Nursing MS (Cardio)

8/14/2019 Nursing MS (Cardio)

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Table of contents:

Objectives..1Methods.1

Anatomy and Physiology..2

History and Assessment5Dysrhythmias and Conduction problems..6

Coronary Vascular Disease...11

Structural, Infectious and Inflammatory Disorders..15Acquired Valvular Disorders

Mitral valve prolapse

Mitral valve regurgitation

Mitral valve stenosisAortic regurgitation

Aortic stenosis

Cardiomyopathies

Dilated CardiomyopathyHypertrophic Cardiomyopathy

Restrictive CardiomyopathyComplications from Cardiac Diseases..21

Heart failure

Cardiogenic Shock

Hypertension23References... 26


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Objectives:

The general objective of the module is to discuss the cardiovascular system anddisorders to the students.

Specifically, after being done with the module the students will be able to:

1. Discuss various cardiac disorders and their pathophysiology.

2. Enumerate various symptoms specific for each disorder.

3. Give the management options, medical and non-medical treatment of choice.4. Formulate various nursing diagnoses specific for each disease and patient.

5. Create appropriate nursing interventions for each priority cardiac problems

identified, encountered or will be encountered in the future.

Methods:

This lecture module is intended to guide the discussion of the subject andfacilitate the learning experience of the students. The lecturers will facilitate, expound on

some topics and clarify unresolved issues and questions.Evaluation of the effectiveness of teaching will be measured through the students

participation, quizzes, mastery test and/or examination.


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CARDIOVASCULAR SYSTEM

by

Ruby Ruth Roces

I. Anatomy and physiology reviewThe heart is a hollow, muscular organ that lies within the pericardium in the

middle mediastinum. It is pyramidal in shape, with the apex directed downward,

forward and to the left, usually lying in the 5 th intercostals space left mid-clavicular line. It is divided into four chambers by an vertical septa. It is

composed of 3 layers; the outer epicardium, middle myocardium and inner

endocardium.

The 4 chamber of the heart are the right atium, right ventricle, left atrium andleft ventricle. The right side of the heart receives deoxygenated blood from the

peripheral organs and distributes it to the lungs via pulmonary arteries for

oxygenation. The left side of the heart receives oxygenated blood from the lungs

through the pulmonary veins and distributes it to the peripheral organs through theaorta.

There are 4 valves in the heart which permits blood flow in 1 direction. Thesevalves can be classified into atrioventricular and semilunar valves. There are 2 AV

valves; the tricuspid so named because of it has 3 cusps, divides the Right atrium

from the Right ventricle. The bicuspid or mitral valve on the other hand divides

the left atrium from the left ventricle. The semilunar valves- the pulmonic andaortic valves are named according to the vessels theyre located in.

The blood supply of the heart is given by the right and left main coronary

arteries.


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The peripheral vascular system


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Conduction systemSA node--AV node--Left and Right Bundle of His--Purkinje fibers


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Cardiac Cycle

Cardiac Output- is the amount of blood pumped by each ventricle during a given

period.

Stroke volume- is the amount of blood ejected per heartbeat.

Control of HR

Cardiac output is responsive to changes in metabolic demands of thetissues. Changes in the heart rate are accomplished by reflex controls mediated by

autonomic nervous system. The parasympathetic slows the heart rate, the

sympathetic speeds it up. The heart rate is also influenced by the central nervoussystem and baroreceptor activity.


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I. History and PE

1. HistoryGeneral data

- age and sex

History of present Illness- symptoms of cardiovascular disease

- patients functional capacity

- history of febrile illness- pregnancy

Past Medical history

- history of systemic diseases such as hypertension, DM, Dyslipidemia,

cerebrovascular disease, Peripheral vascular disease, Thyroid diseases, Bronchialasthma or Chronic obstructive lung disease

- history of allergies and previous and present medications

Family history (up to 1st degree relative)

-Hypertension, ischemic heart disease, DM, dyslipidemiaPersonal and social history

- cigarette smoking( more than 10 sticks/day is a risk factor)- alcohol intake( approx 2 beers/day allowed)

- illicit drug use

- obesity

- athletic history(lack of exercise)- dietary intake( Salt and fat)

- Type A personality( workaholic and obsessive compulsive type)

2. PE- regional examinations

- JVP( best seen at 30-45 degree angle. Normal value is 4-8 cms)

- Arterial pulse- Examination of precordium

- Apex beat palpation

- Heart sounds


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II. Dysrhythmia and Conduction Problems

- These are disorders of the formation or conduction of electrical impulses withinthe heart which can cause disturbances in the heart rate, heart rhythm or both.

