4. Cardiovascular

8/6/2019 4. Cardiovascular

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CARDIO VASCULAR

SYSTEM



CARDIOVASCULAR

SYSTEM Consists: heart, arteries, veins, capillaries

Functions:1. circulation of blood

2. delivery of oxygen and other nutrients to tissuesof the body

3. removal of carbon dioxide and other products of cellular metabolism





CARDIOVASCULARCARDIOVASCULAR

SYSTEM HEART

ANATOMY and PHYSIOLOGY : A. Heart wall

1. pericardiuma. fibrous pericardiumb. serous pericardium

2. epicardium

3. myocardium4. endocardium



CARDIOVASCULAR

SYSTEMB. Chambers

1. Atria a. right

b. left 2. Ventricles a. right

b. left

C. Valves

1. Atrioventricular valves

a. Mitral valve

b. Tricuspid valve



CARDIOVASCULAR

SYSTEMc. Function:

- permit unidirectional flow of blood from

specific atrium to specific ventricle duringventricular diastole

- prevent reflux during ventricular systole

- valve leaflets open during ventricular diastole

and close during ventricular systole; valve closureproduces the first heart sounds (S1)



CARDIOVASCULAR

SYSTEM2. Semilunar valves

a. Pulmonary valve

b.Aortic valve

c. Function:

- permit unidirectional flow of blood fromspecific ventricle to arterial vessel during ventricularsystole

- prevent reflux during ventricular diastole

- valves open when ventricles contract andclose during ventricular diastole; valve closureproduces the second heart sound (S2)



CARDIOVASCULAR

SYSTEMD. Conduction System

1. Sinoatrial (SA) node

2. Internodal Tracts3. Atrioventricular ( A V) node

4. Bundle of His

- right bundle branch

- left bundle branch

5. Purkinje fibers

* Electrical activity of heart can be visualized by ECG



CARDIOVASCULAR

SYSTEME. Coronary Circulation

1. Arteries

a. right coronary arteryb. left coronary artery

2. Veins

a. coronary sinus veins

b. thebesian veins



CARDIOVASCULAR

SYSTEM V ASCULAR SYSTEM

Function:

a. supply tissues with bloodb. remove wastes

c. carry unoxygenated bloodback to the heart



CARDIOVASCULAR

SYSTEM TY PES OF BLOOD VESSELS

A. Arteries

B.

Arterioles

C. Capillaries: the following exchanges occur:

- oxygen and carbon dioxide

- solutes between the blood and tissues

- fluid volume transfer between the plasma andinterstitial spaces

D. Venules

E. Veins



CARDIOVASCULAR

SYSTEM ASSESSMENT

HEALTH HISTORY

A. Presenting problem1. Nonspecific symptoms may include

- fatigue - shortness of breath

- cough - palpitations

- headache - weight loss/gain- syncope - difficulty sleeping

- dizziness - anorexia



CARDIOVASCULAR

SYSTEM2. Specific signs and symptoms

a. chest pain

b. dyspnea (shortness of breath)c. orthopnea / paroxysmal nocturnal dyspnea

d. palpitations: precipitating factors

e. edema

f. cyanosisB. Lifestyle: occupation, hobbies, financial status,

stressors, exercise, smoking, living conditions



CARDIOVASCULAR

SYSTEMC. Use of medications: OTC drugs, contraceptives,

cardiac drugs

D. Personality profile: Type A, manic-depressive,anxieties

E. Nutrition: dietary habits, cholesterol, salt intake,alcohol consumption

F. Past M

edicalH

istoryG. Family history: heart disease (congenital, acute,

chronic); risk factors (DM, hypertension, obesity)



CARDIOVASCULAR

SYSTEMPHYSICAL EXAMINATION

A. Skin and mucous membranes:

- color/texture, temperature, hair distribution onextremities, atrophy or edema, petechiae

B. Peripheral pulses:

- palpate and rate all arterial pulses (temporal,carotid, brachial, radial, femoral, popliteal,

dorsalis pedis and posterior tibial) on scale of:0=absent, 1=palpable, 2=normal, 3=full, 4=fulland bounding



CARDIOVASCULAR

SYSTEMC. Assess for arterial insufficiency and venous

impairment

D. Measure and record blood pressure

E. Inspect and palpate the neck vessels:

a. jugular veins: note location, characteristics, jugular venous pressure

b. carotid arteries: location and characteristics

F. Auscultate heartsounds- normal (S1, S2)

- abnormal (S3, S4)



CARDIOVASCULAR

SYSTEMLABORATORY / DIAGNOSTIC TESTS

A. Blood Chemistry and electrolyte analysis

1. Cardiac enzymes: inMI

a. Troponin T: detected 3-12 hours after chest pain

b. Troponin I: detected 3-12 hrs

c. creatine phosphokinase (CPK MB): 6-12Hrs

d. Aspartate aminotransferase ( AST) (SGOT): 24Hrs after chest pain

e. Lactic dehydrogenase (LDH): 36 Hrs



CARDIOVASCULAR

SYSTEM2. Electrolytes

a. Sodium (Na) 135-148meq/L

- hyponatremia: fluid excess- hypernatremia: fluid deficit

b. Potassium (K) 3.5-5 meq/L

- inc. or dec. levels can cause dysrhythmias

c. Magnesium (Mg) 1.3-2.1 meq/L

- dec. levels can cause dysrhythmias



CARDIOVASCULAR

SYSTEMd. Calcium (Ca) 4.5-5.3 meq/L:

- nec. For blood clotting and neuromuscular

activity- dec. levels cause tetany, inc. levels causes

muscle atony

- dec. and inc. levels cause dysrhythmias

3. Serum Lipidsa. Total Cholesterol 150-200mg/dl:

- high levels predispose to atherosclerotic HD



CARDIOVASCULAR

SYSTEMb. High density lipids (HDL) 30-85 mg/dl

- low levels predispose to CVD

c. Low density lipids (LDL) 50-140 mg/dl:- high levels predispose to atherosclerotic

plaque formation

d. Triglycerides 10-150 mg/dl:

- high levels increase risk of atheroscleroticheart disease



CARDIOVASCULAR

SYSTEMB. Hematologic Studies

1. CBC

2. Coagulation time: 5-15mins; inc. levels indicatebleeding tendency, used to monitor heparin tx.

3. Prothrombin time (PT) 9.5-12sec.; INR 1.0,used to monitor warfarin tx.

4. Activated partial thromboplastin time ( APTT)20-45sec; used to monitor heparin therapy

5. Erythrocyte sedimentation rate(ESR)<20mm/hr; inc. level indicate inflamm. process



CARDIOVASCULAR

SYSTEMC. Urine Studies (routine U/ A)

D. Electrocardiogram (ECG)

1. Noninvasive ECG a graphic record of theelectrical activity of the heart

2. Portable recorder (Holter monitor) providescontinuous recording of ECG for up to 24 hrs.

E. Exercise ECG (stress test): the ECG is recordedduring prescribed exercise; may show heart disease when resting ECG does not

F. Echocardiogram: noninvasive recording of thecardiac structures using ultrasound



CARDIOVASCULAR

SYSTEMG. Cardiac catheterization: invasive, but often

definitive test for diagnosis of cardiac disease.

