Care of Clients with Problems in

Oxygenation (Cardiology)
The Cardiovascular System
 Oxygenation

Transport of O2 to all body

parts and the removal of
CO2.
4 Components of the process
1. Hgb – Oxygen Carrier
2. Blood Vessels – transporting network
3. Heart – pump
4. Lungs – gas exchange
Physiology of Oxygenation
1. Ventilation
2. Alveolar Gas Exchange (oxygen
uptake or external respiration)
3. 02 Transport & Delivery
4. Cellular Respiration
Physiology of Oxygenation

1. Ventilation
The movement of air into and out of
the lungs for the purpose of delivering
fresh air into the lungs’ alveoli.
Regulators of Ventilation
1. Respiratory control centers in the pons &
medulla oblongata.
2. Changes in the concentration of pH &
CO2 in the body’s fluid
3. Decrease in blood O2 concentration
(hypoxemia)
Physiology of Oxygenation

2. Alveolar Gas
Exchange
Oxygen Uptake– the exchange of O2
from the alveolar space into the
pulmonary capillary blood.
Alveolar Gas Exchange
Physiology of Oxygenation

3. O2 Transport and
Delivery
3 Factors Influence The Capacity Of Blood
To Carry O2
1. The amount of O2 dissolved in plasma
2. The amount hemoglobin
3. The tendency of hemoglobin to bind
with O2
Physiology of Oxygenation

4. Cellular Respiration
 Gas exchange at the cellular level (also
called internal respiration) takes place
via diffusion in response to
concentration gradient.
 O2 diffuses from the blood to the
tissues, while CO2 moves from the
tissues to the blood
 Then blood is reoxygenated by the
lungs
Cellular Respiration
The
Structure of
the Heart
 Major Function of the
Cardiovascular System
 Circulation of blood.
 Delivery of O2, nutrients,
hormones and enzymes to
the body.
 Removal of CO2 and other
products of metabolism.
The Heart
 Hollow, Muscular Organ
 Delivers oxygenated blood to
body through arteries
 When blood returns through
veins, pumps it to lungs to be
reoxygenated
The Heart
 Lies obliquely in chest, behind
sternum in mediastinum.
 Located between the lungs in
front of spine.
 Varies in size depending on the
person’s body size.
 Estimated around 5 in long and
3.5 in wide.
The Heart
Changes in the Heart
 In older adult, becomes slightly
smaller and loses contractile
strength and efficiency.
 By 70, cardiac output at rest
has diminished by about 30%
to 35% in many people.
The Heart
Heart Wall
1. Epicardium – outermost layer and
made up of squamous epithelial
cells
2. Myocardium – Made up of
Myocardial cells. Nodal cells - for
pacemaker functions.
3. Endocardium – innermost layer,
consisting of thin layer of
endothelial tissue that lines heart
valves and chambers.
The Heart
Pericardium

 Fluid-filled sac that envelops

heart and acts as tough,
protective coating.
 Consists of fibrous
pericardium (tough, white,
fibrous tissue) and serous
pericardium (two layers
<parietal,visceral>)
The Heart
Pericardium

 Pericardial space separates

the visceral and parietal
layers and contains 10-20ml
of thin, clear, lubricating
pericardial fluid.
The Heart
Functions of the Pericardial Fluid

 Protects & cushions the heart

& great vessels.
 Provides barrier to infectious
processes in adjacent
structures
Chambers of the Heart
Atrium
 Protects & cushions the heart & great vessels.
 Provides barrier to infectious processes in
adjacent structures
Ventricles
 RV receives deoxygenated blood from RA,
pumping it to the lungs for reoxygenation.
 LV receives oxygenated blood from LA,
pumping it into the systemic circulation.
Chambers of the Heart
Septum – a muscular wall
that separates the
chambers of the heart
1. INTERATRIAL septum –
separates the atria
2. INTERVENTRICULAR septum –
separates the ventricles
The Heart Valves

Atrio-ventricular valves
1. Tricuspid
2. Mitral or bicuspid

Semi-lunar valves:
1. Pulmonary
2. Aortic
The Heart Valves
Atrio-ventricular valves
 Tricuspid valve
separates RA fr RV;
mitral valve separates
LA fr LV.
 Closure of AV valves
associated with S1
sound.
The Heart Valves

Semi-lunar valves:

 Pulmonic valve, located

where pulmonary artery
meets right ventricle.
 Aortic valve, located
where left ventricle meets
aorta.
 Closure of semilunar
valves associated with S2
sound.
The Heart Valves
Ventricular Diastole Ventricular Systole
AV valves are open. Semilunar valves are open.
What causes the valves to open and
close?
 Increased pressure within the ventricles during ventricular
systole causes the pulmonic and aortic valves to open,
allowing ejection of blood into the pulmonary and systemic
circulation.
 Loss of pressure as the ventricular chambers empty causes
the valves to close.
Atrial and Ventricular Pressure
The Blood Circulation
Coronary Blood Supply

 Main coronary arteries

lie on surface of heart.
 Heart receives its
blood supply almost
entirely through
coronary arteries.
Coronary Blood Supply
Right Coronary Artery
 Supplies blood to right
atrium, right ventricle,
and inferior wall of left
ventricle.
 Posterior descending
artery supplies
posterior wall of left
ventricle.
Coronary Blood Supply
Left Coronary Artery
 Splits into two major branches:
left anterior descending, left
circumflex.
 Left anterior descending
supplies blood to anterior wall
of left ventricle, anterior
interventricular septum, bundle
of His, right bundle branch, and
anterior fasciculus of left bundle
branch.
Coronary Blood Supply
Left Coronary Artery
 Left circumflex provides
blood to lateral wall of left
ventricle and left atrium.
Cardiac
Physiology
Autonomic Innervation of the Heart

 Sympathetic nerve
stimulation causes release
of norepinephrine, which
increases heart rate and
accelerates AV node
conduction.
Autonomic Innervation of the Heart

 Parasympathetic Nerve
stimulation causes release
of acetylcholine, which
slows heart rate and
conduction through the AV
node.
Role of Baroreceptors and Chemoreceptors in Response
to Blood Loss
Control of Blood
Pressure by
Baroreceptors
 Baroreceptors are stretch
receptors in the wall of some
blood vessels.
 They are involved in the control
of arterial pressure through the
discharge of impulses to the
cardiovascular centre when
there is distension due to a
change in the blood pressure.
Control of Blood
Pressure by
Chemoreceptors
 They are sensitive to any
change in the chemical
composition of the blood, such
as a decrease in oxygen level
and pH of the blood or an
increase in the carbon dioxide
level.
Chemoreceptor Stimulation and the Heart’s
Response
Decreased Blood O2
Increased CO2
Decreased blood Ph

Decreased Increased
Parasympathetic Sympathetic
Stimulation Stimulation

Increased Increased
Heart Rate SV
Increased
BP
Transmission of
Electrical Impulses
Transmission of Electrical Impulses
 In order for the heart to contract and pump blood to the rest of the body, an
electrical stimulus needs to occur first.
 Generation and transmission of electrical impulses depend on the four key
characteristics of cardiac cells: automaticity, excitability, conductivity and
contractility.
Transmission of Electrical Impulses
Four Key Cell Characteristics
1. Automaticity – cell’s ability to spontaneously initiate an electrical impulse.
2. Excitability – cell’s ability to respond to an electrical impulse.
3. Conductivity – cell’s ability to transmit an electrical impulse from cell to another.
4. Contractility – cell’s ability to contract.
Cardiac Conduction System
 Impulses travel from SA node (heart’s
pacemaker) through internodal tracts
and Bachman’s bundle to AV node.
 From AV node, impulses travel through
bundle of His, bundle branches, and to
Purkinje fibers.
Cardiac Conduction System
1. Sinoatrial Node (SA
Node)
 Located in the RA where the superior vena
cava joins the atrial tissue mass.
 Pacemaker of the heart.
 Generates impulses about 60-100 b/min
(resting conditions).
 Impulses travel on specific path but don’t
travel in backward or retrograde direction.
Cardiac Conduction System
2. Atrioventricular Node (AV
Node)
 Located in the inferior right atrium near
ostium of the coronary sinus.
 Does not possess pacemaker cells but the
surrounding tissue does.
 AV node conducts impulses to the
ventricles.
 Firing rate of 40-60 b/min.
Cardiac Conduction System
3. Bundle of His
 Divided into 2 branches ; RBB & LBB
 RBB extends down the right side of the
interventricular septum and through the
right ventricle.
 LBB extends down the left side of the
interventricular septum and through the left
ventricle.
 Firing rate 30-40 b/min
Cardiac Conduction System
4. Purkinje Fibers
 Composed of a diffuse muscle fiber
network beneath the endocardium that
transmits impulses quicker than any other
part of the conduction system.
 Usually doesn’t fire unless SA and AV nodes
fail to generate or when impulse is blocked
in both BB.
 Firing rate 20-40 b/min
Cardiac
Activation
Times
Cardiac Conduction System
SA
(60-100/min)

AV
(40-60/min)