A.ECG Interpretation:

Six Components (mnemonic)

R- RateR- Rhythm

A- Axis

H-HypertrophyI- ischemia and Infarction


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M- misc. findings

1. Rate

Formula:HR= 1500________________________________

No. of small Squares between 1 R-R Interval

300_______________________________

No. of big squares between 1 R-R interval

Mnemonic

HR No.of big squares between R-R interval

300 1

150 2100 3

75 4

60 5

50 6

Normal rate = 60-100Bradycardia = < 60

Tachycardia = > 100

3. Rhythm

Identify the P wave- sinus P

Check relation of P to QRS complex

-should be before QRS (normal)-if buried before or after QRS (SVT, complete heart block)

Check PR interval (normal- 0.12-0.02 secs.)-Short PR (WPW syndrome)-Prolonged PR (1st or2nd degree AV blocks)

Check QRS duration (normal-


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- - Far right or left

5. Hypertrophy

a) LVH- S wave in V1 + R wave in V5 or V6 > 35mm (commonly used)

b) RVH- Right axis deviation or + 110 degrees or more, with any of the following:

Lead V1: R wave > S wave

Deep S wave in leads V5 and V6

ST depression and T wave inversion in V1-V3

c) LAE- Any of the following:

In lead V1: wide terminal component of P wave which is 1mm wide (0.04 sec)

And 1mm deepIn any lead: P wave wider than 0.12 sec (> 3 small squares) or with a 1 mm

Notch in the middle

d) RAE- Any of the following:

In lead V1: tall initial component of P wave which is 2mm wide (0.08 sec)

And 2mm deep

In any lead: P wave 2.5 mm talle) Biventricular hypertrophy

- Any of the following:

The ECG meets one or more of the diagnostic criteria for isolated left and rightventricular hypertrophy

The precordial leads show signs of left ventricular hypertrophy, but the QRS axis

In the frontal plane is greater than + 90 degrees (RAD).

f) Biatrial Enlargement- Any of the following:

In lead V1, the presence of a large diphasic P wave with initial positivecomponent 2 mm tall (RAE) and the terminal negative component

1 mm deep and 0.04 second in duration (LAE).

In any lead, an increase in both the amplitude which is 2.5 mm or greater (RAE)

and duration of 0.12 second or more of the P wave (LAE).

6. Ischemia and Infarction

a) IschemiaAt least 1 mm ST-segment depression

Symmetrically or deeply inverted T waves

Abnormally tall T wavesNormalization of abnormal T waves

Prolongation of the QT interval in addition to the above

Others: arrhythmias, bundle branch blocks, AV blocks, or electrical alternans

b) Infarction- Any of the following:

ST elevation 2 mm in 2 or more chest leads or 1 mm in 2 or more limb leads


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Q waves 0.04 sec (1 small square)

7. Miscellaneousa) Hypokalemia

U wave as tall as or taller than the T wave at leads V2 and V3.

b) HyperkalemiaIn the chest leads, height of T waves > 10 mm in most leads.

In limb leads, height of T waves > 5 mm in most leads.

c) HypocalcemiaProlonged Qt interval, i.e. longer than half of the RR interval by eyeballing.

d) Hypercalcemia

Shortened QT interval.

B. Types of dysrhythmias

1. Sinus node dysrhythmias

a) Sinus bradycardia- occurs when the sinus node creates an impulse at lower thannormal.

b) Sinus tachycardia- occurs when the sinus node creates an impulse at faster thannormal.

c) Sinus arrhythmia- occurs when the sinus node creates an impulse at an irregular

rhythm.The rate usually increases with inspiration and decreases with expioration.

