HEART

D pump blood through

the arteries, capillaries
and veins
D creates blood
pressure, circulates
oxygen, nutrients and
other substance
 Location & Size
D weighs 300g or size of
the fist
D cone like
in
appearance.
D Located in the
MEDIASTINUM
D enclosed by
pericardium
 Two Layers Pericardium
Visceral pericardium
D thin serous inner
layer which surrounds
the heart.
Parietal pericardium
D outer layer, and serves
to prevent over
distension of the heart.
 Layers of the Heart
Epicardium
▪ outermost layer, a
smooth outer surface
of the heart
Myocardium
▪ thick middle layer
⚫ Responsible for the
heart’s ability to
contract
 Layers of the Heart
Endocardium
⚫ Innermost layer
of the heart
⚫ It lines the
chambers and
covers the heart
valves of the heart
 CHAMBERS OF THE HEART
⚫ RIGHT ATRIUM
⚫ RIGHT VENTRICLE
⚫ LEFT ATRIUM
⚫ LEFT VENTRICLE
 RIGHT ATRIUM
⚫ receives deoxygenated
blood from the body by
way of the Superior
vena cava (SVC) and
inferior vena cava (IVC).
 RIGHT VENTRICLE
⚫ Receives blood from
the RA and ejects this
blood into the lungs
via Pulmonary artery.
 LEFT ATRIUM
⚫ Receives oxygenated
blood from the lungs
by way of four
pulmonary veins.
LEFT VENTRICLE
⚫ Receives blood from
the left atrium and
ejects blood into
systemic arterial
circulation.
 VALVES of the Heart
ATRIOVENTRICULAR valves
⚫ allow blood to flow from the atria into the ventricles
⚫ Effective in preventing backflow of blood into the ATRIA.
⚫ Tricuspid- 3 cups located between RA and RV
⚫ MITRAL/Bicuspid- 2 cups, located at LA and LV
SEMILUNAR VALVES
⚫ Prevent backflow of blood into the ventricles
⚫ Aortic valve and Pulmonic valve.
⚫ Aortic valve- lies between the LV and the aorta.
⚫ Pulmonic valve- lies between RV and
pulmonary artery.
During ventricular Systole- the AV valves are CLOSE and
the Semilunar valves are OPEN

During Ventricular Diastole- the semilunar valves are

CLOSE and the AV valves are OPEN
 VEINS
⚫ blood vessels that carries deoxygenated blood
towards the heart.
⚫ SUPERIOR VENACAVA- Drains blood from the head
to the neck
⚫ INFERIOR VENACAVA- Collects blood from
the lower portion of the body.
PATHWAY OF BLOOD
 Cardiac Cycle
SYSTOLE
D Contraction and emptying
of the atria and ventricles
D Aortic and pulmonic valve
are open, the mitral and
tricuspid valve are close
DIASTOLE
D relaxation and filling of
atria and ventricle
D Aortic and pulmonic
(Semilunar) valve are
close and the mitral
and tricuspid (AV) are
open
 TWO HEART
Lub
SOUNDS
Dub
D the first, loudest and D the second sound caused
longest sound caused by by the closure of aortic
ventricular systole and pulmonary semilunar
closing the AV valves. valves.
 CARDIAC OUTPUT
D The volume of blood ejected from the left ventricle into
the Aorta per minute
D CO=Stroke Vol(SV) x Heart Rate(HR)
D Stroke Volume= the amount of blood ejected from one
of the ventricle/beat, Normal=60-130ml, average 70ml
D Normal-5-6 L/minute
D Determine by preload, contractility and afterload
 PRELOAD
⚫ Is the degree or amount of stretch of the ventricular
cardiac muscle fiber or ventricles at the end of the
diastole.
⚫ Related to the volume of blood distending the
ventricles at the end of the diastole
⚫ It is determined by the amount of venous return to
the heart
⚫ It is also called the End-Diastolic Volume (EDV).
 FRANK STARLING’s LAW
⚫ Starling’sLaw conceptualizes that the
greater the myocardial stretch within
physiologic limit, the more forceful the
ventricular contraction resulting to
increase Stroke volume.
What can increase cardiac preload?
⚫ IV fluids
⚫ Sympathetic nervous
system stimulation
⚫ Vasopressor
 Reasons for increasing cardiac preload
⚫ Hypovolemic Shock- by administering
intravenous (IV) fluids, Vasopressor
 What Can Decrease Pre Load?
⚫ Diuretics(Furosemide)
⚫ Vasodilators (Nitroglycerine)
 AFTERLOAD
⚫ The amount of tension in the ventricle during contraction to
eject blood from the left ventricle into the aorta.
⚫ the pressure the ventricles must work against to open the
semilunar valves and pump blood out of the heart.
⚫ the ventricles must overcome VASCULAR RESISTANCE
comes from either the lungs (Pulmonary vascular resistance
and deals the RV ) or the body’s circulation (Systemic vascular
resistance and deals with LV).
⚫ If high resistance, it increase the afterload. If resistance
is low, it will decrease the afterload.
 What can Increase Cardiac Afterload?
⚫ Vasoconstriction: this will cause narrowing of
vessels in the body and increase blood
pressure.
⚫ Valve issues: Ex: Aortic stenosis. This is
narrowing of the aortic valve, which will lead to
an obstruction of outflow of blood.
 What can decrease cardiac afterload?
⚫ Vasodilation: this will widen vessels and decrease vascular
resistance, hence decreasing cardiac afterload.
ANS influences on Cardiac Activity
SNS PNS
D responsible for ▪ regulates the calmer
preparation of the body (Rest and Digest)
for physical activity functions
(Fight or Flight). ▪ Acetylcholine -
D Norepinephrine- slows the HR and
increase HR and the slight decrease
force of contraction in ventricular
of the heart contractility
 Baroreceptors
⚫ Found in the carotid arteries and aortic arch
are sensitive to change in BP
⚫ Decreased BP causes a reflex SNS response-
increase pulse, increase contractility and
vasoconstriction
⚫ Increased BP- causes reflex vagal responses
-decreased heart rate and passive vasodilation in
the systemic arterioles (Known as Marcy’s Law of
the Heart)
 CHEMORECEPTORS
⚫ Medulla Oblongata and special receptors are found in
the carotid and aortic bodies which can regulate
respiratory ACTIVITY.
⚫ A decrease pH or increase in paCO2 level causes
a reflex SNS response - tachycardia,
vasoconstriction and increased myocardial
contractility
⚫ Decreased paCO2 and increased pH -
vasodilation
 CARDIAC INDEX
D More accurate indicator of tissue perfusion
D It represents the CO in terms of liters per minute per
square meter of the body surface area
D Norman CI: 2.4 to 4 L/min
D CI= CO (L/min)
Body Surface area (m2)
 Two Basic Myocardial Cell Groups
MYOCARDIAL WORKING CELLS
D primary function is both CONTRACTION and
RELAXATION
SPECIALIZED PEACEMAKER CELLS
D Responsible for generating and conducting of
electrical impulses
D It controls the heart rate and the rhythm of the
heart
 Primary Cardiac Cell
Characteristics
Automaticity
D is the ability of the heart to initiate impulses
repetitively and spontaneously.
Excitability
D the ability of the cardiac cells to respond to a
stimulus by initiating a cardiac impulse.
 Primary Cardiac Cell
Characteristics
Conductivity
D the ability of the cardiac cells to receive to an
impulse by transmitting the impulse along
cell membranes.
Contractility
D the ability of the cardiac cells to shorten and
cause cardiac muscle contraction in response to
electrical stimulus. Known as rhythmicity.
ELECTRICAL CONDUCTION SYSTEM
ELECTRICAL CONDUCTION SYSTEM
1. Sinoatrial (SA) Node
D Located in the upper portion of
the Right Atrial wall of the heart.
D natural peacemaker of the
heart
D capable of generating
impulses travel
throughout the muscle
fibers of both atria
resulting in
DEPOLARIZATION
D firing rate: 60-100 bpm
D Represent p wave (Atrial
Contraction
 INTERNODAL PATHWAYS
D distribute the electrical impulse from the SA
node throughout the ATRIA to the AV node
D The transmission of impulses from the SA
node to the AV node and to the rest of atrial
myocardium brings ATRIAL SYSTOLE
 2.AV (Atrioventricular) Node
D Located on the floor of the
right atrium just above the
tricuspid valve
D Known as “Gate Keeper”
D It delays electrical impulse
so that the Atrium can fully
contract and fills the
ventricles with blood
D Beats at 40-60 BPM.
AV JUNCTION
⚫ Region where the AV node joins the Bundle of His
⚫ AV Junctional tissue contain fibers that can
depolarize spontaneously forming an electrical
impulse that can spread to the heart chambers
 3. BUNDLE OF HIS
D The conduction pathway that leads out of
the AV node
D Called as Bundle Branches (Right and
Left)
D Two main branches conduct electrical
activity from the Bundle of His down to
Purkinje Network
 4. PURKINJE’S NETWORK
⚫ Spread the impulse
throughout the
ventricles resulting
ventricular contraction
⚫ Possessed the intrinsic
ability to serve as peace
maker
⚫ Firing rate: 20-40BPM
 Blood vessels
ARTERIES
D It carries oxygenated blood AWAY from the heart
LAYERS of ARTERIES
D Tunica intima- Innermost layer and consist of endothelium and
elastic membrane
D Tunica Media- Middle layer and consist of smooth muscle cells
D Tunica Adventitia- Outermost layer and made up of connective
tissue
 VEINS
D Carries UNOXYGENATED blood BACK to the heart
D Two largest veins:
D Superior Vena cava and Inferior venacava
 CAPILLARIES
D Tiny blood vessels that allow for the
exchange of O2, nutrients, and waste
products between the blood and body
tissues
D Connectors between arteries and veins
 BLOOD Components
1. PLASMA
D 55% of total blood
D Fluid portion of blood
D Contain proteins, glucose, fats and gases
D Transport nutrients and maintain acid base balance,
transport waste from the tissues
D 91% water, 7% proteins, 1.5 % other solutes,
D Proteins- Albumin, Globulins, Fibrinogen
 Plasma Proteins
Albumin
▪ 58% of plasma proteins
▪ helps maintain water balance
Globulins
▪ 38% of plasma proteins
▪ helps immune system (antibodies)
Fibrinogen
▪ 4% of plasma proteins
▪ aids in clot formation
 Formed Elements
D 45% of total blood
D Erythrocytes, Leukocytes, Thrombocytes
(Platelets)
Composition of Blood

