Adult Nursing

Dr. ABDALLAH ALWAWI RN, CMH, CNS, PhD

ECG LEC.

Al-Quds University

aalwawi@staff.alquds.edu
 Conduction System
(electrical + mechanical )
• The right coronary artery provides
oxygenated blood to the SA node in about
50% of people and to the AV node in about
90% of people.
• Therefore, patients with occlusion of the right
coronary artery are at high risk for rhythm
disturbances involving the function of the AV
node, such as first-, second-, and third-
degree heart blocks.
 ‫كهرباء القلب عندما تذهب الى اتجاه الليد تجعله يصعد‬
‫لالعلى وهذا يعنى ان ‪ R‬تكون اكبر من ‪S‬‬
‫وعندما تذهب الكهرباء بالبعد عن الليد تجعله لالسفل يعني‬
‫عكس السابق‬
V1 Big S and Small
R
V6 Big R and Small
S

In V 3 and V4 equal
S and R
This important to
recognize cardiac
hypertrophy
 T wave is always upright in leads I, II,
V3-6, and always inverted in lead aVR.
 In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted
in lead aVR.
The other leads are variable depending on the direction of the QRS and the age of the
patient.
T wave is always upright in leads I, II, V3-6, and
always inverted in lead aVR.
T wave is always upright in leads I, II, V3-6,
and always inverted in lead aVR.
 Heart regions
• I Avl
• The nurse is caring for a group of clients who have sustained
myocardial infarction (MI). The nurse observes the client with which
type of MI most carefully for the development of left ventricular
heart failure?
1. Inferior wall
2. Anterior wall
3. Lateral wall
4. Posterior wall
• 2. Owing to the large size of the anterior wall, the amount of tissue
infarction may be large enough to decrease the force of contraction,
leading to heart failure. with the inferior wall, the client is more likely
to develop right ventricular MI. regarding clients with obstruction of
the circumflex artery may experience a lateral wall or posterior wall
MI and sinus dysrhythmias.
 WHICH WALL IS INVOLVED ??

AV P V
II AVR O V1 V4
V4
R S
T
E
1
R
I
O
LATERAL SEPTAL
R

AV
II
II AVL V2
V2 V5
V5
L

INFERIOR
II AV
III AVF V3
V3 V6
V6
I F

ANTERIOR
 Heart regions
• I Avl
 ‫قاعدة سال‬
• SAL
• V1 V2 ………..SEPTAL
• V3 V4 …………ANTERIOR
• V5 V6 …………….LATERAL
Each 5 big box equals one sec.
So one min equal 5*60 = 300
 PR Interval
(From the beginning of the P wave to the onset
of the QRS complex)

Normally: 0.12 – 0.20 second ‫كم مربع؟؟؟؟؟؟؟؟؟؟‬

0.04 0.04 0.04 0.04 0.04

This interval includes impulse transmission

time through the atria and the delay of the
impulse of the AV node

Prolongation: 1st Degree Heart Block

 QRS Complex
Normally: 0.06 – 0.10 second (The normal QRS
duration, is therefore less than 0.10 seconds.)
‫كم مربع؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟؟‬

The amplitude of this wave is great as a result of the

large muscle mass traversed by the electric impulse.

Widening occurs when the ventricles become

hypertrophied
or
when there is disease involving the bundle branches
or their fascicles.
 ST segment
• Interval Between the Wave of Ventricular Depolarization and
Repolarization ..........‫قطعة تكون بين االنقباض واالنبساط البطيني‬

• The ST segment is normally iso-electric because little

potential difference exists during the 'resting' plateau phase
prior to repolarization.

• The ST segment is definitely abnormal when depressed or

elevated more than 1.0 mm from the baseline.

• ST Depression (MORE THAN 1 mm FROM Iso-Electric

Line): Myocardium Ischemia

• ST Elevation (MORE THAN 1 mm FROM Iso-Electric Line):

Myocardium Infarction
 T wave
Represents Ventricular Repolarization

T Wave Inversion : Ischemia

Hyperkalemia: Peaking and Elevation

 U wave

• The normal U wave has the same polarity as the T wave

and is usually less than one-third the amplitude of the T
wave.

• U waves are usually best seen in the right precordial

leads especially V2 and V3.

• Prominent upright U waves in

Sinus bradycardia highlights the U wave ‫يبرز‬

Hypokalemia
Quinidine and heroine effects
Summary of wave formation
 0.2 sec
The ECG Paper

0.04 sec
 0.04
sec

0.04 + 0.04 + 0.04 + 0.04 + 0.04 =

0.20 sec

0.2 + 0.2 + 0.2 + 0.2 + 0.2 = 1 sec

 Determining HR & Rhythm
Calculating Heart Rate
-- Regular Rhythms
Every 5 boxes are one sec.
•(5 Box X 60 sec = 300)

•Count number of small boxes between two R waves

and divide into 1500
 Determining HR & Rhythm
Calculating Heart Rate
-- Regular Rhythms
* Count number of large boxes between two R
waves and divide into 300 (5 Box X 60 sec = 300)
* Count number of small boxes between two R
waves and divide into 1500
• Irregular rhythms
30 boxes equal 6 sec
Count number of R-R intervals in a 6-second strip
and multiply by 10

‫ ثوان كم مربع؟؟‬6 ‫ ثانية وبالتالي‬0.2 ‫كل مربع كبير يساوي‬

 ECG has its limitations

SO IT IS INCONCLUSIVE EVIDENCE

Normal ECG does not rule out

ischemic event
Symptoms of ischemic heart disease

Chest palpitati Dizzine Sweatin

pain SOB on ss g
Compressing
Squeezing lightheadadness
Burnining

Pain Insomn Feet &

Cough Fatigue radiatio leg
ia
n to neck, swelling
jaw, LT UL
Common heart attack warning signs
1 Chest pai & discomfort
2
3
1 4 2 Lightheadedness, nausea/ vomiting

5
3 Jaw and/or Back pain

4 Left arm or shoulder pain

5 Shortness of breath
Modifiable Risk Non-Modifiable
Factors Risk Factors
Steps in Rhythm Interpretation
RR P PR QRS
 ‫‪AXIS‬‬
‫• يعني اتجاه الكهرباء في القلب الى اين يذهب‬

‫• اذا الليد ‪ 1‬وقع فهذا يعني ان القلب ‪RIGHT AXIS‬‬

‫‪DIVATION‬‬

‫• اذا الليد ‪ 2‬و ‪ 3‬وقعوا فهذا يعني ان القلب ‪LEFT AXIS‬‬

‫• لو فرضنا انه حدث تضخم في عضلة القلب واصبح اتجاه‬
‫الكهرباء الى اليمين سوف يصبح كالتالي وسوف يصعد‬
‫ليد ‪ 2‬و ‪ 3‬الن الكهرباء أصبحت باتجاههما‬
‫• لو فرضنا انه حدث تضخم في عضلة القلب واصبح اتجاه‬
‫الكهرباء الى اليسار سوف يصبح كالتالي وسوف يصعد‬
‫ليد ‪ 1‬الكهرباء وتذهب من ليد ‪ 2‬و ‪ 3‬والن الكهرباء‬
‫أصبحت باتجاه ‪ 1‬فسوف يصعد ويسقط االخريين‬
Overview of cardiac rhythmicity
(S & S)
 Sinus rhythm
* Normal sinus rhythm
HR
Regular
P wave
PR interval
QRS shape and size
• Sinus tachycardia/////Sinus bradycardia

• Sinus arrhythmia
 Atrial Flutter
1

2
‫سنان المنشار‬
 Atrial Fibrilation
1

2
Atrial Fibrilation
Atrial Fibrilation
Supraventricular Tachycardia
(SVT)
with a heart R, of about 150<
 Ventricular arrhythmias
• Premature ventricular contractions
• Unifocal PVC’s
• Clinical Tip: Patients may sense the occurrence of PVCs
as skipped beats.
• Because the ventricles are only partially filled, the PVC
frequently does not generate a pulse.
VENTRICULAR TACHYCARDIA (V. TACH)
AREST RETHYM AND NEED CPR & DEFIB

• 2 TYPE…….PULSLESS, PULS
6

7
VENTRICULAR TACHYCARDIA (V. TACH)

Clinical Tip: It is important to confirm the

presence or absence of pulses because VT
may be perfusing or nonperfusing.
♥ Clinical Tip: VT will probably deteriorate
into VF or unstable VT if sustained and not
treated.
♥ Clinical Tip: Consider electrolyte
abnormalities as a possible etiology. (Mg++)
VENTICULAR FIBRILATION (V. FIB)
V.T……V.F
Atrioventricular (AV)block
(Dropped beats))
 Atrioventricular (AV)block
(Dropped beats))

1st degree
PR PROLONGATION

But fixed

More then one big box

IHD
Digoxin toxicity
RH Disease

(2nd degree
(mobitz 1)
PR PRON.. THEN DROP QRS
 2nd degree
(mobitz 2) SAME NORMAL PR BUT DROP QRS

Clinical Tip: This rhythm may be caused by medication such as beta

blockers, digoxin, and calcium channel blockers. Ischemia involving the right
coronary artery is another cause.

