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WRITTEN REPORT

IN

MEDICAL-SURGICAL NURSING

Disturbances in Blood Pumping Mechanism

Presented to

Prof. Joan Oyangoren

Pamantasan ng Lungsod ng Maynila

By:

Baraquiel, Patricia Elaine

Huilar, Faith Anne

Iguia, Shiena Mae

Racelis, Glomarie Alyssa

Saldo, Jan Robert

June 2011

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REVIEW OF ANATOMY & PHYSIOLOGY OF THE HEART AND

BLOOD VESSELS

The heart is a hollow, muscular organ about a size of a closed fist, located in the center of thethorax, where it occupies the space between the lungs (mediastinum) and rests on the diaphragm.

It weighs approximately 300g (10.6 oz); the weight and size of the heart are influenced by age,

gender, body weight, extent of physical exercise and conditioning, and heart disease. The Heart

spans the area from the 2nd to the 5th intercostal space. The heart pumps blood to the tissues,

supplying them with oxygen and other nutrients.

The heart is composed of three layers. The inner layer, endocardium, consists of endothelial

tissue and lines the outside of the heart and valves. The middle layer, myocardium, is made up

of muscle fibers and is responsible for the pumping action. The exterior layer is called the

epicardium.

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The heart is incased in a thin, fibrous sac called the pericardium, which is composed of 2 layers.

Adhering to the epicardium is the visceral pericardium. Enveloping the visceral pericardium is

the parietal pericardium, a tough fibrous tissue that attaches to the great vessels, diaphragm,

sternum, and vertebral column and supports the heart in the mediastinum. The space between

these 2 layers (pericardial space) is normally filled with about 20ml of fluid, which lubricates

the surface of the heart and reduces friction during systole.

As blood travels through the heart, it enters a total of four chambers and passes through four

valves. The two upper chambers, the right and left atria, are separated longitudinally by

the interatrial septum. The two lower chambers, the right and left ventricles, are the pumping

machines of the heart and are separated longitudinally by the interventricular septum. A valve

follows each chamber and prevents the blood from flowing backward into the chamber from

which the blood originated. Two prominent grooves are visible on the surface of the heart:

The coronary sulcus (artioventricular groove) marks the junction of the atria and

ventricles.

The anterior interventricular sulcus and posterior interventricular sulcus mark the

junction of the ventricles on the front and back of the heart, respectively.

The right atrium, located in the upper right side of the heart, and a small appendage, the

right auricle, act as a temporary storage chamber so that blood will be readily available for

the right ventricle. Deoxygenated blood from the systemic circulation enters the right

atrium through three veins, the superior vena cava, the inferior vena cava, and the coronary

sinus. During the interval when the ventricles are not contracting, blood passes down

through the right atrioventricular (AV) valve into the next chamber, the right ventricle. The

AV valve is also called the tricuspid valve because it consists of three flexible cusps

(flaps).

The right ventricle is the pumping chamber for the pulmonary circulation. The ventricle,

with walls thicker and more muscular than those of the atrium, contracts and pumps

deoxygenated blood through the three-cusped pulmonary semilunar valve and into a large

artery, the pulmonary trunk. The pulmonary trunk immediately divides into two pulmonary

arteries, which lead to the left and right lungs, respectively. The following events occur in

the right ventricle.

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When the right ventricle contract, the right AV valve closes and prevents

blood from moving back into the right atrium. Small tendon like cords, the chordae

tendineae, is attached to papillary muscles at the opposite, bottom side of the

ventricle. These cords limit the extent to which the AV valve can be forced closed,

preventing it from being pushed through and into the atrium.

When the right ventricle relaxes, the initial backflow of blood in the pulmonary

artery closes the pulmonary semilunar valve and prevents the return of blood to the

right ventricle.

The left atrium and its auricle appendage receive oxygenated blood from the lungs

though four pulmonary veins (two from each lung). The left atrium, like the right atrium, is

a holding chamber for blood in readiness for its flow into the left ventricle. When the

ventricles relax, blood leaves the left atrium and passes through the left AV valve into the

left ventricle. The left AV valve is also called the mitral or bicuspid valve, the only heart

valve with two cusps.

The left ventricle is the pumping chamber for the systemic circulation. Because a greater

blood pressure is required to pump blood through the much more extensive systemic

circulation than through the pulmonary circulation, the left ventricle is larger and its walls

are thicker than those of the right ventricle. When the left ventricle contracts, it pumps

oxygenated blood through the aortic semilunar valve, into a large artery, the aorta, and

throughout the body. The following events occur in the left ventricle, simultaneously and

analogously with those of the right ventricle.

When the left ventricle contract, the left AV valve closes and prevents blood

from moving back into the right atrium. As in the right AV valve, the chordae

tendineae prevent overextension of the left AV valve.

When the left ventricle relaxes, the initial backflow of blood in the aorta

closes the aortic semilunar valve and prevents the return of blood to the

left ventricle.

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The pathway of blood through the chambers and valves of the heart.

Two additional passageways are present in the fetal heart:

The foramen ovale is an opening across the interatrial septum. It allows blood to bypass

the right ventricle and the pulmonary circuit, while the nonfunctional fetal lungs are still

developing. The opening, which closes at birth, leaves a shallow depression called the fossa

ovalis in the adult heart.

The ductus arteriosus is a connection between the pulmonary trunk and the aorta. Blood

that enters the right ventricle is pumped out through the pulmonary trunk. Although some

blood enters the pulmonary arteries (to provide oxygen and nutrients to the fetal lungs),

most of the blood moves directly into the aorta through the ductus arteriosus.

The coronary circulation consists of blood vessels that supply oxygen and nutrients to the

tissues of the heart. Blood entering the chambers of the heart cannot provide this service

because the endocardium is too thick for effective diffusion (and only the left side of the heart

contains oxygenated blood). Instead, the following two arteries that arise from the aorta and

encircle the heart in the artioventricular groove provide this function:

The left coronary artery has the following two branches: The anterior interventricular

artery (left anterior descending, or LAD, artery) and the circumflex artery.

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The right coronary artery has the following two branches: The posterior

interventricular artery and the marginal artery.

Blood from the coronary circulation returns to the right atrium by way of an enlarged blood

vessel, the coronary sinus. Three veins, the great cardiac vein, the middle cardiac vein, and the

small cardiac vein, feed the coronary sinus.

Contractions of the heart occur in a rhythm, the cardiac cycle. And are regulated by impulses that

normally begin at the sinoatrial (SA) node, the hearts pacemaker. From there the impulses are

conducted throughout the heart. Impulses from the autonomic nervous system affect the SA node

and alter its firing rate to meet the bodys needs.

The cardiac cycle consists ofsystole, the period when the heart contracts and sends blood on its

outward journey, and diastole, the period when the heart relaxes and fills with blood. During

diastole the mitral and tricuspid valves are open, and the aortic and pulmonic valves are closed.

There are various kinds of blood vessels:

Arteries

Aorta (the largest artery, carries blood out of the heart)
http://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Artery

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Branches of the aorta, such as the carotid artery, the subclavian artery, the celiac

trunk, the mesenteric arteries, the renal artery and the iliac artery.

Arterioles

Capillaries (the smallest blood vessels)

Venules

Veins

Large collecting vessels, such as thesubclavian vein, the jugular vein, the renal

vein and the iliac vein.

Venae cavae (the 2 largest veins, carry blood into the heart)

They are roughly grouped as arterialand venous, determined by whether the blood in it is

flowing away from (arterial) ortoward(venous) the heart. The term "arterial blood" is

nevertheless used to indicate blood high in oxygen, although the pulmonary arterycarries

"venous blood" and blood flowing in thepulmonary vein is rich in oxygen. This is because they

are carrying the blood to and from the lungs, respectively, to be oxygenated.

Structure Functions

Arteries The walls (outer structure)

of arteries contain smooth

muscle fibre that contract

and relax under the

instructions of the

sympathetic nervous

system.

Transport blood away

from the heart;

Transport oxygenated

blood only (except in the

case of the pulmonary

artery).

Arterioles Arterioles are tiny branches

of arteries that lead to

capillaries. These are also

under the control of thesympathetic nervous

system, and constrict and

dilate, to regulate blood

flow.