1. A catheter is inserted into the right or left sideof the heart to obtain information

2. Purpose: to measure intracardiac pressuresand oxygen levels in various parts of the heart;with injection of a dye, it allows visualization of

the heart chambers, blood vessels and blood flow(angiography)



CARDIOVASCULAR

SYSTEM3. Nursing care: prior to the test

- informed consent

- any allergies esp. to iodine- keep client on NPO for 8-12 hrs

- record height, weight, V/S

- inform client that a feeling of warmth and

fluttering sensation as catheter is inserted



CARDIOVASCULAR

SYSTEM4. Nursing care: post test

- assess circulation to the extremity used for

catheter insertion- check peripheral pulses, color, sensation of

affected extremity

- if protocol requires, keep affected ext.straight for approx. 8 hrs.

- observe catheter insertion site for swelling,bleeding

- assess V/S and report for sig. changes



CARDIOVASCULAR

SYSTEMH. Coronary arteriography

1. visualization of coronary arteries by injection

of radiopaque contrast dye and recording on amovie film.

2. Purpose: evaluation of heart disease andangina, location of areas of infarction and extent of lesions, ruling out coronary artery disease in

clients with MI.

3. Nursing care: same as cardiaccatheterization



ANALYSIS

Nursing diagnosis for the client with CVD include

A. Fluid volume excess

B. Decreased cardiac output

C. Altered peripheral tissue perfusion

D. Impairment of skin integrity

E. Risk for activity intolerance

F. PainG. Ineffective coping

H. Fear

I. Anxiety



PLANNING AND

IMPLEMENTATIONGOALS

A. Fluid imbalance will be resolved, edema minimized

B. Cardiac output will be improved.C. Cardiopulmonary and peripheral tissue perfusion

will be improved

D. Adequate skin integrity will be maintained

E. Activity intolerance will progressively increaseF. Pain in the chest will be diminished

G. Clients level of fear and anxiety will be decreased



PLANNING AND

IMPLEMENTATIONINTERVENTIONS

CARDIAC MONITORING

A. ECG 1. strip: small square: 0.04secs.

large square: 0.2secs.

2. P wave: produced by atrial depolarization;

indicates SA node function



PLANNING AND

IMPLEMENTATION3. P-R interval (N= 0.12 - 0.20 secs.)

a. indicates A V conduction time or the time it

takes an impulse to travel from the atria downand through the A V node

b. measured from beginning of P wave tobeginning of QRS complex

4. QRS complex (N= 0.06-0.10 secs.)

a. indicates ventricular depolarization

b. measured from onset of Q wave to end of S wave



PLANNING AND

IMPLEMENTATION5. ST segment

a. indicates time interval between complete

depolarization of ventricles and repolarization of ventricles

b. measured after QRS complex to beginning of T wave

6. T wave

a. represents ventricular repolarization

b. follows ST segment



PLANNING AND

IMPLEMENTATIONHEMODYNAMIC MONITORING

(Swan Ganz Catheter)

A. A multilumen catheter with a balloon tip that isadvanced through the superior vena cava into theRA, R V, and P A. When it is wedged it is in thedistal arterial branch of the pulmonary artery.

B. Purpose:

1. Proximal port: measures RA pressure

2. Distal port:

a. measures P A pressure and PCWP



PLANNING AND

IMPLEMENTATIONb. normal values: P A systolic and diastolic less

than 20mmHg; PCWP 4-12mmHg

C.N

ursing care1. a sterile dry dressing should be applied to siteand changed every 24 hours; inspect site dailyand report signs of infection

2. if catheter is inserted via an extremity,immobilize extremity to prevent catheterdislodgment or trauma.



PLANNING AND

IMPLEMENTATION3. Observe catheter site for leakage

4. Ensure that balloon is deflated with a syringe

attached except when PCWP is read5. Continuously monitor P A systolic and diastolicpressures and report significant variations

6. Irrigate line before each reading of PCWP

7.M

aintain client in same position for eachreading

8. Record P A systolic and diastolic readings at least every hour and PCWP as ordered.



PLANNING AND

IMPLEMENTATIONCENTRAL VENOUS PRESSURE (CVP)

A. Obtained by inserting a catheter into the external

jugular, antecubital, or femoral vein andthreading it into the vena cava. The catheter isattached to an I V infusion and H2O manometerby a three way stopcock

B. Purposes:

1. Reveals RA pressure, reflecting alterations inthe R V pressure



PLANNING AND

IMPLEMENTATION2. Provides information concerning blood volumeand adequacy of central venous return

3. Provides an I V route for drawing bloodsamples, administering fluids or medication, andpossibly inserting a pacing catheter

C. Normal range is 4-10 cmH20;

elevation indicates hypervolemia,

decreased level indicates hypovolemiaD. Nursing care

1. Ensure client is relaxed



PLANNING AND

IMPLEMENTATION2. Maintain zero point of manometer always at level of right atrium (midaxillary line)

3.D

etermine patency of catheter by openingI Vinfusion line

4. Turn stopcock to allow I V solution to run intomanometer to a level of 10-20cm above expectedpressure reading

5. Turn stopcock to allow I V solution to flow frommanometer into catheter; fluid level inmanometer fluctuates with respiration



PLANNING AND

IMPLEMENTATION6. Stop ventilatory assistance duringmeasurement of CVP

7. A

fter CVP reading, return stopcock toI Vinfusion position

8. Record CVP reading and position of client

EVALUATION



DISORDERS OF THE

CARDIOVASCULAR SYSTEMHEART

CORONARY ARTERY DISEASE (CAD)

A. General Information1. refers to a variety of pathology that causenarrowing or obstruction of the coronary arteries,resulting in decreased blood supply to themyocardium

2. major causative factor: Atherosclerosis

3. bet 30-50 y.o., men>women

4. may manifest as angina pectoris or MI



CORONARY ARTERY

DISEASE5. Risk factors:

- family history of C AD - DM

- el. Serum lipoproteins - hypertension- cigarette smoking - obesity

- el serum uric acid - lifestyle

B. Medical management, assessment findings andnursing interventions Angina pectoris and MI



ANGINA PECTORIS

A. Gen. info:

1. transient, paroxysmal chest pain produced by

insufficient blood flow to the myocardiumresulting in myocardial ischemia

2. Risk factors:

- C AD - DM

- hypertension - aortic insufficiency- severe anemia - atherosclerosis

- thromboangiitis obliterans



ANGINA PECTORIS

3. Precipitating factors:

- physical exertion - sexual activity

- strong emotions - cigarette smoking- consumption of a heavy meal

- extremely cold weather

B. Medical mgt:1. Drug therapy: nitrates, beta adrenergicblocking agents, and/or calcium blocking agents,lipid reducing drugs if cholesterol is elevated



ANGINA PECTORIS

2. Lifestyle modification

3. Surgery: coronary bypass surgery

C. Assessment Findings:

1. Pain: substernal with possible radiation to theneck, jaw, back and arms, relieved by REST

2. Palpitations, tachycardia, dyspnea, diaphoresis3. el. serum lipid levels



ANGINA PECTORIS

4. Diagnostic tests:

- ECG may reveal ST segment depression and T-

wave inversion during chest pain- Stress test may reveal an abnormal ECG duringexercise

D.