Clinical Tip: Resulting bradycardia can compromise cardiac output and lead
to complete AV
block. This rhythm often occurs with cardiac ischemia or an MI.(II)
2:1 ‫يعني بعض النبضات من ب تتوصل للبطين وبعضها ال‬
3:1 ‫ ب وبعدها واحد بطين‬3 ‫ ب وبعدها واحد بطين او‬2 ‫نشاهد ان هناك‬
 ‫‪3rd degree AV block‬‬
‫‪(complete heart block) NO CORDINATION BETWEEN PR & QRS‬‬

‫هذا يعني انه ال يوجد أي توصيل بين االذين والبطين وكل واحد شغال لوحده‬
‫معدل ب منتظم بمعدل ثابت تقريبا ‪ 90‬وال دخل لها بالبطين‬
‫أيضا ‪ qrs‬واسعه يعني مصدرها من البطين وال دخل لالذين بها‬
 3rd degree AV block

Rate: Atrial: 60–100 bpm; ventricular: 40–60 bpm if

escape focus is junctional, 40 bpm if
escape focus is ventricular
Rhythm: Usually regular, but atria and ventricles act
independently
P Waves: Normal (upright and uniform); may be
superimposed on QRS complexes or T waves
PR Interval: Varies greatly
QRS: Normal if ventricles are activated by junctional
escape focus; wide if escape focus is
ventricular
 Athletes, Respiratory, Sleep
Physiological
C Medications
Sinus Arrhythmia,
B Blocers, Ca C Blockers, Digoxin,
Amiodarone,

a Toxins OPP
Ischaemia, myocarditis,
Cardiac disease
u Metabolic/Endocrine
cardiomyopathies
Anorexia, hyperkalaemia,
hypothyroidism

s Neurological Raised ICP

e Autoimmune SLE, sarcoidosis, amyloidosis

Infections Lyme disease, diphtheria, typhoid fever

s Hypoxia/Hypothermia. surgery
 Bradicardia
Asymptomatic & Symptomatic

Asymptomatic Symptomatic
Heart rate less than 60 Heart rate less than 60

Symptoms
Signs &
beats/min beats/min
• Common in healthy, • Hypotension
active patients & • Ischemic chest pain
patients on B • CHF
Blockers medication • Altered mental status
• Signs of shock
Basics
 Bradicardia
Treatment

Asymptomatic Symptomatic

Just Observe Atropine 1 mg IV/IO

Q 3 – 5 min
Max dose 3mg
TCP

Dopamine infusion
5 – 20 mcg/kg/min
Epi infusion
2 – 10 mcg/min

Search for & treat underlying cause

 TCP
• Trans Cutaneous Pacemaker
• 2nd line treatment in symptomatic bradycardia after
Atropine
 TCP

How To Operate TCP

 2
Sedation
& Pain
control

1- Attach pads

3-Turn on
Pacer
4-Adjust
Capture Failure
Firing Rate

5- Start

100% Capture rate Increase output in milliamper

Increment by 2 Starting from 60 M/A
 Bundle branch blocks
Clinical Tip: Commonly, BBB occurs in coronary artery disease

Right bundle branch

Left bundle branch block block
Rt BBB
RSR pattern •
‫ وممكن في ليد‬1 V‫• في ليد‬
v2 and v 3
Lt BBB
M pattern •
‫ وممكن في ليد‬V6 ‫• في ليد‬
v4 and v 5
Lt BBB
Rt BBB
Clinical Tip:

Potential causes of PEA are pulmonary embolism,

MI, acidosis, tension pneumothorax, hyper- and
hypokalemia, cardiac tamponade, hypovolemia,
hypoxia, hypothermia, and drug overdose (i.e., cyclic
antidepressants, beta blockers, calcium channel
blockers, digoxin).
PEA
Asystole
• Electrical activity in the ventricles is completely absent

Rate: None
Rhythm: None
P Waves: None
PR Interval: None
QRS: None
Clinical Tip: Rule out other causes such as loose leads, no power, or insufficient signal gain.
Clinical Tip: Seek to identify the underlying cause as in PEA. Also, search to identify VF
• Single-Chamber Pacemaker Rhythm––Atrial

Pacemaker spike

• Single-Chamber Pacemaker Rhythm—Ventricular

Pacemaker spike
Dual-Chamber Pacemaker Rhythm—Atrial and
Ventricular

Atrial pacemaker spike Ventricular pacemaker spike

• 60-Cycle Interference

• Muscle Artifact

Regular R-R
intervals

Clinical Tip: Never confuse muscle artifact with A-fib if

the rhythm is regular
 Location of MI

Depends on which artery is affected

LV receives most of the CA supply and so it is the most

affected

Left Anterior Descending (LAD)

Left Circumflex artery (LCA)

Right Coronary Artery (RCA)

Progression of an Acute Myocardial Infarction
• An acute MI is a continuum that
extends from the normal state to a
full infarction:
• ■ Ischemia—Lack of oxygen to the
cardiac tissue, represented by ST
segment depression, T wave
inversion, or both
• ■ Injury—Arterial occlusion with
ischemia, represented by ST
segment elevation
• ■ Infarction—Death of tissue,
represented by a pathological Q
wave
C Cl li in ni ic ca al l T Ti ip p: : Once the acute MI has
ended, the ST segment returns to baseline and the T
wave becomes upright, but the Q wave remains
abnormal because of scar formation.
ECG changes on Ischemia and
infarction
ST segment depression,
Ischemia Twave flattened or
inversion

Infarction ST segment elevation

Q wave

Necrosis Q wave
prominence(OLD)
ST segment normalizes
 Timing of ECG changes on
infarction
Immediate ST elevation

Within a few hours Peaked ‫مدبب‬T waves

ST segment normalizes
Several hours
, T wave inversion

Several hours to days Q waves reduced for

life.
 ECG changes during MI
Anterior wall • V---3-4 ,Q wave ,ST ,T
Inferior wall • II, III, AvF, Q wave ,ST ,T
Septal wall • V1-2 ,Q wave ,ST ,T
Lateral wall • V5-6,I , aVL , Q wave ,ST ,T
Posterior wall • ST ,T V7-9, TALL R V1-3
Right ventricle • V4R-V6R, ST
Anterior Myocardial Infarction
• ■ Occlusion of the left coronary
artery—left anterior descending
branch
• ■ ECG changes: ST segment elevation
with tall T waves and taller-than
normal R waves in leads V3 and V4.;
reciprocal changes in II, III, and aVF

Clinical Tip: Anterior MI frequently involves a large

area of the myocardium and can present with
cardiogenic shock, second-degree AV block type II, or
third-degree AV block.
Inferior Myocardial Infarction
• ■ Occlusion of the right coronary
artery—posterior descending branch
PDA
• ■ ECG changes: ST segment elevation
in leads II, III, and aVF; reciprocal ST
segment depression in I and aVL

C Cl li in ni ic ca al l T Ti ip p: : Be alert for symptomatic

sinus bradycardia, AV blocks, hypotension, and
hypoperfusion.
Lateral Myocardial Infarction
• ■ Occlusion of the left coronary
artery—circumflex branch
• ■ ECG changes: ST segment
elevation in leads I, aVL, V5, and V6;
reciprocal ST segment depression in
V1, V2, and V3
C Cl li in ni ic ca al l T Ti ip p: : Lateral MI is often
associated with anterior or inferior wall MI. Be alert for
changes that may indicate cardiogenic shock or
congestive heart failure.
Septal Myocardial Infarction
• ■ Occlusion of the left coronary
artery—left anterior descending
branch
• ■ ECG changes: pathological Q
waves; absence of normal R
waves in leads V1 and V2

C Cl li in ni ic ca al l T Ti ip p: : Septal MI is often associated

with an anterior wall MI
Posterior Myocardial Infarction
• ■ Occlusion of the right coronary
artery (posterior descending
branch) or the left circumflex
artery
• ■ Usually, tall R waves and ST
segment depression in leads V1,
V2, V3, and V4; possible left
ventricular dysfunction
• ■ You may need to view the true
posterior leads, V8 and V9 (used
in the 15-lead ECG), for definite
diagnosis of an acute posterior
MI. These leads show ST segment
elevation
C Cl li in ni ic ca al l T Ti ip p: : Diagnosis may require a 15-lead ECG
because a standard 12-lead does not look directly at the posterior
wall.
2142
Left Bundle Branch Block
• ■ QRS complex greater than
0.10 sec
• ■ QRS predominantly negative
in leads V1 and V2
• ■ QRS predominantly positive in
V5 and V6 and often notched ■
Absence of small, normal Q
waves in I, aVL, V5, and V6
• ■ Wide monophasic R waves in
I, aVL, V1, V5, and V6
C Cl li in ni ic ca al l T Ti ip p: : Patients may have underlying
heart disease, including coronary artery disease,
hypertension, cardiomyopathy, and ischemia
MI in aVR with DEVUSED ST
DEPRESSION

