Negative in lead I, negative or positive in lead II
Positive in lead III (pathological in any adult)
Indicative of posterior hemiblock
Extreme right (“
(“No man’
man’s land”
land”) when QRS
deflection is negative in all three leads
¾
Rhythm is ventricular in origin
Pulseless Electrical Activity
z
Absence of detectable pulse and presence of
rhythm other than VT or VF
z
Prognosis is poor unless underlying cause is
identified and corrected
z
Priority of care is to maintain circulation with
basic and advanced life support
z
Search for correctable cause
121
Correctable causes
z
¾
¾
¾
¾
¾
¾
¾
Cardiac tamponade
Tension pneumothorax
Hypoxemia
Acidosis
Hyperkalemia
Hypothermia
Drug overdoses
z
Less correctable causes
¾
¾
¾
¾
¾
Massive myocardial damage
Prolonged ischemia
Profound hypovolemia
Massive pulmonary embolism
Profound shock
z
Management
Effective CPR
ALS
¾ Epinephrine
¾ Atropine if HR <60 bpm
¾ Identify and correct specific causes
¾
¾
Various PEA Rhythms as Seen in Lead II
122
Preexcitation Syndromes
z
Clinical condition with abnormal conduction
pathway between atria and ventricles
Bypasses AV node and/or bundle of His
Allows electrical impulses to depolarize ventricles
earlier than usual
¾ Several accessory pathways
¾
¾
z
Most common preexcitation syndrome is
WolffWolff-ParkinsonParkinson-White (WPW) syndrome
WolffWolff-ParkinsonParkinson-White Syndrome
z
Bundle of Kent connects lateral wall of atrium and
ventricle
¾
Bypasses AV node
z
LifeLife-threatening if tachycardia develops
z
Rate: Normal unless associated with rapid
supraventricular tachycardia
z
PR interval <0.12 sec
¾
Normal delay at AV node does not occur
WolffWolff-ParkinsonParkinson-White Syndrome
z
ECG findings
¾
¾
¾
Short PR interval
Delta wave
QRS widening
z
Susceptible to PSVTs
z
Amiodarone, procainamide
z
May be harmful:
¾
¾
Adenosine, calcium channel blockers
Beta blockers, digoxin
123
WPW
(A) Appearance of WPW
syndrome in leads where QRS
complex is upright
(B) Appearance of WPW
syndrome with QRS complex
predominantly negative
Acute Coronary Syndromes
z
Acute myocardial infarction (AMI)
Unstable angina (UA)
z
Treatment goals
z
Reduce myocardial necrosis
Prevent major adverse cardiac events
¾ Treat acute complications of ACS
¾
¾
Atherosclerosis
z
Progressive narrowing of lumen of medium and
large arteries
¾
z
Aorta and its branches, cerebral arteries, coronary
arteries
Development of thick, hard, atherosclerotic
plaques called atheromas or atheromatous
lesions
¾
Commonly found in areas of turbulent blood flow
124
Atherosclerosis—
Atherosclerosis—Risk Factors
z
z
z
z
z
z
z
Age
Earlier in men than women
Family history
Diabetes
Smoking
Hypertension
Hypercholesterolemia
Atherosclerosis—
Atherosclerosis—Effects
z
Disrupts intimal surface, causing loss of
vessel elasticity and increase in
thrombogenesis
¾
¾
Atheroma reduces diameter of vessel lumen
Decreases blood supply to tissues
Angina Pectoris
z
Symptom of myocardial ischemia
z
“Choking”
Choking” pain in the chest
z
Imbalance between myocardial oxygen supply and
demand
z
Accumulation of lactic acid and carbon dioxide in
ischemic tissues of myocardium
¾
Metabolites irritate nerve endings and produce pain
125
Angina Pectoris
z
Causes
¾
¾
Atherosclerotic disease of the coronary arteries
Temporary occlusion due to coronary artery
spasm with or without atherosclerosis
• Prinzmetal's angina
Angina Pectoris
z
Pain described as pressure, squeezing, heaviness, or
tightness in chest
¾
¾
z
30% feel pain only in chest
Others describe as radiating to shoulders, arms, neck, and
jaw and through to back
Associated signs and symptoms
¾
¾
¾
¾
Anxiety
Shortness of breath
Nausea or vomiting
Diaphoresis
Stable Angina
z
Usually caused by physical exertion or emotional
stress
z
Pain lasts 11-5 min
¾