Nursing interventions:1. administer oxygen

2. give prompt pain relief with nitrates or narcoticanalgesics as ordered.



ANGINA PECTORIS

3. Monitor V/S, status of cardiopulmonaryfunction, monitor ECG

4. place patient in semi-high Fowlers position5. provide emotional support, health teachingsand discharge instructions.

6. Instruct client to notify physician immediately if pain occurs and persists, despite rest andmedication administration.



MYOCARDiAL

INFARCTiON A. General information:

1. The death of myocardial cells from inadequate

oxygenation, often caused by a sudden completeblockage of a coronary artery; characterized bylocalized formation of necrosis (tissuedestruction) with subsequent healing by scarformation and fibrosis.

2. Risk factors:- atherosclerotic C AD - DM

- thrombus formation - hypertension



MYOCARDiAL

INFARCTiONB. Assessment findings:

1. Pain same as in angina, crushing, viselike with

sudden onset; UNRELIE

VED

by rest or nitrates2. nausea/vomiting, dyspnea

3. skin: cool, clammy, ashen

4. elevated temperature

5. initial increase in BP and pulse, with gradualdrop in BP

6. Restlessness



MYOCARDiAL

INFARCTiON7. Occasional findings: rales or crackles; presence of

S4; pericardial friction rub; split S1, S2

8.D

iagnostic tests:a. elevated WBC, cardiac enzymes (troponin,CPK-MB, LDH, SGOT)

b. ECG changes (specific changes dependent onlocation of myocardial damage and phase of the

MI; inverted T wave and ST segment changesseen with myocardial ischemia

c. inc. ESR, el. serum cholesterol



MYOCARDiAL

INFARCTiONC. Nursing interventions:

1. establish a patent I V line

2. provide pain relief; morphine sulfate I V (poorperipheral perfusion, false + for enzymes)

3. Administer O2 as ordered to relieve dyspneaand prevent arrhythmias

4. Provide bed rest with semi fowlers position5. Monitor ECG and hemodynamic procedures

6. Administer anti-arrhythmias as ordered.



MYOCARDiAL

INFARCTiON7. Monitor I & O, report if UO <30 ml/hr

8. Maintain full liquid diet with gradual increase to

soft, low salt 9. Maintain quiet environment

10. Administer stool softeners as ordered

11. Relieve anxiety associated with CCU

environment 12. Administer anticoagulants, thrombolytics (tpaor streptokinase) as ordered and monitor for S /E



MYOCARDiAL

INFARCTiON13. Provide client teaching and discharge instructionconcerning

- effects of MI

, healing process and treatment regimen- Medication regimen: name, purpose, schedule, dosage,S /E

- Risk factors with necessary lifestyle modification

-D

ietary restrictions: low salt, low cholesterol, avoidanceof caffeine

- Resumption of sexual activity as ordered (usually 4-6weeks)



MYOCARDiAL

INFARCTiON- Need to report the ff. symptoms:

* increased persistent chest pain

* pain, dyspnea, weakness, fatigue* persistence palpitations, light headedness

- Enrollment of client in a cardiac rehabilitationprogram



DYSRHYTHMIAS

An arrhythmia is a disruption in the normalevents of the cardiac cycle. It may take a varietyof forms.

Treatment varies on the type dysrhythmias

SINUS TACHYCARDIA

A. General Information:

1. A heart rate of over 100 beats/min, originatingin the SA node



DYSRHYTHMIAS

2. May be caused by:

- fever - anemia

- apprehension - hyperthyroidism- physical activity - myocardial ischemia

- caffeine - drugs (epi., theo)

B. Assessment findings:1. Rate: 100-160 beats /min

2. Rhythm: regular



DYSRHYTHMIAS

3. P wave: precedes each QRS complex withnormal contour

4. P-R interval: normal (0.08 sec)

5. QRS complex: normal (0.06 sec)

C. Treatment;

- correction of underlying cause, elimination of stimulants, sedatives, propranolol (Inderal)



DYSRHYTHMIAS

SINUS BRADYCARDIA


1. A slowed heart rate initiated by SA node2. Caused by:

- excessive vagal or decreased sympathetic tone

- MI - IC tumors

- meningitis - myxedema- cardiac fibrosis

- normal variation of the heart rate in well trainedathletes



DYSRHYTHMIAS

B. Assessment findings:

1. Rate: <60 beats/min

2. Rhythm: regular3. P wave: precedes each QRS with a normalcontour

4. P-R interval: normal

5. QRS complex: normalC. Treatment: usually not needed

- if cardiac output is inadequate: atropine andisoproterenol; pacemaker



DYSRHYTHMIAS

ATRIAL FIBRILLATION

A. General information

1. An arrhythmia in which ectopic foci causerapid, irregular contractions of the heart

2. seen in clients with

- rheumatic mitral stenosis - thyrotoxicosis

- cardiomyopathy - pericarditis- hypertensive heart disease - CHD



DYSRHYTHMIAS


1. Rate: atrial: 350-600 beats/min

ventricular: varies bet. 100-160 beats /min2. Rhythm: atrial and ventricular regularly

irregular

3. P wave: no definite P wave; rapid undulationscalled fibrillatory waves

4. P-R interval: not measurable

5. QRS complex: generally normal



DYSRHYTHMIAS

C. Treatment: digitalis preparations, propanolol,verapamil in conjunction with digitalis; direct current cardioversion

PREMATURE VENTRICULAR CONTRACTIONS


1. Irritable impulses originate in the ventricles

2. Caused by:

- electrolyte imbalance (hypokalemia)

- digitalis drug therapy



DYSRHYTHMIAS

Contd: (causes)

- stimulants( caffeine, epinephrine, isoproterenol)

- hypoxia- CHF


1. Rate: varies according to no. of PVCs2. Rhythm: irregular because of PVCs

3. P wave: normal; however, often lost in QRS complex



DYSRHYTHMIAS

4. P-R interval: often not measurable

5. QRS complex: greater then 0.12secs, wide

C. Treatment:

1. I V push of Lidocaine (50-100mg) followed byI V drip of lidocaine at rate of 1-4 mg/min

2. Procainamide, quinidine3. Treatment of underlying cause



DYSRHYTHMIAS

VENTRICULAR TACHYCARDIA

A. General information:

1. 3 or more consecutive PVCs; occurs fromrepetitive firing of an ectopic focus in theventricles

2. caused by:

- MI - C AD

- digitalis intoxication - hypokalemia



DYSRHYTHMIAS


1. Rate: atrial: 60-100 beats/min

ventricular: 110-250 beats/min2. Rhythm: atrial(regular), ventricular (occly.irregular)

