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CARDIOVASCULAR

SYSTEM
Claire R. Hatton, RN, MAN
Learning objectives:
1. Identify the components of cardiovascular
system.
2. State the functions of the cardiovascular system
3. Determine the different parts of the heart
4. Explain the Cardiac cycle
5. Analyze the electrophysiologic function of the
heart
6. Apply the nursing process to clients with
cardiovascular disturbances.


FUNCTIONS
1. Contractions of the heart generate blood
pressure in the arteries.
2. The heart and blood vessels keep O
2
-rich
blood separate from O
2
-poor blood.
3. One-way valves in the heart and veins
keep the blood flowing in one direction.
4. The heart and blood vessels regulate
blood flow according to the needs of the
body.
5. Exchange across capillary wall refreshes
blood and tissue fluid.

Heart structures can be described
with respect to 3 major categories of
function:
1. STRUCTURAL SUPPORT OF HEART TISSUES AND
CIRCULATION OF PULMONARY AND BLOOD
THROUGH THE HEART.
2. MAINTENANCE OF HEART CELLS
3. STIMULATION AND CONTROL OF HEART ACTION

1. STRUCTURAL SUPPORT OF HEART
TISSUES AND CIRCULATION OF
PULMONARY AND BLOOD THROUGH THE
HEART.

HEART WALL AND FIBROUS SKELETON
Which enclosed and support the heart
Divide it into 4 chambers
THE HEART VALVES
Direct flow through the chambers
THE GREAT VESSELS OF THE HEART
Conduct blood to and from the heart
2. MAINTENANCE OF HEART CELLS
VESSELS OF THE CORONARY
CIRCULATION
THE ARTERIES AND VEINS
SERVES THE METABOLIC NEEDS OF HE HEART CELLS
THE LYMPHTIC VESSELS OF THE HEART
3. STIMULATION AND CONTROL OF HEART
ACTION
NERVES
SPECIALIZED MUSCLE CELLS
Direct the rhythmic contraction and relaxation of
heart muscles
Propelling blood throughout the pulmonary and
systemic circulatory system
A.) HEART WALLS
LAYERS OF THE HEART
Epicardium (visceral
pericardium)
Essential layer of the heart
Coronary arteries are found in
this layer
Myocardium
Middle and thickest layer of
the heart (CBQ)
Responsible for contraction of
the heart
Endocardium
Innermost layer of the heart
Lines the inside of the
myocardium
Covers the heart valves
B.) CHAMBERS OF THE HEART
The heart also has four chambers- two atria and two
ventricles
The Left atrium and the right atrium
LOW PRESSURE CHAMBERS
SMALLER HAVE THINNER WALLS
The left ventricle and the right ventricle
HAVE THICKER MYOCARDIAL LAYER
CONSTITUTE MUCH OF THE BULK OF THE HEART
SEPTUMseparates right and left sides of the heart.

The heart chambers are guarded by valves
The atrio-ventricular valves- Tricuspid and bicuspid
The semi-lunar valves- Pulmonic and aortic valves

C.) The Valves of the Heart

Valve Type Name Location
Atrio-ventricular
(AV)
(LUB sound when
closing)
Tricuspid
Separates right atrium and
right ventricle
Mitral (Bicuspid)
Separates left atrium and
left ventricle
Semilunar
(DUB sound
when closing)
Pulmonic
Between right ventricle and
pulmonary artery
Aortic
Between left ventricle and
aorta
D.) Fibrous skeleton of the heart
Refers to the connective tissue in the heart
that separates the atria and the ventricles
fibrous rings of the heart
Surrounds the atrioventricular and arterial
orifices
Provide support and structure for the heart
anulus fibrosus dexter cordis
anulus fibrosus sinister cordis
E.) THE GREAT VESSELS
1. Pulmonary circuitpowered by the right ventricle.
Pulmonary arteriescarry O
2
-poor blood to
the lungs.
Pulmonary veinscarry O
2
-rich blood from
lungs to the left atrium.
2. Systemic circuitpowered by the left ventricle.
Aortacarries O
2
-rich blood to all body
tissues.
Vena cavareturns O
2
-poor blood to the
right atrium.

ArteriesALWAYS carry blood away from the
heart and usually carry O
2
-rich blood.
* Aortalargest artery.
* Arteriolessmallest arteries (whether
constricted or dilated affects blood pressure).
VeinsALWAYS returns blood to the heart and
usually carry O
2
-poor blood (blood reservoirs).
* Vena cavalargest veins in the body.
* Venulessmallest veins.