BUNDLE OF HIS
(30-40/min)

PURKINJE FIBERS
(20-30/min)
Abnormal Impulse Conduction
Causes include:
 Altered Automaticity
 Retrograde Conduction of
Impulses
 Reentry Abnormalities and
Ectopy
Stroke Volume
Stroke Volume

 VentricularStroke volume is the

difference between ventricular end-
diastolic volume (EDV) and end-systolic
volume (ESV).
SV = EDV - ESV
 In
a normal heart, EDV-ESV is the same
volume of blood as ejected into the
aorta during each systole.
Factors affecting the Stroke Volume
1. Preload
 The distending force that
stretches the ventricular
muscle during ventricular
relaxation (Woods, 2010).
 Can be compared to the
stretching of a rubber
band.
Factors affecting the Stroke Volume
1. Preload
 The vol of blood in the
ventricles at the end of
diastole, before the next
contraction.
 Proportional to the end-
diastolic volume (EDV).
Factors Affecting Preload
1. Venous Return
The volume of blood that enters the ventricle during
diastole.
e.g. Fluid Overload

2. Ventricular Compliance
The elasticity when blood enters ventricle.
e.g. Hypertrophy, post MI, cardiac tamponade
Frank Starling’s Law of the Heart

 The > the volume, the > the stretch of the

cardiac muscle, the > the force of
contraction to accomplish emptying.
 Has physiologic limit
 Overstretching of the cardiac muscle fibers
eventually results in ineffective contraction.
Conditions that Decreases Preload

Hemorrhage
Fluid
shifting to 3rd
space
Vasodilation
Conditions that Increases Preload
 CHF
 Renal Disease
 Vasoconstriction
 Hypervolemia
 Regurgitation of cardiac
valves
Factors affecting the Stroke Volume

2. Contractility
 The forcefulness of
contraction of ventricular
muscle fibers.
 Poor contractility will result
to decrease in Cardiac
Output.
Blockage of Coronary Artery and the
Heart’s Contractility
Factors affecting the Stroke Volume

3. Afterload
 The force that the
ventricles must generate
to eject blood.
 Amount of pressure left
ventricle must work
against to eject blood
during systole.
Factors affecting the Stroke Volume

Factors Affecting
Afterload
 Diameter of the aorta &
pulmonary artery.
 Opening and
competence of the
pulmonary & aortic valves.
 Determinants of LV Afterload
✓Resistance Systemic Vascular

⇘ Resistance (SVR)

HPN

⇖
Aortic Valve
Stenosis

✓The FORCE
Determinants of RV Afterload
Pulmonary vascular
resistance (PVR

⇙ CONGESTED
LUNGS
Pulmonic Valve

⇗
The FORCE
Stenosis
PULMONARY
EMBOLISM
Ejection Fraction
Ejection Fraction (EF) is the fraction of
blood ejected by the ventricle relative to
its filled volume (end-diastolic volume).
𝐄𝐅=𝐒𝐕/𝐄𝐃𝐕=(𝐄𝐃−𝐄𝐒𝐕)/𝐄𝐃𝐕
EF is a measure of the ability of the heart
to eject blood.
EF is normally about 0.55-0.65 (55%-65%)
Cardiac Output
Cardiac Output is the amount of blood
the left ventricle pumps into the aorta per
minute.
𝐂𝐎=𝐇𝐑 𝐱 𝐒𝐕
Normalcardiac output is 4-8L per minute,
depending on body size.
Sample Computation
(Compute the SV, EF & CO)
HR = 70/min
End diastolic volume = 120 ml
End systolic volume = 50 ml
Ejection volume (stroke volume) = 70 ml

Ejection fraction = 70ml/120ml

= 58%
(normally 60%)

If heart rate (HR) is 70 beats/minute, what is cardiac output?

Cardiac output = HR x SV = 70/min * 70 ml

= 4900ml/min
GENERAL NURSING INTERVENTION
DIAGNOSTIC TESTS INVOLVING THE
CARDIOVASCULAR SYSTEM
NURSING INTERVENTION

 •Ensure the patient understood the procedure.

 •Sign as a witness in consent forms.
 •Scheduling the test.
 •Providing any necessary care (e.g. adjustments in medications and special diets)
 •Promoting maximal emotional and physical comfort.
COMPLETE BLOOD COUNT

 •A complete blood count, also known as a full blood count, is a set of medical laboratory tests that provide
information about the cells in a person's blood.
 •The CBC indicates the amounts of white blood cells, red blood cells and platelets, the concentration of
hemoglobin, and the hematocrit.
 •⇩RBC’s suggest inadequate tissue oxygenation.
 •⇧WBC may indicate infectious heart disease & MI.
ERYTHROCYTE SEDIMENTATION RATE

 The erythrocyte sedimentation rate is the rate at which red blood cells in anticoagulated whole blood descend in
a standardized tube over a period of one hour.

 •Normal range:
 Male-15-20 mm/hr
 Female 20-30 mm/hr
 •↑in infectious heart disorder & MI
CARDIAC BIOMARKERS

 This test measures the levels of cardiac biomarkers in your blood. These markers include enzymes, hormones,
and proteins.
 •Cardiac biomarkers show up in your blood after your heart has been under severe stress because it isn't getting
enough oxygen.
MYOGLOBIN

 •O₂-binding protein found in myocardium & skeletal muscle.

 •Released after damage of heart or skeletal muscle.
 •Earliest marker detected as early as 1-3 hours after an MI.
 •Normal value = < 90 mcg/L
TROPONIN

 •This protein is by far the most commonly used biomarker. It has the
highest known sensitivity.
 •It enters into your bloodstream soon after a heart attack.
 •It also stays in your bloodstream days after all other biomarkers go back
to normal levels.
CREATININE KINASE

 •This enzyme can also be measured several times over a 24-hour period. It will usually at least double if you've had a
heart attack.
 •Present in heart muscle, skeletal muscle & brain tissue.

 ISOENZYMES:
 1. CK-MM–skeletal muscle
 2. CK-BB –brain
 3. CK-MB–myocardial muscle
 CK :Male: 12-80 u/L
 Female: 10 –70 u/L
ASPARTATE AMINOTRANSFERACE

 It is an enzyme found in cells throughout the body but mostly in the heart and liver and, to a lesser extent, in the
kidneys and muscles.

 •Elevated level indicates tissue necrosis (MI)

 •Normal range: 5-40 IU/L
LACTIC ACID DEHYDROGENASE (LDH)

 •It is an enzyme that helps produce energy. It is present in almost all of the tissues in the body and becomes
elevated in response to cell damage.
 •LDH levels are measured from a sample of blood taken from a vein.
 •Normal LDH levels range from 140 units per liter (U/L) to 280 U/L or 2.34 mkat/L to 4.68 mkat/L.
 •Isoenzymes LDH₁ and LDH₂ are cardiac-specific.
 •If LDH₁ is elevated & exceeds LDH₂= “flipped” ratio
 •A reliable indicator of acute MI.
LACTIC ACID DEHYDROGENASE (LDH)

 •LDH₁& LDH₂
 •Onset: 8 -12 hrsafter acute MI
 •Peak: 24 -48 hrs
 •Return to normal: 10-14 days
 •Normal range: 20-200 IU/L
CARDIAC BIOMARKERS
LIPID PROFILE

 •Lipid profile or lipid panel is a panel of blood

tests that serves as an initial screening tool for
abnormalities in lipids, such as cholesterol and
triglycerides.
 High Density Lipoproteins (HDL)
 •Protective, carries “bad” cholesterol from
arteries to liver for excretion.
 •Increases w/ exercise, ⇩low fat.
 •HDL <35mg/dL assow/ ⇪CHD risk
 •LDL)
LOW DENSITY
LIPOPROTEINS (LDL)

 “bad” cholesterol
 •Deposits cholesterol on artery
walls.
 •The primary carriers of
cholesterol
Triglycerides
 •Compounds of fatty acids.
 •Having a high level may raise
the risk of heart disease,
especially in women.
LIPID PROFILE
BLOOD COAGULATION TEST

 •Coagulation tests measure your blood’s ability

to clot, and how long it takes to clot.
 •Drug-induced anticoagulation is a routine
procedure in the cardiac care unit.
 •Close monitoring required!
PROTHROMBIN TIME (PT) OR FACTOR II

 •plasma CHON produced by the liver.