2. Atrial dysrhythmiasa) Premature atrial complex- is a single ECG complex that occurs when an electrical

impulse starts in the atrium before the next normal impulse of the sinus node.

b) Atrial flutter- occurs in the atrium and creates impulses at an atrial rate between250 and 400 times per minute. Due to the faster atrial rate than the AV node can

conduct, all atrial impulses are conducted into the ventricle causing a therapeutic

block.3. Junctional dysrhythmias

a) Premature junctional complex- is an impulse that starts in the AV nodal area before

the next normal sinus impulse reaches the AV node.b) Junctional rhythm- occurs when the AV node instead of the SA node becomes the

pacemaker of the heart.

d) Atrioventricular nodal reentry tachycardia- occurs when an impulse is conducted to

an area in the AV node that causes the impulse to be rerouted back into the same areaover and over again at a very fast rate.

4. Ventricular dysrhythmias

a) Premature ventricular complex- is an impulse that starts in a ventricle and isconducted through the ventricles before the next normal sinus impulse.

b) Ventricular tachycardia- is defined as 3 or more PVCs in a row occurring at a rate

exceeding 100 beats per minute.c) Ventricular fibrillation- is a rapid but disorganized ventricular rhythm that causes

ineffective quivering of the ventricles. There is no atrial activity seen on ECG.


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d) Ventricular asystole- commonly called flatline is characterized by absent QRS

complexes, although P waves may be apparent for a short duration in 2 different

leads.

5. Conduction abnormalitiesa) First-degree AV block- occurs when all the atrial impulses are conducted through

the AV node into the ventricles at a rate slower than normal.

b) Second-degree AV block, type 1- occurs when all but one of the atrial impulses areconducted through the AV node into the ventricles.

c) Second-degree AV block, type 2- occurs when only some of the atrial impulses are

conducted through the AV node into the ventricles

d) Third-degree AV block- occurs when no atrial impulse is conducted through the AVnode into the ventricles.

C. Nursing Diagnoses:

- Decreased cardiac output- Anxiety related to fear of the unknown

- Knowledge deficiency about dysrhythmia and its treatment

D. Adjunct modalities and management

Pacemaker Therapy

- Pacemakers are electronic devices which provide electrical stimuli to the heart. Itcan be permanent or temporary.

Cardioversion and defibrillation

- Are treatments for tachydysrhythmias. They are used to deliver electrical currentin order to depolarize a critical mass of myocardial cells.

- Cardioversion involves the delivery of a timed electrical current to terminate a

tachydysrhythmia.- Defibrillation is used in emergency situations aas the treatment of choice for

ventricular fibrillation and pulseless VT. Defibrillation depolarizes a critical mass

of myocardial cells at once; when they repolarize, the sinus node usually capturesits role as the pacemaker.


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III. Coronary Vascular Diseases

1. CADIt is the most prominent type of cardiovascular disorder.

a. Coronary Atherosclerosis

- It is the most common heart disease in U.S.A.- It is due to an abnormal accumulation of lipid on fatty substances and fibrous

tissues in the vessel wall creating blockage or narrow the vessel in a way that

reduces blood flow to the myocardium.

- Risks factors:Major risk factors;

Age

Male sex

Hypertension DM

Dyslipidemia

Smoking

Family history of ischemic heart disease

Minor risk factors

obesity

decrease physical activity

Type A personality

Diet high in cholesterol

Pathophysiology (Coronary diseases)

Fatty streaks, lipids

deposited

intimal wall of arteries

Infiltration of T lymphocytes and monocytes

Ingest lipids then die

Vascular smooth muscles then proliferate + formation of fibrous cap over

the fatty core

Atheroma

rupture


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Thrombus emboli

Occlusion of coronary artery(s/sxs of ischemia)

Conversion to anaerobic metabolism (dec. pH)

Conduction system disorders

Dysrhythmias

Decreases cardiac contractility

Myocardial cells will necrose (check for enzyme markers- these enzymes

will be introduced to the blood stream at this time)

Clinical manifestations:

- produces symptoms and complications according to the location and degree of

narrowing

b. Angina Pectoris- clinical syndrome usually characterized by episodes or paroxysms of pain or

pressure in the anterior chest

- Cause is usually insufficient coronary blood flow resulting in decrease O2 supply

not enough to meet the myocardial demand for O2 esp. during physical exertionor stress.