BLOOD FLOW DURING CARDIAC CYCLE
PUMPING ACTIONS:
CONTRACTION (systole)
RELAXATION (diastole)
Of the myocardial layer of the heart wall
1 CARDIAC CYCLE= Contraction + Relaxation
END OF 1 Cardiac cycle: expulsion of blood
from the ventricles
PHASES OF CARDIAC CYCLE
1. Atrial systole
2. Isovolumetric ventricular contraction
Ventricular volume remains constant as pressure
increases rapidly
3. Ejection
4. Isovulumetric ventricular relaxation
Both sets of valves are closed and ventricles are
relaxing
5. Passive ventricular filling
AV valves are forced open and the blood rushes in the
relaxing ventricles
2. STRUCTURES THAT SUPPORT
CARDIAC METABOLISM
CORONARY VESSELS
CORONARY ARTERIES
COLLATERAL ARTERIES
CORONARY CAPILLARIES
CORONARY VEINS AND LYMPHATIC VESSELS
2.A) CORONARY ARTERIES
Coronary Artery
and its Branches
Portion of
Myocardium
Supplied
Portion of
Conduction System
Supplied
Right
Posterior
descending
Right margin (AV
nodal)
Right atrium
Inferior wall of
right ventricle
anterior surface
of left ventricle
AV node (90% of
population)
SA node ( > 55%)
Bundle of His
Posterior division
of left bundle
branch
Left
Anterior
descending (LAD)
Circumflex (LCX)
Anterior surface of
left ventricle
Left atrium
Lateral wall of left
ventricle
Part of right
ventricle
AV node (10%)
SA node (45%)
All bundle
branches
2.B) COLLATERAL ARTERIES
Connections or anastomoses bet. 2 branches of the same or
opposite coronary arteries
Epicardium more collateral vessels than
endocardium
Gradual coronary occlusion--- results in growth of coronary
collaterals.
COLLATERAL CIRCULATION is responsible for supplying blood
and O2 to the myocardium that has been deprived
of O2 following severe narrowing and reduced
function of major coronary artery.
ANGIOGENESIS- the process of formation of new
collateral vessels
- stimulated by: a.) HYPOXIA
b.) VASCULAR ENDOTHELIAL
GROWTH FACTOR

2.C )CORONARY CAPILLARIES
Capillariessmallest blood vessels
connecting arterioles to venules.
* Arteriole endexit of O
2
, water, and nutrients.
* Venus endentrance of CO
2
, water, and wastes.

2.C )CORONARY CAPILLARIES
The heart has extensive capillary network
Blood arteries arterioles capillaries
exchange of O2 and other nutrients
At rest the heart extracts 70%- 80% of the O2
delivered to it
CORONARY BLOOD FLOW- is directly related
to the myocardial oxygen
consumption
- is affected by any alteration of the
cardiac muscle
2.D )CORONARY VEINS
Travels alongside the arteries
Blood flow from the coronary arteries drains
into the cardiac veins
Most of the venous drainage of the heart occurs
through veins in the visceral pericardium
The venous drainage of the heart
Cardiac veins
Coronary sinus


2.E) LYMPHATIC VESSELS
Extensive in the myocardium
Important in protecting the myocardium
against injuries
With cardiac contraction, this drain fluids to
lymph nodes in anterior mediastinum and
empty in the superior vena cava.

3. STRUCTURES THAT CONTROL HEART
ACTION
3.A) CARDIAC ACTION POTENTIALS
Transmission of electrical impulse through the
myocardium.
The continuous, rhythmic repetition of the cardiac
cycle depends on it.
The muscle fibers of the myocardium are uniquely
joined sot that action potentials pass from cell to
cell rapidly and efficiently.
3.B) CONDUCTION SYSTEM
These are specialized cells contained in the
myocardium that enable it to generate and
transmit action potentials without stimulation
from the nervous system.
Myocardial Cell Types
Kinds of
Cardiac Cells
Where Found Primary
Function
Primary
Property
Myocardial cells Myocardium Contraction and
Relaxation
Contractility
Specialized
cells of the
electrical
conduction
system

Electrical
conduction
system
Generation and
conduction of
electrical impulses
Automaticity
Conductivity
The CONDUCTING SYSTEM OF THE
HEART Consists of the:
SA node- the pacemaker
AV node- slowest conduction
Bundle of His branches into the Right and the
Left bundle branch
Purkinje fibers- fastest conduction
A. Intrinsic Conduction System:
* SA node (pacemaker)initiates the heartbeat
and causes the atria to contract.
* AV nodecauses the ventricles to contract.
B. Extrinsic Control of Heartbeatthe autonomic
nervous system and hormones can modify the
rate of the heartbeat.