 •measures the time required for a clot to form after adding calcium ions & thromboplastin (Factor III).
 •Valuable for evaluating effectiveness of coumadin (warfarin).
 •Warfarin inhibits Vit K-dependent synthesis of clotting factors II, VII, IX& X.
 Normal Range: 10-14 seconds
 Therapeutic range 1.5-2x of NV
 Q: What is the target PT?
 A: 5-21 to 20-28 secs
 Q: What will you do w/ warfarin dose if PT is >28 secs? Why?
 A: ⇩dose. PT >2x poses risk for bleeding.
INTERNATIONAL NORMALIZED RATIO (INR)

 •Best means of standardizing

measurement of PT to monitor oral
anticoagulant therapy.
 •The PT and INR are used to monitor the
effectiveness of the anticoagulant
warfarin.
 NormalValue:2.0-3.0
 For patients w/ prosthetic heart valves =
INR –2.5 to 3.5
PARTIAL THROMBOPLASTIN TIME (PTT)

 Time (PTT)
 •Use to determine the effectiveness of heparin
 •Therapeutic range: 1.5-2.5x the patient’s baseline value.
 •Normal Value = 60-70 seconds
 •Usually drawn 30-60 mins before the next dose of heparin.
 •For PTT & aPTTless <50 seconds, an increase in heparin dose should be considered.
 •For PTT & aPTT>100 seconds, dose should be decreased.
ACTIVATED PARTIAL THROMBOPLASTIN TIME (PTT)

 •Same purpose as PTT.

 •Therapeutic range: 1.5 –2.5 x the patient’s baseline value
 •Normal Value =
 •35 –45 seconds
STRESS TEST

 •An exercise stress test is used to learn how

well your heart responds when it's working
hard. You will be asked to exercise while
hooked up to an EKG machine.
 •The test involves the use of an
electrocardiogram (ECG) test.
STRESS TEST

 Nursing Education for clients undergoing Stress test

 •Get enough sleep before the test.
 •Avoid tea, coffee, alcohol on the day of test.
 •Avoid smoking, taking NTG 2 hrsprior to the test.
 •Wear comfortable loose-fitting clothes & rubber shoes.
 •Light meal at least 2 hours prior.
STRESS TEST

 •Provide baseline v/s

 •During exercise, client’s BP, HR, and ECG are closely monitored
 •Inform MD for unusual sensation that develop during the test
 •Rest after the test
 •Stress test result is positive if changes occur during stress test.
WHEN TO TERMINATE THE STRESS TEST:

 •Chest pain or fatigue

 •Greatly increased heart rate
 •Failure of systolic BP to rise or a drop in BP
 •Sudden development of bradycardia
 •Serious cardiac dysrrythmia
 •Severe HPN
 •Severe dyspnea
 •ST depression.
PHARMACOLOGIC STRESS TEST

 The use of Dobutamine (increases heart contractility) or adenosine (coronary artery

dilator) instead of exercise.
 •This is used when clients cannot tolerate exercise
 •NPO for 3-6 hours before the test except for sips of water with medications.
 •IV access, BP and pulse are monitored continuously.
ECHOCARDIOGRAPHY

 •A non-invasive diagnostic procedure to

evaluate structural & functional changes of
the heart
 •No special preparation
 •Takes 30-60 minutes to complete
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)
 Examines cardiac structure and function with an ultrasound
transducer placed behind the heart in the esophagus and
stomach.
 Nursing Responsibilities
 1.Assess history of esophageal surgery, malignancy or allergy
to anesthetic or surgery
 2.Informed consent
 3.NPO 6 to 8 hours before the procedure
 4.Encourage to void before the procedure
 5.Remove dentures and other oral prosthetics
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)

 6.Administer sedatives as ordered.

 7.Suction and resuscitation should be readily available.
 8.Cardiac monitoring.
 9.Topical spray anesthetic is administered to depress gag reflex.
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)

 Nursing Responsibilities
 (Post-Procedure)
 1.NPO until gag reflex return.
 2.Lateral or semi fowler’s position.
 3.Encourage to cough.
 4.May give throat lozenge.
 5.Watch out for complication –pharyngeal bleeding, cardiac dysrythmias, vasovagal rxn, transient hypoxemia.
CHEST X-RAY
STUDIES

 To determine the size and

configuration of the heart and
size of the chambers
 •Nursing Preparation:
 ✓Remove metal objects
 ✓Inhale deeply and hold
breath
 ✓Contraindication: Pregnancy
CARDIAC
CATHETERIZATION

 •Left sided –brachial or femoral

artery.
 •Right sided –medial cubital or
brachial vein.
 Right Cardiac Catheterization
 •Femoral vein or antecubital
vein & inferior vena cava into
the RA to the PA
SWAN-GANZ
CATHETERIZATION

 •Swan-Ganz catheterization is
the passing of a thin tube
(catheter) into the right side of
the heart and the arteries
leading to the lungs. It is done
to monitor the heart's function
and blood flow and pressures
in and around the heart.
LEFT CARDIAC CATHETERIZATION

 •brachial or femoral artery➙aorta ➙coronary arteries or LV

 Preparation during procedure
 •Maintain on NPO status for 6-8 hours before the test.
 •Check for dye allergy, especially allergy to iodine and shellfish.
 •Record quality of distal pulses for comparison after test.
 •Record height and weight
 •Obtain baseline v/s.
 •Have client void.
 •Provide psychosocial support.
LEFT CARDIAC CATHETERIZATION

 Client Education
 •Awake during procedure
 •Report any chest pain
 •Lie still
 •May experience warm or flushing sensation as the contrast medium is injected, fluttering sensation as catheter
enters the chambers of the heart, under local anesthesia.
 •Do cardiac monitoring.
LEFT CARDIAC CATHETERIZATION

 Nursing Care after Procedure

 •Evaluate catheterization entry for hematoma formation (usually Femoral).
 •Evaluate pulses distal to catheterization site.
 •Monitor extremities for color, temperature, and tingling sensation.
 •Maintain bed rest; catheter insertion site is in the upper extremity –until v/s are stable; if it is in lower extremity,
for 24 hours.
MAGNETIC RESONANCE IMAGING

 •Strong magnetic field and radio waves are used

to detect and define differences bet healthy
and diseased tissues. Can show the heart
beating and blood flowing over 3 spatial
dimensions.
 •Used for examining aorta, tumors,
cardiomyopathies, and pericardiac diseases.
MRI

 Nursing Responsibilities
 •Secure written consent
 •Inform client about the procedure
 •Assess for claustrophphobiaa.
 •Remove all metal items
 •Instruct client to remain still during procedure
 •No client with pacemakers, prosthetic valves, recently implanted clip or wires
 •Loud knocking noise.
CENTRAL VENOUS PRESSURE (CVP)

 An IV catheter is placed on the superior

vena cava or RA via the subclavian vein or
jugular vein.
 •A CVP reading may also be obtained from
the proximal lumen of the PA catheter.
 •Catheter is secured and sterile dressing
applied
 •Catheter placement confirmed by CXR.
 It is the blood pressure in the venae cava,
near the right atrium of the heart. CVP
reflects the amount of blood returning to
the heart and the ability of the heart to
pump the blood back into the arterial
system.
CVP

 •Normal reading: 5-10 cm H20

 •Increased CVP ➙hypervolemia, HF
 •Decreased CVP ➙hypovolemia
BASIC ELECTROCARDIOGRAPHY (ECG)
 BASIC ELECTROCARDIOGRAPHY (ECG)

 An electrocardiogram (ECG or EKG) records the electrical

signal from your heart to check for different heart conditions.
 Electrodes are placed on your chest to record your heart's
electrical signals, which cause your heart to beat.
 The signals are shown as waves on an attached computer
monitor or printer.
 BASIC ELECTROCARDIOGRAPHY (ECG)

 Graphic display of electrical activity of the heart, which is

analyzed by the time intervals and segments.
 Noninvasive study, measures the electrical currents/ impulses
that the heart generated during a cardiac cycle
 BASIC ELECTROCARDIOGRAPHY (ECG)

Types of ECG
1. Resting electrocardiography
2. Ambulatory ECG/ Holter monitoring
3. Exercise ECG or Stress Test
 BASIC ELECTROCARDIOGRAPHY (ECG)

Holter Monitoring Device

1. recording of cardiac activity usually 24 hrs, while the
client is performing ADLs
2. Instruct keep a diary to note the time of activities
(eating, sleeping, walking, working) and record symptoms
such as chest pain, lightheadedness and palpitation.
BASIC ELECTROCARDIOGRAPHY (ECG)
 BASIC ELECTROCARDIOGRAPHY (ECG)

Provides information about:

1. cardiac dysrhythmias
2. myocardial ischemia
3. site and extent of MI
4. cardiac hypertrophy
5. electrolyte imbalances.
BASIC ELECTROCARDIOGRAPHY (ECG)

Small
Box Big Box
Box
Horizontal
Time 0.04 sec 0.20 sec

Vertical 1 mm or 5 mm or
Voltage
0.1mV 0.5 mV
 BASIC ELECTROCARDIOGRAPHY (ECG)

 Normal Sinus rhythm occurs when an impulse starts in the sinus node and progresses
to the ventricles through a normal conduction pathway –from Sinus Node, Atria, AV node, bindle of His, to the
bundle branches, and on to the Purkinje fibers.
 BASIC ELECTROCARDIOGRAPHY (ECG)

P wave - represents atrial depolarisation.

Location: precedes the QRS complex
Amplitude: 2-3 mm high
Duration: 0.06-0.12 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

P-R Interval - Tracks atrial impulse from atria to AV node,

bundle of His, and RBB and LBB.
Location: from beginning of P wave to the beginning of the QRS complex.
Duration: 0.12-0.60 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

Q-Wave - represents depolarization in the septum.