ST-Elevation in aVR with diffuse ST-

Depressi
 Causes of Arrhythmias
▪ Hypoxia: Lung disease
▪ Ischemia: CAD, angina (local hypoxia)
▪ Sympathetic Stimulation: Nervous, exercise, CHF,
hyperthyroidism
▪ Drugs: Caffeine, cocaine, stimulants…many
antiarryhtmic drugs…
▪ Electrolyte Disturbances: K+, Ca++, Mg+
▪ Stretch: CHF, hypertrophy, valve disease
‫يوجد ‪ P‬غريبه عن االخريات وكذلك ‪QRS‬التي تتبعها غريبة ايضا‬
caused by enlargement of the right atrium.
https://www.youtube.com/watch?v=iBnqiU
hM8hI
 RBBB

A. Normal V1 tracing B. RBBB in V1 (RSR’)

Small narrow R & deep narrow wide QRS complex & double-
S wave peaked R wave
 LBBB

C. Normal V6 tracing D. LBBB in V6

Tall narrow R wave & absent Wide QRS complex &double-
S wave peaked R wave
https://ecglibrary.com/ecghome.php
Inferior myocardial infarction

•ST elevation in the inferior leads II, III and aVF

•reciprocal ST depression in the anterior leads
Acute anterior myocardial infarction

ST elevation in the anterior leads V1 - 6, I and aVL

reciprocal ST depression in the inferior leads
 Chapter

Acute Myocardial Infarction

AMI
 Coronary Arteries

• Blood supply to the

myocardium is by Rt & Lt
main coronary arteries.
• The left coronary artery
branches into; left anterior
descending (LAD) & the
left circumflex artery (LCA)
• The LAD perfuse the
anterior two thirds of the
ventricular septum,
anterior left ventricle &
most of bundle branches.
• The right coronary artery
• Left circumflex perfuse left
(RCA) perfuse the right
lateral & left posterior
ventricle, & the inferior
walls.
wall of the left ventricle.
 Coronary Atherosclerosis

• Atherosclerosis is the abnormal accumulation of lipid

deposits & fibrous tissue within Arterial walls & lumen.
• In coronary atherosclerosis, blockages & narrowing of
the coronary vessels reduce blood flow & decreasing
oxygen supply to the myocardium.
• The inflammatory response involved with the
development of atherosclerosis begins with injury to
the vascular endothelium & progress over many years.
• Endothelium stop producing the normal Antithrombotic
& vasodilating agents.
• Symptoms occur with 75% or more occlusion (thanks
to the collateral circulation).
 Atherosclerosis—Pathophysiology

• Triglycerides, hypertension, &

cigarette smoking cause damage
to the endothelium.
• Fatty substances, cholesterol,
cellular waste products, calcium,
& fibrin pass are deposited
forming lipid plaque (atheroma).
• WBC, smooth muscle cells, &
platelets to aggregate at the site,
forming a fibrous plaque.
• The plaque may rupture & a
thrombus might form, obstructing
blood flow leading to ACS which
may result in an AMI.
Atherosclerosis—Pathophysiology
 Acute Coronary Syndrome

• Unstable angina
– Unexpected chest pain/discomfort occurring at
rest
• MI
– ST-segment elevation MI (STEMI)
– Non–ST-segment elevation MI (NSTEMI)
Atherosclerotic Plaque
Copyright © 2018 Wolters Kluwer • All Rights Reserved
 Myocardial Infarction (MI)

▪ MI is precipitated by an imbalance between

oxygen supply & oxygen demand, most
commonly R/t a coronary artery thrombosis
• Other causes include embolism, anemia, coronary
artery spasm, arrhythmias
• Thrombus formation occurs most often at the site of
an atherosclerotic plaque.
• Dysfunctioning endothelium—activation of the
inflammatory response---- formation of atherosclerotic
plaque --- rupture of plaque --- thrombus formation --
occlusion of the coronary artery --- Irreversible
damage (necrosis) within 20 - 40 min.
 MI

• Transmural MI infarction implies an infarction that resulted

in necrosis of the tissue in all the layers of the myocardium
(up to the epicardium)
• Transmural MI infarction compromises CO as area of
infarction may become dyskinetic with small infarction, or
akinetic with a large infarction.
• Determinants of ventricular function post MI include
infarction size, location, & type
❑ Size of Infarction is determined by:
o Extent, severity, & duration of ischemia
o Size of the vessel; & amount of collateral circulation
o Status of the intrinsic fibrinolytic system; & the metabolic
demands of the myocardium.
 MI

❑ MIs Location:
▪ Anterior left ventricle
o Occlusion of left anterior descending (LAD)
▪ Lateral & posterior left ventricle
o Left circumflex artery
▪ Inferior left ventricle
o Occlusion of right coronary artery
▪ Inferior Right ventricle
o Occlusion of right coronary artery
 Types of MI Infarction

▪ STEMI= ST-segment elevation MI

• More common
• Usually the affected coronary artery is completely
occluded
• Mostly ends up with Q wave thus causing Q-wave
MI
• The primary goal of initial treatment is early
reperfusion therapy through administration of
fibrinolytics or mechanical reperfusion.
 Types of MI Infarction

❑ NSTEMI = non ST-segment elevations MI

• Related to partially or intermittently occluding thrombus.
• Unstable angina (UA) & NSTEMI are difficult to distinguish
initially, both presented with similar symptoms & ECG
changes (significant ST-segment depression & T-wave
inversions)
• An elevated biomarker is detected with NSTEMI but not UA
• Management strategies for UA/NSTEMI include
Antiplatelet, Antithrombin, & Antianginal
• Fibrinolysis is contraindicated with NSTEMI & UA
• An invasive strategy is indicated in patients with positive
biomarkers or unstable clinical features.
 Assessment/History

• Chest discomfort or pain, described as heaviness,

squeezing, or choking (the most common complaint)
• Patients describe as “someone sitting on my chest.”
• The substernal pain radiate to the neck, left arm, back, or
jaw
• Unlike the pain of angina, the pain of an MI is often more
prolonged & unrelieved by rest or sublingual nitroglycerin
• Nausea & vomiting, thus patients may initially seek relief
of the gastrointestinal symptoms through antacids & other
home remedies.
• Diaphoresis, dyspnea, weakness, fatigue, anxiety,
restlessness, confusion, shortness of breath, or a sense of
impending death.
 Assessment/ Physical Examination

• May appear restless, agitated, in distress

▪ Cool pale moist skin & diaphoreses

• VS, low-grade fever, hypertension, & tachycardia or

hypotension & bradycardia
• Labored & rapid breathing, crackles
• Diminished heart sounds, murmurs, pericardial
friction rub
• JVD, heart failure, pulmonary edema
 Diagnostic Tests/ECG

▪ An ECG can be used to detect patterns of ischemia,

injury, & infarction
• Ischemia—T-wave inversion, ST-segment depression
• Injury—ST-segment elevation
• Infarction—T-wave, ST-segment, & Q-wave changes
• Myocardial ischemia is caused by 70% occluded
coronary artery with & oxygen demand exceeding
oxygen supply
• uncorrected ischemic state leads to injury
• uncorrected injury leads to MI
• Ischemia & injury are reversible but infarction is
irreversible.
Effects of Ischemia, Injury, Infarction on
ECG

• Involve changes in the

T wave, the ST
segment, & the Q
wave in the leads
overlying the infarcted
area.
 ECG Changes in AMI/Infarction

▪ Stage 1: Hyperacute or peaked T waves phase:

• T waves become tall & narrow, after a few hours,
these hyperacute T waves invert
 ECG Changes during AMI

• Hyperacute T waves may precede ST segment

elevation (A) or seen at the same time with ST
elevation (B) during this acute phase.
 ECG Changes in AMI/Infarction

▪ Stage 2: the ST segments elevate from several hours

to several days in the leads of the ECG facing the
infracted heart.
• In the normal ECG, the ST segment should not be
elevated more than 1 mm in the standard leads or
more than 2 mm in the precordial leads.
• The leads facing away from the injured area may show
ST segment depression (reciprocal changes), most
likely to be seen at the onset of infarction & disappear
later
 ECG Changes in AMI/Infarction

▪ Stage 3: development of Q waves

• Q waves compatible with an MI are usually 0.04
second or more in width or one-fourth to one-third the
height of the R wave
• Small, narrow Q waves may be seen in the normal
ECG in leads I, II, III, aVR, aVL, V5, & V6
• Q waves develop within the fist 24 to 48 hours after
the infarction
ECG Changes during AMI