Electrical conduction system of the
heart
1. Sinoatrial node
2. Atrioventricular node
3. Bundle of His
4. Left bundle branch
5. left posterior fascicle
6. left-anterior fascicle
7. Left ventricle
8. Ventricular septum
9. Right ventricle
10. Right bundle branch


This electrical activity is recorded by the
Electrocardiogram (ECG)
a. P wave results from
depolarization of the atrial
myocardium
b. QRS complex results from
depolarization of the ventricles
c. T wave represents
repolarization of the ventricles
d. PR interval the time
between the beginning of the P
wave and the beginning of the
QRS complex

















P=P wave, PR=PR interval,
QRS=QRS complex, QT=QT
interval, ST=ST segment, T=T
wave

Electrophysiologic properties of the
heart

1. Excitability
2. Automaticity (rhythmicity)
3. Contractility
4. Refractoriness
5. Conductivity

Electrophysiologic system
1. Excitability is the ability of cardiac muscle cells
to depolarize in response to a stimulus
excitability is influenced by hormones,
electrolytes, nutrition, oxygen supply,
medications, infection & autonomic nerve
activity.
2. Automacity (Rhythmicity) ability of cardiac
pacemaker cells to initiate an impulse
spontaneously & repetitively, without external
neurohormonal control.
- The sinoatrial (SA) node pacemaker cells have
the highest rate of automacity of all cardiac cells.


3.Contractility

Muscle contraction is initiated through action potential
Through the release of Ca
2+

through the T tubules of the
cell membranes
Intracellular calcium diffuses to
myofibrils & binds with troponin

Actin filaments becomes activated &
myosin filaments are attracted to the active actin sites

Contraction then occurs by power stroke repetition

Free calcium ions are pumped back into
sarcoplasmic reticulum after contraction

muscle relaxation begins


4. Refractoriness is the hearts ability to respond
to a new stimulus while still in a state of
depolarization from an earlier stimulus.
- it develops when sodium channels of the
cardiac cell membrane become inactivated &
unexcitable during an action potential
Two periods of Refractoriness
a. Absolute Refractory period occurs during
depolarization & the first part of repolarization. During
this period cardiac cells do not respond to any stimuli.
b. Relative refractory period occurs in the final stages
of repolarization; refractoriness diminishes & a
stronger-than-normal stimulus can excite the heart
muscle to contract.
5. Conductivity is the ability of heart muscle fibers
to propagate electrical impulses along & across
cell membranes.

Regulation of heart function

a. Cardiac output
- is the volume of blood pumped by either ventricle of the heart
each minute.
- can be calculated by multiplying the stroke volume times the
heart rate.
b. Stroke Volume
- is the volume of blood pumped per ventricle each time the
heart contracts
c. Heart rate
- the number of times the heart contracts each minute.
CO (mL/min) = SV (mL/beat) x HR (beats/min
d. Preload
- is the degree to which muscle fibers in the ventricles are
stretched at the end of the relaxation period.
- Frank-Starling law of the heart
e. Afterload
- is the resistance against which the heart must pump to eject
the blood into the circulation.

When the Cardiac Output is multiplied by the Total
Peripheral Resistance, it becomes the BLOOD
PRESSURE
Blood pressure = Cardiac output X Peripheral resistance
Blood pressure
Control is neural (central and peripheral) and hormonal
Baroreceptors in the carotid and aorta
Hormones - ADH, Adrenergic hormones, Aldosterone
and ANF

Terminologies in regulation of cardiac
function
CHRONOTROPIC
EFFECT
- Refers to a change in heart rate
- A positive chronotropic effect refers to
an increase in heart rate
- A negative chronotropic effect refers to a
decrease in heart rate
DROMOTROPIC
EFFECT
- Refers to a change in the speed of
conduction through the AV junction
- A positive dromotropic effect results in
an increase in AV conduction velocity
- A negative dromotropic effect results in
a decrease in AV conduction velocity
INOTROPIC
EFFECT
- Refers to a change in myocardial
contractility
- A postive inotropic effect results in an
increase in myocardial contractility
- A negative inotropic effect results in a
decrease in myocardial contractility