Whilst the electrical stimulus passes through the bundle of His, and before it
separates down the two bundle branches, it starts to depolarise the septum
from left to right.
 BASIC ELECTROCARDIOGRAPHY (ECG)

R-Wave - represents the electrical stimulus as it passes

through the main portion of the ventricular walls
(Ventricular Depolarization).
 BASIC ELECTROCARDIOGRAPHY (ECG)

S-Wave - represents depolarisation in the Purkinje fibres.

 The S wave travels in the opposite direction to the large R wave
because, the Purkinje fibres spread throughout the ventricles from
top to bottom and then back up through the walls of the ventricles.
 BASIC ELECTROCARDIOGRAPHY (ECG)

QRS Complex - represents depolarization of ventricles.

Location: follows PR interval
Amplitude: 5-30 mm high (differs for each lead used)
Duration: 0.06-0.10 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

ST Segment- represents end of ventricular depolarization and

onset of ventricular repolarization.
Location: extends from the S wave to the beginning of the T wave.
Duration: 0.08 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

T Wave - represents relative refractory period of repolarization or

ventricular recovery.
Location: follows ST segment
Amplitude: 0.5 mm in leads I, II, and III and up to 10 mm in precordial leads
Duration: 0.06-0.12 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

QT Interval - measures timed needed for ventricular depolarizaton

and repolarization.
Location: extends from beginning of QRS complex to the end of the T
wave.
Duration: varies; usually lasts 0.36-0.44 sec
 BASIC ELECTROCARDIOGRAPHY (ECG)

U Wave- repolarization of His-purkinje system.

The U wave may not appear on an ECG. A prominent U wave
may be due to hypercalcemia, hypokalemia, or digoxin toxicity.
 BASIC ELECTROCARDIOGRAPHY (ECG)

ECG Waveform Components

 BASIC ELECTROCARDIOGRAPHY (ECG)

Common Lead Placement Used

1. 12 Lead ECG
2. 5 Lead ECG
3. 3 Lead ECG
 BASIC ELECTROCARDIOGRAPHY (ECG)

3-Lead Monitoring System

 BASIC ELECTROCARDIOGRAPHY (ECG)

5-Lead Monitoring System

 BASIC ELECTROCARDIOGRAPHY (ECG)

12 Lead Placement
 There are 10 wires on an ECG machine that are
connected to specific parts of the body. These
wires break down into 2 groups:
1. 6 chest leads
2. 4 limb or peripheral leads (one of these is
"neutral")
 BASIC ELECTROCARDIOGRAPHY (ECG)
Placement of the 6 Chest
Leads
Electrodes should be placed on the flat surface above
the wrists & ankles
 V1 – 4th ICS right sternal border
 V2 – 4th ICS left sternal border
 V3 – between V2 and V4
 V4 – 5th ICS midclavicular line
 V5 – 5th ICS anterior axillary line
 V6 – 5th ICS midaxillary line
 BASIC ELECTROCARDIOGRAPHY (ECG)

Placement of the Limb Leads

 Limb leads are made up of 4 leads
placed on the extremities: left
and right wrist; left and right
ankle.
 Right ankle is a neutral lead.
 BASIC ELECTROCARDIOGRAPHY (ECG)
Meaning of the Label

Meaning of Position of lead

Label
label on body
AVr Augmented Right wrist
vector right
AVL Augmented Left wrist
vector left
AVf Augmented Left foot
vector foot
NURSING RESPONSIBILITIES IN
CLIENTS FOR ECG
NURSING RESPONSIBILITIES

PRETEST
 Inform pt
 Obtain hx (cc, sx, CV status)
 Obtain hx (previous cardiovascular diagnostic procedures/tests)
 List of pt’s meds
 Review procedure to the pt
 Record baseline VS
 No food, fluid/ med restrictions unless by medical direction
NURSING RESPONSIBILITIES

PRETEST
 SENSITIVITY TO CULTURAL & SOCIAL ISSUES, as well as concern for modesty, is important in providing
psychological support before, during & after the procedure.
NURSING RESPONSIBILITIES

INTRATEST
 Have patient remove clothing to the waist & shoes & any hosiery. May have gown open to front.
 Observe standard precautions & follow general guidelines.
 Instruct pt to lie very still in a relaxed (supine) position & to refrain tensing muscles after electrode placement.
 Breathe normally & avoid touching bed/couch.
 Expose & appropriately drape chest, arms and legs.
 Prepare skin surface with alcohol & clip excess hair. Dry skin sites.
 Apply electrodes in proper position.
 BASIC ECG INTERPRETATION

NORMAL FINDINGS
 Normal HR according to age
 Normal regular rhythm & wave deflections with normal
measurement of ranges of cycle components & ht, depth &
duration of complexes:
 P wave:0.12 secs or 3 sm blocks with amplitude of 2.5 mm
 Q wave: less than 0.04 mm
 BASIC ECG INTERPRETATION

NORMAL FINDINGS
 R wave: 5-27 mm amplitude, depending on lead

 T wave: 1-13 mm amplitude depending

on lead
 QRS complex: 0.12 seconds or 3 small
blocks
 ST segment: 1 mm
 BASIC ECG INTERPRETATION

ABNORMAL FINDINGS
 Arrhythmias
 Atrial/ventricular hypertrophy
 Bundle branch block
 E- imbalances
 MI / ischemia
 Pericarditis
 Pulmonary infarction
 BASIC ECG INTERPRETATION

ABNORMAL FINDINGS
 ST segment:
✓ Depressed= MI
✓ Elevated=acute MI / pericarditis
✓ Prolonged= hypocalcemia
✓ Short = hypokalemia

 T wave:
✓ Flat / inverted = MI, infarction or hypokalemia
✓ Tall = hyperkalemia
 BASIC ECG INTERPRETATION

ABNORMAL FINDINGS
 P wave:
✓ enlarge deflection=atrial enlargement
✓ absent/altered=electrical impulse not
✓ from SA node
 P-R interval:
✓ Increased=conduction delay (AV node)

 QRS complex:
✓ Enlarged=old infarction
✓ Enlarged deflection =ventricular hypertrophy
✓ Increased time duration = BBB
 BASIC ECG INTERPRETATION

ABNORMAL FINDINGS
BASIC ECG INTERPRETATION
ANALYZING A RHYTHM STRIP
ANALYZING A RHYTHM STRIP

Box Small Box Big Box

Horizontal
Time 0.04 sec 0.20 sec
Vertical
Voltage 1 mm or 0.1mV 5 mm or 0.5 mV
ANALYZING A RHYTHM STRIP

The ECG Strip

ANALYZING A RHYTHM STRIP
• HOW MANY SMALL SQUARES in 1 big square
(horizontally)? 5
✓1 BIG SQUARE represents:
Horizontally? 0.20 SEC
Vertically? 0.5 mV or 5 mm

✓1 SMALL SQUARE represents:

Horizontally? 0.04 SEC
Vertically? 0.1 mV or 1 mm
ANALYZING A RHYTHM STRIP
STEPS TO RHYTHM STRIP ANALYSIS
1. Determine Regularity (Rhythm)
2. Calculate Rate
3. Examine P waves
4. Measure PR Interval
5. Measure QRS Complex
STEPS TO RHYTHM STRIP ANALYSIS
STEP 1

Determine the regularity (rhythm) of the R waves.

Regular or Irregular
STEPS TO RHYTHM STRIP ANALYSIS

STEP 1

Determine the regularity (rhythm) of the R waves.

Regular or Irregular
STEPS TO RHYTHM STRIP ANALYSIS
STEP 1

Determine the regularity (rhythm) of the R waves.

Regular or Irregular
STEPS TO RHYTHM STRIP ANALYSIS
STEP 2

Calculate the heart rate.

 Count the number of R waves in a 6-second strip and multiply
by 10.
 This method provides an approximate heart rate in beats per
minute, is fast and simple, and can be used with both regular
and irregular rhythms
STEPS TO RHYTHM STRIP ANALYSIS
STEP 2

Calculate the heart rate. Regular or Irregular?

Heart Rate?
STEPS TO RHYTHM STRIP ANALYSIS
STEP 2

Calculate the heart rate.

Regular or Irregular?
Heart Rate?
STEPS TO RHYTHM STRIP ANALYSIS

STEP 2

Calculate the heart rate (Precise rate calculation).