⚫ Figure 11.1

⚫ ©liquidlibrary/PictureQuest RF
 RBC/ERYTHROCYTES
D Transport O2 and CO2
to and from tissues.
D Biconcave disc
D Mature RBC consist
of Hemoglobin
D Has a lifespan
of 90-120days
D Normal: Men=4.7-6.1
M/Cu.mm and
women= 4.2-5.4
M/cu.mm
 Hemoglobin
D Main component of erythrocytes
D Transports O2
D O2 binds to iron
⚫ Oxyhemoglobin
D hemoglobin with an O2 attached
D Normal Hgb- Male 14-18 g/dl, Female=12-
16 g/dl
D Normal Hgb= 15g/100ml (Fishbach, 2018)
 Erythropoiesis- Production of Erythrocytes
1. Decreased blood O2 levels cause kidneys to
increase production of Erythropoietin.
2. Erythropoietin stimulates RBM to produce
more erythrocytes.
3. Increased erythrocytes cause an increase
in blood O2 levels.
Red Blood Cell Production

Figure 11.5
 Leukocytes
▪ White blood cells (WBC)
▪ Lack hemoglobin
▪ Larger than erythrocytes
▪ Contain a nucleus
▪ Normal: 4000-11,000 cells/mm3 or 5000-
10000 cu/mm
⚫ Functions:
• fight infections
• remove dead cells and debris by phagocytosis
 TYPES OF LEUKOCYTES
1. Granulocytes
D contain specific granules
D includes neutrophils, eosinophils, and
basophils
D Body’s first line of cellular defense against
foreign organism
1. Neutrophils
D most common
D remain in blood for 10 to 12 hours
then move to tissues
D Phagocytes- they engulf, ingest, and
digest foreign materials during early
phase of inflammation
2. Eosinophils
D reduce inflammation and destroy parasites
D Participate in allergic and parasitic response
3. Basophils
D least common
D release histamine and heparin
 Types of Leukocytes
2.Agranulocytes- no specific granules
1. Monocytes
D largest sized white blood cells
D Enlarge and mature- macrophages- phagocytosis
2. Lymphocytes
D immune response
D several different types (T cells and B cells)
D lead to production of antibodies
PLATELETS
D are produced in the red bone marrow from
large cells called megakaryocytes.
D Small fragments break off from the
megakaryocytes and enter the blood as
platelets.
D play an important role in preventing blood loss.
 PLATELETS
D Smallest cells in the blood
D Essential for coagulation of blood
D Plug damaged blood vessels
D Promote blood clotting
D Life span 5-9 days
D 150,000-360,000/μl
 Assessment of Clients with
Cardiovascular Disorders
▪ History, Physical Exam, clinical
manifestations, Diagnostic test