Transport blood from

arteries to capillaries;

Arterioles are the main

regulators of blood flow

and pressure.
http://en.wikipedia.org/wiki/Carotid_arteryhttp://en.wikipedia.org/wiki/Subclavian_arteryhttp://en.wikipedia.org/wiki/Celiac_trunkhttp://en.wikipedia.org/wiki/Celiac_trunkhttp://en.wikipedia.org/wiki/Mesenteric_arteryhttp://en.wikipedia.org/wiki/Mesenteric_arteryhttp://en.wikipedia.org/wiki/Renal_arteryhttp://en.wikipedia.org/wiki/Iliac_arteryhttp://en.wikipedia.org/wiki/Arteriolehttp://en.wikipedia.org/wiki/Capillaryhttp://en.wikipedia.org/wiki/Venulehttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Subclavian_veinhttp://en.wikipedia.org/wiki/Subclavian_veinhttp://en.wikipedia.org/wiki/Jugular_veinhttp://en.wikipedia.org/wiki/Renal_veinhttp://en.wikipedia.org/wiki/Renal_veinhttp://en.wikipedia.org/wiki/Iliac_veinhttp://en.wikipedia.org/wiki/Venae_cavaehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_veinhttp://en.wikipedia.org/wiki/Pulmonary_veinhttp://en.wikipedia.org/wiki/Carotid_arteryhttp://en.wikipedia.org/wiki/Subclavian_arteryhttp://en.wikipedia.org/wiki/Celiac_trunkhttp://en.wikipedia.org/wiki/Celiac_trunkhttp://en.wikipedia.org/wiki/Mesenteric_arteryhttp://en.wikipedia.org/wiki/Renal_arteryhttp://en.wikipedia.org/wiki/Iliac_arteryhttp://en.wikipedia.org/wiki/Arteriolehttp://en.wikipedia.org/wiki/Capillaryhttp://en.wikipedia.org/wiki/Venulehttp://en.wikipedia.org/wiki/Veinhttp://en.wikipedia.org/wiki/Subclavian_veinhttp://en.wikipedia.org/wiki/Jugular_veinhttp://en.wikipedia.org/wiki/Renal_veinhttp://en.wikipedia.org/wiki/Renal_veinhttp://en.wikipedia.org/wiki/Iliac_veinhttp://en.wikipedia.org/wiki/Venae_cavaehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_vein

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Capillaries Capillaries are tiny

(extremely narrow) blood

vessels, of approximately 5-

20 micro-metres

(one micro-metre =

0.000001metre) diameter.

There are networks of

capillaries in most of the

organs and tissues of the

body. These capillaries are

supplied with blood by

arterioles and drained by

venules. Capillary walls are

only one cell thick (see

diagram), which permits

exchanges of material

between the contents of the

capillary and the

surrounding tissue.

Function is to supply

tissues with components

of, and carried by, the

blood, and also to

remove waste from the

surrounding cells ... as

opposed to simply

moving the blood around

the body (in the case of

other blood vessels);

Exchange of oxygen,

carbon dioxide, water,

salts, etc., between the

blood and the

surrounding body tissues.

Venules Venules are minute vessels

that drain blood from

capillaries and into veins.

Many venules unite to form

a vein.

Drains blood from

capillaries into veins, for

return to the heart

Veins The walls (outer structure)

of veins consist of three

layers of tissues that are

thinner and less elastic than

the corresponding layers of

arteries.

Veins include valves that

Transport blood towards

the heart;

Transport deoxygenatedblood only (except in the

case of the pulmonary

vein).

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aid the return of blood to

the heart by preventing

blood from flowing in the

reverse direction.

Arteries Veins

Transport blood away from the heart; Transport blood towards the heart;

Carry Oxygenated Blood

(except in the case of the Pulmonary

Artery);

Carry De-oxygenated Blood

(except in the case of the Pulmonary

Vein);

Have relatively narrow lumens (see

diagram above);

Have relatively wide lumens (see

diagram above);

Have relatively more muscle/elastictissue;

Have relatively less muscle/elastictissue;

Transports blood under higher pressure

(than veins);

Transports blood under lower pressure

(than arteries);

Do not have valves (except for the

semi-lunar valves of the pulmonary

artery and the aorta).

Have valves throughout the main

veins of the body. These are to

prevent blood flowing in the wrong

direction, as this could (in theory)

return waste materials to the tissues.The central opening of a blood vessel, the lumen, is surrounded by a wall consisting of three

layers:

The tunica intima is the inner layer facing the blood. It is composed of an

innermost layer of endothelium (simple squamous epithelium) surrounded by variable

amounts of connective tissues.

The tunica media, the middle layer, is composed of smooth muscle with variable

amounts of elastic fibers.

The tunica adventitia, the outer layer, is composed of connective tissue.

The cardiovascular system consists of three kinds of blood vessels that form a closed system of

passageways:

Arteries carry blood away from the heart. The three kinds of arteries are

categorized by size and function:

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Elastic arteries (conducting arteries) are the largest arteries and include the

aorta and other nearby branches. The tunica media of elastic arteries contains a

large amount of elastic connective tissue, which enables the artery to expand as

blood enters the lumen from the contracting heart. During relaxation of the heart,

the elastic wall of the artery recoils to its original position, forcing blood forward

and smoothing the jerky discharge of blood from the heart.

Muscular arteries (conducting arteries) branch from elastic arteries and

distribute blood the various body regions. Abundant smooth muscle in the thick

tunica media allows these arteries to regulate blood flow by vasoconstriction

(narrowing of the lumen) or vasodilation (widening of the lumen). Most named

arteries of the body are muscular arteries.

Arterioles are small, nearly microscopic, blood vessels that branch from

muscular arteries. Most arterioles have all three tunics present in their walls,

with considerable smooth muscle in the tunica media. The smallest arterioles

consist of endothelium surrounded by a single layer of smooth muscle.

Arterioles regulate the flow of blood into capillaries by vasoconstriction and

vasodilation.

Capillaries are microscopic blood vessels with extremely thin walls. Only the

tunica intima is present in these walls, and some walls consist exclusively of a single

layer of endothelium. Capillaries penetrate most body tissues with dense interweaving

networks called capillary beds. The thing walls of capillaries allow the diffusion of

oxygen and nutrients out of the capillaries, while allowing carbon dioxide and wastes

into the capillaries.

Metarterioles (precapillaries) are the blood vessels between arterioles and

venules. Although metarterioles pass through capillary beds with capillaries,

they are not true capillaries because metarterioles, like arterioles, have smooth

muscle present in the tunica media. The smooth muscle of a metarteriole allows

it to acts as a shunt to regulate blood flow into the true capillaries that branch

from it. The thoroughfare channel, the tail end of the metarteriole that connects

to the venule, lacks smooth muscle.

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True capillaries form the bulk of the capillary bed. They branch away

from a metarteriole at its arteriole end and return to merge with the metarteriole

at its venule end (thoroughfare channel).

Some true capillaries connect directly from an arteriole to a metarteriole or

venule. Although the walls of true capillaries lack muscle fibers, they possess a

ring of smooth muscle called a precapillary sphincter where they emerge from

the metarteriole. The precapillary sphincter regulates blood flow through the

capillary. There are three types of true capillaries:

Continuous capillaries have continuous, unbroken walls consisting of cells

that are connected by tight junctions. Most capillaries are of this type.

Fenestrated capillaries have continuous walls between endothelial cells,

but the cells have numerous pores (fenestrations) that increase their permeability.

These capillaries are found in the kidneys, lining the small intestine, and in other

areas where a high transfer rate of substances into or out of the capillary is

required.

Sinusoidal capillaries (sinusoids) have large gaps between endothelial

cells that permit the passage of blood cells. These capillaries are found in the

bone marrow, spleen, and liver.

Veins carry blood toward the heart. The three kinds of veins are listed here in the

order that they merge to form increasingly larger blood vessels:

Postcapillary venules, the smallest veins, form when capillaries merge as

they exit a capillary bed. Much like capillaries, they are very porous, but with

scattered smooth muscle fibers in the tunica media.