May last as long as 15 min
z
Relieved by rest, nitroglycerin, or oxygen
z
“Attacks”
Attacks” are usually similar in nature
z
Always relieved by same therapy
126
Unstable Angina
z
Preinfarction angina
z
Anginal pattern that has changed in its ease of onset,
frequency, intensity, duration, or quality
z
Includes “new onset”
onset” anginal chest pain
z
May occur during exercise or at rest
z
Pain lasts >10 min
z
Less promptly relieved than stable angina
Unstable Angina—
Angina—Management
z
Place patient at rest
z
Administer oxygen
z
Administer aspirin (per protocol)
z
IV therapy
z
Pharmacological therapy
¾ Nitroglycerin
¾ Morphine
z
Monitor ECG
z
Transport as soon as possible
Myocardial Infarction
z
Sudden and total occlusion or nearnear-occlusion of
blood flowing through affected coronary artery
z
Ischemia, injury, and necrosis of myocardium distal to
occlusion
z
Often associated with atherosclerotic heart disease
(ASHD)
z
Precipitating events
127
Types and Locations of Infarcts
z
Infarction distal to occluded artery
z
Size of infarct determined by:
Metabolic needs of tissue supplied by occluded
vessel
¾ Collateral circulation
¾ Time until flow is reestablished
¾
z
Emergency care
Increasing oxygen supply
Decreasing metabolic needs
¾ Providing collateral circulation
¾ Reestablishing perfusion to ischemic myocardium
quickly
¾
¾
z
Most AMIs involve ventricle or
interventricular septum, which is supplied
by either of two major coronary arteries
¾
Some patients sustain damage to right ventricle
128
z
Anterior, lateral, or septal wall infarction
¾
z
Usually left coronary artery occlusion
Inferior wall infarction
¾
Usually right coronary artery occlusion
Myocardial Infarction
z
Three ischemic syndromes
z
Based on rupture of an unstable plaque in an
epicardial artery
Unstable angina
NonNon-STST-elevation myocardial infarction
¾ STST-elevation myocardial infarction
¾
¾
Infarction
z
Unstable angina
Thrombus has not completely obstructed coronary
flow
¾ Intermittent ischemic episode
¾ May lead to complete occlusion and AMI
¾
z
NonNon-STST-elevation MI
¾
¾
STST-segment depression
T-wave abnormalities
129
Infarction
z
STST-elevation MI
¾
Q-wave MI
• Pathological Q waves
h
h
> 5 mm in depth
> 0.04 sec in duration in
>2 contiguous leads
Death of Myocardium
z
After blood flow to myocardium stops, cells
switch to anaerobic metabolism
¾
Produces ischemic pain (angina)
z
Cells begin to swell and depolarize
z
If collateral flow and reperfusion are
inadequate, much of muscle dies distal to
occlusion
Area of Infarction
130
Myocardial Infarction—
Infarction—Deaths
z
z
z
Lethal dysrhythmias
• VT
• VF
• Cardiac standstill
Pump failure
• Cardiogenic shock
• CHF
Myocardial tissue rupture
• Ventricle, septum, or papillary muscle
MI—
MI—Signs and Symptoms
Pain is similar to angina
May radiate to arms, neck, jaw, or back
Dyspnea
Anxiety
Agitation
Sense of impending doom
Nausea and vomiting
Diaphoresis
Cyanosis
Palpitations
z
z
z
z
z
z
z
z
z
z
MI—
MI—Signs and Symptoms
z
Chest pain often constant
z
Not altered by nitroglycerin or medications,
rest, changes in body position, or breathing
patterns
¾
¾
Onset of pain at rest in >50% of MI patients
Most have experienced warning anginal pain
(preinfarction angina) hours or days before
131
Infarction—ECG Findings
z
Heart muscle unable to contract effectively
z
Remains in depolarized state
¾
Current flow between pathologically depolarized
and normally repolarized areas can produce:
• Abnormal ST segment elevation
• Ischemic ST segment depression
• Normal or nonnon-diagnostic ECG changes
Infarction—ECG Findings
z
STST-Segment Elevation MI (STEMI)
¾
¾
z
HighHigh-Risk UA/nonUA/non-STST-Elevation MI (NSTEMI)
¾
¾
z
ST segment elevation >1 mm in 2 adjacent leads
new LBBB
ST segment depression >0.5 mm lasting 20 min.