▪ Last stage: few days after the MI

• The elevated ST segments return to baseline.
o Persistent elevation of the ST segment may indicate the
presence of a ventricular aneurysm.
• The T waves may remain inverted for several weeks,
indicating areas of ischemia near the infarcted region.
Eventually, the T waves should return to their upright
configuration.
• The Q waves do not disappear and therefore always
provide ECG evidence of a previous MI.
o Abnormal Q waves accompanied by ST segment
elevations indicate an acute MI.
o Abnormal Q waves accompanied by a normal ST segment
indicate a previous MI.
 ECG Changes in AMI

Figure 21-8
Evolution of the electrocardiogram (ECG) in a patient with MI. A: Tall peak T waves
known as hyperacute T waves. B: Symmetrical T-wave inversions. C: ST-segment
elevation. D: Development of the Q wave.
The 12-lead ECG: Correlation of lead with the view
of the heart
The 12-lead ECG: Correlation of lead with the view
of the heart
Correlation of lead with the view of the heart
 Coronary
MI Location ECG leads Clinical impact
artery
Anteroseptal LAD V1 –V4 Significant
MI hemodynamic
ventricular Q waves and Compromise:
most septum, ST
common anterior left segment CHF, pulmonary
ventricle & elevations edema, cardiogenic
most of shock;
bundle intraventricular
branches. conduction
disturbances (e.g.,
RBBB, LBBB)
 Anterior MI

•
 Septal MI

Acute septal MI is associated with ST elevation, Q wave formation and T wave

inversion in the leads overlying the septal region of the heart (V1 & V2)
 MI Location Coronary artery ECG leads Clinical impact

Lateral wall MI Left circumflex I, aVL, V5, V6, Some

hemodynamic
Perfuse the SA Q waves, ST Changes
node in 45% of segment
people and AV elevations dysrrhythmias
node in 10% of such as sinus
people arrest and
junctional
rhythm
 Lateral wall MI

Figure 21-10
Twelve-lead ECG showing an acute lateral wall MI. ST-segment elevations can be seen in leads I, aVL, V5 &
V6. Note also the deep Q waves in II, III, and aVF & normal ST segments, indicating a previous inferior wall
MI.
 Coronary
Location ECG leads Clinical impact
artery

Posterior wall MI Left V1 and V2 Some hemodynamic

circumflex all upright R changes;
waves
Perfuse with ST segment dysrrhythmias
the SA depression such as sinus arrest
node in (reciprocal and junctional
45% of changes) rhythm
people and
AV node in V7 - V9 (15
10% of lead ECG) : Q
people waves and ST
segment
elevation
Posterior MI
 MI Location Coronary artery ECG leads Clinical impact

Inferior wall RCA II, III, aVF Some

hemodynamic
less common Supplies SA Q waves and ST changes
than node in 50% of segment
anteroseptal people and the elevation Potential for
AV node in 90% significant
more common of people arrhythmias caused
than lateral or by SA and AV node
posterior dysfunction
 Inferior wall MI

Figure 21-11
ECG showing an acute inferior wall MI. Note the ST-segment elevations in II, III, and aVF. The posterior
wall infarction is evidenced by a tall R wave, ST-segment depression, and inverted T wave in V1 and V2.
Location Coronary artery ECG leads Clinical impact

Types of MI
Right RCA right precordial Some
ventricular chest leads hemodynamic
wall Supplies blood to (RV1 through changes
the SA node in RV6)
50% of 50% of people Potential for
patients will and the AV node Q waves and significant
have also in 90% of people ST segment arrhythmias
inferior MI elevations caused by SA
and AV node
dysfunction
 Inferior and RV MI

 Right ventricular
infarction. The six chest
leads have been
positioned on the right
side of the chest.
 Note the ST segment
elevation in RV4, RV5, &
RV6.
 ST segments in the
inferior leads (II, III,
aVF) indicating inferior
wall MI

Figure 21-13
Twelve-lead ECG showing right ventricular infarction. The six chest leads have been positioned on the right side of the
chest. Note the ST-segment elevation in RV4, RV5, and RV6. The ECG also shows elevated ST segments in the inferior
leads (II, III, aVF). Patients with an inferior wall MI often also have an infarction in the right ventricle.
 Diagnostic tests/ Lab tests

• Cardiac Troponins
– Preferred biomarker
– Are proteins with two subforms (troponin T & troponin I,)
that are highly specific for cardiac muscle. (Troponin C
which is not sensitive to MI)
– Troponin levels are not detected in the healthy person &
not affected by skeletal muscle injury.
– Troponin I levels rise in about 3 to 12 hours, peak at 24
hours & remain elevated for 5 to 10 days.
– Troponin T levels rise in 3 to 12 hours, peaks in 12 hours-
2 days & remains elevated for 5 to 14 days.
– Excellent diagnostic markers for patients who present late
with symptoms of MI.
 Diagnostic tests/ Lab tests

▪ Creatine Kinase (CK)

• CK is an enzyme found mainly in heart & skeletal
muscles. When heart muscle is damaged, CK is released
into the blood.
• Onset 6 to 8 hours after the MI, peaks within 12 to 28
hours, & returns to normal in 24 to 36 hours
• The isoenzyme (CK MB) offers a more definitive
indication of myocardial cell damage than total CK alone.
• CK-MB appears in the serum in 6 to 12 hours, peaks
between 12 & 28 hours, & returns to normal levels in
about 72 to 96 hours.
• In the patient with an MI, the CK-MB2 level rises
resulting in a CK-MB2 to CK-MB1 ratio greater than one
 Diagnostic tests/ Lab tests

• Myoglobin
– Myoglobin is an oxygen-binding protein found in
skeletal & cardiac muscle (thus it is not specific to
the heart)
– Onset within 1 to 2 hours of acute MI & peaks
within 3 to 15 hours
– The early release of myoglobin makes it valuable
in helping to detect MI
Laboratory Tests
 Management

▪ Early management
• An initial evaluation (Hx, PE, ECG, monitor) of the patient
should occur ideally within the first 10 minute
• Continuous cardiac monitoring & Serial ECGs required
• Administer Aspirin, 160 to 325 mg chewed, to diminishes
platelet aggregation
• Give oxygen by nasal cannula , use pulse oximeter, &
draw ABG.
o hypoxemia often occurs in patients with a myocardial
infarction because of pulmonary edema.
o If severe pulmonary edema is present & the patient is in
respiratory distress, intubation may be necessary
o Serum cardiac markers, CBC, chemistry, and lipid profile
 Management

• Administer sublingual Nitroglycerin (unless the systolic BP

is less than 90 mm Hg or the heart rate is less than 50 or
greater than 100 beats/minute)
• Nitroglycerin promotes vasodilation but is relatively
ineffective in relieving pain in the early stages of a MI.
• Intravenous nitroglycerin is recommended for the first 24 to
48 hours for patients with acute MI & heart failure, large
anterior wall infarctions, persistent ischemia, or hypertension.
• Morphine is the drug of choice to relieve the pain of a MI.
o given intravenously in small doses (2–4 mg) & can be
repeated every 5 minutes until the pain is relieved.
o Close respiratory monitoring is indicated because morphine
can depress respirations
 Management

▪ Percutaneous Transluminal Coronary

Angioplasty (PTCA)
• It is the RECOMMENDED method of reperfusion
• PTCA is an invasive procedure in which the infarct-
related coronary artery is dilated with a balloon catheter
and possibly stent placement after balloon dilatation
• PTCA is used for patients who present within 12 hours of
the onset of symptoms, with persistent ischemic
symptoms, OR for patients ineligible for thrombolytic
therapy
• A dose of 162 to 325 mg of Aspirin is given to the
patient before the primary PCI and the aspirin is
continued indefinitely
• Complications include retroperitoneal or vascular
hemorrhage, early acute reocclusion, & late restenosis
 Management
• Fibrinolytic therapy
– Lyse coronary thrombi by converting plasminogen to
plasmin which degrade fibrin and fibrinogen
– The ideal door to drug time for these patients is 30
minutes. Once the patient is stabilized, the patient is
evaluated for transfer to a hospital for angiography and
revascularization within 3 to 24 hours.
– Thrombolytic therapy provides maximal benefit if given
within the first 3 hours after the onset of symptoms.
– Significant benefit still occurs if therapy is given up to 12
hours after the onset of symptoms, if PCI can not be
performed within 120 minutes
– Fibrinolytic therapy also is recommended for patients with
STEMI who are unable to receive PCI if there is clinical
and/or electrocardiographic evidence of ongoing ischemia
within 12 to 24 hours of symptom onset and a large area
of myocardium is at risk or hemodynamically unstable
 Management