 Count the numbers of small squares between two consecutive
R waves and refer to conversion table.
 Use conversion table for the equivalents.
STEPS TO RHYTHM STRIP ANALYSIS
Conversion Table
STEPS TO RHYTHM STRIP ANALYSIS
STEP 3
Identify and Examine the P waves

 Analyze the P waves – one P

wave should precede each QRS
complex. All P waves should be
identical (or near identical) in
size, shape, and position.
STEPS TO RHYTHM STRIP ANALYSIS
STEP 3
Identify and Examine the P waves

P waves…
Abnormal or Normal
STEPS TO RHYTHM STRIP ANALYSIS

STEP 4
Measure the PR interval.
 Measure from the beginning of the P wave as it leaves
baseline to the beginning of the QRS complex. Count
the number of squares contained in this interval and
multiply by 0.04 sec.
STEPS TO RHYTHM STRIP ANALYSIS

STEP 5
Measure the QRS Complex.
 Measure from the beginning of the QRS complex as it
leaves baseline until the end of the QRS complex
when the ST segment begins.
 Count the number of squares in this measurement
and multiply by 0.04 sec.
Management of
Patients
With Dysrhythmias and
Conduction Problems
Dysrhythmias

 Are disorders of the formation or conduction (or both) of the

electrical impulse within the heart.
 These disorders can cause disturbances of:
 Rate
 Rhythm
 Both rate and rhythm

 Potentially can alter blood flow & cause hemodynamic

changes.
 Diagnosis by analysis of ECG waveform.
Influences on Heart Rate and Contractility

 Sympathetic stimulation
 Positive chronotropy – increases heart rate
 Positive dromotropy- increases conduction through AV node
 Positive inotropy- increases force of myocardial contraction

 Parasympathetic stimulation
 Negative chronotropy – decreases heart rate
 Negative dromotropy- decreases conduction through AV node
 Rev. Components of
Electrocardiogram strip
Determining Heart Rate from the Electrocardiogram: 1st
method (more accurate)

 1-minute rhythm strip- 300 big boxes / 1500 small boxes

 Count small boxes between RR interval then 1500 by that
number.
 i.e. 1500/ 25 = 60 bpm
6 second method: less
accurate, for irregular rhythm

 Count the R in a 6 second strip then multiply by 10.

 i.e. 7x10 = 70 bpm
  Ventricular and atrial rate: 60 to 100 bpm in the adult
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal, but may be regularly

Normal 


abnormal
P wave: Normal and consistent shape; always in front of the QRS

Sinus 


PR interval: Consistent interval between 0.12 and 0.20 seconds
P:QRS ratio: 1:1

Rhythm
Types of
Dysrhythmias
 Sinus Bradycardia

 Ventricular and atrial rate: Less than 60 bpm in

the adult
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal, but
may be regularly
 abnormal
 P wave: Normal and consistent shape; always in
front of the QRS
 PR interval: Consistent interval between 0.12
and 0.20 seconds
 P:QRS ratio: 1:1
Medical Management

 First line: 0.5 mg of atropine may be given

rapidly as an intravenous (IV) bolus and
repeated every 3 to 5 minutes until a
maximum dosage of 3 mg is given.
 Second line:
 emergency transcutaneous pacing
 Dopamine
 Catecholamines
Sinus
Tachycardia  Ventricular and atrial rate: Greater than 100 bpm in the adult, but
usually less than 120 bpm
Physiologic &  Ventricular and atrial rhythm: Regular

psychologic  QRS shape and duration: Usually normal, but may be regularly
abnormal
Stress  P wave: Normal and consistent shape; always in front of the QRS,
but may be buried in the preceding T wave
Medication  PR interval: Consistent interval between 0.12 and 0.20 seconds
Enhanced  P:QRS ratio: 1:1

Automaticity
of SA node
Autonomic
dysfunction
Management

 Treatment of choice: Cardioversion

 Vagal maneuvers: carotid sinus massage, gagging, bearing down against a
closed glottis (as if having a bowel movement), forceful and sustained coughing,
and applying a cold stimulus to the face (such as immersing the face in ice water).
 Adenosine (Adenocard)- increase parasympathetic stimulation
 Calcium channel and beta blockers: narrow QRS tachy
 Adenosine- wide QRS, monophormic QRS, VR regular
 Procainamide, amiodarone= wide QRS
Management

 Treatment of choice: Cardioversion

 Vagal maneuvers: carotid sinus massage, gagging, bearing down against a
closed glottis (as if having a bowel movement), forceful and sustained coughing,
and applying a cold stimulus to the face (such as immersing the face in ice water).
 Adenosine (Adenocard)- increase parasympathetic stimulation
 Calcium channel and beta blockers: narrow QRS tachy
 Adenosine- wide QRS, monophormic QRS, VR regular
 Procainamide, amiodarone= wide QRS
Sinus Arrythmia

 Ventricular and atrial rate: 60 to 100 bpm in

the adult
 Ventricular and atrial rhythm: Irregular
 QRS shape and duration: Usually normal,
but may be regularly abnormal
 P wave: Normal and consistent shape;
always in front of the QRS
 PR interval: Consistent interval between
0.12 and 0.20 seconds
 P:QRS ratio: 1:1
Atrial
Dysrhythmias
Premature Atrial Complex (PAC)

 Ventricular and atrial rate: Depends on the underlying rhythm (e.g., sinus tachycardia)
 Ventricular and atrial rhythm: Irregular due to early P waves, creating a PP interval that is
shorter than the others.
 QRS shape and duration: The QRS that follows the early P wave is usually normal, but it
may be abnormal (aberrantly conducted PAC). It may even be absent (blocked PAC).
 P wave: An early and different P wave may be seen or may be hidden in the T wave;
other P waves in the strip are consistent.
 PR interval: The early P wave has a shorter-than-normal PR interval, but still between
0.12 and 0.20 seconds.
 P:QRS ratio: Usually 1:1
Premature Atrial Complex
Normal PP interval=0.60-1.04 sec
Atrial Fibrillation

 Ventricular and atrial rate: Atrial rate is 300 to

600 bpm; ventricular rate is usually 120 to 200
bpm in untreated atrial fibrillation.
 Ventricular and atrial rhythm: Highly irregular
 QRS shape and duration: Usually normal, but
may be abnormal
 P wave: No discernible P waves; irregular
undulating waves that vary in amplitude and
shape are seen and referred to as fibrillatory or f
waves
 PR interval: Cannot be measured
 P:QRS ratio: Many:1
  Antithrombotic Medications-
anticoagulants & anti-platelet
 Low stroke risk = Aspirin 75 to 325 mg
daily.
Management
 Mod stroke risk= Warfarin (Coumadin)
 Control the HR = Beta or calcium
channel blockers – decrease
ventricular rate less than 80 bpm
 Convert heart rhythm- cardioversion
(electric or pharmacologic) if no
thrombus formation.
 Pharmacologic- Dofetilide (side effects:
renal & QT prolongation) in hospital
setting
 Flecainide- recurrent Afib, “pill on the
pocket)
 Atrial Flutter

 Ventricular and atrial rate: Atrial rate ranges between 250 and
400 bpm; ventricular rate usually ranges between 75 and 150
bpm.
 Ventricular and atrial rhythm: The atrial rhythm is regular; the
 ventricular rhythm is usually regular but may be irregular
because of a change in the AV conduction.
 QRS shape and duration: Usually normal, but may be
abnormal or may be absent.
 P wave: Saw-toothed shape; these waves are referred to as F
waves.
 PR interval: Multiple F waves may make it difficult to
determine the PR interval.
 P:QRS ratio: 2:1, 3:1, or 4:1
Management

 Adenosine IV followed by 20
ml of NSS for flushing –
elevate arm
 Antithrombotic, rate control,
rhythm control medications
(same with atrial fibrillation)
 Cardioversion
Ventricular
Dysrhythmias
  Ventricular and atrial rate: Depends on the underlying
rhythm (e.g., sinus rhythm)
Premature  Ventricular and atrial rhythm: Irregular due to early QRS,
creating one RR interval that is shorter than the others. The
Ventricular PP interval maybe regular, indicating that the PVC did not
depolarize the sinus node.
Complex  QRS shape and duration: Duration is 0.12 seconds or longer;
shape is bizarre and abnormal.
 P wave: Visibility of the P wave depends on the timing of
the PVC; may be absent (hidden in the QRS or T wave) or in
front of the QRS. If the P wave follows the QRS, the shape of
the P wave may be different.
 PR interval: If the P wave is in front of the QRS, the PR
interval is
 less than 0.12 seconds.
 P:QRS ratio: 0:1; 1:1
PVCs

1 2 3 4
 Ventricular Tachycardia

 Ventricular and atrial rate: Ventricular rate is

100 to 200 bpm; atrial rate depends on the
underlying rhythm (e.g., sinus rhythm).
 Ventricular and atrial rhythm: Usually regular;
atrial rhythm may also be regular.
 QRS shape and duration: Duration is 0.12
seconds or more; bizarre, abnormal shape.
 P wave: Very difficult to detect, so the atrial
rate and rhythm may be indeterminable.
 PR interval: Very irregular, if P waves are seen
 P:QRS ratio: Difficult to determine, but if P
waves are apparent, there are usually more
QRS complexes than P waves.
Management
Procainamide- Stable VT , no MI or Severe HF
Amiodarone- Medication of choice for with
cardiac dysfunction & acute MI
Sotalol- monomorphic VT
Lidocaine- most common for short term
therapy; no significant effect on both short-
and long-term efficacy.
Cardioversion- conscious, elective
Defibrillation- unconscious, pulse less= Action
of choice
  A polymorphic VT preceded by a prolonged QT
interval, which could be congenital or acquired
 Causes: [Cipro], erythromycin [Zmax, Zithromax,