Nursing History
RISK FACTORS
1. Non-Modifiable Risk Factors
D Gender, Race, Age, Heredity
 MODIFIABLE RISK FACTORS
D Stress
D Diet
D Lack exercise
D Cigarette smoking
D Alcohol
D Hypertension
D Hyperlipidemia
 MODIFIABLE RISK FACTORS
D Obesity
D Personality Type/ Behavior
Factors-Type A- impatient, competitive,
aggressive, and time urgency
D Contraceptive pills
D DM
 PHYSICAL EXAM
INSPECTION
D SKIN COLOR-cyanosis, pallor or jaundice.
D Neck vein distension
D Respirations
D Neck veins distension
D Peripheral Edema
 PALPATION
Peripheral Pulses
D 0, 1, 2, 3
D Weak or bounding pulse and irregular pulses
D Examine the pulses bilaterally.
Apical Pulse
D it is assessed at the POINT OF MAXIMUM
IMPULSE (4th to 5th mid left clavicular line)
PALPATE CAROTID ARTERY
✔ reveals character of pulse in the proximal aorta
PERCUSSION
D To detect DULLNESS on percussion of the chest due
to Pulmonary Edema (Cor Pulmonale)
AUSCULTATION
D Heart Sounds
D LOW PITCHED sounds, use the BELL of the
stethoscope
D HIGH pitch sounds, used DIAPGRAM of the
stethoscope.
 Patient Positioning for
Heart Auscultation
Supine or sitting-up
D Use the diaphragm and
listen at all 5
auscultation sites
(noting S1 and S2)
 Patient Positioning
for Heart Auscultation
LEFT
LATERAL
RECUMBENT
POSITION
D best suited for hearing
LOW PITCHED
sounds
D Use the BELL of the
stethoscope at the
APEX area
D listen for S3, S4,mitral
 Patient Positioning for
Heart Auscultation
FORWARD LEANING
D to hear HIGH pitch
sounds.
D used DIAPGRAM of
the stethoscope at the
aortic and pulmonic
sites for murmurs.
5 AREAS of AUSCULTATION
 Heart Sounds
S1 S2
D is produced by D asynchronous closure of
asynchronous closure of AORTIC and PULMONIC
MITRAL and VALVES
TRICUSPID VALVE D High pitch, described as
“DUB”
D Dull, low pitch sound, D Best heard at the base
described as “LUB” of the heart
D It signals the onset of
ventricular systole
D louder at the apex.
 S3/ Ventricular S4/Atrial Diastolic
Diastolic Gallop Gallop
D a faint, low pitch D Heard over
sound produced by tricuspid or mitral
rapid ventricular area, lying on left
filing in early side
diastole after S2. D Low
D Best heard at the frequency
Apex, pt lying on sounds
his Left SIDe D Described as
D Indicates CHF “Ten-nes-see”
in older adults or
D heard after S2 and
 Ta-Lub-Dub sound
D It is abnormal in all
ages
 MURMUR
D Blowing/swooshing noise from blood
turbulence in the chambers of the
heart (wall defect) or valve problem
D Valves or chambers are affected
D Incompetent and stenotic valves.
 Types of Murmurs
Systolic Murmur
D It occurs during a heart muscle contraction.
Diastolic Murmur
D It occurs during heart muscle relaxation
between beats.
Continuous Murmur
D It occurs throughout the cardiac cycle.
 GRADING OF MURMURS
1: Hard to hear
2: Faint but heard
3: Easily to hear
4: Loud with a chest thrill
5: Louder
6: Loudest
 Pericardial Friction Rub
D extra heart sound originating from
the pericardial sac
D Short, High pitch and scratch
sound
D Indicates Pericarditis
 COMMON MANIFESTATION OF
HEART DISEASE
CHEST PAIN
❖ due to decrease
coronary
tissue
perfusion and
oxygenation
 CHARACTERIZATION
Nature and Intensity
D Dull, sharp, burning, heaviness
D Rate the pain using PRS 1-10.
Onset and duration
D when did the pain start?
D how long did the pain episode last
 CHARACTERIZATION
Location and radiation
D Ask the patient to point where it hurt most?
D Ask the patient if the pain seem to travel.
Precipitating and relieving factors
D What activity was patient doing just before
pain?
D What relieves the pain?
 POSITIVE LEVINE’S SIGN
⚫ clenched fist brought
to patient’s chest.
 SIGNIFICANCE of PAIN
D Levine’s sign- Ischemia- reversible,
D Levine’s sign- Heart attack-
irreversible/ Myocardial necrosis
D Excruciating pain-radiating to back
or plank- Aneurysm of the Aorta
D Sharp pericardial pain-Acute
Pericarditis
 DYSPNEA/Shortness of Breath
D Difficulty of breathing
D Left
ventricular
failure/ CHF
 CAUSES
D Heartattack/ L CHF
D Low blood pressure
D Pulmonary embolism
D Emotional distress or a panic attack
D Carbon monoxide poisoning
D Asthma and COPD
D Pneumonia,
 ASK:
D What precipitates or relieves dyspnea?
D How many pillows does the patient sleep
with at night?
D How far can patient walk or how many
flights of stairs can patient climb before
becoming dyspneic?
 Types of Dyspnea
EXERTIONAL ORTHOPNEA
D Breathlessness on D DOB when lying down
moderate exertion D Relieve by upright
D relieve by REST position
D Several pillows
is needed.
D Sign of More Advance
HF
 Paroxysmal Nocturnal Dyspnea
D Sudden dyspnea occurs at night 2-5 hours
after the onset of sleep.
D Awakens the client with feeling
of SUFFOCAtion
D During waking hours- client is in UPRIGHT
 PALPITATION
D unpleasant awareness of the heart
beat
SIGNIFICANCE
D Tachydysrhythmias
D Premature or ventricular beats,
anemia, heart failure, thyrotoxicosis
 EDEMA
D Increased hydrostatic
pressure in the venous
system causes shifting
of plasma results to
abnormal
accumulation of serous
fluid in soft tissues
D LATE SIGN OF
HEART
FAILURE
 Grade of Edema
Grade Indentation Rebound time
0 No pitting edema
1 2 mm in immediate
depression
2 3–4 mm, 10-15 seconds.
3 5–6 mm 60 seconds
4 8 mm or deeper more than 60 sec
SYNCOPE/DIZZINESS
D generalized weakness with inability to stand
upright followed by transient loss of
consciousness.
SIGNIFICANCE
D Decrease Tissue Perfusion
D Fall of Cardiac output
D Problem in Electrical Conduction
 FATIGUE
D weakness or lack
of energy
D Due to low
cardiac output
 CYANOSIS
D Bluish discoloration of the skin and
mucous membrane.
D Indicate poor cardiac output and
tissue perfusion
D Types: Central cyanosis and
Peripheral cyanosis
 TYPES OF CYANOSIS
Central cyanosis
❖ Low oxygen
saturation of arterial
blood
❖ Tongue,
buccal
mucosa, lips
 TYPES OF CYANOSIS
Peripheral Cyanosis
❖ due to vasoconstriction
❖ Distal aspect of the
extremities, tip of
the nose and
earlobes
❖ Cold exposure and
peripheral vascular
disease
 JAUNDICE
D Yellowish
discoloration of the
sclera of the eyes
D Sign of Right Sided
Heart Failure/
chronic hemolysis
 FATTY SKIN DEPOSITS
❖ Associated with
hyperlipidemia and
CAD
 CLUBBING of the NAIL BEDS
⚫ Swollen nail base
and loss of
normal angle
⚫ Low oxygen in the
blood and a sign
of lung disease.
LABORATORY and DIAGNOSTIC TEST

Complete Blood Count

❖ For evaluation of general status
❖ RBC,WBC, platelets, Hgb, ESR
 RBC
D Male 4.5-5.5M/cu.mm;
D Female: 4.1-5 M/cu.mm
D HYPOXIA stimulate renal secretion of
erythropoietin.
D Elevated RBC = inadequate tissue perfusion
Hemoglobin
D substance in red blood cells that makes for the blood to
transport (carry) oxygen
D Male: 13-18g/dl
D Female=12-16g/dl
 WBC
D 5000-10000/cu.mm;
D Increase- MI, infectious heart disease
D Decrease- Leukemia, anemia, autoimmune disease
ESR
D a measurement of the rate at which RBC’s
“settle out” of anticoagulated blood in an hour.
D Male: 15-20 mm/hr
D Female: 20-30mm/hr
 PLATELET
D thrombocytes, are small, colorless cell
fragments in our blood that form clots and stop
or prevent bleeding.
D 150-450k/cu.mm
D INC: poly vera; DIC: viral infections, SLE, dengue
 BLOOD COAGULATION TEST
Pro-thrombin Time (PT, Pro TIME)
D A protein produced by the liver for clotting
of blood.
D Valuable in evaluating the effectiveness
of COUMADINE
D Normal range is 11-16 sec
D Increase PT- at risk for bleeding
D Decrease PT- thrombophlebitis
 Partial Thromboplastin Time (PTT)
D It measures the time required for clotting to
occur after a partial thromboplastin reagent
is added to the blood plasma.
D The best single screening test for disorders in
coagulation
D Used to evaluate the effectiveness of HEPARIN
D Normal values: 60-70 secs
 Activated Partial Thromboplastin Time
(APTT)
D Same purpose of PTT
D Most specific test to evaluate
the effectiveness of Heparin
D 30-45sec.
 BLOOD LIPIDS
Serum cholesterol
D NPO for 10-12 hrs
D 150-200mg/dl
Serum
triglycerides D NPO
for 10-12 hrs D 140-
200 mg/dl
 Blood Urea Nitrogen (BUN)
▪ An indicator of renal function
▪ Elevated BUN is due Decreased cardiac output
leads to low renal tissue perfusion and reduction
in GFR.
▪ Normal Value: 2.1 to 8.5 mmol/L
 SERUM ENZYME STUDIES
ASPARTATE AMINO D Initial elevation: 4-6 hours
TRANSPERASE
D Peak: 24-46 hours
❖ Formerly SGOT D Back to normal: 4-7 days
❖ Elevated indicates
tissue necrosis, liver
injury
❖ Found in liver, heart
and skeletal muscle
❖ Range:
⚫ Men= 10-40 U/L
⚫ Women= 9-25 U/L
 CREATININE PHOSPHOKINASE
(CK-MB)
D Is the most cardiac specific enzyme
D The accurate indicator of myocardial damage.
D Normal range
⚫ Male: 50-325 mu/ml
⚫ Female: 50-250mu/ml
⚫ Onset: 3-6 hrs
⚫ Peak: 12-18 hrs
D Returns to normal in 3-4 days
 SERUM ENZYME STUDIES
CREATININE KINASE (CK)
D Found in the heart muscles, brain,
skeletal muscles.
D Normal range: 35-232 IU
D rise in 12 hrs
D peak in 36-72 hrs
D normalize in 3-5 days
LACTIC DEHYDROGENASE (LDH)
D LDH 1 the most sensitive indicator of
myocardial damage
D Normal range: 100 -225 mU/ml
D Onset: rise in 12 hrs
D Peak: 24-48 hrs
D Returns to normal: 10-14 days
 HYDROXYBUTYRATE
DEHYDROGENASE (HBD)
❖ Elevation of HBD is always accompanied by
elevation of LDH levels
❖ Valuable in detecting “SILENT MI”
⚫ Normal Range: 140-350 ug/L
⚫ Onset: 10-12 hrs
⚫ Peak: 48-72 hrs
⚫ Normal: 12-13 days
 CARDIAC TROPONINS
D are a group of proteins found in skeletal and
heart (cardiac) muscle fibers that regulate
muscular contraction.
D Most specific test to detect MI
D three Components: Troponin C, troponin T,
and troponin I
 CARDIAC TROPONINS
Troponin I
D Modulates the contractile state
D Rise in 3-5 hrs
D Peak: 14-18 hrs
D NV: 0- .04 ng/ml
D Remain elevated (1.5 ng/ml) for 4-7
days indicates MI
Troponin T
D Sensitive as CK MB in detecting myocardial
injury
D Rise in 3-5 hrs
D Remains elevated (above 0.1 ng/ml) in for 14-
21 days