Venules form when postcapillary venules join. Although the walls of

larger venules contain all three layers, they are still porous enough to allow

white blood cells to pass.

Veins have walls with all three layers, but the tunica intima and tunica

media are much thinner than in similarly sized arteries. Few elastic or muscle

fibers are present. The wall consists of primarily of a well-developed tunica

adventitia. Many veins, especially those in the limbs, have valves, formed from

folds of the tunica intima that prevent the backflow of blood.

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Many regions of the body receive blood supplies from two or more arteries. The points where

these arteries merge are called arterial anastomoses. Arterial anastomoses allow tissues to receive

blood even after one of the arteries supplying blood has been blocked.

ASSESSMENT OF CLIENT WITH DISEASES OF THE

CARDIOVASCULAR SYSTEM

I. Assessment

Health history

Elicit a description of the clients present illness and chief complaints, including onset, course,

duration, location, and precipitating and alleviating factors. Cardinal signs and symptoms

indicating altered cardiovascular function include:

Pain over the lower sterna region and the upper abdomen characterized by heavy vicelike,

belt-squeezing pain that may radiate to the shoulders, neck, and down the arms. (Associated

symptoms may include electrocardiogram [ECG] changes and arrhythmias. This pain may

indicate myocardial ischemia)

Palpitations characterized by rapid irregular or pounding heart beat. (This symptoms may be

associated with arrhythmias or ischemia).

Intermittent claudication characterized by extremity pain with exercise (This may indicate

peripheral vascular disease).

Dyspnea characterized by difficult breathing or shortness of breath with activity (i.e. dyspnea

on exertion), in the supine position (i.e. orthopnea), or sudden onset at night (i.e paroxysmal

nocturnal dyspnea). (This is commonly associated with compromised cardiac function).

Fatigue with or without activity (This may be associated with decreased carbon dioxide).

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Syncope with or without dizziness (This can result from a sudden decrease in cardiac output)

Diaphoresis with associated clamminess and cyanosis (This reflects decreased cardiac output

and decreased peripheral perfusion).

Edema or weight gain greater than 3 lbs in 24 hours (This may indicated heart failure)

Explore the clients history for risk factors associated with cardiovascular disease

(atherosclerosis):

Positive family history for cardiovascular disease

Age (the incidence of cardiovascular disease increases after age 40)

Gender (mortality from cardiovascular disease is greater than men than in women; however,

this difference decreases after menopause)

Race (mortality is greater than nonwhites than whites)

Smoking (the risk of cardiovascular diseases is two to four times greater than cigarette

smokers than nonsmokers)

Hypertension, particularly elevated systolic pressure

Hyperlipidemia (the ratio of high-density lipoproteins [HDL] to low-density lipoproteins

[LDL] is the best predictor)

Obesity (contributes to the severity of other risk factors)

Sedentary lifestyle

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Diabetes (uncontrolled elevated blood glucose level increases risk)

Stress (may contribute to developing coronary artery disease)

Hormonal contraceptives

Physical Examination

Vital signs

Assess vital signs, particularly pulse rate, blood pressure, and respirations. Increased blood

pressure and pulse may indicate cardiovascular disease.

Inspection

Observe general appearance for signs of distress, anxiety, and altered level of consciousness.

Inspect the lips and buccal mucosa for central cyanosis, which reflects hypoxia.

Inspect the peripheral extremities for cyanosis and a capillary refill time of less than 3

seconds.

Assess jugular venous pressure and observe for venous distention.

Palpation

Palpate all peripheral pulses including carotid, brachial, radial, femoral, popliteal, dorsalis

pedia, and anterior tibial. Grade 0 (no pulse), 1+ (weak), 2+ (normal), 3+ (increased), 4+

(bounding)

Palpate the pericardium to locate the point of maximal impulse or the apical impulse.

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Auscultation

Systematically auscultate the heart for normal and abnormal sounds, murmurs, and friction

rub, covering four main areas: aortic, pulmonary, mitral and tricuspid.

Perform a respiratory assessment.

Findings pointing to cardiovascular problems may include cough (possibly reflecting

pulmonary congestion); crackles or wheezing (reflecting airway narrowing, atelactasis, or left

ventricular failure); hemoptysis (possibly pointing to acute pulmonary edema), Cheyne-stokes

respiration (possibly associated with severe left ventricular failure)

Perform abdominal assessment

Noting liver enlargement and ascites (indicating decreased venous return secondary to right

ventricular failure); bladder distention (pointing to decrease cardiac output); and bruits just above the

umbilicus (reflecting abdominal aortic obstruction or aneurysm).

LABORATORY AND DIAGNOSTIC PROCEDURES

A. Erythrocyte Sedimentation Rate (ESR)

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It is a measurement of the rate at which RBCs settle out of anticoagulated blood in an hour.

It is elevated in infectious heart disorders or myocardial infarction.

Normal range is as follows:

Males: 15-20 mm/hr.

Females: 20-30 mm/hr.

B. Enzyme Studies

Aspartate Aminotransferase (AST)

Formerly SGOT.

Elevated ievels indicate tissue necrosis. Normal range is 10 40 u/ml

Range in MI

Initial Elevation: 4-6 hrs

Peaks: 24-36 hrs

Returns to normal: 4-7 days

Creatinine Phosphokinase (CK-MB)

It is the most cardiac specific enzyme

It is an accurate indicator of myocardial damage

Normal range

Males: 50-325 mU/mL

Females: 50-250 mU/mL

Range with MI

Onset: 3-6 hrs

Peaks: 12-18 hrs


Lactic Dehydrogenase (LDH)

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Among the five LDH isoenzymes, LDH 1 is the most sensitive indicator of

myocardial damage.

Normal range is 100-225 mU/mL.

Range with Myocardial Infarction

Onset: 12 hrs

Peaks: 48 hrs


Hydroxybutyrate Dehydrogenase (HBD)

Elevation of HBD is always accompanied by elevation of LDH levels.

It is valuable in detecting silent MI. Normal range is 140-350 mU/mL.

Range with Myocardial Infarction

Onset: 10-12 hrs

Peaks: 48-72 hrs


Troponin

Best indicator for myocardial infarction (MI).

Negative result is normal.

Troponin I greater than 1.5 ng/ ml. indicates MI.

Troponin T greater than .1 to .2 ng/ ml. indicates MI.

C. Electrocardigraphy (ECG, EKG)

It is the graphical recording of the electrical activities of the heart.

It is the first diagnostic test done when cardiovascular disorder is suspected.

P wave. Depolarizatin of atria. Duration is .04 to .11 secs.

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PR interval. Time of impulse transmission from SA node to the AV node. Duration is .12-.20

secs.

ST segment. Represents the plateau phase of the action potencial.

T wave. Ventricular repolarization. Should not exceed 5 mm amplitude.

Common ECG Changes

Hypokalemia

U-wave

Depressed ST segment

Short T wave

Hyperkalemia

Prolonged QRS Complex

Elevated ST segment

Peaked T wave

Pathologic Q wave

D. SONIC STUDIES

Echocardiography

Uses ultrasound to assess cardiac structure and mobility

The client is to remain still, in supine position slightly turned to the left side, with HOB

elevated 15-20 degrees

Transesophageal Echocardiography (TEE)

Allows ultrasonic imaging of the cardiac structures and great vessels via esophagus.

Nursing Interventions before TEE

Ascertain history of esophageal surgery, malignancy or allergy to anesthetics or

sedatives.

NPO for 4-6 hours before the procedure.

Encourage to void before the procedure.

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Administer sedatives as ordered.

Keep suction and resuscitation equipment available.

Cardiac monitoring is done throughout the procedure.

Topical anesthetics to depress gag reflex.

Place the patient in chin to chest position to facilitate passage of endoscope.

Nursing interventions After TEE

NPO until gag reflex returns. To prevent aspiration.

Place patient in lateral or semi-fowlers position. To promote drainage from the

mouth and to enhance ventilation.

Encourage to cough.

Throat lozenges to relieve throat soreness.

Phonocardiography

Involves the use of electrically recorded amplified cardiac sounds.

It is helpful in assessing the exact timing and characteristics of murmurs and extra heart sounds.