Torsades
Biaxin], haloperidol [Haldol], lithium (Eskalith,
Lithobid), methadone [Dolophine, Methadose]); or

de
low levels of potassium, calcium, or magnesium
and , congenital QT prolongation.

pointes
  IV magnesium
 Isoproterenol- Beta 1 & 2
adrenergic agonist
Management  Pacing- if bradycardic
 Ventricular Fibrillation

 Ventricular rate: Greater than 300

bpm
 Ventricular rhythm: Extremely
irregular, without a specific pattern
 QRS shape and duration: Irregular,
undulating waves with changing
amplitudes. There are no
recognizable QRS complexes
Management

 Early Defibrillation
 CPR
 Amiodarone
 Epinephrine
Ventricular
Asystole
 aka flat line
 Absent of QRS
 No audible heart beat,
no pulse, no respiration
Management

 CPR- 2 inches deep, 100-120

compressions per minute
 Epinephrine- 1 mg every 3-5 minutes
IV or Intraosseous route.
 Followed by peripheral IV
administration with 20 ml flush and
elevate extremities for 10-20 seconds.
Conduction
Abnormalities
AV BLOCKS
 First-Degree Atrioventricular Block

 Ventricular and atrial rate: Depends on the

underlying rhythm
 Ventricular and atrial rhythm: Depends on the
underlying rhythm
 QRS shape and duration: Usually normal, but
may be abnormal
 P wave: In front of the QRS complex; shows
sinus rhythm, regular shape
 PR interval: Greater than 0.20 seconds; PR
interval measurement is constant.
 P:QRS ratio: 1:1
Second-Degree Atrioventricular Block,
Type I (Wenckebach)
 Ventricular and atrial rate: Depends on the underlying rhythm, but the ventricular rate is lower
than the atrial rate.
 Ventricular and atrial rhythm: The PP interval is regular if the patient has an underlying normal
sinus rhythm; the RR interval characteristically reflects a pattern of change. Starting from the
RR that is the longest, the RR interval gradually shortens until there is another long RR interval.
 QRS shape and duration: Usually normal, but may be abnormal
 P wave: In front of the QRS complex; shape depends on underlying rhythm.
 PR interval: The PR interval becomes longer with each succeeding ECG complex until there is a
P wave not followed by a QRS. The changes in the PR interval are repeated between each
“dropped”
 QRS, creating a pattern in the irregular PR interval measurements.
 P:QRS ratio: 3:2, 4:3, 5:4, and so forth
Second-Degree Atrioventricular Block, Type I
(Wenckebach)
Third-Degree Atrioventricular Block
 Ventricular and atrial rate: Depends on the escape rhythm (idionodal or
idioventricular) and underlying atrial rhythm, but the ventricular rate is lower
than the atrial rate.
 Ventricular and atrial rhythm: The PP interval is regular and the RR interval is
regular, but the PP interval is not equal to the RR interval.
 QRS shape and duration: Depends on the escape rhythm; with junctional rhythm,
QRS shape and duration are usually normal; with idioventricular rhythm, QRS
shape and duration are usually abnormal.
 P wave: Depends on underlying rhythm
 PR interval: Very irregular
 P:QRS ratio: More P waves than QRS complexes
 2nd degree-Degree Atrioventricular Block type
2
 Ventricular and atrial rate: Depends on the underlying
rhythm, but the ventricular rate is lower than the atrial
rate.
 Ventricular and atrial rhythm: The PP interval is regular if
the patient has an underlying normal sinus rhythm. The
RR interval is usually
 regular but may be irregular, depending on the P:QRS
ratio.
 QRS shape and duration: Usually abnormal, but may be
normal
 P wave: In front of the QRS complex; shape depends on
underlying rhythm.
 PR interval: The PR interval is constant for those P waves
just before QRS complexes.
 P:QRS ratio: 2:1, 3:1, 4:1, 5:1, and so forth
3 rd degree AV block
Management

 Initial treatment of choice- Atropine IV bolus (not

effective on 2nd degree AV type 2, & 3rd
degree).
 Transcutaneous pacing- does not respond to
Atropine & for advanced AV blocks.
 If pulseless- same treatment with ventricular
asystole
 Permanent pacemakers
Care of patients with dysrhythmias
 • Assess indicators of cardiac output and oxygenation,
especially changes in level of consciousness.
 • Physical assessment includes:
 Rate and rhythm of apical and peripheral pulses
 Assess heart sounds
 Blood pressure and pulse pressure
 Signs of fluid retention
 Health history: include presence of coexisting conditions
and indications of previous occurrence
 • Medications
Nursing Diagnosis

 Decreased cardiac output related to inadequate

ventricular filling or altered heart rate
 Anxiety related to fear of the unknown outcome of
altered health state
 Deficient knowledge about the dysrhythmia and its
treatment
Potential Complications

 Cardiac arrest
 Heart failure
 Thromboembolic event, especially with
atrial fibrillation
Planning

•Goals may include eradicating or

decreasing the occurrence of the
dysrhythmia to maintain cardiac
output, minimizing anxiety, and
acquiring knowledge about the
dysrhythmia and its treatment.
Decrease CO

 ECG monitoring
 Assessment of signs and symptoms
 Administration of medications and
assessment of medication effects •
 Adjunct therapy: cardioversion,
defibrillation, pacemakers
Reducing Anxiety

 Use a calm, reassuring manner.

 Measures to maximize patient control to make
episodes less threatening
 Communication and teaching
 Teaching self-care
 Include family in teaching
Pacemakers

An electronic device
that provides electrical
stimuli to the heart
muscle Types :
 Permanent

 Temporary
Transcutaneous pacemaker
Complications of pacemakers

 Infection
 Bleeding or hematoma formation
 Dislocation of the lead
 Skeletal muscle or phrenic nerve stimulation
 Cardiac tamponade
 Pacemaker malfunction
Diagnosis

• Risk for infection

• Risk for ineffective coping
• Knowledge deficiency
Planning

 absence of infection,
 adherence to self-care program,
 effective coping, and
 maintenance of device function.
Intervention

 • Risk for ineffective coping

 • Support of patient and family coping
 • Setting of realistic goals
 • Allow patient to talk, share feeling and experiences
 • Support groups or referral
 • Stress reduction techniques
 • Knowledge deficiency
 • Patient and family teaching (See home care checklist
chart 26-9, pp. 2036-2038).
Electric
Cardioversion
 Electrical cardioversion is indicated for
patients with atrial fibrillation that is
hemodynamically unstable (e.g., acute
alteration in mental status, chest
discomfort, hypotension) and does not
respond to medications .
 Flecainide, propafenone, amiodarone,
dofetilide, or sotalol may be given prior
to cardioversion to enhance the success
of cardioversion and maintain sinus
rhythm (January et al., 2014).
 Safety Measures

 Ensure good contact between skin and pads or paddles.

 Use a conductive medium and 20-25 pounds of pressure.
 • Place paddles so that they do not touch bedding or clothing and are not near
medication patches or oxygen flow.
 • If cardioverting, turn the synchronizer on.
 • If defibrillating, turn the synchronizer off.
 • Do not charge the device until ready to shock.
 • Call “clear” three times; follow checks required for clear and ensure that no one is in
contact with the patient, bed, or equipment.
Paddle Placement for Defibrillator
Cardioversion & Defibrillation

 • Treat tachydysrhythmias by
delivering an electrical current that
depolarizes a critical mass of
myocardial ceils. When cells repolarize,
the sinus node is usually able to
recapture its role as heart pacemaker.
•
 In cardioversion, the current delivery is
synchronized with the patient’s ECG.
 • In defibrillation, the current delivery
is unsynchronized.
Implantable Converter
Defibrillator (ICD)

 • A device that detects

and terminates life-
threatening episodes
of tachycardia or
fibrillation
 • Anti-tachycardia
pacing
Catheter Ablation Therapy

 Catheter ablation destroys specific cells that are the cause of a

tachydysrhythmia
 Treatment for atrial fibrillation, although it may also be useful in treating
atrioventricular nodal reentry tachycardia (AVNRT) and recurrent
ventricular tachycardia (VT) .
 In moderate sedation
 Heparin – given prior to the procedure to reduce the risk of periprocedural
thromboembolism
 Monitor closely
 WOF for complications: AV block, pericardial tamponade, phrenic nerve
injury, stroke, hematoma, retroperitoneal bleeding, pulmonary vein
stenosis, and atrioesophageal fistulas
Maze Procedure

 The maze procedure is an open heart surgical

procedure for refractory atrial fibrillation.
 Usually done together with other procedure
to correct another heart problem.
Diseases of Myocardial
Perfusion
Cardiovascular Disease

A generic term for disorders of the heart

& blood vessels.
Coronary Artery Disease (CAD)

• A condition w/
reduced blood
flow going to the
heart muscle.
• ♥ Other term:
Coronary Heart
Disease (CHD)
 Coronary Artery Disease (CAD)