Factors affecting Oxygenation

a. Non-modifiable risk factors
1. Age
Changes of aging affect the Respiratory system and
Cardiovascular system:
- Chest wall and airways become more rigid and less
elastic
- Cough reflex and cilia action are decreased.
- dilation of cardiac chambers and lessening of
contractility
2. Gender
- Estrogen has a protective effect in women, slowing the
progress of atherosclerosis and reducing the risk of
cardiovascular disease.
3. Heredity
-CAD, asthma
Factors affecting Oxygenation

b. Modifiable risk factors
1. Environment
- Exposure to air pollution, high altitude, heat, cold
2. Lifestyle
- diet, exercise, vices
3. Stress
- some people may hyperventilate in response to stress. Arterial
PO
2
rises & PCO
2
falls & the person may experience light-headedness,
numbness & tingling of the fingers, toes, and around the mouth.
4. Health Status

5. Medications
- a variety of medication can decrease the rate & depth of respiration


NURSING PROCESS
Assessment:

1. History (Comprehensive Health History)
Nursing history for Cardiac function
a.Chest pain common symptom
Characteristics strange feeling as indigestion, dull heavy
pressure, burning, crushing, constricting, aching, stabbing
or a tightness
Location substernal pain, localized or diffuse, may
radiate to the jaw, teeth, neck, arms, shoulders, elbows or
the back
Duration note the time the pain begins and ends
Severity
Aggravating factors
Associated symptoms
Alleviating factors
Differential Diagnosis of Episodic Chest
Pain Resembling Angina Pectoris
b.Shortness of breath
c. Dyspnea
d. Fatigue easy fatigability on mild exertion is a
frequent problem for clients experiencing cardiac
disease.
e. Palpitations sensation of rapid heart beats,
skipping, irregularity, thumping, or pounding and
may be accompanied by anxiousness.
f. Syncope momentary loss of consciousness
resulting from a reduction in cerebral blood flow.
g. Weight gain a sensitive indicator of water and
sodium retention
h. Past health history
i. Cardiac risk factors

2. Physical examination
(Cardiovascular status)

- Take note of:
Rate and rhythm of heart rate
Signs of hypoxia
Level of consciousness
Edema
V/S, determine pulse pressure
Assess pressence of orthostatic hypotension
hypoxemia (cyanosis in conjunctiva, skin
discoloration)
vasoconstriction (cyanosis of extremities, nail
beds)
clubbing
Contd : PE
- Percussion:
Change in density of lungs and surrounding tissues
- Palpation
Position of the PMI
- Ausculatation
Abnormal heart sounds: (murmurs, Pericardial
friction rub, murmurs, gallops, thrills, bruits)


Grading of cardiac murmurs
Grade Description
I Faintest audible; can be heard only with special
effort
II Faint, but easily audible
III Moderately loud
IV Loud; associated with a thrill
V Very loud; associated with a thrill; may be heard
with a stethoscope off chest
VI Maximum loudness; associated with a thrill; heard
without a stethoscope
Diagnostic Evaluation

Laboratory Tests
a. Complete blood count
b. Cardiac enzymes
- CK,CPK-MB
- LDH
- Cardiac Troponin (T & I)
-myoglobin levels
c. Serum lipids
d. Serum electrolytes Potassium -
Calcium
- Sodium Magnesium
e. BUN
f. Blood Glucose level


Radiology and Imaging
Chest x-ray
doppler ultrasound
Myocardial imaging
Stess echocardiography
Phlebography
Cardiac MRI
Treadmill stress testing
Plethysmography(PVR) pulse volume recording
Digital subtraction angiography

Other diagnostic studies

Electrocardiogram
Electrophysiology studies
Cardiac catherization
Hemodynamic monitoring
Heart rate measurement
Intracranial pressure
Cardiac output
Central venous pressure
Pulmonary artery pressure
Pulmonary artery wedge pressure

Alterations in Cardiopulmonary
Functioning

1. Disturbances in conduction
- caused by interruption in normal conduction
process
- accompanied by alterations in myocardial tissues,
automaticity, regularity, and excitability which
can result in hemodynamic alterations affecting
the force of contraction and overall cardiac
output.