Troponin C
D Binds with calcium
MYOGLOBIN
❖ Is a low molecular weight heme protein found in
cardiac and skeletal muscle.
❖ A sensitive indicator of early MI.
❖ Elevation occurs as early as 30-60 minutes after
injury but declines rapidly 7 hours
URINALYSIS
D To assess the defects of cardiovascular
diseases, renal function and the existence of
concurrent renal and systemic diseases
D Albuminuria-indicates malignant, HPN and CHF
D Myoglobinuria- supports MI
 Serum Electrolytes
D Electrolytes affects
cardiac contractility
D Na=135 to 145 mEq/L
D K=3.5-5 mEq/L
D Ca=4.5 to 5.5 mEq/L
ELECTROCARDIOGRAPHY (ECG/EKG)
D Itis a graphical recording of the electrical
activities of the heart.
D The procedure is PAINLESS.
 INDICATIONS OF ECG
D MI and other CAD
D Cardiac Dysrhythmias
D Heart enlargement
D Electrolytes imbalances- especially CA, NA
and K levels
D Inflammatory diseases of the heart
D Effects of drugs on the heart
ELECTRODE
D An adhesive pad that contains conductive gel and
designed to be attached to the patients skin
LEADS
D Electrodes connected to the monitor or EKG
machine by wires
D Wires are color coded (Red, Black, Yellow and
Green)
RHYTHM STRIP
D The printed record of the electrical activity of the
 The Standard ECG consist of 12 leads
D (I, II, III, AVR, AVL, 3 lead ECG
AVF, V1, V2, V3, D is use to
V4, V5, V6) detect life-
threatening
dysrhythmias
 CHEST LEADS
D from V1-V6
D knows as Unipolar leads or Precordial
leads
D Chest leads look at the heart via horizontal
(transverse plane)
D proper placement of the V leads is
important to the correct interpretation of
the 12 lead ECG strip
NORMAL PLACEMENT OF ECG LEADS
 NURSING INTERVENTIONS
1. Clean the area with an alcohol swab and allow the
area to dry
2. Shave excess hair as indicated
3. If the patient is diaphoretic, attempt to dry the area
or use antiperspirant
4. Use conductive gel to ensure proper conduction
5. Proper placement of the leads
 WAVES, COMPLEXES and INTERVAL
P-WAVE
D Depolarization of the
Atria
D SA node is responsible
for this.
D Represents Atrial
Depolarization
D Duration: 0.04-0.11sec
D Normal P wave is 3mm
or less
 PR INTERVAL
D Time of impulse
transmission from the SA
node to AV node through
the intermodal pathways
in the atria downward to
the ventricles
D Starts at the P-wave
and ends at
the beginning of the
QRS complex
 PR INTERVAL
D Shortened PR interval-
indicates that the impulse
was outside the normal
route
D Prolonged PR interval-
delay in the electrical
conduction pathway or
AV block
 QRS COMPLEX
D Depolarization or
contraction of
the ventricles
D The bundle of His,
bundle branches, and
Purkinje fibers are
responsible
D Duration: 0.05-0.10
sec
 QRS COMPLEX
Q
WAVE
D The first negative
deflection after the P
wave
D The first down stroke
after the P wave
D 3mm in depth
D Pathologic Q wave
indicates MI
Pathologic Q wave
WAVES, Complexes and Interval
R wave
D first positive
deflection after the Q
wave
D 5-10mm in height

S Wave
D The second negative
deflection after the R
wave
 WAVES, Complexes and Interval
ST Segment
D Beginning of ventricular
repolarization or when
the ventricles are relax.
 ST Segment Abnormality
ST SEGMENT DEPRESSION
D Due to myocardial
ischemia secondary to
myocardial tissue hypoxia
 ST Segment Abnormality
ST Segment Elevation
D Due to myocardial injury
secondary to acute
myocardial infarction
D Other causes coronary
artery spasm,pericarditis
and ventricular aneurysm
 WAVES, Complexes and Interval
T wave
D Repolarization of the
ventricles or
ventricular relaxation
D Resting phase
of cardiac cycle
 WAVES, Complexes and Interval
U-wave
D sometimes is seen after
the t-wave.
D caused by the
relaxation of the
Purkinje fibers.
 COMMON ECG CHANGES
Hypokalemia
D D-epressed ST segment
D U-wave
D S- hort T-Wave
HYPERKALEMIA
D P-rolonged QRS
complex
D E-levated ST segment
D P-eak T wave
 Myocardial Infarction
D Elevated ST segment
D Inverted T wave
D Pathologic Q wave
 HOLTER MONITORING
DA continuous 24 hr
ECG monitoring
D To assess the activities
that precipitates
dysrhythmias and the
TIME when the client
experiences
dysrhythmias
 HEMODYNAMIC MONITORING
1. CENTRAL VENOUS
PRESSURE
D Monitors the pressures within
the right atrium and SVC
D Monitors the blood volume,
adequacy of venous return to
the heart, pump function of the
right side of the heart
D To serve as guide for
fluid replacement
 CENTRAL VENOUS PRESSURE
D To administer blood
products, TPN
D To obtain venous access
when peripheral vein sites
are inadequate
D To insert a temporary
peacemaker
D To obtain central venous
sample
 CENTRAL VENOUS PRESSURE
D thread the catheter into a
large central vein
D The catheter tip is positioned
in the RA, or upper portion of
SVC
D The level of water
manometer should be
placed at the right, mid
axillary, 4th ICS.
D SUPINE Position during the
 CENTRAL VENOUS PRESSURE
D Strict asepsis
D Normal reading: SVC= 0-12 cm H2O, RA= 5-12 cm H2O
D CVP near zero- hypovolemia/ DHN- hypotension, oliguria
and rapid, weak, thread pulse
D High CVP (15-20cm H2O)- hypervolemia-hypertension.
Polyuria, bounding pulse.
 NURSING RESPONSIBILITIES
D Evaluate patients PT, PTT, CBC
D Informed consent
D Explain to do Vasalva Manuever
D Position the pt SUPINE
D Arm vein- extend arm and secure arm board
D Neck Veins- TRENDELENBURG position
D Place pt on ECG
D The catheter should be suture in place
D Place a sterile dressing over the site
D Obtain a chest x ray.
D Monitor Complications: Pneumothorax,
Hemothorax, air embolism, hematoma, Cardiac
tamponade
Pulmonary Artery Pressure & PCWP
D Monitor pressure in the RA, RV, PA, and distal
branches of pulmonary artery (PCWP)
D It reflects pressure in the LEFT Atrium
D Swan Ganz catheter
D Normal range: PAP= 4-12mmHg, PCWP=
4-12mm Hg
D Elevated PAP and PCWP-indicate LSCHF
 PCWP
D PCWP above 25mm Hg- PULMONARY EDEMA