- Types:

1. Stable2. Unstable- with new or worsening symptoms.

3. Refractory angina- with severe incapacitating chest pain

4. Variant or Prinzmetals angina- with pain at rest

c. Myocardial infarction

- Refers to the process by which areas of myocardial cells in the heart arepermanently destroyed.

Clinical presentation:

- severe chest pain usually > 30 mins. Unrelieved by nitroglycerin, may radiate as

high as occipital area but not lower than the umbilicus.- May be painless (25%)

Assessment and Diagnosis:

- by a typical rise and gradual fall (troponin) and /or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least 1 of the following

myocardial symptoms: ischemic symptoms, pathologic Q waves on ECG, ECG

findings indicative of ischemia.- Or a pathological finding of an acute myocardial infarction.

Management:

- Objectives of treatment are to reduce the O2 demand and to increase O2 supply to

the myocardium


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Pharmacologic:

1. Nitrates- mainstay of treatment. Acts as vasodilators and decrease myocardial O2

demand in turn decreasing ischemia and relieving pain.2. B-blockers- decrease myocardial O2 consumption by blocking B-adrenergic

stimulation, resulting in decrease HR, BP and contractility.

3. Ca channel blocking agents- have different effects. Some decrease HR andstrength of contractility, others increase O2 supply by relaxing blood vessels.

4. Antiplatelet and anticoagulant medications- administered to prevent platelet

aggregation which impedes blood flow. (e.g. aspirin, Clopidogrel, Ticlopidineand Heparin)

5. Thrombolytics

The first four medications are also used as treatment of angina except

thrombolytics.Non pharmacologic

1. Invasive Interventional procedures

> Percutaneous Transluminal Angioplasty- used to treat patients who do not

experience angina but are at risk for a cardiac event. Its purpose is to improve bloodflow within the artery by cracking the atheroma. Possible complications during the

procedure are dissection, perforation abrupt closure and vasospasm of the coronaryartery. Post procedure care involves monitoring for bleeding since patients received

large amounts of heparin during the procedure.

> Coronary artery stent- placed to overcome the risks that the coronary artery may

recoil and the tissue will remodel and form restenosis.> Transmyocardial revascularization- those who have ischemia and are not candidates

for CABG may benefit from this procedure.

2. Surgical Procedures> Coronary artery revascularization

Coronary artery bypass graft- a surgical procedure in which a blood vessel fromonother body part is grafted to the occluded coronary artery so that blood can flowbeyond the occlusion. The coronary artery must have at least 70% occlusion for this

procedure to be considered. Complications of this procedure include Mi,

dysrhythmias and hemorrhage.- Goals of the Plan of care after procedure are: restoration of cardiac output to

maintain/ attain desired lifestyle; to achieve adequate gas exchange; to improve fluid

and electrolyte balance; to reduce symptoms of sensory perceptual imbalance and

prevention of postcardiotomy psychosis; to promote relief of pain and to be able toperform self-care.

Nursing Diagnoses:1. Ineffective myocardial tissue perfusion secondary to CAD, as evidenced by chest

pain

2. Anxiety related to fear of death3. Potential ineffective air exchange related to fluid overload

4. Potential ineffective peripheral tissue perfusion related to decreased cardiac

output.


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IV. Structural, Infectious and Inflammatory cardiac disorders

1. Acquired Valvular disorders

a) mitral valve prolapse- is a deformity which usually produces no symptoms

- In this disorder, a portion of the mitral valve leaflet balloons back into the atrium

during systole, blood then regurgitates from the left ventricle back into the leftatrium.