• The patient is closely monitored during and after the

infusion of a thrombolytic agent
• The nurse assesses the patient for resolution of chest
pain, normalization of elevated ST segments,
development of reperfusion dysrhythmias (accelerated
idioventricular rhythm, ventricular tachycardia, and AV
heart block) any allergic reactions, evidence of bleeding,
and the onset of hypotension
• The nurse monitor the development of complications
such as reocclusion of the coronary artery (chest pain,
ST segment elevation, and hemodynamic instability),
bleeding (urine and stool for blood or altered levels of
consciousness due to intracranial bleeding)
 Absolute Contraindications to Fibrinolytic
Therapy
• Previous intracranial hemorrhage or cerebrovascular
events within 1 year
• Known malignant intracranial neoplasm (primary or
metastatic)
• Known structural cerebral vascular lesion (e.g.,
arteriovenous malformation)
• Active bleeding or bleeding diathesis (excluding menses)
• Suspected aortic dissection
• Significant closed-head or facial trauma within 3 months
• Intracranial or intraspinal surgery within 2 months
• For streptokinase/anistreplase: prior treatment within the
previous 6 months or prior allergic reaction
 Relative Contraindications to Fibrinolytic
Therapy

• Severe uncontrolled hypertension on presentation (blood

pressure >180/110 mm Hg)
• History of prior ischemic stroke greater than 3 months
• Known intracranial pathology not covered in contraindications

• Current use of anticoagulants in therapeutic doses

(international normalized ratio [INR] ≥2:3); known
bleeding diathesis
• Recent (within 2–4 weeks) internal bleeding
• Head trauma or traumatic or prolonged (>10 minutes)
• (CPR) or major surgery (<3 weeks)
• Pregnancy/ Dementia/ Active peptic ulcer
 Management/ Pharmacological therapy

▪ For management of dysrhythmias

o Easy access to atropine, lidocaine, amiodarone,
transcutaneous pacing patches, transvenous pacing
wires, a defibrillator, & epinephrine is essential
o Prophylactic Antidysrhythmics during the first 24
hours of hospitalization are NOT recommended
• IV Nitroglycerin is continued for 24 to 48 hours
• IV beta blocker therapy should be administered within
the initial hours of the evolving infarction, followed by
oral therapy (they reduce oxygen demand by
decreasing the heart rate and contractility)
 Management/ Pharmacological therapy

• β Blockers & ACE inhibitors are initiated in the first 24

hours unless contraindicated.

• β Blockers are continued during & after hospitalization

• Angiotensin-converting enzyme (ACE) inhibitors are

administered to patients with anterior wall MI and to
patients who have an MI with heart failure in the absence
of significant hypotension (they prevent ventricular
remodeling (dilation) & preserve ejection fraction)

• Calcium channel blockers may be given to patients in

whom beta blocker therapy is ineffective or
contraindicated
 Management/ Pharmacological therapy

• Heparin (IV or low molecular weight) is given to patients

MI because of the high risk of embolism

• Daily aspirin is continued on an indefinite basis.

• Clopidogrel is added to the aspirin regimen for patients

with an STEMI and is continued for 14 days.

• Thrombotic thrombocytopenic purpura is associated

with the prolonged use of Clopidogrel

• During the first several days after STEMI, it is important

to normalize the patient’s blood glucose levels.

– An insulin infusion may be required to achieve this

goal.

• Lipid management therapy is initiated if indicated.

 Management

▪ Other interventions
• Hemodynamic monitoring
– Use of a pulmonary artery catheter (check
volume status, CO) .
– Invasive arterial monitoring is indicated
 Complications

▪ Ventricular dysrhythmias that occur in the prehospital

phase cause the majority of sudden cardiac deaths.

▪ Recurrent myocardial ischemia

• Efforts are made to lower myocardial oxygen demand, to
relieve pain. Emergent PTCA or surgical revascularization
may be considered
▪ Cardiogenic shock
• Is the most serious myocardial complication of MI.
• Occurs because of the loss of contractile forces in the
heart (necrosis involves 40% or more of the left ventricle),
• Is the most common cause of in-hospital death for
patients with MI, with a mortality rate of nearly 80%.
 Complications

▪ Manifestations: rapid, thready pulse, narrow pulse

pressure, dyspnea, tachypnea, inspiratory crackles,
distended neck veins, chest pain, cool, moist skin, oliguria,
and decreased mentation. Decreased PaO2 and respiratory
alkalosis, systolic BP <85 mm Hg, a mean arterial blood
pressure <65 mm Hg, PAWP >18 mm Hg (should be =18).
• Interventions to cardiogenic shock include oxygen supply,
IV dopamine, nitroprusside with a vasopressor (to reduce lt
ventricle workload), use of an intra-aortic balloon pump
(IABP)
• Other complications: ventricular septal wall rupture, left
ventricular wall rupture, pericarditis, DVT, pulmonary
embolism, ventricular dysrhythmias and conduction
disturbances
 Nursing DX

• Chest Pain related to myocardial infarction, angina

• Decreased Cardiac Output: Electrical factors affecting
rate, rhythm, or conduction
• Decreased Cardiac Output: Mechanical factors related
to preload, afterload, or left ventricular failure
• Knowledge Deficit related to illness and impact on
patient’s future
• Anxiety, stress related to fear of illness, death, and
critical care environment
• Activity Intolerance related to decreased cardiac output
or alterations in myocardial tissue perfusion
• Risk for Ineffective Tissue Perfusion related to
thrombolytic therapy impact on myocardial tissue
ACLS
<3 hours
 Chapter 15

Cardiac Surgery
 Cardiac Surgery/ CABG

• Cardiac surgery is necessary in two common

conditions: CAD & Valvular disease.
❑ Coronary Artery Bypass Graft Surgery (CABG)
• Is a surgical procedure in which one or more blocked
coronary arteries are bypassed by a blood vessel graft
to restore normal blood flow to the heart.
• It is also called a bypass graft.
• Native vessels or conduits are “harvested” & used to
bypass blood flow past diseased areas of coronary
artery.
➢ Recommended for patient with coronary arteries
occlusion of 70% or more (60% left main artery).
Coronary Artery Bypass Grafts
 4
Coronary Artery Bypass Grafts

❑ Major Indications for CABG:

▪ Left main coronary (stenosis) occlusion of 70% or more
▪ Three-vessel disease with poor left ventricular function
▪ Two vessel disease with significant stenosis in the
proximal left anterior descending.
▪ Alleviation of Angina that cannot be controlled with
medications or PCI.
▪ Treatment for complications from unsuccessful PCI.
➢ CABG performed under general anesthesia, patient are
connected to the cardiopulmonary bypass (CPB)
machine.
Cardiopulmonary Bypass System
 Desired Characteristics of Graft

• Diameter similar to coronary arteries

• No disease or vessel wall abnormalities
• Adequate length
▪ Commonly used grafts:
– Saphenous vein graft
– Internal mammary artery grafts
 Saphenous Vein Graft

• Used to bypass the obstruction in the coronary artery.

▪ Bypass is done by:
– Proximal anastomoses: anastomosing one end of
the vein to aorta.
– Distal anastomoses: anastomosing the other end of
the vein to the coronary artery past obstruction.
• May be simple or sequential (also called skip)
• May be taken from above or below (preferred same
diameter) the knee.
• About 50% occluded after 10 years due to vein failure:
o Thrombosis (most common, occurs between first month &
first year).
o Fibrointimal hyperplasia (between first month & 5 years).
o Atherosclerosis (between first year- 5 years).
 Greater and Lesser Saphenous Veins Are
Commonly Used for Bypass Graft Procedures

Figure 22-1
Aortocoronary bypass grafts using saphenous vein.
A: Simple graft from aorta to right coronary artery.
B: Sequential graft from aorta to left anterior descending
coronary artery to diagonal or circumflex artery.
 Saphenous Vein Graft

▪ The vein is removed by making along incision along

the inner aspect of the leg or by making a small
incisions in the area of the vein with use of flexible
fiberoptic scope to visualize & remove the vessel.
• Advantages
– Easy to remove
– Longer length allow for several grafts
• Disadvantages
– Less long-term patency compared with IMA
– Leg incision has high chance of edema & infection
 Internal Mammary Artery Grafts

• Preferred alternative to Saphenous.