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ANGINA PECTORISAngina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of

pain or pressure in the anterior chest. The cause is usually insufficient coronary blood flow. The

insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand

for oxygen in response to physical exertion or emotional stress. In other words, the need for

oxygen exceeds the supply.

Etiology and Risk Factors

Angina pectoris is associated with atherosclerotic lesions and is a manifestation of CHD.

Angina can be caused either by chronic or acute blockage of a coronary artery or by coronary

artery spasm. Chronic blockages are associated with fixed calcified (type Vb) or fibrotic (type

Vc) atherosclerotic lesions that occlude more than 75% of the vessel lumen.

When fixed blockages are present in the coronary arteries, conditions that increase

myocardial oxygen demand (e.g., physical exertion, emotion, exposure to cold) may precipitate

episodes of angina. Because the severely stenosed arteries cannot dilate to deliver enough

oxygen to meet the increased demand, ischemia results. In contrast, acute blockage of a coronary

artery results from rupture or disruption of vulnerable atherosclerotic plaques that cause platelet

aggregation and thrombus formation. Acute blockages are associated with unstable angina and

AMI.

Primary prevention is through the lifelong commitment to reducing the risk factors of

CHD. Secondary prevention is through recognition and early treatment of angina attacks.

Tertiary prevention consists of resolution of angina before myocardial damage occurs.

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Risk Factors of CHD

Nonmodifiable Risk Factors

Heredity (Including Race)

Children whose parents had heart disease are at higher risk for CHD. This increased risk is

related to genetic predisposition to hypertension, elevated lipid levels, diabetes, and obesity, all

of which increase the risk of CHD.

Increasing Age

Age influences both the risk and the severity of CHD. Symptomatic CHD appears predominantly

in people older than 40 years of age, and 4 of 5 people who die of CHD are age 65 years or older.

Angina and MI, however, can occur in a persons 30s and even in ones 20s. At older ages,

women who have heart attacks are twice as likely as men to die from the heart attack.

Gender

Coronary heart disease is the number one killer of both men and women. In 1999 mortality from

CHD was almost equal for men and women. Although men are at higher risk for heart attacks at

younger ages, the risk for women increases significantly at menopause, so that CHD rates in

women after menopause are two to three times that of women the same age before menopause.

Women who take oral contraceptives and who smoke or have high blood pressure are at greater

risk for CHD. Women with an early menopause are also at higher risk than women with a normal

or late menopause.

Modifiable Risk Factors

Smoking

Both active and passive smoking have been strongly implicated as a risk factor in the

development of CHD. Currently 23 % of men and 18 % of women are smokers. The prevalence

of smoking is higher in people with 11 years of education or less. Smoking triples the risk of

heart attack in women and doubles the risk of heart attack in men. It also doubles the risk of

dying from a heart attack and may quadruple the risk of sudden death. Nonsmokers who are

exposed to second-hand tobacco smoke at home or work may also have a higher death rate from

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CHD. The risk of CHD is decreased by 50% 1 year after smokers quit. The risk is further

reduced to that of non-smokers within 5 to 10 years after smoking cessation.

Tar, nicotine, and carbon monoxide contribute to the damage. Tar contains hydrocarbons and

other carcinogenic substances. Nicotine increases the release of epinephrine and norepinephrine,

which results in peripheral vasoconstriction, elevated blood pressure and heart rate, greater

oxygen consumption, and increased likelihood of dysrhythmias. In addition, nicotine activates

platelets and stimulates smooth muscle cell proliferation in the arterial walls. Carbon monoxide

reduces the amount of blood available to the intima of the vessel wall and increases the

permeability of the endothelium.

Hypertension

High blood pressure afflicts nearly 1 in 3 adults in the United States. It increases the workload of

the heart by increasing the afterload, enlarging and weakening the left ventricle over time. As

blood pressure increases, the risk of a serious cardiovascular event also escalates. When clients

have hypertension, obesity, tobacco use, high cholesterol levels, and diabetes, the risk of heart

attack increases significantly.

More men than women have hypertension until the age of 45, when it is more prevalent in

women. The prevalence of hypertension in African Africans is among the highest in the world.

In addition, African Americans have hypertension at an earlier age and it is more severe at any

age. Consequently, the rate of heart disease in African Americans is 1.5 times greater than that of

white Americans. Although hypertension cannot always be prevented, it should be treated to

lower the risk of CHD and premature death.

Elevated Serum Cholesterol Levels

The risk of CHD increases as blood cholesterol levels increase. This risk increases further when

other risk factors are present. In adults total cholesterol levels of 240 mg/dl are classified as

borderline high. At young and middle ages, men have higher cholesterol levels. In women

cholesterol levels contimue to increase up to about age 70. A high intake of cholesterol and

saturated fats is associated with the development of CHD.

Physical Inactivity

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In the United States about 25 % of adults report no leisure time physical activity, even though

regular aerobic exercise is important in preventing heart and blood vessel disease. There is an

inverse relationship between exercise and the risk of CHD. Those who exercise reduce their risk

of CHD because they have (1) higher HDL levels; (2) lower LDL cholesterol, triglyceride, and

blood glucose levels; (3) greater insulin sensitivity; (4) lower blood pressure; and (5) lower body

mass index. The AHA recommends 30 to 60 minutes of physical activity on most days of the

week.

Obesity

Obesity places an extra burden on the heart, requiring the muscle to work harder to pump enough

to support added tissue mass. In addition obesity increases the risk for CHD because it is often

associated with elevated serum cholesterol and triglyceride levels, high blood pressure, and

diabetes.

Distribution of body fat is also important. A waist measurement is a way to estimate fat. For men

a high-risk waistline measurement is more than 40 inches, and for women a high-risk waist

measurement is more than 35 inches. Body mass index (BMI) is another measure to estimate

body fat. A BMI from 18.5 to 24.9 is considered healthy. Extreme obesity, or a BMI greater than

40, is estimated to occur in 4.9 % of the population. People can lower their heart disease risk by

losing as little as 10 to 20 pounds. An alternating pattern of weight gain and weight loss,

however, is associated with an increased risk for CHD.

Diabetes

A fasting blood glucose level of more than 126 mg/dl or a routine blood glucose level of 180

mg/dl and glucosuria signals the presence of diabetes and represents an increased risk for CHD.

Clients with diabetes have a two-to four-fold higher prevalence, incidence, and mortality from all

forms of CHD.

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Pathophysiology

Three coronary arteries normally supply the myocardium with blood to meet its metabolic needs

during varying workloads. The right coronary artery supplies arterial blood to the right side of

the heart; the left coronary artery divides into the left circumflex artery, which feeds the posterior

heart muscle, and the anterior descending artery, which supplies the anterior myocardium,

especially the left ventricle. The coronary vessels are usually efficient and perfuse the

myocardium during diastole. When the heart needs more blood, the vessels dilate. As the vessels

become lined and eventually occluded with atherosclerotic plaques and thrombi, the vessels can

no longer dilate properly.

If the coronary vessels slowly become occluded, collateral vessels develop to provide the

myocardium with needed arterial blood. Collateral vessels are more common in clients with

long-term coronary artery disease.

Myocardial ischemia develops if the blood supply through the coronary vessels or oxygen

content of the blood is not adequate to meet metabolic demands. Disorders of the coronary

vessels, the circulation, or the blood may lead to deficits in supply.

Myocardial ischemia occurs when either supply or demand is altered. In some people, the

coronary arteries can supply adequate blood when the person is at rest; when the person attempts

activity or is taxed in some manner, however, angina develops. Myocardial cells become

ischemic within 10 seconds of coronary artery occlusion. After several minutes of ischemia, the

pumping function of the heart is reduced. The reduction in pumping deprives the ischemic cells

of needed oxygen and glucose. The cells convert to anaerobic metabolism, which leaves lactic

acid as a waste product. As lactic acid accumulates, pain develops. Angina pectoris is transient,

lasting for only 3 to 5 minutes. I f blood flow is restored, no permanent damage myocardial

damage occurs.