3. P wave: often lost in QRS complex

4. P-R

interval usually not measurable5. QRS complex: greater than 0.12 secs, wide



DYSRHYTHMIAS

C. Treatment:

1. I V push of lidocaine (50-100mg), then I V dripof lidocaine 1-4 mg/min

2. Procainamide via I V infusion of 2-6 mg/min

3. direct current cardioversion

4. bretylium, propanolol

PERCUTANEOUS



PERCUTANEOUS

TRANSLUMINAL CORONARY

ANGIOPLASTY (PTCA) A. General information:

1. PTC A can be performed instead of coronaryartery bypass graft surgery in various clients withsingle vessel C AD.

2. Aim: revascularize the myocardium

decrease angina increase survival

3. a balloon tipped catheter is inserted into thestenotic, diseased coronary artery. The balloon isinflated with a controlled pressure and therebydecreases the stenosis of the vessel



CORONARY ARTERY

BYPASS SURGERY A. General information:

1. A coronary artery bypass graft is the surgery of choice for clients with severe C AD

2. new supply of blood brought todiseased/occluded coronary artery by bypassingthe obstruction with a graft that is attached tothe aorta proximally and to the coronary artery

distally3. Procedure requires use of extracorporealcirculation (heart-lung machine, cardiopulmonarybypass)



CORONARY ARTERY

BYPASS SURGERYB. Nursing interventions: preoperative

1. Explain anatomy of the heart, function of coronary arteries, effects of C AD

2. Explain events of the day of surgery

3. Orient to the critical and coronary care unitsand introduce to staff

4. Explain equipments to be used (monitors,hemodynamic procedures, ventilators, ET, etc)

5. Demonstrate activity and exercise

6. Reassure availability of pain medications



CORONARY ARTERY

BYPASS SURGERYC. Nursing interventions: post-operative

1. Maintain patent airway

2. Promote lung re-expansion3. monitor cardiac status

4. maintain fluid and electrolyte balance

5. maintain adequate cerebral circulation

6. provide pain relief 7. prevent abdominal distension



CORONARY ARTERY

BYPASS SURGERY8. Monitor for and prevent the ff. complications:

a. Thrombophlebitis / pulmonary embolism

b. Cardiac tamponadec. arrhythmias

d. CHF

9. Provide client teaching and discharge planning

concerning:a. limitation with progressive increase in

activities



CORONARY ARTERY

BYPASS SURGERYb. sexual intercourse can usually be resumed

by 3rd or 4th week post-op

c. medical regimen

d. meal planning with prescribed modifications

e. wound cleansing daily with mild soap andH2O and report for any signs of infection

f. Symptoms to be reported:

- fever, dyspnea, chest pain with minimalexertion



CONGESTIVE HEART

FAILURE A. Gen. Info:

- Inability of the heart to pump an adequatesupply of blood to meet the metabolic needs of the body

B. Types:

1. Left sided heart failure

2. Right sided heart failure



CONGESTIVE HEART

FAILURE1. LEFT SIDED HEART F AILURE

a. Left ventricular damage causes blood to backup through the left atrium and into the pulmonaryveins. Increased pressure causes transudationinto the interstitial tissues of the lungs withresultant pulmonary congestion

b. Caused by:

- left ventricular damage (MI, C AD)

- hypertension, aortic valve disease ( AI, AS)

- mitral stenosis, cardiomyopathy



CONGESTIVE HEART

FAILUREc. Assessment findings:

Signs:

- easy fatigability, dyspnea on exertion, PND

,orthopnea, cough, nocturia, confusion

Symptoms:

-S3 gallop, tachycardia, tachypnea, rales,wheezing, pleural effusion



CONGESTIVE HEART

FAILUREd. Diagnostic tests:

- ECG, chest x-ray (cardiomegaly, pleuraleffusion), echocardiography, cardiaccatheterization, dec. PO2, inc. PCO2

2. RIGHT SIDED HEART F AILURE

a. weakened R V is unable to pump blood into thepulmonary system; systemic venous congestionoccurs as pressure builds up.



CONGESTIVE HEART

FAILUREb. caused by:

- left sided heart failure

-R V infarction

- atherosclerotic heart disease

- COPD, pulmonic stenosis, pulmonary embolism

c. Assessment findings:Symptoms:

- easy fatigability, lower extremity swelling, earlysatiety, RUQ discomfort



CONGESTIVE HEART

FAILURESigns:

- elevated jugular venous pressure,hepatomegaly, ascites, lower extremity edema

d. Diagnostic tests:

- chest x-ray: reveals cardiac hypertrophy

- echocardiography: indicates inc. size of cardiacchambers

- elevated CVP, dec. PO2, inc. ALT(SGPT)



CONGESTIVE HEART

FAILUREC. Medical Management:

1. determination and elimination/control of underlying cause

2. Drug therapy:

- Diuretics: Furosemide, Spironolactone

- Dilators: ACE inhibitors, nitrates

-D

igitalis: digoxin3. Diet: low salt, low cholesterol

* If medical therapies unsuccessful, mechanical assist devices (intra-aortic balloon pump), cardiac transplantation or mechanical heartsmay be employed.



CONGESTIVE HEART

FAILURED. Nursing Interventions:

1. Monitor respiratory status and provideadequate ventilation (when CHF progresses topulmonary edema)

2. Provide physical and emotional rest

3. Increase cardiac output

4. Reduce/eliminate edema




CARDIAC ARREST

A. General Info:

- sudden, unexpected cessation of breathing andadequate circulation of blood by the heart

B. Medical management:

1. Cardiopulmonary resuscitation (CPR)

2.D

rug therapy:a. lidocaine, procainamide, verapamil

b. Dopamine, isoproterenol, Norepinephrine



CARDIAC ARREST

c. Epinephrine to enhance myocardial automaticity,

excitability, conductivity, and contractility

d. Atropine sulfate to reduce vagus nerves control over

the heart, thus increasing the heart ratee. Sodium bicarbonate: administered during first fewmoments of a cardiac arrest to correct respiratory andmetabolic acidosis

f. Calcium chloride: calcium ions help the heart beat

more effectively by enhancing the myocardium's contractileforce

3. Defibrillation



CARDIAC ARREST

C. Assessment findings:

- unresponsiveness, cessation of respiration,pallor, cyanosis, absence of heart rate/ BP/pulses,dilation of pupils, ventricular fibrillation

D. Nursing interventions:

1. Begin precordial thump and if successful,administer lidocaine

2. If unsuccessful, defibrillation - CPR

3. Assist with administration of and monitoreffects of emergency drugs



CARDIOPULMONARY

RESUSCITATION A. General info: process of externally supporting the

circulation and respiration of a person who hashad a cardiac arrest

B. Nursing interventions: unwitnessed cardiac arrest

1. Assess LOC

a. Shake victims shoulder and shout

b. if no response, summon for help

2. Position victim supine on a firm surface



C P R

3. Open airway

a. Use head tilt, chin lift maneuver

b. Place ear nose and mouth- look to see if chest is moving

- listen for escape of air

- feel for movement of air against face

c. If no respiration, proceed to #44. Ventilate twice, allowing for deflation betweenbreaths