• Used as a pedicle graft to bypass diseased artery
• When used, the proximal end of the artery remains
attached to the subclavian artery while the other end
bypass diseased coronary arteries.
• Both left & right can be used.
• Left internal mammary artery longer & larger
– Used to bypass LAD
• Right internal mammary artery is
used for right coronary artery or LCX.
• 90% patency at least for 10 years
 Internal Mammary Artery Grafts

• Advantages:
– Has the ability to adapt size to provide blood flow
according to myocardial demand.
– Improved short & long term patency rates over
saphenous vein grafts.
– Has diameter close to diameter of coronary arteries
• Disadvantages:
– Greater postoperative pain.
– Higher risk of postoperative bleeding & requires
pleural chest tube.
– Requires longer time which means longer
cardiopulmonary bypass.
 Other Grafts

• Radial artery
– More prone to spasm
– Postoperative add Nitroglycerin followed by oral
Nitrates to help reduce spasms
• Right gastroepiploic artery
• Homologous (nonnative) grafts
– Saphenous, umbilical, or
bovine ‫ي‬
ّ ‫ بَقَ ِر‬internal mammary artery
 Newer Technique

• Off-pump CABG surgery (OPCABG)

– Decreased length of stay.
– Incidence of stroke 48 to 72 hours (vs.
immediately after surgery if on
cardiopulmonary bypass).
• Minimally invasive direct coronary
artery bypass grafting (MIDCABG)
– Number of grafts restricted
Off-pump CABG surgery (OPCABG)
Copyright © 2018 Wolters Kluwer • All Rights Reserved
 ❖ Valvular Disease

• Cardiac valves maintain the uni-directional flow of blood

• Valvular stenosis or insufficiency (regurgitation) cause
disturbances of blood flow across valves & may occur
alone or in combination, in the same valve, or in more
than one valve.
• Can affect the tricuspid, pulmonic, mitral, & aortic valve
• The stenotic valve has a narrowed orifice that creates a
partial obstruction to blood flow, resulting in increasing
pressure behind the valve & decreasing forward blood
flow.
• The insufficient valve (regurgitation) is
incompetent or leaky; blood flows backward,
increasing pressure & volume behind the valve.
 Valvular Disease DX

• Diagnosis is confirmed by echocardiography &

catheterization of both sides of the heart, at which time
valvular gradients are measured.
▪ Mitral Valve:
– To determine the gradient across the mitral valve, left
atrial & left ventricular pressures are measured during
diastole.
• A gradient > 15 - 20 mm Hg means that severe
mitral stenosis exists.
– Valve area is also calculated during cardiac
catheterization. The normal mitral valve area is 4 to 6
cm2.
• An area less than 1.5 cm2 signifies critical mitral
stenosis, & surgery is indicated.
 Valvular Disease DX

▪ Aortic Valve:
– To determine the gradient across the aortic valve,
the left ventricular & aortic root pressures are
measured during systole.
– Significant aortic stenosis:
• Gradient greater than 50 mm Hg
• Aortic valve area less than 1 cm2
• Normal 2.6 to 3.5 cm2
– Valvular insufficiency is diagnosed by regurgitation
of the contrast medium backward through the
incompetent valve.
 Pathophysiology

▪ Mitral Stenosis
• Rheumatic disease causes fusion of the commissures &
fibrotic contraction of valve leaflets, commissures, &
chordae tendineae
▪ Mitral Insufficiency
o Valve dysfunction is caused by thickening or stretching of
the leaflets, resulting in backward blood flow.
▪ Aortic Stenosis
o Calcific degeneration results in fusion of the commissures &
fibrous contractures of the cusps & leads to a decreased
valve area size & obstruction of left ventricular outflow.
▪ Aortic Insufficiency
o Rheumatic disease results in thickened & retracted valve
cusps, whereas aortic aneurysm causes annular dilation.
Valvular Disease
Surgical Treatment for Valvular Disease

• Goals
– Relieve symptoms
– Restore hemodynamics
• Indicated
– Left ventricular function deterioration
– Activity becomes severely limited.
– Surgical intervention consists of either valve
reconstruction or valve replacement
 Valve Reconstruction

• Most valve reconstruction procedures are performed on

the mitral valve.
• Advantages
– Eliminates need for long-term Anticoagulation
– Decreases risk of thromboembolism & endocarditis
– Decreases need for reoperation
– Increases survival rates
– Not successful in aortic valve disorders (insufficiency
& restenosis)
• Reconstruction procedures are more likely to be
successful if performed early in the course of the disease,
before left ventricular function deteriorates.
 Balloon Valvuloplasty

Valve Leaflet Resection and Repair With Ring Annuloplasty

 Surgical Treatment for Valvular Disease

▪ Mitral Stenosis
o By reconstruction (Commissurotomy) the fused commissures
are surgically divided, calcified tissue is debrided.
▪ Mitral Insufficiency
o By reconstruction the valve leaflets are repaired.
o Anticoagulation is not usually needed after valve repair
unless an annuloplasty ring is used, In such cases,
anticoagulants are given for only 3 months.
o If reconstruction cannot be accomplished, valves are replaced
Surgical Treatment for Valvular Disease

• Done through a median sternotomy incision with the use

of cardiopulmonary bypass.
• Two major types of prosthetic valves are available;
mechanical & biological.
Box 22-1 Advantages and Disadvantages of Prosthetic Cardiac Valves

Mechanical Valves
• Good long-term durability
• Adequate hemodynamics
• High risk for thromboembolism; necessity for long-term anticoagulation
• Increased risk for bleeding complications

Biologic Valves
• Limited long-term durability
• Better hemodynamics than mechanical valves (except in small sizes)
• No hemolysis
• Low incidence of thromboembolism; possibly no necessity for
anticoagulation
• Fewer bleeding
 Surgical Treatment for Valvular Disease

• Patients with a long life expectancy may receive mechanical

valves because they are particularly durable.
• Older patients may receive biological valves because less
calcification & deterioration occur in older people, long-term
durability is less important, & the risk of anticoagulation
may increase with advancing age.
• Biological valves are indicated for patients who are unable
to comply with an anticoagulation regimen, for those in
whom a long-term anticoagulation regimen is
contraindicated, & for women who plan to become pregnant
(the anticoagulant Warfarin crosses the placental barrier).
• Patients in chronic atrial fibrillation undergoing mitral valve
replacement frequently receive long-term anticoagulation
therapy even with a biological prosthesis.
Mechanical Valves
 Cardiac Surgery

• Preoperative care
– Typical preparation
• Intraoperative phase
– Surgical approach
– Cardiopulmonary bypass
– Cold or warm cardioplegia
– Topical hypothermia
 Cardiac Surgery/Preoperative Phase

• Includes history taking, physical examination, chest

radiography, & ECG.
• Laboratory tests include CBC, electrolytes, PT, PTT, KFT,
pulmonary function tests & ABG.
▪ Preoperative teaching:
o Equipment to point out, incisions & dressings to expect,
patient’s immediate postoperative appearance (yellow or
pale, & cool skin, generalized “puffiness, discomfort
(medications, relief mechanisms), postoperative
respiratory care (incentive spirometry, early mobilization,
use of pillow to splint median sternotomy incision).
 Cardiac Surgery/Intraoperative Phase

• Median sternotomy is commonly used

for myocardial revascularization &
valve surgery.
• The sternum is split with a sternal saw
from the manibrium to below the
xiphoid process, & the ribs are spread
to expose the anterior mediastinum &
pericardium.
• Once the pericardium is opened & the
heart & aorta are exposed, the patient
is placed on cardiopulmonary bypass
machine (also called a pump
oxygenator).
Bypass Machine
Cardiac Surgery/Blood flow in Bypass Machine

• (1) Patient’s deoxygenated

blood enters the bypass
circuit from the venous
cannulas in the SVC superior
vena cavae & IVC.
• (2) The reservoir holds the
blood temporarily.
• (3) The oxygenator removes
carbon dioxide from & adds
oxygen to the patient’s blood.
• (4) The heat exchanger
initially cools the blood &
then rewarms the blood.
Figure 22-7
Blood flow through the circuit of the cardiopulmonary bypass machine: (1) Patient’s deoxygenated blood enters the
bypass circuit from the venous cannulas in the superior and inferior vena cavae. (2) The reservoir holds the blood
temporarily. (3) The oxygenator removes carbon dioxide from and adds oxygen to the patient’s blood. (4) The heat
exchanger initially cools the blood & then rewarms the blood. (5) Roller pumps pump the blood through the circuit &
back to the patient. (6) Oxygenated blood is returned to the ascending aorta by way of the aortic cannula.
Cardiac Surgery/Blood flow in Bypass Machine

• (5) Roller pumps pump the

blood through the circuit &
back to the patient.

• (6) Oxygenated blood is

returned to the ascending
aorta by the aortic cannula.