Clinical Manifestations

Characteristics of Angina

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Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or

arm. Angina pectoris produces transient paroxysmal attacks of substernal or precordial pain with

the following characteristics:

o Onset. Angina can develop quickly or slowly. Some clients ignore the chest pain,

thinking that it will go away or that it is indigestion. Ask what the client was doing when

the pain began.

o Location.Nearly 90 % of clients experience the pain as retrosternal or slightly to the left

of the sternum.

o Radiation. The pain usually radiates to the left shoulder and upper arm and may then

travel down the inner aspect of the left arm to the elbow, wrist, and fourth and fifth

fingers. The pain may also radiate to the right shoulder, neck, jaw, or epigastric region.

On occasion, the pain may be felt only in the area of radiation and not in the chest. Rarely

is the pain localized to any one single small area over the precordium.

o Duration. Angina usually lasts less than 5 minutes. However, attacks precipitated by a

heavy meal or extreme anger may last 15 to 20 minutes.

o

Sensation. Clients describe the pain of angina as squeezing, burning, pressing, choking,aching, or bursting pressure. The client often says the pain feels like gas, heartburn, or

indigestion. Clients do not describe angina pain as sharp or knife-like.

o Severity. The pain of angina is usually mild or moderate in severity. It is often called

discomfort, not pain. Rarely is the pain described as severe.

o Associated characteristics. Women, older adults, and clients with diabetes may have

atypical presentations of CHD that are equivalent to angina. In women, CHD may be

manifested as epigastric pain, dyspnea, or back pain, whereas older adults frequently

experience dyspnea, fatigue, syncope.

o Relieving and aggravating factors. Angina is aggravated by continued activity, and

most anginal attacks quickly subside with the administration of nitroglycerine and rest.

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The typical exertion-pain, rest-relief pattern is the major clue to the diagnosis of angina

pectoris.

o Treatment. Treatments to reduce the demand on the heart, such as rest, or treatments that

dilate the coronary arteries will commonly reduce the pain. The client may have used

nitroglycetrine and the client should be asked if the angina subsided.

Patterns of Angina

Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest

Unstable angina (also called preinfarction angina or crescendo angina): symptoms occur more

frequently and last longer than stable angina. The threshold for pain is lower, and pain may occur

at rest.

Intractable or refractory angina: severe incapacitating chest pain

Variant angina (also called Prinzmetals angina): pain at rest with reversible ST-segment

elevation; thought to be caused by coronary artery vasospasm

Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a

stress test), but patient reports no symptoms

Medical Management

Medical management of clients with angina pectoris focuses on three goals: (1) relieve the acute

pain, (2) restore coronary blood flow, and (3) prevent further attacks to reduce the risk of AMI.

The diagnosis of angina pectoris is confirmed by history and various tests. A complete history of

the pain and its pattern is collected to discriminate angina from other causes of chest pain.

Clients are encouraged to describe the pain in their own words. Record a complete analysis of

manifestations. This description provides a baseline that can be used in ongoing care.

Relieve acute pain and restore coronary blood flow

The primary goal of pharmacologic treatment of angina is to balance myocardial oxygen supply

and demand by altering the various components of the process, thereby increasing oxygen supply

to the myocardium or reducing myocardial oxygen demand. The components of myocardial

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oxygen consumption that can be pharmacologically treated are (1) blood pressure, (2) heart rate,

(3) contractility, and (4) left ventricular volume.

The major types of medications used to treat the acute attack in angina pectoris are as follows:

o Opiates analgesics are used to relieve or reduce acute pain. By reducing pain, the heart

rate often lowers and the need for oxygen by the myocardium also is reduced.

o Vasodilators help reduce acute pain and prevent further attacks by widening the diameter

of coronary arteries and increasing the supply of oxygen to the myocardium.

Nitroglycerin, a short acting nitrate, has been the treatment of choice against angina

attacks since 1867. Administered sublingually, per tablet, or via transligual spray,

nitroglycerin helps relieve or reduce angina pain within 1 to 2 minutes. Long-acting

nitrates, given orally or transdermally, help maintain coronary artery vasodilation,

thereby promoting greater flow of blood and oxygen to the heart muscle.

o Beta-adrenergic blockers help reduce the workload of the heart, decrease myocardial

oxygen demand, and may decrease the number of angina attacks.

o Calcium-channel blockers are used to dilate coronary arteries, thereby increasing

oxygen supply to the myocardium.

o Antiplatelet agents inhibit platelet aggregation and reduce coagulability, thus preventing

clot formation.

Prevent further attacks

Education and counselling regarding modification of risk factors are necessary to reduce the

progression of CHD and to prevent further attacks.

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ASSESSMENTNURSING

DIAGNOSISINFERENCE PLANNING INTERVENTION RATIONALE EVALUATI

Subjective:

Sumasakit

ang dibdibko, as

verbalized by

the patient

Objective:

(+)Diaphoresis(+)Facial

grimace

-Pain scale of8 out of 10

-v/s taken as

follows:

PR: 112 cpmBP:140/100

mmHg

Acute painrelated to

myocardial

ischemiaresulting

from

coronary

arteryocclusion

Occlusion ofcoronary

artery

Impaired

coronary

blood flow

Ischemia

Shift from

aerobic to

anaerobicmetabolism

Lactic

acidosis

Sensitization

to pain

After 20minutes of

effective

nursingintervention,

the client

will

experienceimproved

comfort in

the chest, asevidenced

by

-decrease in

the pain

rating-have

reducedanxiety

-the abilityto rest and

sleep

comfortably

> Establishrapport with

patient.

>Assess the

characteristics of

chest painincluding

location,

duration,intensity etc.

Have the client

rate pain on ascale of 0 to 10.

> Assessrespirations,

blood pressure,and heart rate

with each episodeof chest pain.

> Obtain a 12-lead ECG on

admission and

then each timechest pain recurs

for evidence of

further infarction

> Monitor the

response to drugtherapy. Notify

physician if pain

does not abate15-20 minutes

> Provide care in

a calm, efficientmanner that

reassures the

client andminimizes

anxiety. Staywith the client

until discomfort

> To gaincooperation and

trust from the

client.

> To ascertain

clients present

situation

> To determineany significant

changes

> To monitorfurther cardiac

damage and

location ofmyocardial

ischemia

> Pain control is

a prioritybecause it

indicates

ischemia

> External

stimuli mayworsen anxiety

and increase

cardiacworkload as

well as limitcoping abilities

> Goal met.

After 20

minutes ofeffective

nursing

intervention

the clientspain was les

as evidenced

by

-pain scale o

-respiratoryrate, cardiac

rate, and blo

pressurereturned to

prediscomfolevel

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ACUTE MYOCARDIAL INFARCTION

An AMI is also known as a heart attack, coronary occlusion, or simply a coronary, which is a

life-threatening condition characterized by the formation of localized necrotic areas within themyocardium. AMI usually follows the sudden occlusion of a coronary artery and the abrupt

cessation of blood and oxygen flow to the heart muscle. Because the heart muscle must function

continuously, blockage of blood to the muscle and the development of necrotic areas can be

lethal.

Etiology and Risk Factors

The most common cause of AMI is complete or nearly complete occlusion of a coronary artery,

usually precipitated by rupture of a vulnerable atherosclerotic plaque and subsequent thrombus

formation. Plaque rupture can be precipitated by both internal and external factors.

Internal factors include plaque characteristics, such as the size and consistency of the lipid core

and the thickness of the fibrous cap, as well as conditions to which it is exposed, such as

coagulation status and degree of arterial vasoconstriction.

External factors result from actions of the client or from external conditions that affect the

client. Strenuous physical activity and severe emotional stress, such as anger, increase

sympathetic nervous system responses, that may lead to plaque rupture. At the same time,

sympathetic nervous system responses increase myocardial oxygen demand. Scientists have

reported that external factors, such as exposure to cold and time of day, also affect plaque

rupture. Acute coronary events occur more frequently with exposure to cold and during the

morning hours. Researchers hypothesize that the sudden increases in sympathetic nervous system

responses associated with these factors may contribute to plaque rupture. The role of

inflammation in triggering plaque rupture is currently being studied.

Regardless of the cause, rupture of the atherosclerotic plaque results in (1) exposure of the

plaques lipid-rich core to flowing blood, (2) seepage of blood into the plaque, causing it to

expand, (3) triggering of thrombus formation, and (4) partial or complete occlusion of the

coronary artery.