Clinical Manifestations:

- fatigue, shortness of breath, light-headedness, dizziness, syncope, palpitations, chest

pain and anxiety. May also be asymptomatic.Assessment and Diagnostics-

- On physical exam extra heart sound referred to as Mitral click

Management- symptomatic relief and control. In advance cases mitral valve repair

and replacement may be necessary.

b) Mitral Regurgitation- involves flowing back from the let ventricle to the left atrium

- Maybe caused by problems in one of more leaflets, chorda tendinae, annulus or

the papillary muscles. Regardless of the cause, blood regurgitates back into the

atrium during systole.Assessment and diagnostics:

- (+) systolic murmur, high pitched blowing sound at the apex. Echocardiography is

used to diagnose and monitor progression of mitral regurgitation.Management:

-medical management used is the same as those used for congestive heart failure.

Surgical interventions consist of mitral valve replacement or valvuloplasty.

c) Mitral stenosis

- It is an obstruction of blood flowing from the left atrium to the left ventricle.- It is most often caused by the rheumatic endocarditis, which progressively

thickens the leaflets and chorda tendinae. Leaflets often fuse together narrowing

the orifice and progressively obstructing blood flow into the ventricle.

Clinical manifestations- first symptom often is difficulty breathing on exertion. They may expectorate blood,

cough and with repeated respiratory infections due to venous pulmonary

hypertension.Assessment and Diagnosis:

- PE-weak, irregular pulse, low pitched rumbling diastolic murmur heard at the

apex. - Echocardiography is used to diagnose.- ECG and cardiac catheterization are used to determine severity.

Management:


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- antibiotic prophylaxis use to prevent recurrence of infections. Anticoagulants may

be given to decrease risk for developing atrial thrombus. Surgical interventions

consist of valvuloplasty.

d) Aortic Regurgitation- It is the flow of blood back from the aorta back into the left ventricle during

diastole.

- It maybe caused by inflammatory lesions that deform the leaflets preventing themfrom closing the orifice.


- develops without symptoms usually. Some may have forceful heartbeat in the head

and neck, visible or palpable temporal pulsations, followed by exertional dyspnea andfatigue.

Assessment and Diagnostics

- (+)high pitched, blowing sound diastolic murmur heard at the 3rd to 4th intercostals

space at left sternal area.(+) widened pulse pressure, water-hammer pulse.- Diagnosis confirmed by echocardiography, radionucleide imaging, ECG, MRI

and cardiac catheterization.Management:

- use of antibiotic prophylaxis prior to any invasive and dental procedure. Heart

failure treatment will be discussed in the next topic. Dysrhythmias will be treated as

previously described. Surgery is recommended for any patients with left ventricularhypertrophy regardless of the presence or absence of symptoms.

e) Aortic Stenosis- It is the narrowing of the orifice between the left ventricle and the aorta. In adults,

stenosis may involve congenital leaflet malformation or abnormal number of

leaflets or it may result from rheumatic endocarditis or cusp calcification ofunknown cause.


- Many are asymptomatic. After symptoms developed, patients usually first haveexertional dyspnea caused by left ventricular failure. Other s/sxs are dizziness,

syncope due to reduced blood flow to the brain, angina pectoris results from increased

O2 demand of a hypertrophied left ventricle.

Assessment and diagnostics:- PE- loud, rough systolic murmur heard at the aortic area (systolic crescendo-

decrescendo).

- Echocardiography is used to diagnose and monitor progression.Management:

- Antibiotic prophylaxis to prevent endocarditis. Dysrhhythmia medications ma also

be required. Definitive treatment for aortic stenosis is valve replacement.