➢ Heparin is administered throughout cardiopulmonary

bypass to prevent massive extravascular coagulation as
the blood circulates through the mechanical parts of the
bypass system.
 Cardiac Surgery

• During bypass, the patient’s core body temperature is

lowered to 28°C to 32°C to protect the major organ
systems from possible ischemic injury.
• The aorta is cross-clamped just above the coronary
arteries, then cold cardioplegia solution at 4°C (39.2°F)
is infused into the aortic root . It’s high Potassium
concentration causes immediate asystole & relaxation.
Asystole & hypothermia protect against myocardial
ischemia by decreasing the metabolic needs of
myocardial tissue.
• After surgery is completed, the heat exchanger rewarms
the blood to return the patient’s core temperature to
37°C , aortic cross-clamp is removed so that blood again
perfuse the coronary arteries, warming the myocardium.
 Cardiac Surgery

• As perfusion & rewarming continue, a spontaneous

cardiac rhythm may resume, ventricular fibrillation may
develop (necessitating internal defibrillation), or pacing
may be used to initiate a rhythm.
• After a reliable rhythm with a rate adequate to
maintain the cardiac output & blood pressure is
established, cardiopulmonary bypass is gradually
reduced.
• Heparinization is reversed by the administration of
Protamine Sulfate.
• If adequate cardiac output cannot be maintained,
positive inotropic agents or intra-aortic balloon
counterpulsation can be instituted.
 Cardiac Surgery

• If the need for postoperative cardiac pacing is

anticipated, temporary pacing electrodes are placed
on the epicardial surface of the heart & brought out
through the chest wall.
• Chest tubes placed in the mediastinum & pericardial
space for drainage & pleural tubes are also placed if
the pleural space has been entered.
• After adequate hemostasis is obtained, the edges of
the sternum are approximated with wires, the
incision is closed, & dressings are applied.
 Effects of Cardiopulmonary Bypass

• The interface between blood & bypass circuit

(nonphysiological surfaces) leads to:
– Increased capillary permeability, thus the patient
becomes edematous.
– Hemodilution, thus Hb, HCT & coagulation factors
are decreased.
– Altered coagulation.
– Increased risk of microemboli.
– Increased systemic vascular resistance (SVR)
related to Catecholamine secretion during bypass
surgery.
 Postoperative Phase

• In the immediate post operative period in ICU, patient is

attached to cardiac monitor, ventilator, hemodynamic
monitoring lines.
▪ Nursing Care
– Monitor chest tubes & character of drainage: amount,
color, flow & check for air leaks.
– Measure body temperature & initiate rewarming if
temperature < 36°c.
– Apply end-tidal carbon dioxide device to ventilator
circuit, measure urine output, take a 12-lead ECG,
obtain routine blood work, assess neurological status,
test pacemaker function by assessing capture &
sensing.
 Postoperative Phase

• Prevention of Hypothermia
o Core temperature to decline as warmed blood begins to
circulate to the periphery, heat transfer to the
surrounding tissues.
• Prevent Shivering:
o Shivering often occurs between 90 & 180 minutes.
o Increases metabolic rate, oxygen consumption, CO2
production, & myocardial workload
– Increasing the room temperature & using radiant
heat, blankets, or a warming blanket
– Rewarming should occur slowly to prevent
hemodynamic instability due to rapid vasodilation.
 Postoperative Phase

• Monitoring for systemic inflammatory response

syndrome (SIRS), natural defense mechanism that is
initiated when tissue or vessels are injured, inflammation
at the level of the entire “body”.

• Causes endothelial dysfunction & increased capillary

permeability & alteration in coagulation.

• Symptoms & signs include fever, tachycardia, tachypnea,

& an increased white blood cell count.

• Nursing responsibilities focus on early detection of

embolic events in any system, especially the
cardiovascular, pulmonary, & renal system.
 Postoperative Phase

• Preventing Pulmonary Complications

– Effective oxygenation is monitored using pulse
oximetry with intermittent ABG sampling.
– Positive end-expiratory pressure (PEEP) help keeping
the alveoli open & improve oxygenation.
– Prepare for weaning from mechanical ventilation
– Use of incentive spirometry, encourage physical
mobility.
– Auscultation of breath sounds at frequent intervals,
diminished breath sounds may indicate atelectasis
– Observation work of breathing, tachypnea, use of
accessory muscles, bronchodilator therapy may indicated
 Postoperative Phase

▪ Controlling Pain
• Pain results from the chest or leg incision, the chest tubes,
rib spreading during surgery & care activities.
• The ICU environment may accentuate the pain
physiologically because of light & noise, & psychologically
because of separation & fear.
• Angina after CABG may indicate graft failure.
• Pain often stimulates the sympathetic nervous system,
increasing heart rate & blood pressure, decrease chest
expansion, increase atelectasis, & retention of secretions.
• Nursing management: assessment of the patient’s pain
using a pain scale; administration of analgesics based on
the reported pain intensity; provision of adequate pain relief
as reported by the patient; & alleviation of factors that
enhance pain perception, such as anxiety & fear.
 Postoperative Phase

• Monitoring for Arrhythmias

– Sinus tachycardia is very common & may result from
Sympathomimetic drugs, SIRS, hypovolemia, fever, &
pain.
– Sinus bradycardia may occur, In many cases,
preoperative beta blockade may be the cause.
– Premature atrial contractions PACs are usually Rt
electrolyte disturbances, ischemia or infarction, or
hypoperfusion, treated by replacement of Potassium &
Magnesium.
– Atrial fibrillation, heart block & , Vtach arrhythmias are
also possible.
– Refers to ACLS guidelines for management
 Postoperative Phase

• Preventing Neurological Complications

▪ Neurologic Assessment
– Assesses the level of consciousness, motor and
sensory ability, & CN injury.
– The family of the patient may be helpful in detecting
any subtle changes
– Confirmation of a stroke can be performed with CT
scan or MRI of the head
– Thrombolytic therapy cannot be used after surgery in
the patient who has just had CABG surgery because of
bleeding concerns.
 Postoperative Management

• Monitoring Postoperative Bleeding

– Monitor chest tube output.
– Reverse Anticoagulant.
– Rewarm the patient.
– Administer blood products.
– Administer Antifibrinolytics.
 Postoperative Management

▪ Monitoring Postoperative Bleeding

 If the chest tube output continues to be greater than
200 mL/hour, Protamine sulfate is the first level of
intervention & given at 1 mg for every 100 units of
Heparin.
 Monitor PT & PTT
 Rewarming is important as coagulation cascade
cannot function properly at hypothermic temperatures
 Infusion of platelet, fresh frozen plasma (usually 4 to 6
units/infusion), coagulation factors such as
cryoprecipitate (factors I & VIII) & factor VII
 Surgical reexploration with chest tube bleeding > 500
mL/hour.
Bleeding Complication: Cardiac Tamponade

• Excessive accumulation of blood in pericardial space

• Warning signs:
– Decreased chest tube output
– Decreased cardiac output & BP
– A-line demonstrates pulsus paradoxus.
• Increase & equalization of pressures
• Definitive diagnosis: Echocardiogram
 Postoperative Phase

• Preventing Renal Complications

– Autodiurese with depletion electrolytes
– Slight metabolic acidosis
– Decreasing urine output
• Fluid or loop diuretics
• Preventing Endocrine Complications
– Strict glycemic control
– Adrenal insufficiency
• Preventing Gastrointestinal Complications
 Postoperative Care

• Controlling BP
– Maintain between 120 & 170 mm Hg
• Wound Care
• Assessment of operative site
• Monitoring for Infection
– SIRS or overshoot rewarming
 Patient Teaching and Discharge

• Hospitalization after CABG usually 4 to 7 days.

• Discharge planning begins on admission.
• Discharge medications typically include
– Aspirin, -Blocker, ACE inhibitor, & Statin
• Smoking cessation interventions
• Risk factor reduction
• Incision care
• Neurologic changes
• Medication education
• Follow-up physician appointments
Postoperative Care
 Chapter 6

Basic Life Support

(BLS)
The New Trends
Sudden Cardiac Death or Cardiac Arrest

 The cessation of breathing & circulation is known

as cardiopulmonary arrest, also referred to as sudden
cardiac arrest.
 Cardiac arrest can occur without warning, &
requires rapid detection & resuscitation.
 Immediate, high quality cardiopulmonary
resuscitation (CPR) must be initiated within 4 to 6
minutes, to increase patient’s chances of survival &
prevent irreversible brain injury.
 Causes of Cardiopulmonary Arrest

 Cardiac Causes: MI, HF, Dysrhythmia, Coronary

vasospasm, Cardiac tamponade.
 Pulmonary Causes: Respiratory failure, Airway
obstruction, Impaired gas exchange (ARDS), Impaired
ventilation, (Pneumothorax), Pulmonary embolus (PE)
 Electrolyte Imbalances: Hyperkalemia,
Hypomagnesemia, Hypercalcemia/hypocalcemia.
 Procedural Causes: Pulmonary artery
catheterization, Cardiac catheterization & Surgery.
 Miscellaneous: Drug toxicity & drug side effects,
Trauma—myocardial contusion or aortic tear.
 Cardiopulmonary Resuscitation
CPR

 The American Heart Association (AHA) separates

care of adult cardiac arrest patients into three tiers:
 Basic Life Support (BLS)
 Advanced Cardiac Life Support (ACLS)
 Post–cardiac arrest care
The sequence of events in CPR:

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

 CPR

 Basic Life Support (BLS): includes emergency

care interventions for:
 CPR
 Choking
 Rescue breathing
 Use of an Automated External Defibrillator (AED)

 Advanced Cardiac Life Support (ACLS)

 Is an advanced set of intra- & postarrest
interventions.
 The cause of the arrest can be searched for, &
specific interventions designed to correct the
underlying cause.
Assessment & Management of the Patient
in Cardiopulmonary Arrest

 Initial assessment should take no more than 10 seconds.