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Unstable angina is associated with short-term partial occlusion of a coronary artery, whereas

AMI results from significant or complete occlusion of a coronary artery that lasts more than 1

hour. When blood flow ceases abruptly, the myocardial tissue supplied by the artery dies.

Coronary artery spasm can also cause acute occlusion. The risk factors that predispose a client to

a heart attack are the same as for all forms of CHD.

Pathophysiology

AMI can be considered the end-point of CHD. Unlike the temporary ischemia that occurs with

angina, prolonged unrelieved ischemia causes irreversible damage to the myocardium. Cardiac

cells can withstand ischemia for about 15 minutes before they die. Because the myocardium is

metabolically active, manifestations of ischemia can be seen within 8 to 10 seconds of decreased

blood flow. When the heart does not receive blood and oxygen, it converts to anaerobic

metabolism, creating less adenosine triphosphate (ATP) and more lactic acid as a by-product.

Myocardial cells are very sensitive to changes in pH and become less functional. Acidosis

causes the myocardium to become more vulnerable to the effects of the lysosomal enzymes

within the cell. Acidosis leads to conduction system disorders, and dysrhythmias develop.

Contractility is also reduced, decreasing the hearts ability to pump. As the myocardial cells

necrose, intracellular enzymes are introduced into the bloodstream, where they can be detected

by laboratory tests.

Cellular necrosis occurs in one layer of myocardial tissue in subendocardial, intramural, and

subepicardial infarctions. In a transmural infarction, cellular necrosis is present in all three layers

of myocardial tissue. The infarct site is called thezone of infarction and necrosis. Around it is a

zone of hypoxic injury, also called a penumbra. This zone can return to normal but may also

become necrotic if blood flow is not restored. The outermost zone is called the zone of ischemia;

damage to this area is irreversible.


The clinical manifestations associated with AMI result from ischemia of the heart muscle and the

decrease in function and acidosis associated with it. The major clinical manifestation of AMI is

chest pain which is similar to angina pectoris but more severe and unrelieved by nitroglycerine.

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The pain may radiate to the neck, jaw, shoulder, back, or left arm. The pain also may present

near the epigastrium, simulating indigestion. AMI may also be associated with less common

clinical manifestations, including the following:

o Atypical chest, stomach, back, or abdominal pain

o Nausea, or dizziness

o Shortness of breath

o Unexplained anxiety, weakness, or fatigue

o Palpitations, cold sweat, or paleness

Women experiencing AMI frequently present with one or more of the less common clinicalmanifestations.

Medical Management

Major goals of care for clients with AMI include the following:

o Initiating prompt care

o Determining the type of AMI (STEMI vs NSTEMI)

o Reducing pain

o Delivering successful treatment for the acute pain and reperfusion of the myocardium

o Preventing complications

o Preventing remodelling and heart failure

o Rehabilitating and educating the client and significant others

Treat the acute attack immediately

Clients with manifestations of AMI must receive immediate treatment. Delays may increase

damage to the heart and reduce the chance of survival. The goal for treatment of AMI is door to

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needle in less than 30 minutes, or specifically from onset of pain till thrombolytic therapy

within 30 minutes or percutaneous angioplasty within 1 hour.

Until EMS personnel arrive, keep the client quiet and calm. It is recommended that, if conscious,

a client chew an aspirin at the onset of manifestations, because mortality is reduced 23 % with

this action alone.

While waiting for EMS to arrive, elevate the clients head and loosen any tight clothing around

the neck. Once EMS workers arrive, the client is assessed and transported quickly to an

emergency department.

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ASSESSMENTNURSING


S/O:

-(+) Dyspnea

-(+) Crackles-(+) Cyanosis

- Impaired

capillary refill

-PaO2:60

mmHg

Impairedgas

exchange

related todecreased

cardiac

output as

evidencedby cyanosis

Occlusion ofcoronary

artery

Impairedcoronary

circulation

Decreased

cardiac output

Ischemia

Decreasedexchange of

O2 and CO2

Anaerobic

metabolism

Decreasedoxygenation

Cyanosis

After 1 hourof effective

nursing

intervention,the client

will

demonstrate

improvedgas

exchange, as

evidencedby

-absence ofdyspnea,

crackles

-absence ofcyanosis

-briskcapillary

refill- ABG

levels

withinnormal

limits

> Establishrapport with

patient.

>Administer

oxygen as

ordered; maintaincontinuous

oximetry

> Monitor ABGsas ordered

> Continue toassess clients

skin, capillary

refill, and thelevel of

consciousness

every 2-4 hoursas needed

> Assess

respiratory statusfor dyspnea and

crackles

> Provide care in

a calm, efficientmanner that

reassures the

client andminimizes

anxiety. Staywith the client

until discomfort

> To gaincooperation and

trust from the

client.

> To increase

amount of

oxygenavailable for

myocardial

uptake ;measures

peripheral

oxygensaturation

> To monitordata on

adequacy oftissue perfusion

andoxygenation

> Capillaryrefill greater

than 3 seconds

indicates poorperfusion and

hypoxia

> Dyspnea may

indicateinadequate

oxygenation

> External

stimuli mayworsen anxiety

and increase

cardiacworkload as

well as limitcoping abilities

> Goal met.

After 1 hour

effectivenursing

intervention

the clients

breath soundwere clear a

the ABG

values arewithin norm

limits

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ENDOCARDITIS

- A microbial infection of the endothelial surface of the heart.

- It is most common in older people, who are more likely to have degenerative or calcific

valve lesions, reduced immunologic response to infection, and the metabolic alterations

associated with aging.

Pathophysiology

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- The primary presenting symptoms of infective endocarditis are fever and heart murmur.

- Fever may be intermittent or absent, especially in patients who are receiving antibiotics or

corticosteroids, in those who are elderly, or those who have heart failure or renal failure.

- Heart murmur may be absent initially but develops in almost all patients. Murmurs that

worsen over time indicate progressive damage from vegetations or perforation of the valve

or the chordae tendineae.

- Clusters of petechiae may be found on the body.

- Small, painful nodules (Osler nodes) may be present in the pads of finger or toes.

- Irregular, red pr purple, painless, flat macules (Janeway lesions) may be present on the

palms, fingers, hands, soles, and toes.

- Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi

of the eyes.

- Splinter hemorrhages (ie, reddish-brown lines and streaks) may be seen under the

fingernails and toenails, and petechiae may appear in the conjunctiva and mucous

membranes.

- Cardiomegaly, heart failure , tachycardia, or splenomegaly may occur.

- CNS manifestations of infective endocarditis include headache; temporary or transient

cerebral ischemia; and strokes, which may be caused by emboli to the cerebral arteries.

- Valvular stenosis or regurgitation, myocardial damage, and mycotic (fungal) aneurysm are

potential cardiac complications.

- First-degree, second-degree, and third degree atrioventricular blocks may occur and are

often a sign of a valve ring abscess.

Assessment and Diagnostic Findings

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- Vague complaints of malaise, anorexia, weight loss, cough, and back and joint complain

may be mistaken for influenza.

- A definitive diagnosis is made when a microorganism is found in two separate blood

cultures, in a vegetation, or in an abscess.

- Three sets of blood cultures (with each set including oneaerobic and one anaerobic culture)

drawn over a 24-hour period (or every 30 minutes if the patients condition is unstable)

should be obtained before administration of any antimicrobial agents.

- Negative blood cultures do not definitely rule out infective endocarditis.

- Patients may have elevated WBC counts.

- In addition, patients may be anemic and have a positive rheumatoid and an elevated

erythrocyte sedimentation rate (ESR) or C-reactive protein.

- Micrscopic hematuria may be present on urinalysis.

- Doppler echocardiography may assist in the diagnosis by demonstrating a mass on the

valve, prosthetic valve, or supporting structures and by identifying vegetations, abscesses,

new prosthetic valve dehiscence, or new regurgitation.

Medical Management

- The objective of treatment is to eradicate the invading organism through adequate doses of

an appropriate antimicrobial agent.

- Antibiotic therapy is usually administered parenterally in a continuous IV infusion for 2 to

6 weeks.