C P R

5. Assess circulation: if not present, proceed to #6

6. Initiate external cardiac compressions

a. Proper placement of hands: lower half of thesternum

b. Depth of compressions: 1½ - 2 in. for adults

c. One rescuer: 15 compressions (80-100/min) with2 ventilations

d. Two rescuers: 5 compressions (80-100/min)

with 1 ventilation

INFLAMMATORY



INFLAMMATORY

DISEASES OF THE HEARTENDOC ARDITIS

A. General Info:

1.Inflammation of the endocardium; plateletsand fibrin deposit on the mitral and/or aortic

valves causing deformity, insufficiency or stenosis

2. caused by bacterial infection:

- commonly S. aureus. S. viridans, B hemolyticstreptococcus, gonococcus

3. Precipitating factors: RHD, open heart surgery,GU/OB Gyn surgery, dental extractions



ENDOCARDITIS


1. Drug therapy:

a. antibiotics specific to sensitivity or organismcultured

b. PenG and streptomycin if org. not known

c. antipyretics

2. Cardiac surgery to replace valve



ENDOCARDITIS


1. Fever, malaise, fatigue, dyspnea and coughacute upper quadrant pain, joint pain

2. petechiae, murmurs, edema, splenomegaly,hemiplegia and confusion, hematuria

3. elevated WBC & ESR, decreased Hgb & Hct.

4. Diagnostic tests: positive blood culture forcausative organism



ENDOCARDITIS


1. antibiotics as ordered

2. control temperature

3. assess for vascular complications and pulm.embolism


- types of procedures, antibiotic therapy

- S /S to report: persistent fever, fatigue, chills,anorexia, joint pains

- avoidance of individuals with known infections



MYOCARDITIS

A. General Info: an acute or chronic inflammation of the myocardium as a result of pericarditis,systemic infection or allergic response.

B. Assessment:

- fever, pericardial friction rub, gallop rhythm

- murmur, signs of heart failure, fatigue, dyspnea

- tachycardia, chest pain



MYOCARDITIS

C. Implementation:

1. Assist client to assume a position of comfort

2. Administer analgesics, salicylates, NSAIDS

3. Administer O2, provide adequate rest periods

4. Limit activities, to dec. workload of heart

5. Treat underlying cause

6. Administer meds. as ordered:- antibiotics, diuretics, ACE inhibitors, digitalis

7. Monitor complications: thrombus, heart failure,cardiomyopathy



PERICARDITIS

A. General Info:

1. An inflammation of the visceral and parietalpericardium

2. caused by bacterial, viral, or fungal infection;collagen diseases; trauma; acute MI, neoplasms,uremia, radiation, drugs (procainamide,hydralazine, Doxorubicin HCL)



PERICARDITIS


1. Determination and elimination/control of underlying cause

2. Drug therapy

a. Medication for pain relief

b. Corticosteroids, *salicylates (aspirin),indomethacin, to reduce inflammation

3. Specific antibiotic therapy against the causativeorganism may be indicated



PERICARDITIS


1. chest pain with deep inspiration (relieved bysitting up), cough, hemoptysis, malaise

2. tachycardia, fever, pericardial friction rub,cyanosis or pallor, jugular vein distension

3. Elevated WBC and ESR, normal or inc. SGOT

4. Diagnostic test:

a. chest x-ray may show increased heart size

b. ECG: ST elevation, T wave inversion



PERICARDITIS

D. Nursing Interventions:

1. Ensure comfort, bed rest with semi- or highFowlers position

2. Monitor hemodynamic parameters

3. Administer medications as ordered and monitoreffects

4. Provide client teaching and discharge planning:

- S /S of pericarditis indicative of recurrence (chest pain intensified by lying down and relieved whensitting up; medication regimen

CONGENITAL HEART



CONGENITAL HEART

DISEASE (CHD) A. General Info:

1. CHDs are structural defects of the heart, great vessels, or both that are present from birth

2. 2nd only to prematurity as a cause of death inthe first year of life

B. Clinical Classification of Congenital heart disease

1. Acyanotic: PD A, ASD, VSD

2. Cyanotic: TOF, TG V, Truncus arteriosus

3. Obstructive: Coarctation of Aorta, AS, PS



ACYANOTIC CHD (PDA)

ACYANOTIC CHD

A. P ATENT DUCTUS ARTERIOSUS (PD A)

- results when the fetal ductus arteriosus fails toclose completely after birth

1. Pathophysiology

- blood flows from the aorta through the PD A andback to the pulmonary artery and lungs, causinginc. L V workload and increase pulmonary vascularcongestion



ACYANOTIC CHD (PDA)

2. Assessment findings:

a. Clinical manifestations:

1. if defect is small, child may be aysmptomatic

2. a loud machine like murmur is characteristic3. child may have frequent resp. infections

4. child may have CHF with poor feeding,fatigue, hepatosplenomegaly, poor weight gain,

tachypnea and irritability5. widened pulse pressure and bounding pulse

rate maybe detected



ACYANOTIC CHD (PDA)

b. Laboratory and diagnostic findings:

1. ECG normal but may show ventricle enlargement if the

shunt is large

3. Nursing management:

a. Provide family teaching abt. treatment options

- some close spont; others can be closed surgically or

nonsurgically

b. In premature infants, PD A sometimes can beclosed using prostaglandin synthetase inhibitors(Indomethacin) w/c stimulate closure of the ductus

arteriosus



ACYANOTIC CHD (ASD)

B. ATRIAL SEPTAL DEFECT

- an abnormal communication between the toatria; results when the atrial septal tissue does

not fuse properly during embryonic devt.

1. Pathophysiology

a. pressure is higher in the left atrium than the

right, causing blood to shunt from left to right

b. the R V and P A enlarge because they arehandling more blood



ACYANOTIC CHD (ASD)


a. Clinical manifestations:

- most infants tend to be aysmptomatic until earlychildhood and many defects close spont. By 5y.o.

- symptoms vary with the size of the defect,fatigue and dyspnea on exertion are the mc

- slow weight gain and frequent respiratory

infections may occur

- systolic ejection murmur may be auscultated,usually most prominent at the 2nd ICS



ACYANOTIC CHD (ASD)

b. Laboratory and diagnostic study findings:

- echocardiography with doppler gen. reveals the

enlarged R side of the heart and the inc. pulmonary circulation

- cardiac catheterization demonstrates the separation of

the R atrial septum and the inc. oxygen saturation in the R atrium


a. Provide family teaching abt. treatment options:- defects are usually repaired in girls due to possibility of clot formation during child bearing years

- small ASDs are left open in boys, larger ones are repaired

- surgical closure is performed during the school age years



ACYANOTIC CHD (VSD)

C. VENTRICULAR SEPTAL DEFECT

- the most common CHD, is an abnormal openingbetween the right and left ventricles

- the degree of this defect vary from a pinholebetween the R & L ventricles to an absent septum

1. Pathophysiology

a. pressure from the L V causes blood to flowthrough the defect to R V, resulting in increasedpulmonary vascular resistance and right heart enlargement



ACYANOTIC CHD (VSD)

b. R V and P A pressures increase, leadingeventually to obstructive pulmonary vasculardisease


- symptoms vary with the size of the defect, ageand amt of resistance, usually the child is asymp.