2 Categories
1. Chronic Ischemic Heart
Dse
✓ Stable angina
2. Acute Coronary
Syndromes
✓ Unstable Angina Pectoris
✓ Myocardial Infarction
a. NSTEMI b. STEMI
✓ Sudden cardiac death
 Myocardial Oxygen Demand
• Q: What is the
relationship bet
contractility, HR &
wall tension
(preload/afterload)
and O₂ demand?
 Myocardial Oxygen Supply

Determined by:
Coronary Blood Flow & O2 Carrying Capacity
( Flow = Pressure / Resistance)

▪ Coronary perfusion pressure ▪ O2 saturation of the blood

▪ Coronary vascular resistance ▪ Hemoglobin content of the
blood
☞ What happens when
myocardial O₂ demand
exceeds myocardial O₂
supply?
Answer: Myocardial Ischemia
Atherosclerosis
➳ abnormal
accumulation of
lipid deposits &
fibrous tissue within
arterial walls & lumen
➳ the most common
form of
arteriosclerosis.
Classification of Atherosclerosis
Atherosclerosis
Atheroma (Plaque)
• ➳ complex
lesion consist of
lipids, fibrous
tissue, collagen,
calcium, cellular
debris &
capillaries.
 Atheroma (Plaque)
STABLE PLAQUE
➳ a plaque gradually
occluding the vessel
lumen.
UNSTABLE PLAQUE
➳ plaque prone to
rupture & thrombus
formation.
Effects of the Plaque
Formation
Myocardial ISCHEMIA
➳ insufficient tissue oxygenation.
Myocardial INJURY
➳ damage to the area when ischemia is
prolonged.
Myocardial INFARCTION/NECROSIS
➳ death of heart tissue d/t lack of oxygenated
blood flow or obstruction in circulation.
 Lipids and their Role
HDL
a CHON-bound lipid that
transports cholesterol to
the liver for excretion in
the bile.
LDL
➳ a CHON-bound lipid that
transports cholesterol to
tissues in the body.
Risk Factors
Nonmodifiable:
Gender (male)
Race (African-American)
Age (>45yo men; >55yo women
(+) Family history
Risk Factors
Modifiable:
• Stress
• Hyperlipidemia/HPN
• Obesity
• Physical inactivity
• DM
• Estrogen (lack in women)
• Cigarette smoking
 Angina Pectoris

➙ Chest pain resulting

from reduced coronary
blood flow.
ETIOLOGY:
➳ CHD or CAD
(atherosclerosis)
➳ Coronary vessel
constriction
Precipitating Events of
Angina Pectoris
4 E’s
• Exertion – vigorous sporadic exercise,
sexual activity
• Emotions - Excitement , stress
• Eating a heavy meal
• Environment – exposure to cold
Types of Angina
1. Stable
Pattern:
➳ Predictable
(Precipitated)
Relieving Factors:
➳ Rest or
Nitroglycerin
Duration:
➳ less than 15 mins
Types of Angina
2. Unstable Angina
"pre-infarction
angina”
“crescendo angina”
Pattern:
➳ unpredictable,
may occur at rest
➳ occurs w/ ⇪
frequency, intensity
& duration
Relieving factors:
➳ NTG & REST
 Types of Angina
3. Prinzmetal's angina
OTHER TERM:
”variant angina”
PATTERN:
➳ Unrelated to activity
➳ coronary artery
vasospasm
➳ prolonged and severe;
occurs same time each day
Assessment Findings
Pain in the chest
✓Tight, squeezing, constricting or heavy
sensation
✓ Burning, choking, dull or constant
✓substernal or precordial, may radiate to
neck, arms, jaw, or shoulders.
✓Usually relieved w/in 5-15mins by rest, w/
or w/o use of vasodilators
Classic Sequence

PRECIPITATING EVENT
Associated Manifestations
✓Dyspnea
✓Pallor, diaphoresis
✓Anxiety, fear
✓Faintness
✓Palpitations,
tachycardia
✓Digestive
disturbances
 Atherosclerosis

Stable Plaque formation

Gradual narrowing of coronary arteries

PRECIPITATING EVENT

Temporary ↓ O2 to myocardium

↓myocardial pump function

Further ↓ in O2 & glucose

Anaerobic metabolism

Lactic acid formation

Chest pain (STABLE ANGINA PECTORIS)

Diagnostic Tests
Blood Chemistry
✓ ↑ Cholesterol Levels, ↓ HDL, ↑LDL, ↑ triglycerides
ECG or Holter monitor
✓ ST segment depression and T wave inversion
Stress Test
✓ST segment changes and provokes chest discomfort
Cardiac catheterization / Coronary angiography ✓
extent & exact location of obstructions in the coronary
arteries
Dx Evaluation (MI)
Diagnosis (2 out of 3 of the ff:)
1. Hx of prolonged chest pain
2. ECG changes consistent w/
ischemia or necrosis
3. Elevated cardiac enzymes
(CKMB, LDH, Troponin I & T)
Nursing Intervetions
GOAL OF TREATMENT (ANGINA):

➳ REDUCE myocardial O₂ demand

or
➳ INCREASE O₂ supply to the
myocardium.
➳ to relieve chest pain.
Nursing Intervetions
GOAL OF TREATMENT (MI):

➳ relieve chest
pain
➳ stabilize heart
rhythm
➳ reduce cardiac
workload
Nursing Interventions
1. Assessment
2. Administer as ordered:
• Oxygen
• Nitroglycerine
• Betablockers (olol)
• Calcium-channel blockers (ine)
3. CBR, activity restriction
4. Diet
Low fat, low Na, low chol diet
5. Provide continuous cardiac monitoring.
Collaborative Interventions
1. Vasodilators
Isosorbide dinitrate (Isordil),
Nitroglycerin
Action: VASODILATION
Q: What are the effects?
1. decreased BP
2. increased coronary blood flow
Nursing Responsibilities
Nitroglycerin (drug of choice)

✓ Take max. of __ doses; _____ interval

✓ Route: ____
✓ Onset of 1-2 min, duration of 30min
✓ Store in a: _____________________________
✓ Replace stock q ____ months
 Nursing Responsibilities
Nitroglycerin (drug of choice)

Q: What side effects shld be observed?

Dizziness
Headache
Hypotension
Nausea
✓ Nitropatch applied OD in AM, rotating site;
wear gloves
Collaborative Interventions
2. Beta-adrenergic blocker
Metoprolol (Lopressor), Propranolol (Inderal),
Nadolol (Corgard), Esmolol
Q: Give ACTIONS of betablockers.
✓It blocks the cardiac-stimulating effects of
NE & E
What are the EFFECTS???
Q: What should be assessed before
administering betablockers?
 Nursing Responsibilities

Beta-adrenergic blocker
➢Administer w/ food.
➢Contraindicated to clients w/
severe COPD...why?
➢What will it do to DM patients?
➢ WHAT are non-selective
betablockers?
Collaborative Interventions
3. Anticoagulant
✓ heparin, coumadin
Action:
✓ Prevents clot
formation & clot
extension
Collaborative Interventions
Heparin Sodium
Guidelines: 5 A’s
➢ Avoid massage.
➢ Avoid IM injection
➢ Avoid same site
➢ Avoid
aspirin/dipyridamole
➢ Avoid alcohol intake
Collaborative Interventions
Heparin Sodium
Assess for
_______________
Q: What is the
antidote?
A: Protamine
Sulfate
Nursing Responsibilities
(Heparin Na)

Q: What determines the

effectiveness of heparin?
A: PTT
Therapeutic range: 1.5-2.5x
the patient’s baseline value.
NV = 60-70 seconds
Nursing Responsibilities
✓Usually drawn 30-60 mins before the
next dose of heparin.
– Q: For PTT <50 seconds...what
will you do w/ heparin dose?
– A: Increase heparin dose
– Q: For PTT >100 seconds…
– A: decrease Heparin dose
Collaborative Intervention
Coumadin ➙ Guidelines: 4 A’s
✓ Avoid aspirin
✓ Avoid/minimize green, leafy veg
✓ Administer in advance 3 days before
discontinuation of heparin therapy.
✓ Assess & report for s/sx ______________
Q: What is the antidote?
A: Vitamin K
Q: What determines its effectiveness?
A: PT
Collaborative Intervention
Coumadin
✓Monitor Prothrombin time.
✓Normal: 12 – 15 seconds
✓Therapeutic Level: 1.5 -2 x of NV.
Collaborative Intervention
4. Platelet aggregation inhibitors
Aspirin, Dipyridamole (persantin),
Ticlopidine (ticlid)
✓inhibit platelet aggregation
✓Assess for s/s of bleeding
✓Take with food.
✓Do not give w/ coumadin.
✓Observe for aspirin toxicity – tinnitus
Collaborative Intervention
5. Cholesterol-lowering drugs:
Atorvastatin (Lipitor)
Cerivastatin (Baycol)
Prevastatin (Prevachol)
Simvastatin (Zocor)
Collaborative Intervention
6. Calcium channel Blocker
Nifedipine (Procardia), Diltiazem (Cardizem),
Verapamil (Calan)
 Inhibit the flow of Ca+ ions across the cell
membrane of vascular & cardiac cells.
➙ relax ARTERIAL smooth muscles
1. Assess HR and BP.
2. Monitor hepatic & renal function.
3. Food delays absorption.
Surgical Management
Percutaneous
Coronary Intervention
(PCI)
1. Percutaneous
Transluminal
Coronary Angioplasty
(PTCA)
2. Stenting
 Surgical Management
Coronary Artery
Bypass Graft (CABG)
 severe/multivessel
involvement
Common source of graft:
1. saphenous vein
2. internal mammary
artery
MYOCARDIAL INFARCTION
Early Warning Signs
What Happens During a Heart
Attack
Types Of MI According To Location
Of Damage