NURSING INTERVENTIONS
⚫ Inflate balloon only for PCWP readings,
deflate between reading.
⚫ Observe catheter insertion site; culture site q 48 hrs
as ordered
⚫ Assess extremity for color, temp, capillary filling
and sensation
 ECHO CARDIOGRAPHY
D Uses ultrasound to assess cardiac structure and
mobility such as valvular structure, chambers size and
contents, ventricular muscle, thickness and septal
motion, pericardial sac and ascending aorta
D measure the ejection fraction (EF) or the percentage of
end diastolic blood volume ejected during systole.
D Normal ejection fraction: 50% to 75% (AHA)
D A borderline ejection fraction can range between 41%
and 50%.
ECHO CARDIOGRAPHY
 NURSING INTERVENTIONS
D No special preparation.
D Painless and takes 30 to 60 minutes to complete
D The client has to remain still, in supine position
slightly turned to the left side, with HOB
elevated 15 to 20 degrees
 Transesophageal Echocardiography
⚫ Allows ultrasonic imaging of the cardiac
structures and great vessels of the esophagus
 Nursing Interventions Before TEE
⚫ Ascertain history of esophageal surgery, malignancy, allergy to
anesthesia or sedatives
⚫ NPO 4-6 hours before the test
⚫ Void before the procedure
⚫ Remove dentures and other oral prosthetics
⚫ Administer sedative as ordered
⚫ Keep suction and resuscitation equipment available
⚫ Cardiac monitoring
⚫ Topical anesthesia is administered
⚫ Place patient in chin to chest position
 POST TEE
⚫ NPO until gag reflex return
⚫ Place in Lateral or Semi Fowler’s position
⚫ Encourage to cough
⚫ Throat lozenges or rinses
observe signs of complications: pharyngeal bleeding,
cardiac dysryhtmias, and hypoxemia
 STRESS OR EXERCISE / TREADMILL TEST
⚫ ECG is monitored
during exercise on
a treadmill or a
bicycle-like device
 PURPOSE OF STRESS TEST
D Identify ischemic heart disease
D Evaluate patients with chest pain
D Evaluate effectiveness of therapy
D Develop individual fitness program during cardiac
rehabilitation
 Health Teachings
D Get adequate sleep the night before the test
D Avoid tea, coffee and alcohol on the day of the test.
D No smoking and taking nitroglycerine 2 hours before
the test
D Wear comfortable loose clothes
D Eat light breakfast or lunch 2 hours before the test
D Wear low heeled rubber soled shoes for comfort during
the test
D Inform the physician if any usual sensations develop
 RADIOLOGIC TEST
Chest X ray
- To determine the size and configuration of
the heart and size of the chambers
- Avoid wearing metals
Cardiac Fluoroscopy
- Facilitates observation of the heart from
varying views while the heart is in motion
 Cardiac Catheterization
D a procedure in which a thin, flexible tube (catheter)
is guided through a blood vessel to the heart to
diagnose or treat certain heart conditions such
as clogged arteries or irregular heartbeats
D A thin, long, flexible tube is inserted, usually in the
arm or groin, and is guided to the blood vessels of
your heart.
Routes of Cardiac Catheterization
Right Sided Heart Catheterization
▪ done by insertion of catheter via cutdown
into a large vein (Median cubital or brachial)
Left Sided Heart Catheterization
▪ is done by passing a catheter into the aorta
via brachial or radial artery
 PURPOSES
D Assess oxygen levels, pulmonary blood flow,
CO, heart structures
D Visualization of coronary arteries for blockages
and to assess heart muscle function and the
structure and function of your heart valves.
D to assess and treat various heart rhythm
disturbances.
D For Diagnostic and Therapeutic Uses
 Diagnostic Uses
⚫ take between 30 minutes to over an hour
⚫ atherosclerosis or coronary artery disease
⚫ show your overall heart function and the condition
of individual cardiac chambers
⚫ heart valves impairment (narrow, stiff, or leaky)
⚫ done preoperatively for planning cardiac procedures
⚫ to take a sample of tissue
 Diagnostic Uses
D to measure oxygen levels for assessment of cardiac and
pulmonary disease, or
D to determine the pressure in various areas of the heart
D heart valve disease, congestive heart failure,
cardiomyopathy, or heart failure.
 Therapeutic Uses
⚫ to relieve blockages in the coronary arteries
with angioplasty (widening the arteries)
⚫ to remove obstructive material (thrombectomy)
⚫ for stent placement (a tube that remains in place to
keep the artery open).
⚫ treat heart valve conditions such as mitral stenosis
and aortic stenosis (valvuloplasty) and heart
rhythm irregularities (cardiac ablation), or to repair
patent foramen ovale.
⚫ for the diagnosis and treatment of a heart attack
CARDIAC CATHETERIZATION
Nursing Interventions (Before)
D Assess for allergy to iodine/seafood
D VS
D NPO before the procedure
D CBC, PT and PTT, ECG, X-ray
D Withhold blood thinners
D Have the client to void.
D Administer sedative as order
D Do cardiac monitoring
D Inform that warm or flushing sensation
will be feel as the contrast medium is
injected
D Fluttering sensation is felt
 During the Test
D IV fluids will be infuse
D Local anesthesia is given, a catheter is inserted in one of the blood
vessels (groin, arm, wrist, or neck.)
D Catheters are typically maneuvered to various locations within the
heart, and the pressures within the chambers of the heart are
measured
D Dye is injected through the catheter while a series of rapid X-ray
images are recorded.
D Once the procedure is completed, the catheter is removed.
 After the Procedure
D Bed rest
D Monitor VS especially peripheral pulses
D Monitor EKG
D Apply pressure dressing/ice pack
D Immobilized affected extremity in extension
D Monitor extremities for color, temp,
pulse and sensation
 Possible Complications
D Common-Minor bleeding at the site of catheter
insertion (the arm or the groin) temporary heart rhythm
disturbances and changes in the blood pressure
D Serious: Allergic Reaction to dye, artery damage,
Dysrhythmia, Perforation of great vessels of the
heart, Cardiac tamponade, Sudden blockage of
the artery, pulmonary edema, severe bleeding,
stroke
 ANGIOGRAPHY
D contrast medium is injected into the vascular
system to outline the heart and blood vessels
D almost always done during the procedure, which
involves injecting dye into your vessels so they can be
visualized with imaging, typically an X-ray or an
intravascular ultrasound.
D It is done to see any restriction in blood flow
going to the heart.
D It may be done during cardiac catheterization
 D EAS---
A,\'\ osclf:.i<.os\s
 Coronary Artery Disease
□Accumulation of fatty
deposits or plaques
(ATHEROSCLEROSIS)
along the innermost layer of
the coronary arteries
leading to restriction of blood
flow to the heart and
inadequate oxygen supply to
the heart muscle.
 Coronary Artery Disease
□LDL known as “bad
cholesterol” that irritate
and damage the inner
layer of the coronary
vessel
 Main Arteries of the Heart
Left Coronary Artery
Left circumflex artery-
provides blood to left atrium &
side and back of the left
ventricle

Left anterior descending

artery-provides blood to
the front and bottom of the
left ventricle and front of the
septum
 Main Arteries of the Heart
Right Coronary Artery
□provides blood to the
right atrium and ventricle
and to the bottom part of
the left ventricle and back
of the septum and
branches off to:
□Right marginal artery and
Posterior descending
artery
 RISK FACTORS
□Age □Diet
□Gender □Sedentary lifestyle
□Race. □Smoking
□Heredity or family history □Alcohol
□Stress □Hypertension
□Obesity
□DM
R
I
S
K

F
A
C
T
O
R
S
 Etiology/ Risk Factors
P
ATHOPHYSIOLOG
y
LDL adhere to the artery wall

Plaque formation/ Athersclerosis

Blood restriction into the heart

Signs and symptoms of Ischemia, MI

 Signs and Symptoms of CAD
□Chest pain- STABLE and Unstable Angina
□Shortness of breath, Substernal pain, Burning,
squeezing pain
□Very tired, feeling run down especially with activity
□Diaphoresis
□Nausea
□Tachycardia
 STABLE ANGINA (UNSTABLE ANGINA)
□ Precipitated by physical □Occurring at rest
exertion and emotional stress
□Pain is less than 15 minutes □Last longer than 15 minutes

