CARDIOVASCULAR SYSTEM

Claire R. Hatton, RN, MAN

Learning objectives:

1. Identify the components of cardiovascular system.

2. State the functions of the cardiovascular system3. Determine the different parts of the heart4. Explain the Cardiac cycle5. Analyze the electrophysiologic function of the

heart6. Apply the nursing process to clients with

cardiovascular disturbances.

FUNCTIONS1. Contractions of the heart generate blood

pressure in the arteries.2. The heart and blood vessels keep O2-rich

blood separate from O2-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 CELLS3. 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 WALLSLAYERS 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

• SEPTUM—separates 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 VESSELS1. Pulmonary circuit—powered by the right ventricle.

Pulmonary arteries—carry O2-poor blood to the lungs.

Pulmonary veins—carry O2-rich blood from lungs to the left atrium.

2. Systemic circuit—powered by the left ventricle. Aorta—carries O2-rich blood to all body

tissues. Vena cava—returns O2-poor blood to the

right atrium.

• Arteries—ALWAYS carry blood away from the heart and usually carry O2-rich blood.

* Aorta—largest artery.* Arterioles—smallest arteries (whether

constricted or dilated affects blood pressure).• Veins—ALWAYS returns blood to the heart and

usually carry O2-poor blood (blood reservoirs).

* Vena cava—largest veins in the body.* Venules—smallest 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 systole2. Isovolumetric ventricular contraction

• Ventricular volume remains constant as pressure increases rapidly

3. Ejection4. 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 ARTERIESCoronary Artery and its Branches

Portion of Myocardium

Supplied

Portion of Conduction System

SuppliedRightPosterior descendingRight margin (AV nodal)

Right atrium Inferior wall of

right ventricle ½ anterior surface

of left ventricle

AV node (90% of population)

SA node ( > 55%) Bundle of His

Posterior division of left bundle branch

LeftAnterior 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• Capillaries—smallest blood vessels

connecting arterioles to venules.* Arteriole end—exit of O2, water, and nutrients.

* Venus end—entrance of CO2, water, and wastes.

2.C )CORONARY CAPILLARIESThe 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 VEINSTravels alongside the arteriesBlood flow from the coronary arteries drains

into the cardiac veinsMost 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 VESSELSExtensive in the myocardiumImportant in protecting the myocardium

against injuriesWith 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 SYSTEMThese 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

AutomaticityConductivity

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 node—causes the ventricles to contract.

B. Extrinsic Control of Heartbeat—the autonomic nervous system and hormones can modify the rate of the heartbeat.

Electrical conduction system of the heart

1. Sinoatrial node2. Atrioventricular node3. Bundle of His4. Left bundle branch5. left posterior fascicle6. left-anterior fascicle7. Left ventricle8. Ventricular septum9. Right ventricle10. 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 complexP=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. Contractility4. Refractoriness5. 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 Ca2+

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 heart’s 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 potentialTwo 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 functiona. 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/mind. 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 functionCHRONOTROPIC 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 rateDROMOTROPIC 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 factors1. AgeChanges 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

PO2 rises & PCO2 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 breathc. Dyspnead. 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 historyi. 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

Cont’d : 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 murmursGrade 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 countb. Cardiac enzymes

- CK,CPK-MB- LDH- Cardiac Troponin (T & I)-myoglobin levels

c. Serum lipidsd. Serum electrolytes – Potassium - Calcium - Sodium Magnesiume. BUNf. 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 Functioning1. 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 Arrhythmiasa. 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 Arrhythmiasc. 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 patient’s 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 test’s purpose, performance and after-care.

Expected outcome: Client and family will demonstrate sufficient knowledge in

performing self- care after procedures.Interventions:• Assess client’s and family’s knowledge of the

diagnostic procedure.• Provide both verbal and written information

concerning th test’s 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 client’s 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