- failure to thrive, excessive sweating, fatigue

- more susceptible to pulmonary infections

- may exhibit s/s of CHF



ACYANOTIC CHD (VSD)


- Echocardiography with Doppler U/S or MRI reveals R VH and possible P A dilatation from the inc. blood flow

- ECG shows R VH

3. Nursing management

a. provide family teaching abt treatment options

- some VSDs close spontaneously

- others are closed with a Dacron patch, recommended for largedefects, P A hypertension, CHF, recurrent resp. infxns. FTT



CYANOTIC CHD (TOF)

ACYANOTIC CHD ACYANOTIC CHD

A. TETRALOGY OF F ALLOT (TOF)

- consists of 4 major anomalies:

a. VSD c. PS

b. R VH d. overriding aorta

1. Pathophysiologya. PS impedes the flow of blood to the lungs, causingincreased pressure in the R V, forcing deoxygenatedblood through the septal defect to the L V



CYANOTIC CHD (TOF)

b. the increased workload on the R V causeshypertrophy. The overriding aorta receives blood fromboth right and left ventricles.


a. Clinical manifestations: vary, depending on thesize of the VSD and the degree of PS.

1. Acute episodes of cyanosis (tet spells) andtransient cerebral ischemia. Tet spells are char. Byirritability, pallor, and blackouts or convulsions.

2. Cyanosis occurring at rest (as PS worsens)



CYANOTIC CHD (TOF)

3. Squatting (a char. posture of older children that

serves to decrease the return of poorly oxygenatedvenous blood from the lower extremities and to inc.

S VR, w/c increases pulmonary blood flow and easesrespiratory effort)

4. slow weight gain

5. clubbing, exertional dyspnea, fainting, or fatigueslowness due to hypoxia

6. a pansystolic murmur may be heard at the mid-lower left sternal border



CYANOTIC CHD (TOF)

b. Laboratory and diagnostic study findings

1. echocardiography and ECG show the enlargedchambers of the right side of the heart

2. echocardiography also demonstrates thedecrease in the size of the P A and the reduced bloodflow through the lungs

3. cardiac catheterization and angiography allowdefinitive evaluation of the extent of the defect,particularly the PS and the VSD

4. CBC reveals polycythemia, ABG demonstratereduced oxygen saturation



CYANOTIC CHD (TOF)


a. Provide family teaching about treatment options

1. elective repair is usually performed during the

infants 1st year of life, but palliative repairs may bewarranted for infants who cannot undergo primaryrepair

2. total repair involves VSD closure, infundibularstenosis resection, and pericardial patch to enlarge R Voutflow tract

b. Provide preoperative and postoperative care



CYANOTIC CHD (TGV)

B. TRANSPOSITION OF GREAT VESSELS (TG V)

- in TG V, the P A leaves the L V and the aorta exits theR V, there is no communication between the systemic

and pulmonary circulations

1. Pathophysiology

a. this defect results in two separate circulatory

patterns; the right heart manages systemic circulationand the left manages pulmonary circulation

b. to sustain life, the child must have an associateddefect.



CYANOTIC CHD (TGV)

Associated defects such as septal defects or a PD A,

permit oxygenated blood into the systemic circulationbut cause increased cardiac workload.

c. Potential complications include CHF, infectiveendocarditis, brain abscess, and cerebral vascularaccidents resulting from hypoxia or thrombosis.

2. A

ssessment findings:a. Clinical manifestations vary, depending onassociated defects



CYANOTIC CHD (TGV)

1. In infants with minimal communication (no

associated defects), severe respiratory depression andcyanosis, will be evident at birth

2. In infants with associated defects, there is lesscyanosis but the infant may have symptoms of CHF

3. easily fatigued, FTT

b. Laboratory and diagnostic study findings1. echocardiography reveals an enlarged heart

2. cardiac catheterization reveals low O2 saturationresulting from the mixing of blood in the chambers



CYANOTIC CHD (TGV)


a. Provide family teaching about the treatment options

1. Prostaglandin E is administered to maintain a

PD A and further blood mixing.

2. An arterial switch procedure within the 1st weekof life is the surgical procedure of choice

C. TRUNCUS ARTERIOSUS - failure of normal septation and division of the

embryonic bulbar trunk into the P A and aorta,resulting in a single vessel that overrides bothventricles



CYANOTIC CHD

1. Pathophysiology

a. blood ejected from the ventricles enters thecommon artery and flows either the lungs or aortic

arch.b. pressure in both ventricles is high and blood flow tothe lungs is markedly increased.

2. Assessment findings:a. neonates with this defect appear normal; however,as pulmonary vascular resistance decreases afterbirth, severe pulmonary edema and CHF commonlydevelop



CYANOTIC CHD

2. marked cyanosis, especially on exertion; S /S of CHF; L VH, dyspnea, marked activity intolerance, andretarded growth

3. loud systolic murmur best heard at the lower left sternal border and radiating throughout the chest


- echocardiography reveals the defect


a. surgical repair is necessary in the 1st few months of life, the mortality rate associated with surgery isgreater than 10%; w/o surgery, children die w/in 1 yr.



OBSTRUCTIVE CHD (COA)

OBSTRUCTIVE CHD

A. CO ARCT ATIO N O F AORT A (CO A)

- a defect that involves a localized narrowing of theaorta

1. Pathophysiology

a. CO A is char. by inc. pressure proximal to the defect

and decreased pressure distal to it b. restricted blood flow through the narrowed aortaincreases the pressure on the LV and causes dilationof the proximal aorta and LVH , w/c may lead to LV F




c. eventually, collateral vessels develop to bypass thecoarctated segment and supply circulation to the LE

2. Assessment findings:a. Clinical manifestations

1. the child may be asymptomatic or mayexperience the classic difference in BP and pulse

quality between the upper and lower ext. theBP iselevated in the UE and dec. in the LE while the pulse

is bounding in the UE and dec. or absent in the LE.Thus femoral pulse are weak or absent

( )




2. epistaxis, headaches, fainting and lower legcramps

3. a systolic murmur may be heard over the left

anterior chest and between the scapula posteriorly4. rib notching may be observed in an older child

b. Laboratory and diagnostic findings

1. ECG, echocardiography, and chest x-ray mayreveal left sided heart enlargement resulting fromback pressure

2. the radiograph may also demonstrate ribnotching from enlarged collateral vessels

O S C C (CO )





a. repair involves surgical removal of the stenotic area

b. nonsurgical repair via balloon angioplasty

B. AORTIC STENOSIS ( AS)

- a defect that primarily involves an obstruction to theL V outflow of the valve

1. Pathophysiology

a. L V pressure inc. to overcome resistance of theobstructed valve and allow blood to flow into theaorta, eventually producing L VH