□Relieves by rest □Unrelieved by rest/

and nitroglycerine SL nitroglycerine

□Good prognosis □Can cause sudden death

□Poor prognosis
 DIAGNOSTIC TESTS
□Blood tests: Lipid profile: total cholesterol, LDL, HDL,
triglycerides
□ECG: ST segment depression, ST segment elevation
□Stress testing
□Cardiac catheterization/coronary angiography-
presence, location and extent of coronary lesion
 Goal/Planning
□ to maintain normal blood and oxygen supply
to the heart
□ to eliminate the signs and ss
□ patient can resume his/her ADL
□ prevent further progression of CAD
 Nursing Interventions
□ Assess signs and symptoms
□ Monitoring heart rate and blood pressure and
oxygen saturation
□ Modifying lifestyle: Diet (low fat, low calorie), Exercise ,
Smoking cessation, weight loss
□ Educating patient about treatment, preventive
measure, medications, and management
□ Education about procedures: EKG, stress test, heart cath,
lipid profile blood test
□ Educate about the significance and complications of CAD
 Medical Management
Antiplatelet
□prevent clots from forming or growing which decrease
the chances of ischemia
□Aspirin and Plavix
□Nursing Considerations:
□watching for GI bleeding and monitor Thrombotic
Thrombocytopenic Purpura (TTP)
Nitrates
□ causes vasodilation
□ Sublingual, transdermal
□ One tab or one spray for
maximum of 3 doses,5 min
interval
□ Monitor their blood
pressure
□ SE: dizzy or hot flushing
after taken.
BETA BLOCKERS
□Decrease myocardial oxygen demand by decreasing
the heart rate, BP, myocardial contractility and
calcium output
□Ends in “LOL”
□Propranolol, metropolol, atenolol, pindolol, esmolol
□Monitor the HR, and BP
□SE: Mask hypoglycemia-sweating,
bradycardia, breathing problems
Calcium Channel Blockers
□Inhibit the calcium ions transportation into myocardial
cells to depressed inotropic and chronotropic activity
decreasing cardiac work load
□Promote vasodilation and reduces coronary
vasospasm.
□Verapamil, Nifedipine, Diltiazem,
Amlodipine, Nicardipine
□Monitor HR and BP
 Angiotensin Converting
Enzyme/ACE Inhibitors
□ ends in “pril”
□ Lisinopril, ramipril
□ blocks the conversion of angiotensin I to
angiotensin II which caused vasodilation, lowers
blood pressure, decreases the workload on the
heart.
□ Side effect: nagging dry cough
Statins (tins)
□Simvastatin, Atorvastatin
□helps lower LDL, total cholesterol, triglycerides,
and increase HDL.
□Educate not to replace diet and exercise
□Notify doctor if they develop muscle pain or tenderness
□Monitor CPK (creatine kinase) levels if elevated
□Monitor liver function
 Surgical Management
Percutaneous Transluminal
Coronary Angioplasty
□ A balloon tip catheter is placed
in a coronary vessel narrowed by
plaque
□ The balloon is inflated and
deflated to stretch the vessel
and flatten the lesion
□ Blood flows freely through
the unclogged vessel to the
heart.
 Surgical Management
Intra Coronary Stent
□A diamond mesh
tubular device is placed
in the coronary artery
□Prevents re-stenosis
(after PTCA) by
providing skeletal
support
 Surgical Management
Intra Coronary
Atherectomy
□A blade tip catheter is
guided in a coronary
vessel to the site of
the plaque
□The plaque is cut,
shave, or pulverized
then
removed
 Surgical Management
Coronary Artery Bypass Graft
□ A graft is surgically attached
to the aorta and the other end
of the graft is attached to a
distal portion of a coronary
vessel.
□ By passes obstructive lesion
in the vessel and returns to
adequate blood flow to the
heart muscle supplied by the
artery.
 ANGINA PECTORIS/ MYOCARDIAL
ISCHEMIA
□Insufficient blood
flow resulting to
inadequate oxygen
supply to the
myocardium causing
transient chest pain
due to obstruction or
spasm of coronary
arteries
CAUSES ATHEROSCLEROSIS HYPERTENSION DIABETES MELITUES
THROMBOANGITIS OBLITERANS POLYCYTHEMIA VERA
AORTIC REGURGITATION

REDUCED CORONARY TISSUE

DIMINISHED MYOCARDIAL OXYGENATION

INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS )