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Pathophysiology of the acquired valvular defects and their complication:


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2. Cardiomyopathies:

a) Dilated cardiomyopathy

- It is the most common form of cardiomyopathy. It is distinguished by significant

dilation of the ventricles without concomitant hypertrophy. The microscopicexamination of the muscle tissue will show diminished contractile elements and

diffuse necrosis of myocardial cells resulting in poor systolic function. These

changes decrease the amount of blood ejected from the ventricle in systole,

increasing the remaining blood in the ventricle after contraction. Less blood isthen able to enter the ventricle during diastole, increasing the end-diastolic

pressure and eventually increasing the pulmonary pressure. Echocardiography and

ECG are used to diagnose DCM.

b) Hypertrophic Cardiomyopathy

- It is a genetic disease. In this disorder, the heart muscle increase in size and massespecially along the septum. The increased thickness reduces the size of

ventricular cavity causing longer relaxation time. This makes it difficult for the

ventricles to be filled with blood during the 1st part of diastole and making them

more dependent on atrial contraction for filling.

c) Restrictive cardiomyopathy

- It characterized by diastolic dysfunction caused by rigid ventricular walls thatimpair ventricular stretch and diastolic filling. The systolic function is usually

normal.The cause for this disorder is usually unknown in most cases but in others

can often be attributed to amyloidosis and other infiltrative disease.


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- Usually asymptomatic for years, may have s/sxs of heart failure, exertional

dyspnea, orthopnea, fluid retention, peripheral edema, cough, poor perfusion togit(nausea), chest pain, dizziness and syncope with exertion.

Assessment and Diagnostics:

- PE- tachycardia and extra heart sounds in early stages, symptoms of CHF(pulmonary crackles, vein distention, pitting edema)

- Echocardiogram- ECG

- CXR - Endomyocardial biopsy

Management:

- Determine and manage cause, correction of heart failure with medications, lowsalt diet and exercise.

- Surgical management includes heart transplantation when medical management

fails. A left ventricular assistive device may be used pending the transplant.Nursing Diagnoses:

- Decreased cardiac output related to structural disorders caused by

cardiomyopathy or to dysrhythmia from the disease process and medicaltreatments.

- Ineffective CP, cerebral, peripheral and renal tissue perfusion related to decreased

peripheral blood flow.

- Impaired gas exchange related to pulmonary congestion caused by myocardialfailure

- Activity intolerance related to change in health status

- Powerlessness related to disease process


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3. Infectious diseases of the heart

a) Rheumatic Endocarditis- It occurs most often in school children following a streptococcal pharyngitis.

- Occurs as a result of sensitivity reaction occurring in response to the Streptoccal

infection.Clinical manifestations:

- Signs and symptoms of valvular regurgitation as previously discussed.

Assessment and diagnostics:PE- findings will depend on which side of the heart is involved; severity depends on

the size and location of the lesion, presence of murmur.

Management;

- eradicate microorganism through long term antibiotic regimen( Penicillin).

b) Infective Endocarditis

- It occurs as a direct invasion of the microorganisms to the endocordium.

- Its presentation is similar to the rheumatic endocarditis with the addition ofinfluenza-like symptoms prior to the valvular damage manifestations.

c) Myocarditis

- It is an inflammatory process involving the myocardium.

- Myocarditis results from Viral, bacterial, mycotic, protozoal, spirochetialinfection. It may also be caused by an Allergic reaction. The degree of myocardial

involvement determines the degree of hemodynamic effect and resulting signs and

symptoms.

d) Pericarditis

- refers to inflammation of the pericardium( membranous sac enveloping theheart).. It maybe a primary illness or caused by a variety of medical and surgical

disorders.

- It can lead to pericardial effusion and increased pressure on the heart leading tocardiac tamponade. Frequent or prolonged episodes may also lead to thickening

and decreased elasticity that restricts the hearts ability to fill properly (constrictive

pericarditis).

Clinical manifestations:- Chest pain-most characteristic symptom, usually constant but may worsen with

inspiration or when lying down or turning.

- Friction rub- most characteristic sign- Dyspnea and other signs of heart failure may occur as a result of pericardial

compression.

Assessment and Diagnostic findings:- Echocardiogram

- ECG


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V. Complications from heart disease

1. Heart Failure- It is the inability of the heart to pump sufficient blood to meet the needs of the

tissues for oxygen and nutrients.