T-wave inversion with pain
Normal or nondiagnostic ECG changes
¾
Inconclusive changes
Myocardial Infarction ECG Imposters
z
z
z
z
z
z
Left bundle branch block
Some ventricular rhythms
Left ventricular hypertrophy
Pericarditis
Ventricular aneurysm
Early repolarization
132
Infarction—Management
z
z
z
z
z
z
z
Oxygen
Aspirin
Nitroglycerin
Morphine
1212-lead ECG
Fibrinolytic screening
Transport to appropriate facility
ST Segment Elevation Likely with
Acute Injury
STST-Elevation and Infarct Location
Lead
Location of Infarction
Coronary Artery
Involved
II, III, aVF
Inferior wall
(most common)
Right
V1, V2
Septal wall
Left
V3, V4
Anterior wall
(most lethal)
Left
I, aVL, V5, V6
Lateral wall
Left
V4R, V5R, V6R
Right ventricle
Right
133
Multilead Assessment of the Heart
Left Ventricular Failure (LVF) and
Pulmonary Edema
z
Left ventricle fails to function as an effective
forward pump
z
Causes backback-pressure of blood into pulmonary
circulation
LVF and Pulmonary Edema
z
Caused by heart disease, including:
Ischemic
Valvular
¾ Hypertensive heart disease
¾
¾
z
Untreated LVF leads to pulmonary edema
134
LVF—
LVF—Signs and Symptoms
z
z
z
z
z
z
z
Respiratory distress
Apprehension, agitation, confusion
Cyanosis (if severe)
Diaphoresis
Adventitious lung sounds
JVD
Abnormal vital signs
Pulmonary Edema—
Edema—Management
z
z
z
z
z
z
z
z
Oxygen, IV, monitor
1212-lead ECG
Nitroglycerin (SBP >100)
Furosemide
Morphine
CPAP
Reversible causes
Dobutamine or dopamine for shock
Right Ventricular Failure (RVF)
z
Right ventricle fails as effective forward pump
z
BackBack-pressure of blood into systemic venous
circulation
135
RVF
z
Causes
Chronic hypertension (LVF precedes RVF)
COPD
¾ Pulmonary embolism
¾ Valvular heart disease
¾ Right ventricular infarction
¾
¾
z
RVF usually results from LVF
RVF
z
Signs and symptoms
Tachycardia
Venous congestion
• Engorged liver, spleen, or both
• Venous distention
• Peripheral edema
¾ Fluid accumulation in serous cavities
¾
¾
z
Management
Cardiogenic Shock
z
Most extreme form of pump failure
z
Left ventricular function is so compromised
heart cannot meet metabolic needs of body
z
Extensive myocardial infarction
¾
¾
40% of left ventricle
Diffuse ischemia
136
Cardiac Tamponade
z
Impaired diastolic filling of heart
z
Increased fluid in pericardial space
z
Volume of pericardial fluid encroaches on
capacity of atria and ventricles to fill
adequately
z
Ventricular filling is mechanically limited, and
stroke volume is decreased
Cardiac Tamponade
Acute onset
z
¾
Trauma
z
Presentation
¾
¾
Gradual onset
z
¾
¾
¾
¾
Neoplasm
Infection
Renal disease
Hypothyroidism
Management
z
¾
¾
¾
¾
¾
¾
¾
¾
Chest pain
Tachycardia
Ectopy
JVD
Decreased SBP
Pulsus paradoxus
Muffled heart sounds
ECG changes
Fluid
Pericardiocentesis
Thoracic and Abdominal
Aortic Aneurysms
z
Aneurysm
¾
z
Dilation of a vessel
Causes
¾
¾
¾
¾
Atherosclerotic disease (most common)
Infectious disease (primarily syphilis)
Traumatic injury
Certain genetic disorders (e.g., Marfan's syndrome)
137
Aortic Aneurysms—Signs and Symptoms
z
Hypotension
z
Peritoneal irritation
z
Syncope
z
Urge to defecate
z
Abdominal or back pain
z
Pulsatile, tender mass
z
Distal pulses present or
absent
z
GI bleeding
¾
z
Tearing or ripping
Low back or flank pain
¾
Radiates to thigh, groin,
testicle
Branches of Aorta
Pathogenesis of Dissecting Aneurysms
Medial and intimal degeneration
in aortic wall
Hemodynamic forces produce
tear
Dissecting hematoma
propagated by pulse wave
138
Dissecting Aneurysms—Management
z
Gentle handling
z
Oxygen
z
Monitor
z
IV fluids
¾
Bolus if profound shock
Acute Arterial Occlusion
z
Blockage of arterial flow caused by:
Trauma
Embolus
¾ Thrombosis
¾
¾
z
Severity of episode depends on:
¾
¾
Site of occlusion
Collateral circulation
Acute Arterial Occlusion
z
Signs and symptoms
¾
Pain in extremity
• May be severe and sudden in onset or absent because
of paresthesia