CHEST PAIN
 Types of Angina Pectoris
Stable Angina
□ the most common form of angina
□ characterized by burning, heavy, or
squeezing feeling in the chest.
 Types of Angina Pectoris
Unstable angina
□ chest pains occur with increased frequency
□ requires hospital admission and
more aggressive therapy
 Types of Angina Pectoris
STABLE ANGINA
□ Chest pain last for less
than 15 minutes
□ Recurrence is less frequent
□ Relieved by Rest or
nitroglycerin
UNSTABLE ANGINA
□ Chest pain is last more than
15 minutes but not more than
30 minutes
□ Recurrence is more frequent
□ not relieve by rest
or nitroglycerin.
 Types of Angina Pectoris
Prinzmetal’s or Vasospastic Angina
□Is uncommon pattern of episodic angina that occurs at
rest due to coronary artery spasm.
□Responds promptly to coronary vasodilators
and calcium-channel blockers.
 Intractable Angina
□ Also called Refractory Angina unresponsive
to intervention.
□ Respond poorly invasive procedures such
as angioplasty or by pass surgeries.
 VARIANT ANGINA
□Chest pain is longer duration
□Occur at rest
□Attack occurs in early hours of the day
□May result from Coronary artery spasms
Nocturnal Angina
□Occurs only at night and possibly associated with
REM sleep
Angina Decubitus
□Paroxysmal chest pain that occurs in sitting or
lying down
Post infarction angina
□Occurs after MI, when residual ischemia may
cause episodes of angina.
 Precipitating factors of Angina
4 E’s
□ Exertion
□ Emotion
□ Eating heavy meal
□ Environment
 Clinical Manifestations
Chest pain
□ Transient (temporary), paroxysmal substernal or pre cordial pain,
squeezing, burning, pressing, choking aching or bursting left
sternal chest pain
□ Heaviness or chest tightness
□ The patient often says, “It feels like gas or heartburn or indigestion”
□ Radiates down one or both arms, left shoulder jaw, neck and back
□ Precipitated by physical exertion
□ Relieve by rest and Nitroglycerine
 Clinical Manifestations
□Pallor
□Diaphoresis
□Dyspnea
□Faintness
□Palpitation
□Dizziness
 ANGINA CHEST PAIN
□Sub-sternal
□Anterior chest pain
□Vague ( Radiates)
□Exertion
□Relieved by rest and Nitroglycerine
□Short duration (less than 15 minutes)
 Assessment of Chest Pain
□Precipitating factors of Angina- 4 E’s
□Provocative
□Quality
□Region
□Severity
□Timing and Treatment
 SUBSEQUENT ASSESSMENT
□ Obtain 12 lead ECG
□ Assess patient knowledge on the disease
□ Medical history- previous attacks and
Drug therapy
 Nursing Diagnosis
□Pain related to decreased oxygen supply and
demand
□Decreased cardiac output related to reduced
preload, afterload and contractility
□Anxiety related to chest pain
 NURSING INTERVENTIONS
To Relieve Chest pain
□Assess the level of chest pain and its duration
□Place in comfortable position
□VS q 5-10 minutes until anginal pain subsides
□Administer oxygen and Nitroglycerine as ordered
□Monitor relief of pain
 NURSING INTERVENTIONS
To maintain Tissue Perfusion
□Avoid over fatigue
□Stop activity immediately
□Monitor BP and HR in response to drug therapy
□Monitor ECG- ST segment depression and Elevation
 To Decrease Anxiety
□Minimize emotional outburst, worry and tension
□Verbalize fears and concerns
□Maintain an optimistic outlook
□Explain the reasons for hospitalization, diagnostic test,
and therapies administered
□Teach relaxation techniques such as yoga, DBE
□Administer sedative and tranquilizer.
ACTIVITY
□Encourage within patient’s limitation
DIET
□DASH diet-rich in vegetables, fruits and whole
grains, fat-free or low-fat dairy products, fish,
poultry, beans and nuts.
□Low sodium, low fat and cholesterol, High Fibers
□Avoid saturated fat (animal fats)
□White meat ( chicken without skin, turkey, fish are
low in cholesterol)
□Read labels
 NITROGLYCERINE
□ Promotes venous and arterial relaxation of coronary vessel
and prevention of coronary spasm
□ causes coronary vasodilation and increases blood flow to
the heart
□ Decrease peripheral resistance, decrease systolic pressure
and preload
□ ointment, sublingual, IV, patch, or oral “Imdur”
□ Relief of chest pain or angina and reduce the risk of
heart attack and sudden death.
 NURSING CONSIDERATION IN
NITROGLYCERINE THERAPY
□Administer SL (at the first sign of chest pain.)
□Sitting position when taking the drug.
□Offer sips of water before giving SL nitrates
□Take maximum of 3 doses at 5 minutes interval
□Advise the pt to always carry 3 tablet in his pocket
□Instruct the patient that a burning sensation under
the tongue will be felt.
 NURSING CONSIDERATONS
□Store nitroglycerine in a cool dry place, use
dark/amber colored air tight container.
□Change stock of nitroglycerine every 3 months
□Observe for side effects: Headache, flushed
face, dizziness, faintness, tachycardia.
□Transderm Nitro patch-once a day, usually in
the morning.
 NURSING CONSIDERATONS
□Best taken before any strenuous activity
□Burning sensation is a sign of potency of the drug. Facial
flushing is a side effect.
□Do not chew the tablet.
□Monitor the BP and HR.
□Evaluate the effectiveness- Pain relief
 Beta Adrenergic Blocking Agent
□ ends with “lol”
□ decrease myocardial oxygen demand
by decreasing the heart rate, bp,
myocardial contractility and calcium
output.
□ Propanolol, Atenolol, Metoprolol,
Esmolol, Nadolol, Pindolol, Timolol
 NURSING
CONSIDERATION
(BETA-BLOCKERS)
□Assess the PR before giving the drug.
□Best taken with food
□Do not give to clients with asthma and DM patients
□Observe for SE: NV, mental depression, mild diarrhea,
fatigue, impotence.
□GLUCAGON- antidote for beta blocker poisoning.
 Calcium Channel Blockers
□Norvasc, Cardizem, Verapamil (Isoptin,
Calan), Amlodipine, Nicardipine, Nifedipine,
Diltiazem
□stops the transport of calcium to the myocardium
and into smooth muscle which causes vasodilation
on the coronary arteries to improve oxygen demand
and supply
□Monitoring heart rate, orthostatic hypotension,
□Educate about good oral hygiene
 NURSING CONSIDERATIONS
□Assess HR and BP
□Monitor hepatic and renal function
□Administer 1 hr before or 2 hrs after meal.
□Prepare GLUCAGON- antidote for calcium
channel blocker overdose
 Calcium Channel blockers
□ Inhibit calcium ion transportation into myocardial
cells to depress inotropic and chronotropic
activity, decreasing cardiac work load
□ Vasodilation effect, and reduces coronary spasm
□ Verapamil (Isoptin, Calan), Amlodipine
□ Nicardipine, Nifedipine, Diltiazem
 NSG CONSIDERATIONS
□Assess HR and BP
□Monitor hepatic and renal function
□Administer 1 hr before or 2 hrs after meal.
□GLUCAGON- for calcium channel blocker overdose
 PLATELET AGGREGATE INHIBITORS/
ANTI PLATELET
□ It prevents platelet from clumping and
blood clots from forming
□ ASA, Aspirin, Dypiridamole,
Clopidogril, Ticlopidine, Plavix
 NSG CONSIDERATIONS
□ Watch for signs and symptoms of GI bleeding, especially
if patient has a history.
□ Plavix: taken if can’t take aspirin
□ Assess for ss and sx of bleeding
□ Avoid straining of stool.
□ ASA with food.
□ Observe for TINNITUS. ASA toxicity
□ ASA may cause Bronchoconstriction. Observe for wheezing
 Anti coagulants
□ It prevent blood clotting
□ Inactivates thrombin and other clotting
factors inhibiting conversion of fibrinogen to
fibrin
□ Examples: Heparin, Coumadin
 Heparin Sodium
▪ Assess for signs of bleeding
▪ Keep protamine sulfate at the bedside. Antidote
if bleeding occurs in heparin therapy
▪ If administered SC, do not aspirate, do not massage
the site of heparin injection.
▪ Monitor PTT or APTT levels
▪ Used for maximum of 2 weeks
 Warfarin Sodium (Coumadin)
□Assess for signs of bleeding
□Keep Vit K. Antidote if bleeding occurs in Coumadine
therapy
□Monitor Prothrombin Time
□Minimize green leafy vegetables in the diet.
□Don’t give ASA and Coumadin together to prevent
bleeding.
 MYOCARDIAL INFARCTION (MI)
□Results from prolonged lack of blood flow to a portion
of the myocardial tissue resulting to lack of OXYGEN,
DEATH or NECROSIS to the myocardial tissue.
 CAUSES
ATHEROSCLEROSIS, Thrombosis,

REDUCED CORONARY TISSUE

DIMINISHED MYOCARDIAL OXYGENATION

Left atrium and ventricle

INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS )

CK-MB, troponins, myoglobin production

Ischemia, injury, Necrosis
 What happens to the heart muscle after an MI?
Early signs of an MI
□no physical changes to heart muscle yet (until about 6-8
hours).
□If the myocytes die, cardiac enzymes are released-
CK-MB (4 to 6 hours after MI), troponins (2-4 hour most
regarded) myoglobin (1 hour after injury)
 Within 24-36 hours
□inflammation sets in and neutrophils come on
the scene and congregate at the damaged tissue
site.
□complication is possible pericarditis.
□within 24 hours the heart fails to pump efficiently
resulting to cardiogenic shock and arrhythmias
Within 10 days
□granulation occurs when the macrophages come on
the scene.
□WBCs came to clean up the dead cells and other
components.
□The new tissue formed from granulation is not well
formed and is weak. This increases the chance of
cardiac rupture.
Within 2 months
□ scarring occurs, and the heart is affected in
size and functionality due to increased
collagen.
 ETIOLOGY/CAUSES
□Thrombus formation- the most
common causes of MI
□Severe CAD
□Intramural hemorrhage
□Coronary artery spasm
□Coronary artery embolism
 Degree of Damage to the Heart Muscle
Myocardial
ischemia/Zone of
ischemia
❖ Temporary deprivation
of oxygen and transient
absence of blood supply
and other nutrients to
the heart
Degree of Damage to the Heart Muscle
Myocardial injury/zone of
injury
❖ Inflamed and Damage
to the heart muscle
(myocardium)
❖ Most commonly
results from
myocardial ischemia
Degree of Damage to the Heart Muscle
Myocardial
Necrosis/Zone of
infarction
❖ Death of
myocardial tissue
(MI)
❖ Complete oxygen
deprivation
❖ Irreversible damage
 Classification of MI according to the
Heart muscle involve
Transmural (Q wave) infarction
❖ necrosis occurs throughout the entire thickness of
the heart muscle
❖ extends from endocardium to epicardium
 Classification of MI according to the
Heart muscle involve
Sub endocardial infarction
❖ necrosis is in the innermost layer of the heart
lining chambers.
❖ Affects the endocardial muscles
Intramural infarction
❖ patchy areas of the myocardium associated with
long standing angina pectoris.
 ANGINA AND MI
ANGINA PECTORIS MI
□ Chest pain- usually last less □ Chest pain-last more than
15 minutes 2 hours