 Positioning the Patient: Placed supine on a firm, flat surface.
 Back board is used in a hospital bed when help arrives.
Determining Responsiveness: The first step in assessment
o Unresponsiveness is defined as no response when the patient is
shaken & spoken to loudly (eg, “Are you ok?”).
 Observe the patient’s chest for breathing while
simultaneously palpating the carotid pulse at the same time.
 The patient who is breathing is not in cardiac arrest.
 Unresponsiveness associated with lack of breathing is
considered a cardinal sign of cardiac arrest.
 If patient is unresponsive, not breathing, & has no detectable
carotid pulse, nurse should call for help & request a Code Blue.
 Once help has been requested, CPR should be started.
 Compression, Airway, Breathing (C-A-B) sequence.
8

2020 Adult BLS

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
1
0

Compression, Airway, Breathing (C-A-B) sequence

1
1
Components of High-Quality CPR (C-A-B)
 Circulation
• Determine unresponsiveness & absence of breathing & pulse.
• Place backboard under patient’s chest.
• Start compressions within 10 seconds of finding no breath or pulse
• Push Hard and Fast while:
o Compressing chest at rate of at least 100 to 120/min
o Compressing chest to a depth at least 2 inches (5cm) but no
more than 2.4 inches (6cm).
o Allowing full chest recoil after each compression.
o Minimizing interruptions in compressions to less than 10 seconds
o Rotating staff doing compressions every 2 minutes or after every
5 cycles of 30:2
 Palpate pulses (Carotid or femoral) to determine effectiveness of
compressions.
 Components of High-Quality CPR

 Airway
 Open patients airway using head tilt–
chin lift maneuver (jaw thrust without
head extension for patients with or
suspected to have cervical spine
injuries).
 Place oropharyngeal airway (if possible)
 Provide suction as necessary

Jaw thrust maneuver Head tilt-chin lift maneuver

 Jaw Thrust Maneuver

 The patient’s head & neck not be

moved to ensure that no damage
(or no further damage) is done to
the cervical spine & spinal cord.
 Keeping the head in a neutral
position.
 The rescuer places a hand on each
side of the patient’s head behind
the temporomandibular joint.
 Gently pushing the jaw forward;
this will open the airway to allow
for ventilation.
 Components of High-Quality CPR
 Breathing
 Ventilate effectively using a barrier device
(bag-valve-mask (BVM), face mask)
 Maintain seal around patient’s mouth & nose
 Observe for chest rise & fall
 Avoid excessive ventilations:
o 2 ventilations with each 30 compressions or
o One ventilation every 6 seconds (10 breaths a minute) with an advanced
airway.

o The recommended assisted ventilation rate has been

increased to 1 breath every 2 to 3 seconds (20-30 breaths
per minute) for all pediatric resuscitation scenarios.(2020
guidelines)
o Each of the two ventilations is to be given over 1 second each.
 One & Two person BVM Technique

 The mask is placed on the face of the patient with the narrow end
over the nose, & the wide end positioned just below the lower lip.
 Using the thumb & forefinger of the hand holding the mask (forming
a “C”), the rescuer presses directly down on the mask.
 Using the other three fingers of the same hand (forming an “E”), the
rescuer then grasps the bony part of the mandible, pulling the angle
of the jaw up & back.
 With 2 providers, one opens the airway & seals the mask to the
face while the other squeezes the bag.
 Components of High-Quality CPR
 Defibrillation
• Defibrillate as soon as possible when a shockable rhythm is
detected.
• May terminate Ventricular Fibrillation (VF) or Pulseless
Ventricular Tachycardia (PVT).
• Most effective when delivered within 3 to 5 min of cardiac arrest
• Placement of electrode
patches (paddles):
• One patch on the upper right
chest below the clavicle.
• The second patch on the left
side of the chest in the mid
axillary line.
Automated External Defibrillator (AED)

• Studies have shown that the sooner a patient in Ventricular

Fibrillation is defibrillated, the greater the chance for survival.
• The development of the AED has improved the survivability of
individuals suffering from potentially life-threatening
arrhythmias.
• The AED allows for defibrillation to be performed in a variety of
settings by personnel trained in the use of the AED, but not
trained in BLS/ACLS.
• The AED consists of a computerized detection system that
recognizes the patient’s inherent heart rhythm & delivers a
shock when necessary.
• AEDs are now found in airports, train stations, sports stadiums,
& shopping malls.
High-Quality CPR
 Chest Compression Rate

 2020: at rate of 100 to 120 times/min

Why
 Emphasis on an adequate compression rate & minimizing
interruptions to chest compression.
 The actual number of chest compressions delivered per
minute is determined by the rate of chest compressions
& the number & duration of interruptions (e.g., to open
the airway, deliver rescue breaths, or allow AED analysis)
in compressions.
 Increasing rate to > 120/min negatively affected depth of
compressions (i.e., depth becomes less).
 Adult Chest Compression Depth

• 2020: at least 2 inches (5 cm) but not greater than 2.4

inches (6 cm).
Why
 Studies suggest that compressions of at least 2 inches are
more effective than compressions of 1½ inch.
 Compressions create blood flow primarily by increasing
intrathoracic pressure & directly compressing the heart.
 Rescuers often do not adequately compress the chest
despite recommendations to “push hard.”
 Injuries are more common when compression depth is > 6
cm than when it is between 5 and 6 cm.
 Chest wall Recoil

• 2020: rescuer should allow for full chest wall recoil.

Why
• Full chest wall recoil occurs when the sternum returns
to its natural or neutral position during the
decompression phase of CPR.
• Chest wall recoil creates a relative negative
intrathoracic pressure that promotes venous return &
cardiopulmonary blood flow.
• Leaning on the chest wall (incomplete recoil) between
compressions precludes full chest wall recoil thus it
reduces venous return, coronary perfusion pressure, &
myocardial blood flow.
 Interruptions in Chest Compressions

• Frequency & duration of interruptions in compressions should be

minimized. Chest compression fraction (CCF) should be as high
as possible, with a target of at least 60%
Why
• CCF is a measurement of the proportion of total resuscitation time
that compressions are performed.
• Reduction in interruptions would maximize the number of
compressions delivered per minute.
• The optimal goal for CCF has not been defined in 2015.
• Addition of a target CCF is intended to limit interruptions in
compressions & to maximize coronary perfusion & blood flow
during CPR.
 Ventilation During CPR With an
Advanced Airway

• Once an advanced airway is in place, chest

compressions can be continuous & no longer cycled
with ventilations.
• Rescue breaths can then be provided at about 1
breath every 6 seconds (about10 breaths per
minute).
• 1 breath every 2 to 3 seconds (20-30 breaths per
minute) for all pediatric

• Excessive ventilation should be avoided

• Excessive ventilation rate can compromise venous
return & cardiac output during CPR. resulted in
increased intrathoracic pressures, decreased
coronary perfusion pressures, & reduced survival.
 Hands Position

 Placing the heel of one hand

on the lower half of the
sternum at the nipple line, &
placing the heel of the other
hand over the first hand.
 The shoulders of the rescuer
must be positioned directly
above the sternum, with
arms fully extended &locked
into position.
 Trained Vs Untrained Rescuers
 2020: differentiated between trained versus untrained rescuers
 The trained lay rescuer perform both compressions &
ventilations (ratio of 30 compressions to 2 breaths)
 The not trained rescuer should provide Hands-Only™
(compression-only) CPR for the adult victim who suddenly
collapses ,“push hard & fast” on the center of the chest”
 2020: recommend that laypersons initiate CPR for presumed
cardiac arrest because the risk of harm to the patient is low if the
patient is not in cardiac arrest.
Why
 Hands-Only (compression-only) CPR is easier for an untrained
rescuer to perform & can be more readily guided by dispatchers
over the telephone.
 New evidence shows that the risk of harm to a victim who
receives chest compressions when not in cardiac arrest is low.
Lay rescuers are not able to determine with accuracy whether a
victim has a pulse, and the risk of withholding CPR from a
pulseless victim exceeds the harm from unneeded chest
compressions.
 When can you stop performing CPR

 In the Prehospital Setting

 Return of spontaneous circulation (ROSC)
 You see an obvious sign of life, such as opens their
eyes, makes a movement, sound, or starts breathing.
 Another trained responder or EMS personnel take
over.
 You are too exhausted to continue.
 The scene becomes unsafe (fire, electrical lines, or
Forshootout nearby).
further explanation of the H’s and T’s, see Part 10:
“Special Resuscitation Situations.
27
Copyright © 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
 References

• Kleinman ME, et al. Part 5: adult basic life support and

cardiopulmonary resuscitation quality: 2015 American Heart
Association Guidelines Update for Cardiopulmonary Resuscitation
and Emergency Cardiovascular Care. Circulation. 2015;132(suppl
2):S414–S435
• Highlights of the 2020 American Heart Association Guidelines
Update for CPR and ECC. https://eccguidelines.heart.org/wp-
content/uploads/2020/10/2020-AHA-Guidelines-Highlights-
English.pdf
• Cardiopulmonary Resuscitation and Emergency Cardiovascular
Care Part 1: Executive Summary : 2010 American Heart
Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation 2010, 122:S640-S656