Pallor
¾ Cool skin distal to occlusion
¾ Change in sensory and motor function
¾ Diminished or absent pulse distal to injury
¾ Bruit over affected vessel
¾ Slow capillary filling
¾ Sometimes shock
¾
139
Arterial Occlusion—Management
z
Extremity occlusion is painful and limb threatening if
blood flow is not reestablished within 44-8 hrs
z
Immobilize limb and transport
z
Patients with mesenteric occlusion
¾
¾
Manage for shock:
• Oxygen
• IV fluids
Analgesics for pain control
Common Sites of
Embolic Arterial Occlusion
Venous Thrombosis
z
Predisposing factors
History of trauma
Sepsis
¾ Stasis or inactivity
¾ Recent immobilization
¾ Pregnancy
¾ Birth control pills
¾ Malignancy
¾ Coagulopathies
¾ Smoking
¾ Varicose veins
¾
¾
140
Acute Deep Vein Thrombosis (DVT)
z
Occlusion of deep veins is serious, common
problem
z
May involve any portion of deep venous
system
¾
More common in lower extremities
Acute DVT—
DVT—Risk Factors
z
Lower extremity trauma
z
Previous thrombosis
z
Recent surgery
z
Oral contraceptives
z
Advanced age
z
Cancer
z
Recent MI
z
Obesity
z
Inactivity
z
CHF
Acute DVT—
DVT—Management
z
Risk of pulmonary embolus
z
Hospitalization
z
Bed rest
z
Anticoagulants
141
Common Sites of
Atherosclerotic Occlusive Disease
Hypertension
z
Resting BP: Consistently >140/90 mm Hg
z
Several categories of hypertension based on
level of blood pressure, symptoms, and
urgency of need for intervention
Chronic Hypertension
z
Conditions associated with chronic,
uncontrolled hypertension
Cerebral hemorrhage and stroke
Myocardial infarction
¾ Renal failure (secondary to vascular changes in
the kidney)
¾ Thoracic and/or abdominal aortic aneurysm
¾
¾
142
Hypertensive Emergencies
z
Blood pressure increase leads to significant,
irreversible endend-organ damage within hours if
not treated
z
Organs most at risk are brain, heart, and
kidneys
z
Myocardial ischemia with hypertension
z
Aortic dissection with hypertension
z
Pulmonary edema with hypertension
z
Hypertensive intracranial hemorrhage
z
Toxemia
z
Hypertensive encephalopathy
Hypertensive Emergencies—
Signs and Symptoms
z
z
z
z
z
z
Paroxysmal nocturnal
dyspnea
Shortness of breath
Altered mental status
Vertigo
Headache
Epistaxis
z
z
z
z
z
Tinnitus
Changes in visual acuity
Nausea and vomiting
Seizures
ECG changes
143
Hypertensive Encephalopathy
z
Severe hypertension produces hypertensive
encephalopathy and cerebral hypoperfusion
z
Loss of integrity of bloodblood-brain barrier
z
Fluid exudation into brain tissue
Hypertensive Encephalopathy
z
Progresses from:
¾
z
Severe headache, nausea, vomiting, aphasia,
hemiparesis, and transient blindness
Later
¾
Seizures, stupor, coma, and death
z
z
z
z
z
z
Supportive care
Oxygen
IV
ECG monitoring
Rapid transport
Drugs under medical supervision
144
Techniques for Managing
Cardiac Emergencies
z
z
z
z
z
z
Basic life support
Mechanical CPR devices
MonitorMonitor-defibrillators
Implantable cardiovertercardioverter-defibrillators (ICDs)
Transcutaneous cardiac pacing (TCP)
Advanced cardiac life support (ACLS) system
Basic Life Support
z
z
z
z
z
z
z
CPR within 4 min
Compression/ventilation ratio 30:2
Compressions must be at least 100/min
Depth of 11-1/2 to 2 inches
Allow complete chest recoil
Minimize interruptions of CPR
Externally supports circulation and respiration
Mechanical CPR Devices
z
Designed to:
¾
¾
¾
¾
Standardize CPR technique
Eliminate rescuer fatigue
Free rescuers to perform
ACLS procedures
Provide adequate
compression during patient
transport
145
Impedence Threshold Devices
z
z
Attach to ET or mask
During Pulseless Arrest:
Increases blood flow to
heart and brain
Doubles systolic pressure
Increases survival to
hospital
Increases defibrillation
success
AHA Class IIa in intubated
patients
¾
¾
¾
¾
¾
Automated External Defibrillators
z
Analyze ECG signal
¾
z
Including frequency,
amplitude, and wave
morphology
Designed for use by