□ Relieve by nitroglycerine □ Not relieve by nitroglycerine

□ Nitroglycerine □ Morphine
□ Precipitated by stress □ Not
and exercise
□ Relieve by rest □ Not
□ Maybe accompanied □ Accompanied by dysrhythmias
by dysrhythmias
 Clinical Manifestations
Chest pain (intense, heavy)
Radiating chest pain that goes to left arm, jaw, back
Unrelieved by nitroglycerin or rest (chest pain)
Sweating (cold)
Hard to breathe (shortness of breath)
Increased heart rate, blood pressure or irregular heart rate
Nausea with vomiting
Going to be anxious and scared
 CLINICAL MANIFESTATIONS
□ Shock- hypotension, tachycardia-bradycardia, tachypnea,
lethargy, cold skin and diaphoresis, peripheral cyanosis and
weak pulse.
□ Anxiety and Apprehension
□ Oliguria
□ FEVER
□ Suffocation, dyspnea, orthopnea, gurgling or bubbling
respiration
 Diagnostic Evaluations
ECG changes
□Elevation of ST segment- due to injury area or Acute
MI
□Inverted T wave- From the zone of ischemia
□Pathologic Q wave- Develops due to area of
infarction/tissue necrosis and are permanent
Elevated Troponins
□gold standard now used by most hospitals in
assessing for an MI
□Most specific test to detect MI.
□Elevated Troponin T, I, C- sensitive as CK MB
for the detection of MI
□usually drawn every 6 hours for 3 sets.
CK-MB
□it elevates 4-6 hr after injury
□the most sensitive enzyme for determining for heart
muscle damage
Elevated LDH 1 and LDH 2
□sensitive isoenzyme that indicates myocardial damage
Elevated WBC and ERS
□due to inflammatory process
 OTHER TEST
□Echocardiogram
□Heart Catheterization
□Stress test with Myocardial Perfusion
Imaging
 Nursing Interventions
□Monitoring & Assessing Cardiovascular
system-12-lead EKG, and continuous bedside cardiac
monitoring.
□Semi fowlers
□OXYGEN via nasal cannula- at 2- 4 L/Minute
□Working IV access
□Monitor lung sounds “crackles”
□Bedrest for 24-48hrs
 Nursing Interventions
□Collect cardiac enzymes as ordered by the physician
□Administering medications per MD order:
□Oxygen, Morphine sulphate, MEPERIDINE
(DEMEROL), THROMBOLYTIC
THERAPY
Streptokinase (streptase), Urokinase, and Tissue
plasminogen activator (Activase).
MORPHINE SULFATE
□ Narcotic Agonist, analgesic,
□ DOC of MI
□ Used relieve pain
□ To improve hemodynamics by reducing
pre load and afterload and promotes
venous pooling of blood in the periphery
 NURSING CONSIDERATIONS
□Best taken with Food
□Report nausea and vomiting and respiratory
depression
□Keep Naloxone HCL (antidote) at the bedside
□Instruct the patient to lie down during IV
administration.
□Contraindicated to patient with PANCREATITIS
 MEPERIDINE (DEMEROL)
□Has Vagolytic effect –causing tachycardia
□Narcotic Analgesic
□Negative Pain
□Avoid alcohol
□Keep the antidote: Naloxone hydrochloride
□Supine position- prevent hypotension
 THROMBOLYTIC THERAPY
□Streptokinase (streptase), Urokinase, and
Tissue plasminogen activator (Activase)
□It dissolve obstructing thrombus
□Effectiveness of the drug: Absence of chest pain
□Detect for occult bleeding during and after
thrombolytic therapy
□Assess neurologic status changes
 ANTI-THROMBOTIC AGENTS
□prevent formation of clot
□Lovenox and Heparin
□monitor for bleeding (assess gums of mouth, stool
(dark tarry), drop in blood pressure and increase
in heart rate, blood in urine
□watch platelet count which may start to decrease
after several days
 ANTI PLATELET
□It decrease platelets aggregation and
thrombus formation
□It prevents platelet from clumping and blood clots
from forming
□Aspirin (ASA), Plavix, Dypiridamole, Clopidogril
□Watch for signs and symptoms of GI bleeding, and
Thrombotic Thrombocytopenic Purpura (TTP)
 NSG CONSIDERATIONS
□Watch for signs and symptoms of GI
bleeding, especially if patient has a history.
□Assess for ss and sx of bleeding
□Avoid straining of stool.
□ASA with food.
□Observe for TINNITUS. ASA toxicity
□ASA may cause Bronchoconstriction.
 Anti-Coagulants
□ It prevent blood clotting
□ Inactivates thrombin and other clotting
factors inhibiting conversion of fibrinogen to
fibrin
□ Examples: Heparin, Coumadin
Heparin Sodium
▪ Assess for signs of bleeding
▪ Keep protamine sulfate at the bedside.
▪ If administered SC, do not aspirate and massage
the site of heparin injection.
▪ Monitor PTT or APTT levels
▪ Used for maximum of 2 weeks
 Warfarin Sodium (Coumadin)
□Assess for signs of bleeding
□Keep Vit K. Antidote if bleeding occurs in
Coumadine therapy
□Monitor Prothrombin Time
□Minimize green leafy vegetables in the diet.
□Don’t give ASA and Coumadin together to
prevent bleeding.
 NITROGLYCERINE
□Promotes venous and arterial relaxation of
coronary vessel and prevention of coronary spasm
□causes vasodilation and increases blood flow to the
heart, hence better blood flow to the area
experiencing ischemia
□ointment, sublingual, IV, patch, or oral “Imdur”
□Relief of chest pain
 NURSING CONSIDERATONS
□Best taken before any strenuous activity
□ Place a tablet under the tongue at the first sign of chest pain.
□ Burning sensation is a sign of potency of the drug. Facial flushing
is a side effect.
□ Do not chew the tablet.
□Keep the tablets in dark container.
□ Monitor the BP and HR.
 Ace Inhibitors
□ends in “pril”
□Lisinopril, Ramipril, Enalapril, Captopril
□It work by allowing more blood to get to the
heart muscle
□It does this by blocking the conversion of Angiotensin
I or Angiotensin II
 Beta Adrenergic Blocking Agent
□ ends with “lol”
□ decrease myocardial oxygen demand
by decreasing the heart rate, bp,
myocardial contractility and calcium
output.
□ Propanolol, Atenolol, Metoprolol,
Esmolol, Nadolol, Pindolol, Timolol
 NURSING
CONSIDERATION
(BETA-BLOCKERS)
□Assess the PR before giving the drug.
□Best taken with food
□Do not give to clients with asthma and DM patients
□Observe for SE: NV, mental depression, mild diarrhea,
fatigue, impotence.
□GLUCAGON- antidote for beta blocker poisoning.
 ARBS Angiotensin II Receptor Blockers
□end in “sartan” like Losartan, Valsartan
□It blocks angiotensin II receptors which
causes vasodilation.
□Monitor sodium, K, and blood pressure
Statins (“tins)
□Simvastatin, Atorvastatin,
□helps lower LDL, total cholesterol, triglycerides,
and increase HDL.
□Educate not to replace diet and exercise
□Notify doctor if they develop muscle pain or tenderness
□Monitor CPK (creatine kinase) levels if elevated
□Monitor liver function
 Calcium Channel Blockers
□Norvasc, Cardizem, Verapamil (Isoptin,
Calan), Amlodipine, Nicardipine, Nifedipine,
Diltiazem
□stops the transport of calcium to the myocardium
and into smooth muscle which causes vasodilation
on the coronary arteries to improve oxygen demand
and supply
□Monitoring heart rate, orthostatic hypotension,
□Educate about good oral hygiene
 NURSING CONSIDERATIONS
□Assess HR and BP
□Monitor hepatic and renal function
□Administer 1 hr before or 2 hrs after meal.
□Prepare GLUCAGON- antidote for calcium
channel blocker overdose
 Surgical Management
Percutaneous Transluminal
Coronary Angioplasty
□ A balloon tip catheter is placed
in a coronary vessel narrowed by
plaque
□ The balloon is inflated and
deflated to stretch the vessel
and flatten the lesion
□ Blood flows freely through
the unclogged vessel to the
heart.
 Surgical Management
Intra Coronary Stent
□A diamond mesh
tubular device is placed
in the coronary artery
□Prevents re-stenosis
(after PTCA) by
providing skeletal
support
 Surgical Management
Intra Coronary
Atherectomy
□A blade tip catheter is
guided in a coronary
vessel to the site of
the plaque
□The plaque is cut,
shave, or pulverized
then
removed
 Surgical Management
Coronary Artery Bypass Graft
□ A graft is surgically attached
to the aorta and the other end
of the graft is attached to a
distal portion of a coronary
vessel.
□ By passes obstructive lesion
in the vessel and returns to
adequate blood flow to the
heart muscle supplied by the
artery.
 Self Management Education Guide To Decrease
the Anginal Attack and MI
□Manage Hypertension □Avoid extreme activities such
□Stop active and passive as sudden exertion, walking
smoking against the wind, extreme
temperature, high altitude,
□Avoid alcohol and stress emotionally stressful situations
□ Plan a regular exercise
under medical supervision □ Lose weight if overweight
□Healthy diet.
□ Adequate time to rest and
relaxation