- Parenteral therapy is adminstered in doses that produce a high serum concentration for a

significant period to ensure eradication of the dormant bacteria within the dense

vegetations.

- If there is insufficient bactericidal activity, increased dosages of the antibiotic are

prescribed or a different antibiotic is used.

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- Penicillin is usully the medication of choice.

- Blood cultures are taken periodically to monitor the effect pf therapy.

- In addition, the patients temperature is usually monitored at regular intervals because the

course of the fever is one indication of the effectiveness of treatment.

Surgical Management

- Surgical intervention is required if the infection does not respond to medications, the

patient has a prothetic heart valve endocarditis, has a vegetation larger that 1 cm, or

develops complications such as a septal perforation.

- Surgical interventions include valve debridement or excision, debridement of vegetations,

debridement and closure of an abscess, and closure of a fistula.

- Aortic or mitral valve debridement, excicion, or rreplacement is required in patient who:

Develop congestive heart failure despite adequate medical treatment.

Have more than one serious systemic embolic episode

Develop a periannular (heart valve), myocardial, or aortic abscess

Have uncontrolled infection, persistent or recurrent infection, or fungal endocarditis

- Most patients who have prosthetic valve endocarditis (ie, infected valve replacement)

require valve replacement.

Nursing Management

- The nurse monitors the patients temperature.

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- Heart sounds are assessed. A new or worsening heart murmur may indicate dehiscence of a

prosthetic valve, rupture of an abscess, or injury to valve leaflets or chordae tendineae.

- The nurse montors for signs and symptoms of systemic embolization, or, for patients with

right-sided heart endocarditis, for signs and symptoms of pulmonary infarction and

infiltrates.

- In addition, the nurse assesses signs and symptoms of organ damage such as stroke (ie,

cerebrovascular accident or brain attack), meningitis, heart failure, myocardial infarction,

glomerulonephritis, and splenomegaly.

- Patient care is directed toward management of infection.

-Long-term IV antimicrobial therapy is often necessary; therefore, many patients have

peripherally inserted central catheters or other long-term IV access.

- All invasive lines and wounds must be assessed daily for redness, tenderness, warmth,

swelling, drainage, or other signs of infection.

- The patient and family are instructed about activity restrictions, medications, and signs and

symptoms of infection.

-Patients with infective endocarditis arre at high risk for another episode of infective endo

carditis. The nurse emphasizes the antibiotic prophylaxis previously prescribed.

- If the patient undergone surgical treatment, the nurse provides postoperative care and

instructions.

- The nurse provides the patient and family with emotional support and facilitates coping

strategies during the prolonged course of the infection and antibiotc treatment.

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ASSESSMENTNURSING


Subjective:

Mainit yung

pakiramdamko, as

verbalized by

the patient.

Objective:

Temp: 38.2 C

WBC: 15 000

mg/dl

Fever

related to

increased

WBCproduction.

Fever

WBC of14.4 x 10 9/L,

suggestive of

infection

Production

of heat as

a bodydefense

mechanism

Increased production of

heat

Release of prostaglandins

After 1 hour

of effective

nursing

intervention,the client

will have

stable bodytemperature

as

manifestedby:

Temperature within

normalrange, 36.5to 37.5C.

Establish

rapport

Monitor V/S

q4 hours

Increase fluid

intake, with 1glass of water

q1 1/2 hours

Maintain

protection

against riskfactors (e.g.

Too cold and

too warm

environment)

Encouragepatient to wear

lose clothes

Perform TSB

Administerprescribedmedication.

To establish

good

communicati

on,cooperation

and gain

trust

For baseline

data

To prevent

dehydration

To prevent

from

unwantedeffect of

elevated

body

temperature

To facilitatebody

temperature

To facilitate

the heat of

the body

To facilitate

the present

condition.

GOAL W

MET.

After 1 houeffective

nursing

interventionthe cl

maintained

stable btemperature

manifested b

Temperatur

37.5C

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PERICARDITIS

- An inflammation of the pericardium, the membranous sac enveloping the heart.

- It may be a primary illness or it may develop during various medical and surgical disorders.

- It may be acute, subacute, or chronic. It is classified either as adhesive (constrictive),

because the layers of the pericardium become attached to each other and restrict ventricular

filling, or by what accumulates in the pericardial sac: serous (serum), purulent (pus),

calcific (calciumdeposits), febrinous (clotting protein), or sanguinous (blood).

CAUSES:

Idiopathic or nonspecific causes

Infection: usually viral; rarely bacterial; and mycotic

Disorders of connective tissue: systemic lupus erythematosus, rheumatic fever,

rheumatoid arthritis, polyarthritis, scleroderma

Hypersensitivity state: immune reactions, medication reaction, serum sickness

Disorders of adjacent structures: MI, dissecting aneurysm, pleural and pulmonary

disease (pneumonia)

Neoplastic disease: causes by metastasis from lung cancer or breast cancer, leukemia,

and pimary (mesothelioma) neoplams

Radiation theraphy of chesst and upper torso (peak occurance: 5-9 mos after treatment)

Trauma: chest injury, cardiac surgery, cardiac catheterization, implantation of

pacemaker or implantable cardiverter defibrillator (ICD)

Renal failure and uremia

TB

Pathophysiology

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- May be asymptomatic

- Most characteristic symptom is chest pain, although pain may be located beneath the

clavicle, in the neck, or in the left trapezius (scapula) region.

- The pain or discomfort usually remains fairly constant, but it may worsen with deep

inspiration and when lying down or turning. It may be relieved with a forward-leaning or

sitting position.

- Most characteristic sign of pericarditis is a creaky or scratch friction rub heard most clearly

at the left lower sternal border.

-Other signs may include a mild fever, increased WBC count, anemia, and an elevated ESR

or C-reactive protein level.

- Patients may have a productive or nonproductive cough.

- Dyspnea and other signs and symptoms of heart failure may occur as the result of

pericardial compression due to constrictive pericarditis or cardiac tamponade.


-Diagnosis is most often made on the basis of the history, signs, and symptoms.

- An echocardiogram may detect inflammation, pericardial effusion or tamponade, and heart

failure. It may help confirm the diagnosis and may be used to guide pericardiocentesis

(needle or catheter drainage of the pericardium).

- Computed tomography (CT) may be the best diagnostic tool for determining the size,

shape, and location of the pericardial effusions and may be used to guide

pericardiocentesis.

- MRI may assist with detection of inflammation and adhesions.

Medical Management

- The objective are to determine the cause, administer therapy foor treatment and symptom

relief, and detect sign and symptom of cardiac tamponade.

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- When the cardiac output is impaired, the patient is placed on bed rest until the fever, chest

pain, and friction rub have subsided.

- Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or

ibuprofen (Motrin) may be prescribed for pain relief during the acute phase. These agents

also hasten the reabsorption of fluid in oatients with rheumatic pericarditis. Indomethacin is

contraindicated because it may decrease the coronary blood flow.

- Corticosteroids (e.g. Prednisone) may be prescribed if the pericarditis is severe and the

patient does not respond to NSAIDs.

- Pericardiocentesis, a procedure in which some of the pericardial fluid is removed, is rarely

necessary. It may be performed to assist in the identification of the cause or relieve

symptoms, especially if there are signs and symptoms of heart failure or tamponade.

- Pericardial fluid is cultured if bacterial bacterial, tubercular, of fungal disease is suspected,

and a sample is sent for cytology if neoplastic disease is suspected.

- A pericardial window, a small opening made in the pericardium, may be oerfoemed to

allow continuous drainage inti the chest cavity.

- Surgical removal of the tough encasing pericardium (pericardiectomy) may be necessary to

release both the ventricles from the constrictive and restrictive inflammation and scarring.

Nursing Management

- Patients with acute pericarditis require pain management with analgesics, positioning, and

psychological support.

- Patients with chest pain often benefit from education and reassurance that the pain is not

due to a heart attack.

- To minimize complication, the nurse helps the patient with activity restrictions until the

pain and fever subsude. As the condition of the patient improve, the nurse encourages a

gradual increase of activity. However, if pain, fever, or friction rub reappear, activity

restrictions must be resumed.