Types of Arrhythmias
a. Sinus Tachycardia
- Heart rate 100-180bpm, normal rhythm, normal
P wave, normal QRS complex
- caused by elevated body temp., excessive
sympathetic stimulation, exercise and toxic
conditions.
b. Sinus bradycardia
- Heart rate less than 60bpm, normal P wave,
normal QRS complex, normal PR interval
- Maybe normal response to sleep on a well-
conditioned athlete, excessive vagus nerve
stimulation, nonfunctional SA node, and
pharmacological agents

Types of Arrhythmias

c. Paroxysmal Supravenricular tachycardia (PSVT)/ Paroxsmal
Atrial Tachycardia
- Sudden, rapid onset of tachycardia with the stimulus originating above AV
node
- regular rhythm, rate is 150-250bpm, P wave is uniform, PR interval is
difficult to measure
- caused by emotional stress, caffeine, tobacco, alcohol, COPD, digoxin
toxicity
d. Premature Ventricular contraction
- Prolonged QRS complex, exaggerated voltage because only one ventricle
may depolarize, inverted T wave
- commonly associated with M.I., hypocalcemia
e. Ventricular Tachycardia
- rhythm maybe regular or irregular, rate is 100-200bpm, P wave absent,
QRS complex wide and bizarre
- caused by M.I., Cardiomyopathy, MV prolapse, Heart failure



Alterations in Cardiopulmonary
Functioning
2. Altered Cardiac output
- caused by atherosclerosis, blood clot, hemorrhage
- may result to failure of the myocardial pump
Cardiomyopathy MI Heart failure

3. Altered Breathing Patterns
- Breathing patterns refer to the rate, volume,
rhythm and relative ease or effort of respiration

Alterations in Cardiopulmonary
Functioning
4. Hypoxia
- insufficient oxygen in the body
Factors:
Decreased hemoglobin
Diminished concentration of inspired O2 which may
occur with high altitudes
Inability of the tissues to extract O2 from the blood as
with cyanide poisoning
Decreased diffusion of oxygen from alveoli into the
arterial blood
Poor tissue perfusion with O2 blood as with shock
Impaired ventilation as with multiple rib fracture or
chest trauma

Clinical signs of Hypoxia

Early signs Late signs
- Increased PR - Decreased PR
- Headache -Dyspnea
- Apathy
- Slight increased in SBP -Decreased SBP
- Oliguria -Clubbing of toes,
fingers

DIAGNOSIS, PLANNING,
INTERVENTIONS

ANXIETY related to insecurity.
Expected outcome: Anxiety will be reduced to a
tolerable level.
Interventions:
Greet he client by name and introduce personnel
involved in patients care.
Promote a relaxed environment.
Orient client to surroundings.
Inform the client when tests will begin and how long will
it take.
Keep client informed of unexpected delays.
Remain in view of the client or establish some means of
contact for assistance such as signal light.

DEFICIENT KNOWLEDGE related to the tests purpose,
performance and after-care.
Expected outcome: Client and family will demonstrate
sufficient knowledge in performing
self- care after procedures.
Interventions:
Assess clients and familys knowledge of the
diagnostic procedure.
Provide both verbal and written information
concerning th tests purpose, procedure, and after-
care.
Use language that the client can easily understand.
Ask client, family or both to paraphrase information.

PAIN and ACTIVITY INTOLERANCE related to ischemia.
Expected outcomes: 1. Pain will be relieved or controlled
within a tolerable level during the
diagnostic procedure.
2.Activity will be limited to that which
avoids dyspnea or tachycardia.
Interventions:
Assess pain level frequently before, during, and after the
diagnostic procedure.
Allow for rest periods.
Stop the procedure, assess vital signs, give short-acting
prescribed vasodilator such as nitroglycerine and
administer oxygen if chest pain occurs.
Notify the physician if rest, oxygen, or prescribed
medications d not provide relief.

RISK FOR INJURY related to untoward reactions
during or after diagnostic Tests.
Expected outcome: The clients condition will
remain stable during and after
diagnostic tests.
Interventions:
Assess for dyspnea, hypotension or hypertension,
cardiac dysrhythmias, mental changes, pain or
discomfort, and cyanosis.
Implement nursing measures to stabilize the client
such as ensuring a patent IV access and
administering oxygen and prescribe medications.
Collaborate with the physician to restore client to
a stable condition.
EVALUATION OF EXPECTED
OUTCOMES:

The client is relaxed and feels secure.
The test is performed uneventfully or the
client is stabilized when complications are
managed successfully.
The client and family have an accurate
understanding of the diagnostic testing
process and discharge instructions.

TREATMENT MODALITIES:

Cardiac Pacing
Defibrillation and Cardioversion
Implantable cardioverter defibrillator
Pericardiocentecis
Percutaneous coronary intervention
Intraortic Balloon Pump Counterpulsation
Heart surgery