individuals with minimal
training
Defibrillation
z
Delivery of electrical current through chest
wall to terminate VF and pulseless VT
Shock depolarizes a large mass of myocardial
cells at once
¾ If 75% of cells are in resting state (depolarized)
after shock is delivered, normal pacemaker may
resume discharging
¾
146
Defibrillation
z
Early defibrillation
VF is most frequent initial rhythm in arrest
Treatment for VF is electrical defibrillation
¾ Chance of successful defibrillation diminishes
rapidly over time
¾ VF tends to convert to asystole within a few minutes
¾ If prehospital arrest is unwitnessed, 2 minutes of
CPR may enhance ability to defibrillate
¾
¾
Paddle Electrodes
z
Apex or sternum
z
Place so that the heart
is in path of current and
distance between
electrodes and the
heart is minimized
Stored and Delivered Energy
z
Electrical energy measured in joules
¾
z
Delivered energy about 80% of stored energy
¾
¾
z
Watt seconds
Losses within defibrillator circuitry
Resistance to current flow across chest wall
80% of stored energy approximates amount of
joules delivered to patient
147
Monitor Defibrillator Pacer
Defibrillator Safety
z
Clear all personnel from patient, bed, and
defibrillator before shock delivery
z
Do not make contact with patient except
through defibrillator paddle handles
z
Do not use excessive gel or coupling material
z
Do not discharge paddles over a pacemaker
or ICD generator or nitroglycerin paste
z
Remove nitroglycerin patches before
defibrillation
148
z
Apply gel or paste before turning on defibrillator
z
Do not discharge defibrillator in open air to rid
unwanted charge
z
Turn defibrillator off to dump charge
z
Do not discharge defibrillator with paddles
placed together
z
Do not touch metal electrodes or hold paddles
to your body when defibrillator is on
z
Clean paddles after use
z
Routinely check defibrillator to make sure
equipment is functioning properly
¾
Including batteries
Defibrillator Use in
Special Environments
z
Can defibrillate in wet conditions
¾
¾
Keep chest dry between defibrillator electrode sites
Keep operator's hands and paddle handles as dry
as possible
• In a rainstorm, finding shelter would be safest
149
Defibrillator Use in
Special Environments
Video Clip: Defibrillation
Implantable CardioverterCardioverter-Defibrillator
(ICD)
z
Implanted through median sternotomy
incision
¾
z
Other approaches also used
ICD monitors patient's cardiac rhythm, rate,
and QRS morphology
ICD
150
Synchronized Cardioversion
z
z
Terminates dysrhythmias other than VF and pulseless
VT
Delivers shock about 10 msec after peak of QRS
complex
¾
¾
¾
¾
z
Avoid relative refractory period
May reduce energy needed to end dysrhythmia
Decreases
potential for development of secondary complicating
dysrhythmias
Procedure
Synchronized Cardioversion
Video Clip: Cardioversion
Transcutaneous Cardiac Pacing (TCP)
z
External cardiac pacing
z
Treatment for bradycardia
z
Indications
z
Contraindications
151
TCP—
TCP—Proper Electrode Placement
Preferred anterior-posterior placement
Alternate anterior-anterior placement
TCP—
TCP—Proper Electrode Placement
Video Clip: Transcutaneous Pacing
Cardiac Arrest and Sudden Death
z
Resuscitation in prehospital setting best
chance for survival
z
Rapid ACLS protocol initiated without
delaying transport to hospital
152
Termination of Resuscitation
z
Inclusion criteria
z
Exclusion criteria
z
Procedure
z
Special considerations
Conclusion
About two thirds of cases of sudden death due to
coronary disease take place outside the hospital.
This usually occurs within 4 hours after onset of
symptoms. It is possible that a large number of
these deaths could be prevented by rapid entry
into the EMS system, effective early CPR, and
early defibrillation.
Questions?
153

Sanders: Mosby`s Paramedic Textbook, Revised 3

Transcription

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