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- The educates the patients and the family about a healthy lifestyle to enhance the patients

immune system.

- Nurse must be alert about cardic tamponade

- Nurse monitors the patient for heart failure.

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SSESSMENTNURSING

DIAGNOSISINFERENCE PLANNING INTERVENTION RATIONALE EVALUA

O:)

chycardia

)facialimace

) guarding

havior

Describes

pain at the

chest

From the

pain scale

10 is the

highest, the

patientverbalized

7.

Acute painrelated to

inflammation

ofpericardium.

Tissue trauma

Inflammation

Transportatio

n of

bradykininand histamine

at the site

Hyperemia

Redness

Heat

After 30minutes of

effective

nursingintervention,

the patient will

experience painalleviation as

evidenced by:

- Verbalization

of pain

alleviation- (-)

tachycardia- (-) facial

grimace

- (-) guarding

behavior

- Pain scale

score of 4-5

Establish

rapport

Monitor V/S

q4 hours

Assess pain

location,severity/inten

sity, duration,

and interval

Provide

divertional but non-

energy

exertingactivities

such as

watching tv,

music, etc.

Assist clientwith

positioning

Encourage period of

rests

Administer

prescribed

medication.

To establish

good

communicati

on,cooperation

and gain

trust

For baseline

data

To have an

intensiveassessment

of pain that

the patientfeels.

To divert

patients

attentiontowards pain

and promote

none

pharmacological pain

management.

To have less

energy

consumption

To prevent

fatigue

To facilitatethe present

condition.

GOAL MET.

After minutes

effective

nursinginterventi

the patien

experiencpain

alleviation

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PATHOPHYSIOLOGY OF ACQUIRED VALVULAR DISORDERS

Backward

Heart

Aoritcstenosis limitsforward flow of bloodfrom the left ventricle

Aortic regurgitationpermits blood flowback into the left

Increased bloodvolume and pressure

Left ventricularhypertrophy anddilation; blood from theleft atrium cannot get

Mitral stenosis limits

the forward flow ofblood into the leftventricleMitral regurgitationpermits blood flow back

Forward

Heart

Not enough blood flowsthrough the aorta forthe bodys needs(decreased cardiac

Angina pectoris,postural hypotension,

Increased blood volume and ressure in

Left atrium h ertro h and dilation

Increased blood volume and ressure in the

Pulmonary congestion (shortness of breath andpulmonary edema), increased pulmonary

Increased work for the ri ht ventricle, ri ht

Ri ht ventricular failure

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MITRAL REGURGITATION

Mitral regurgitation involves blood flowing back from the left ventricle into the left atriumduring systole.


Chronic mitral regurgitation is often asymptomatic, but acute mitral regurgitations (eg, that

resulting from a myocardial infarction) usually manifests as severe congestive heart failure.

Dysnpea, fatigue, and weakness are the most common symptoms. Palpitations, shortness of

breath on exertion, and cough from pulmonary congestion also occur.


A systolic murmur is heard as a high-pitched, blowing sound at the apex. The pulse may be

regular and of good volume, or it may be irregular as a result of extrasystolic beats or atrial

fibrillation. Echocardiography is used to diagnose and monitor the progression of mitral

regurgitation

Medical Management

Surgical intervention consists of mitral valve replacement or valvuloplasty (ie, surgical repair of

the heart valves).

MITRAL STENOSIS

Mitral stenosis is an obstruction of blood flowing from the left atrium into the left ventricle. It ismost often caused by rheumatic endocarditis, which progressively thickens the mitral valve

leaflets and chordae tendineae. The leaflets often fuse together. Eventually, the mitral valve

orifice narrows and progressively obstructs blood flow into the ventricle.

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The first symptom of mitral stenosis is often dyspnea on exertion as a result of pulmonary

venous hypertension. Patients with mitral stenosis are likely to show progressive fatigue as a

result of low cardiac output. They may expectorate blood (ie, hemoptysis), cough, and

experience repeated respiratory infections.


The pulse is weak and often irregular because of atrial fibrillation (caused by the strain on the

atrium). A low-pitched, rumbling diastolic murmur is heard at the apex. As a result of the

increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically

unstrable, and the patient experience atrial dysrhythmias. Echocardiography is used to diagnose

mitral stenosis. Electrocardiography (ECG) and cardiac catheterization with angiography are

used to determine the severity of the mitral stenosis.

Medical Management

Antibiotic prophylaxis therapy is instituted to prevent recurrence of infections. Patients with

mitral stenosis may benefit from anticoagulants to decrease the risk for developing atrial

thrombus. They may also require treatment for anemia.

Surgical intervention consists of valvuloplasty, usually commissurotomy to open or rupture the

fused commussures of the mitral valve. Percutaneous transluminal valvuloplasty or mitral valve

replacement may be performed.

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VALVULAR HEART DISORDERS: NURSING MANAGEMENT

Educate the patient regarding the disease:

about the diagnosis, the progressive nature, and treatment plan

to report any new symptoms or changes in symptoms to the health care provider

on emphasis of the need for prophylactic antibiotic therapy before any invasive procedure

that may introduce infectious agents to the patients bloodstream

infectious agent, usually a bacterium, is able to adhere to the diseased heart valve more

readily than to a normal valve. Once attached tot the valve, the infectious agent

multiplies, resulting in endocarditis and further damage tot eh valve

Assessment:

patients vital signs are taken, recorded, and compared with previous data for any

changes

heart and lung sounds are auscultated and peripheral ppulses palpated.

Assess patient for signs and symptoms of heart failure: fatigue, dyspnea with exertion, an

increase in coughing, hemoptysis, multiple respiratory infections, orthopnea, or

paroxysmal nocturnal dyspnea

assess for dysrhythmias by palpating the patients pulse for strength and rhythm (ie,

regular or irregular) and asks if the patient has experienced palpitations or felt forceful

heartbeats

assess for dizziness, syncope, increased weakness, or angina pectoris

Collaborative:

to develop a medication schedule and teaches about the name, dosage, actions, side

effects, and any drug-drug or drug-food interactions of the prescribed medications for

heart failure, dysrhythmias, angina pectoris, or other symptoms

teach the patient to weigh daily and report the gain of 2 pounds in 1 day or 5 pounds in 1

week to the health care provider

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assist the patient with planning activity and rest periods to achieve a lifestyle acceptable

to the patient

If the patient is to have surgical valve replacement or valvuloplasty, teaches the patient

about the procedure and anticipated recovery.

VALVULOPLASTY AND REPLACEMENT: NURSING MANAGEMENT

Patients who have had valvuloplasty or valve replacements area admitted to the intensive care

unit; care focuses on recovery from anesthesia and hemodynamic stability. Vital signs are

assessed every 5 to 15 minutes and as needed until the patient recovers from anesthesia or

sedation and then assessed every 2 to 4 hours and as needed. Intravenous medications to increase

or decrease blood pressure and to treat dysrhythmias or altered heart rates are administered and

their effects monitored. The intravenous medications are gradually decreased until they are no

longer required or the patient takes needed medication by another route (eg, oral, topical). Patient

assessments are conducted every 1 to 4 hours and as needed, with particular attention to

neurologic, respiratory, and cardiovascular systems.

After the patient has recovered from anesthesia and sedation, is hemodynamically stable withoutintravenous medications, and assessment values are stable, the patient is usually transferred to

a telemetry unit, typically within 24 to 72 hours after surgery. Nursing care continues as for most

postoperative patients, including wound care and patient teaching regarding diet, activity,

medications, and self-care.

The nurse educates the patient about long-term anticoagulant therapy, explaining the need for

frequent follow-up appointments and blood laboratory studies, and provides teaching about any

prescribed medication: the name of the medication, dosage, its actions, prescribed schedule,

potential side effects, and any drug-drug or drug-food interactions. Patients with a mechanical

valve prosthesis require education to prevent bacterial endocarditis with antibiotic prophylaxis,

which is prescribed before all dental and surgical interventions. Patients are discharged from the

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hospital in 3 to 7 days. Home care and office or clinic nurses reinforce all new information and

self-care instructions with the patient and family for 4 to 8 weeks after the procedure.

ms wrep ii

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