1. Transmural infarction or Q-
wave MI - ➙ entire thickness of
the myocardium
2. Non-transmural, non-Q-wave
MI, subendocardial MI ➙
innermost layer
Acute Myocardial Infarction
• Occurs when myocardial tissue is abruptly and
severely deprived of O2
• When blood flow is reduced by 80-90% ischemia
develops
• Prolonged ischemia lasting more than 35-45
minutes produces irreversible cellular damage
and necrosis of the myocardium
• ischemic injury evolves over several hours
toward complete necrosis and infarction
The Cause of Infarct and the
ECG

Zone of infarction

Zone of hypoxic
injury
Zone of
ischemia
The Cause of Infarct and the
ECG

Zone of infarction

Zone of hypoxic injury

Zone of ischemia
Pathologic Q
Wave
The Cause of Infarct and the
ECG

Zone of infarction

Zone of hypoxic injury

Zone of ischemia ST Segment

Elevation
The Cause of Infarct and the
ECG

Zone of infarction

Zone of hypoxic injury

Zone of ischemia

T wave
Inversion
Clinical Manifestations
1. Pain - crushing, severe, prolonged,
unrelieved by rest or nitroglycerine,
radiating to one or both arms, neck, back
2. Signs of shock - hypotension, cold
diaphoresis, peripheral cyanosis,
tachy/brady, thready pulse
3. Oliguria
Clinical Manifestations
4. Fever
5. Apprehension
6. Indigestion
7. DOB
8. Nausea and vomiting
9. Pallor, cyanosis, coolness of
extremities
Classic Heart Attack
Symptoms
Diagnostics
1. 12 lead ECG
- ST segment elevation - injury
- ST segment depression / T wave
inversion - ischemia
- Q wave - infarction
- serial ECG’s done x 3 days
Diagnostics
2. Serum Markers of Myocardial Damage
• - Myoglobin – found in both skeletal and
cardiac muscle
- detected 2-3 hours post MI
• - C- reactive protein (CRP)
- correlates with CK-MB levels but it peaks
several days later
• - WBC – increases to 10,000 to 20,000
cells/mm3 on the second day
Causes of MI
PROLONGED OCCLUSION D/T:
1. ATHEROSCLEROSIS
2. THROMBOSIS
3. CORONARY ARTERY STENOSIS OR
SPASM
4. Decreased myocardial O₂ supply and
increased demand for O₂
Myocardial Infarction
Painless MI common in the ff:
a. Post-operative patients
b. Elderly
c. Patients with DM, HPN
Clinical Stratification
Expected
Killips Classification of MI Hospital
Mortality
K-I No signs of Pulmonary or venous congestion.
0-5%
K-II Moderate heart failure or presence of
bibasal rales, S3 gallop, tachypnea, or signs of
right-heart failure including venous (JVP) and 10-20%
hepatic congestion.
K-III Severe heart failure, rales >50% of the Lung
Fields or pulmonary edema. 35-45%
K-IV Shock with systolic pressure <90 mmHg and
evidence of peripheral asoconstriction,
peripheral cyanosis, mental confusion and 85-95%
oliguria.
Myocardial Infarction as
reflected on the ECG
Pathophysiology
Coronary arterial occlusion
↓
Inadequate coronary blood flow
↓
Continuous myocardial ischemia
↓
PAIN
↓
Hypoxia
and pain trigger ANS
↓
Persistent ischemia in tissue region supplied by the artery
Pathophysiology
Cellular injury
↓
Tissue necrosis
Myocardial cell death
↓
Scar formation
↓
Permanent loss of myocardial
contractility in the affected area
MI Leading To
Congestive Heart Failure (CHF)

For example: Massive

MI Left Ventricle

↓ Myocardial Contractility

↓ Cardiac Output

ACTIVATES COMPENSATORY MECHANISMS

SNS STIMULATION
1. Vasoconstriction, ↑ LV afterload
2. ↑ HR
3. ↑ myocardial contractility
= ↑ cardiac workload

STIMULATION RENIN SECRETION

✓Angiotensin II = vasoconstriction
✓Aldosterone = ↑Na & H2O retention
= ↑ cardiac workload

COMPENSATIONS MAINTAIN
CARDIAC OUTPUT FOR A TIME
 Left Ventricle
Weakens

LV DOES NOT EFFECTIVELY PUMP

Further Blood Backs up in

↓Cardiac Output Pulmonary Circulation

FORWARD EFFECT BACKWARD EFFECT

Pulmonary Congestion

LEFT SIDED HF
Myocardial Cell Death Results to:

1. Release of cardiac enzymes →↑CPK MB,

↑ myoglobin, ↑ LDH, Troponin T & I, AST
2. Decreased myocardial contractility →
decreased LV function → increased
preload, S3, ↓CO, ↓tissue perfusion →
cardiogenic shock
3. Switching from aerobic to anaerobic
metabolism → lactic acid production
(pain)
Myocardial Cell Death Results to:

4. Altered repolarization of myocardium

→ elevated ST segment & pathologic Q
wave
5. Formation of thin scar tissue to replace
necrotic tissue → noncompliance, stiff
myocardium, S4
6. Myocardial irritability → dysrrhythmias
→ ↓CO
Thrombolytic therapy
Streptokinase, urokinase
➢ To dissolve bld clots
Q: What are the contraindications?
➙ hemorrhagic CVD
➙ bleeding disorder
➢ administration is crucial between 2-6
hrs from onset of pain.
Complications of MI
1. DYSRHYTHMIAS
2. PUMP FAILURE
HEART FAILURE / CARDIOGENIC SHOCK
3. INFARCT EXTENSION
4. STRUCTURAL DEFECTS
VENTRICULAR ANEURYSM
VALVULAR DEFECTS
5. PERICARDITIS
6. DRESSLER’S SYNDROME (fever, chest pain, dyspnea)
Nursing Diagnosis
Chest pain r/t nerve irritation from
lactic acid 2⁰ to anaerobic
metabolism.
Activity intolerance r/t compromised
oxygen transport 2⁰ MI.
Ineffective breathing pattern
Nursing Diagnosis
Ineffective individual coping
Fear
Ineffective health maintenance
Altered sexuality patterns r/t anxiety,
pain & fear
Risk for ineffective therapeutic
regimen management
Collaborative Management

O - xygen
B - eta blocker M-orphine
A - spirin O-XYGEN
T - hrombolytics N-itroglycerin (NTG)
A-spirin
M - orphine
A - CE
N - itroglycerin
Nursing Responsibilities
• Provide pain relief
• Promote Oxygenation and Tissue
Perfusion
• Promote Adequate Cardiac Output
• Promote rest and minimize unnecessary
disturbances
• Provide rest and relieve anxiety
Nursing Responsibilities
• Provide psychosocial support to patient
and family
• Provide low cholesterol, low Na diet
• Avoid stimulants
• Avoid taking very hot or very cold
beverages & gas forming foods. –
vasovagal stimulation may occur thereby
bradycardia & cardiac arrest
Nursing Responsibilities
• Use of bedpan & straining at stool should
be avoided.
• Valsalva maneuver causes changes in BP
and HR & may trigger dysrrhythmias,
ischemia, or cardiac arrest
• Use bedside commode.
• Administer stool softener as ordered.
 Program of Physical Activities
1. Increase activities gradually after the first 24-48 hours
2. Early mobilization after an MI. May be allowed to sit on a
chair for increasing periods of time and begins ambulation
on the 4th or 5th day
3. Monitor V/S before activities.
4. An exercise session is terminated if any one of the
following occurs: cyanosis, cold sweats, faintness, extreme
fatigue, severe dyspnea, pallor, chest pain, PR > 100,
dysrhythmias, Bp > 160/90
5. Sexual intercourse - 4-6 weeks post MI or when a patient
with uncomplicated MI is capable of walking 2 flights of stairs
without difficulty
Sexual Intercourse of Post-MI
• Nitrogylcerine before sex
• Avoid concomitant use with Sildenafil
• Assume position with less strain – WOMAN on TOP/
SIDE-LYING
• Perform sexual activity in a cool, familiar environment
• Refrain from sexual activity during a fatiguing day, after
eating a large meal, or after drinking alcohol
• If dyspnea, chest pain, dizziness or palpitations occur,
moderation should be observed.
• If symptoms persist stop sexual activity