OBSTRUCTIVE CHD (AS)




b. MI may develop as the inc. O2 demands of the

hypertrophied L V go unmet

2. Assessment findings:a. clinical manifestations:

1. faint pulse, hypotension, tachycardia, and poorfeeding pattern

2. exercise intolerance, chest pain, and dizzinesswhen standing for long periods

3. a systolic ejection murmur may be heard best at the 2nd ICS






1. ECG or echocardiography reveals L VH

2. cardiac catheterization demonstrates degree of

the stenosis


a. if the childs symptoms warrant, surgical aortic

valvulotomy or prosthetic valve replacement isnecessary

b. balloon angioplasty can be used to dilate thenarrow valve

OBSTRUCTIVE CHD (PS)




C. PULMONIC STENOSIS (PS)

- a defect that involves obstruction of blood flow fromthe right ventricle

1. Pathophysiology

a. R V pressure increases leading to R VH andeventually R V failure may occur


a. Clinical manifestations

1. may be asymptomatic or may have mild cyanosisor CHF








a. provide family teaching about treatment options

1. Balloon angioplasty techniques are being widely

used to treat PS2. Surgical valvulotomy may be performed

(although the need for surgery is uncommon due tothe widespread use of balloon angioplasty techniques)

b. provide preoperative and postoperative care

THE BLOOD VESSELS



THE BLOOD VESSELS

A. HY PERTENSION

- persistent elevation of the SBP above 140mmHg andof DBP above 90mmHg (WHO)

Types:

a. Essential (primary, idiopathic): marked by loss of elastic tissue and arteriosclerotic changes in the aorta

and larger vessels coupled with decreased caliber of the arterioles

b. Benign: a moderate rise in BP marked by agradual onset and prolonged course

HYPERTENSION



HYPERTENSION

c. Malignant: characterized by a rapid onset andshort dramatic course with a DBP of >150mmHg

d. Secondary: elevation of the BP as a result of

another disease such as renal parenchymal disease,Cushings disease, pheochromocytoma, primaryaldosteronism, coarctation of the aorta

A. Essential hypertension usually occurs between ages 35-

50; more common in men over 35, women over 45; African- American men affected twice as often as whitemen/women

HYPERTENSION



HYPERTENSION

Risk Factors:

- (+) family history, obesity, stress, cigarette smoking,hypercholesterolemia, inc. sodium intake


1. Diet and weight reduction (restricted sodium, kcal,cholesterol)

2.Lifestyle changes: alcohol moderation, exerciseregimen, cessation of smoking

3. Antihypertensive drug therapy

HYPERTENSION



HYPERTENSION


1. Pain similar to anginal pain; pain in calves of legs afterambulation or exercise (intermittent claudication);

severe occipital headaches, particularly in themorning; polyuria; nocturia; fatigue; dizziness;epistaxis; dyspnea on exertion

2. BP consistently above 140/90, retinal hges andexudates, edema of extremities

3. Rise in SBP from supine to standing position (indicativeof essential hypertension)

4. Diagnostic tests: elevated serum uric acid, sodium,cholesterol levels

HYPERTENSION



HYPERTENSION


1. Record baseline BP in 3 positions (lying, sitting,standing) and in both arms

2. Continuously assess BP and report any variables that relate to changes in BP (positioning, restlessness)

3. Administer antihypertensive agents as ordered; monitorclosely and assess for S /E

4. Monitor intake and hourly output


- risk factors, dietary instructions, compliance of antihypertensive medications, routine follow up w/ MD

ARTERIOSCLEROSIS



OBLITERANS

- a chronic occlusive arterial disease that may affect the abdominal aorta or the LE. The obstruction toblood flow with resultant ischemia usually affects

the femoral, popliteal, aortic and iliac arteries- occurs most often in men ages 50-60

- caused by atherosclerosis

- Risk Factors: cigarette smoking, hyperlipidemia,

hypertension, DM

ARTERIOSCLEROSIS



OBLITERANS


1. Drug therapy

a. Vasodilators: papaverine, Isoxsuprine Hcl

(Vasodilan), Nylidrin Hcl ( Arlidin), nicotinyl alcohol(Roniacol) cyclandelate (Cyclospasmol), tolazoline Hcl(priscoline) to improve arterial circulation;effectiveness questionable

b. Analgesics to relieve ischemic pain c.

Anticoagulants to prevent thrombus formationd. Lipid reducing drug: cholestyramine, colesti[pol

Hcl, dextrothyroxine sodium, clofibrate, gemfibrozil(Lopid), niacin, lovastatin (Mevacor), atorvastatin

ARTERIOSCLEROSIS



OBLITERANS

2. Surgery: bypass grafting, endarterectomy, ballooncatheter dilation, lumbar sympathectomy (to increaseblood flow), amputation may be necessary


1. Pain both intermittent claudication and rest pain,numbness or tingling of the toes

2. Pallor after 1-2 mins. Of elevating feet, and dependent

hyperemia/rubor; diminished or absent dorsalis pedis,posterior tibial and femoral pulses; shiny, taut skinwith hair loss on lower legs

ARTERIOSCLEROSIS



OBLITERANS


a. Oscillometry may reveal decrease pulse volume

b. Doppler U/S reveals decreased blood flow through

affected vesselsc. Angiography reveals location and extent of obstructive process

4. Elevated serum triglycerides; sodium

D. Nursing Interventions:

1. Encourage slow, progressive physical activity

ARTERIOSCLEROSIS



OBLITERANS

2. Administer medications as ordered

3. Assist with Buerger- Allen exercises qid

a. client lies with legs elevated above heart for 2-3

minsb. client sits on edge of bed with legs and feet dependent and exercises feet and toes upward anddownward, inward and outward for 3 mins

c. client lies flat with legs at heart level for 5 mins

4. Assess for sensory function; protect client from injury

5. Provide client teaching and discharge planning: stopcigarette smoking, diet, drug compliance, exercise

THROMBOANGIITIS

OBLITERANS



OBLITERANS(BUERGERS DISEASE)

- Acute inflammatory disorder affecting medium/smallerarteries and veins of the LE. Occurs as focal,obstructive process; results in occlusion of a vesselwith subsequent development of collateral circulation

- Most often affects men ages 25-40; disease is idiopathic;high incidence among smokers

A. Medical management: same as arteriosclerosis

obliterans but only cessation of smoking is effectivetreatment

THROMBOANGIITIS

OBLITERANS





1. Intermittent claudication, sensitivity to cold (skin of extremity may at first be white, changing to blue then

red)2. Decreased or absent peripheral pulses (post. tibial and

dorsalis pedis), ulceration and gangrene (advanced)