Etiology:- most often caused by coronary artery disease, cardiomyopathy or valvular

disorders.

Pathophysiology:


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Left-sided heart failure

-pulmonary congestion, dyspnea, shortness of breath, cough, crackles, lower thannormal O2 saturation levels

Right-sided heart failure

-congestion of viscera and peripheral tissues, distended neck veins and bi-pedaledema.

*Most common cause of right sided heart failure is left-sided heart failure

Assessment and Diagnostic tests:

- PE- s/sxs of left or right-sided heart failure


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- ECG- non-specific findings

- CXR-cardiomegaly and signs of congestion and effusion

- Echocardiogram- Cardiac catheterization- for selected patients to detect presence of CAD

Management:

Nursing Diagnoses:- Activity intolerance related to imbalance between O2 supply and demand

- Excess fluid volume related to excess fluid intake or sodium intake and retention

of fluid due to HF and its medical therapy- Anxiety related to breathlessness and restlessness from inadequate oxygenation

- Powerlessness related to inability to perfoem role responsibilities because of

chronic illness and hospitalizations

2. Cardiogenic shock

- Occurs when the heart can not pump enough blood supply to the amount of oxygenneeded by the tissues.

Pathophysiology of cardiogenic shock

P


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- Tissue hypoperfusion manifested as cerebral hypoxia, low BP, rapid weak pulse,

cold and clammy skin, increased crackles, hypoactive bowel sounds anddecreased urinary output.

Assesment and Diagnostics:

- PA catheter to measure left ventricular pressure and CO.Mangement:

- correct underlying problems

- intubation and ventilation

- High concentration O2- Inotropic agents e.g. dopamine, dobutamine, norepinephrine

- Vasodilators and diuretics as BP permits

- Use of intra-aortic balloon pump

VI. Hypertension

- It is defined as a systolic BP of 140 mmHg and diastolic BP of 90 mmHg over a

sustained period, taken in 2 separate occasions.

Primary hypertension- also called essential, is hypertension without a known cause

Secondary hypertension

- also called the non-essential is a result of a known or definable cause


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Classification:

Pathophysiology:

Clinical Manifestations:- elevated BP

- Retinal changes and papilledema, LVH, pathologic changes in the kidney, stroke

or TIA, all of which are complications of hypertension.Assessment and diagnostics:

- BP monitoring

- CBC, serum K, Ca, FBS, Creatinine, Lipid profile and 12-lead ECGManagement:


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- Pharmacologic therapy involves use of beta-blockers, Ca channel blockers, alpha-

blockers, ACE inhibitors, diuretics.

- Lifestyle modifications involved diet, cessation of smoking and alcohol intake,exercise, lose weight if over weight and minimize stress

Nursing Diagnoses

- Knowledge deficiency regarding treatment regimen and control of disease process- Non compliance to therapeutic regimen related to side effects of prescribed therap

or financial constraints

monitoring for complications should be emphasized

Hypertensive Crises;

2 types:

1. Hypertensive emergency- is a situation in which the BP must be loweredimmediately to halt or prevent damage to target organs. These are acute life-

threatening elevation in BP that requires prompt treatment. Medications of choice are

those with immediate effects such as IV venodilators.

2. Hypertensive urgency- on the other hand is a situation in which the BP must belowered in a few hours. These are usually managed with oral doses of fast-acting

agents such as loop-diuretics, beta-blockers and ACE inhibitors.

References:

o Richard S. Snell. Clinical Anatomy, an illustrated review with questions

and explanations. 2nd edition,1996

o Ong, Willie, Patacsil,Gregorio. Cardiology blue book. 3rd edition, 2004

o Bare, Brenda, Smeltzer, Suzanne. Brunner and Suddarths Medical-

Surgical nursing. 10th edition, 2004


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o Guyton, A., Hall,J. Pocket companion to Textbook of Medical physiology.

10th edition2001

o Ferry, David. Basic Electrocardiography in Ten Days. McGraw-hill,

Singapore, 2001

Documents

Nursing MS (Cardio)