3. Diagnostic tests: same as arteriosclerosis obliteransexcept no elevation in serum triglycerides

C. Nursing Interventions:

1. Prepare client for surgery

THROMBOANGIITIS

OBLITERANS





- drug regimen, avoidance of trauma to the affectedextremity, need to maintain warmth esp. during cold

weathers, importance of stopping smoking

RAYNAUDS



PHENOMENON

- intermittent episode of arterial spasms, most frequentlyinvolving the fingers; most often affects womenbetween the teenage years and age 40; causeunknown

- Predisposing factors: collagen diseases (SLE, RA), trauma(from typing, playing piano)

A. Medical management: vasodilators, catecholamine-

depleting antihypertensive drugs (reserpine,guanethidine monosulfate)

RAYNAUDS



PHENOMENON


1. coldness, numbness, tingling in one or more digits; pain(usually pptd. By exposure to cold, emotional upsets,

tobacco use)2. intermittent color changes (pallor, cyanosis, rumor);

small ulcerations and gangrene tips of digits

C. Nursing interventions

1. provide client teaching concerning:

- importance of stopping smoking; need to maintainwarmth; need to use gloves in handling cold objects;

drug regimen

ANEURYSM



ANEURYSM

- a sac formed by dilation of an artery secondary toweakness and stretching of an arterial wall. Thedilation may involve one or all layers of the arterialwall.

C lassification

1. Fusiform: uniform spindle shape involving the entirecircumference of the artery

2. Saccular: outpouching on one side only, affecting part of the arterial circumference

ANEURYSM



ANEURYSM

3. Dissecting: separation of the arterial wall layers to forma cavity that fills with blood

4. False: the vessel wall is disrupted, blood escapes into

surrounding area but is held in place by surroundingtissue

A. General info:

1. an aneurysm, usually fusiform or dissecting, in the

descending, ascending, or transverse section of thethoracic aorta

2. usually occurs in men ages 50-70; caused by

arteriosclerosis, infection, syphilis, hypertension

ANEURYSM



ANEURYSM


1. control of underlying hypertension

2. Surgery: resection of the aneurysm and replacement

with a Teflon/Dacron graft; client will needextracorporeal circulation


1. Often asymptomatic; deep, diffuse chest pain;hoarseness; dysphagia; dyspnea

2. Pallor, diaphoresis, distended neck veins

ANEURYSM



ANEURYSM


a. Aortography shows exact location of the aneurysm

b. X-rays: chest film reveals abnormal widening of

aorta; abdominal film may show calcification withinwalls of aneurysm

4. Nursing interventions: same as in Cardiac surgery

THROMBOPHLEBITIS



THROMBOPHLEBITIS

A. General info:

1. Inflammation of the vessel wall with formation of a clot (thrombus); may affect superficial or deep veins

2. Most frequent veins affected are the saphenous,femoral, and popliteal.

3. Can result in damage to the surrounding tissues,ischemia and necrosis

4. Risk Factors: obesity, CHF, prolonged immobility, MI,

pregnancy, oral contraceptives, trauma, sepsis,cigarette smoking, dehydration, severe anemias,venous cannulation, complication of surgery

THROMBOPHLEBITIS



THROMBOPHLEBITIS


1. Anticoagulation therapy:

a. Heparin: blocks conversion of prothrombin to

thrombin and reduces formation of thrombus- S /E: spontaneous bleeding, injection site

reactions, ecchymoses, tissue irritation and sloughing,reversible transient alopecia, cyanosis, pain in arms orlegs, thrombocytopenia

b. Warfarin (coumadin): blocks prothrombin synthesisby interfering with vit. K synthesis

- S /E: GI: anorexia, nausea/vomiting, diarrhea,stomatitis

THROMBOPHLEBITIS



THROMBOPHLEBITIS

- hypersensitivity: dermatitis, urticaria, pruritus, fever

- other: transient hair loss, burning sensation of feet,bleeding complications.

2. Surgery

a. Vein ligation and stripping

b. venous thrombectomy: removal of a clot in theiliofemoral region

c. plication of the inf. vena cava: insertion of anumbrella-like prosthesis into the lumen of the venacava to filter incoming clots

THROMBOPHLEBITIS



THROMBOPHLEBITIS


1. Pain in the affected extremity

2. Superficial vein: tenderness, redness, induration along

course of the vein3. Deep vein: swelling, venous distension of limb,

tenderness over involoved vein, (+) Homans sign

4. Elevated WBC and ESR


a. venography (phlebography): inc. uptake of radioactive material

THROMBOPHLEBITIS



THROMBOPHLEBITIS

b. Doppler ultrasonography: impairment of blood flowahead of thrombus

c. Venous pressure measurements: high in affected

limb until collateral circulation is developed

D. Nursing interventions

1. Provide bed rest, elevating involved extremity

2. Apply continuous warm, moist soaks to dec. lymphaticcongestion

3. Administer anticoagulants as ordered

THROMBOPHLEBITIS



THROMBOPHLEBITIS

a. Heparin

1. monitor PTT, use infusion pump to administer I V heparin

2. assess for bleeding tendencies (hematuria;

hematemesis; bleeding gums; epistaxis, melena)3. have antidote ( protamine sulfate) available

b. Warfarin (Coumadin)

1. assess PT

daily, advise client to withhold dose and notifyphysician immediately if bleeding or signs of bleedingoccurs

2. instruct client to use a soft toothbrush and to flossgently, prepare antidote: Vit. K

THROMBOPHLEBITIS



THROMBOPHLEBITIS

4. monitor for chest pain or SOB (possible pulmonaryembolism)


a. need to avoid standing, sitting for long periods;constrictive clothing; crossing legs at the knees;smoking; oral contraceptives

b. importance of adequate hydration

c. use of elastic stockings when ambulatory

d. importance of planned rest with elevation of feet

e. importance of weight reduction and exercise

VARICOSE VEINS



VARICOSE VEINS

A. General info:

1. Dilated veins that occur most often in the lowerextremities and trunk. As the vessel dilates, the valves

become stretched and incompetent with resultant venous pooling/edema

2. most common between ages 30-50

3. predisposing factor: congenital weakness of the veins,thrombophlebitis, pregnancy, obesity, heart disease

B. Medical management: vein ligation (involves ligating thesaphenous vein where it joins the femoral vein andstripping the saphenous vein system from groin to ankle)

VARICOSE VEINS



VARICOSE VEINS


1. Pain after prolonged standing (relieved by elevation)

2. Swollen, dilated, tortuous skin veins

3. Diagnostic tests:a. Trendelenburg test: varicose veins distend veryquickly (less than 35 secs)

b. Doppler U/S: decreased or no blood flow heardafter calf or thigh compression


1. Elevate legs above heart level

VARICOSE VEINS



VARICOSE VEINS

2. Apply knee length elastic stockings

3. Provide adequate rest

4. Prepare client for vein ligation, if necessary

a. Provide routine pre-op careb. keep affected extremity elevated above the level

of the heart to prevent edema

c. apply elastic bandages and stockings, whichshould be removed every 8hrs for short periods.

d. assist out of bed within 24hrs, ensuring that elastic stockings are applied.

e. assess for increased bleeding



Documents

4. Cardiovascular