med surg cardiovascular system

MEDICAL-SURGICAL NURSING

CARDIO

VASCULAR

SYSTEM

Prof. Randy V. Prof. Randy V. Fernandez, RN, MAN, Fernandez, RN, MAN, USRNUSRN

CARDIOVASCULAR SYSTEM

Consists: heart, arteries, veins, capillaries

Functions: 1. circulation of blood

2. delivery of oxygen and other nutrients to tissues of the body 3. removal of carbon dioxide and other products of cellular metabolism

CARDIOVASCULAR CARDIOVASCULAR SYSTEM

HEART ANATOMY and PHYSIOLOGY:

A. Heart wall1. pericardium

a. fibrous pericardium

b. serous pericardium

2. epicardium3. myocardium4. endocardium


B. Chambers1. Atria a. right

b. left2. Ventricles a. right

b. leftC. Valves

1. Atrioventricular valvesa. Mitral valveb. Tricuspid valve


c. Function:- permit unidirectional flow of blood

from specific atrium to specific ventricle during ventricular diastole

- prevent reflux during ventricular systole

- valve leaflets open during ventricular diastole and close during ventricular systole; valve closure produces the first heart sounds (S1)


2. Semilunar valves

a. Pulmonary valve

b. Aortic valve

c. Function:- permit unidirectional flow of blood from

specific ventricle to arterial vessel during ventricular systole

- prevent reflux during ventricular diastole

- valves open when ventricles contract and close during ventricular diastole; valve closure produces the second heart sound (S2)


D. Conduction System1. Sinoatrial (SA) node2. Internodal Tracts3. Atrioventricular (AV) node4. Bundle of His

- right bundle branch- left bundle branch

5. Purkinje fibers* Electrical activity of heart can be visualized by ECG


E. Coronary Circulation1. Arteries

a. right coronary arteryb. left coronary artery

2. Veinsa. coronary sinus veinsb. thebesian veins


VASCULAR SYSTEMFunction: a. supply tissues with bloodb. remove wastesc. carry unoxygenated blood back to the heart


TYPES OF BLOOD VESSELSA. ArteriesB. ArteriolesC. Capillaries: the following exchanges occur:

- oxygen and carbon dioxide- solutes between the blood and tissues- fluid volume transfer between the

plasma and interstitial spacesD. VenulesE. Veins


ASSESSMENT HEALTH HISTORYA. Presenting problem

1. Nonspecific symptoms may include- fatigue - shortness of breath- cough - palpitations- headache - weight loss/gain- syncope - difficulty sleeping- dizziness - anorexia


2. Specific signs and symptomsa. chest painb. dyspnea (shortness of breath)c. orthopnea / paroxysmal nocturnal dyspnead. palpitations: precipitating factorse. edemaf. cyanosis

B. Lifestyle: occupation, hobbies, financial status, stressors, exercise, smoking, living conditions


C. 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 Medical HistoryG. Family history: heart disease (congenital,

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


PHYSICAL EXAMINATIONA. Skin and mucous membranes: - color/texture, temperature, hair distribution

on extremities, atrophy or edema, petechiaeB. 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=full and bounding


C. Assess for arterial insufficiency and venous impairment

D. Measure and record blood pressureE. Inspect and palpate the neck vessels:

a. jugular veins: note location, characteristics, jugular venous pressureb. carotid arteries: location and characteristics

F. Auscultate heartsounds - normal (S1, S2)- abnormal (S3, S4)


LABORATORY / DIAGNOSTIC TESTSA. Blood Chemistry and electrolyte analysis 1. Cardiac enzymes: in MI

a. Troponin T: detected 3-12 hours after chest painb. Troponin I: detected 3-12 hrsc. creatine phosphokinase (CPK – MB): 6-12Hrsd. Aspartate aminotransferase (AST) (SGOT): 24 Hrs after chest paine. Lactic dehydrogenase (LDH): 36 Hrs


2. Electrolytesa. 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

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

- dec. levels can cause dysrhythmias


d. 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


b. 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 formationd. Triglycerides 10-150 mg/dl:

- high levels increase risk of atherosclerotic heart disease


B. Hematologic Studies1. CBC2. Coagulation time: 5-15mins; inc. levels indicate bleeding 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 therapy5. Erythrocyte sedimentation rate(ESR) <20mm/hr; inc. level indicate inflamm. process


C. Urine Studies (routine U/A)D. Electrocardiogram (ECG)

1. Noninvasive ECG – a graphic record of the electrical activity of the heart2. Portable recorder (Holter monitor) – provides continuous recording of ECG for up to 24 hrs.

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

F. Echocardiogram: noninvasive recording of the cardiac structures using ultrasound


G. Cardiac catheterization: invasive, but often definitive test for diagnosis of cardiac disease.1. A catheter is inserted into the right or left side of the heart to obtain information2. Purpose: to measure intracardiac pressures and 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)


3. 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


4. 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


H. Coronary arteriography1. visualization of coronary arteries

by injection of radiopaque contrast dye and recording on a movie film.

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

3. Nursing care: same as cardiac catheterization

ANALYSIS

Nursing diagnosis for the client with CVD includeA. Fluid volume excessB. Decreased cardiac outputC. Altered peripheral tissue perfusionD. Impairment of skin integrityE. Risk for activity intoleranceF. PainG. Ineffective copingH. FearI. Anxiety

PLANNING AND IMPLEMENTATION

GOALSA. Fluid imbalance will be resolved, edema

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

will be improvedD. Adequate skin integrity will be maintainedE. Activity intolerance will progressively increaseF. Pain in the chest will be diminishedG. Client’s level of fear and anxiety will be

decreased


INTERVENTIONSCARDIAC MONITORINGA. ECG 1. strip: small square: 0.04secs.

large square: 0.2secs.2. P wave: produced by atrial depolarization;

indicates SA node function


3. P-R interval (N˚= 0.12 - 0.20 secs.)a. indicates AV conduction time or the time it takes an impulse to travel from the atria down and through the AV nodeb. measured from beginning of P wave to beginning of QRS complex

4. QRS complex (N˚= 0.06-0.10 secs.)a. indicates ventricular depolarizationb. measured from onset of Q wave to end of S wave


5. ST segmenta. indicates time interval between complete depolarization of ventricles and repolarization of ventriclesb. measured after QRS complex to beginning of T wave

6. T wavea. represents ventricular repolarizationb. follows ST segment


HEMODYNAMIC MONITORING(Swan Ganz Catheter)A. A multilumen catheter with a balloon tip that is

advanced through the superior vena cava into the RA, RV, and PA. When it is wedged it is in the distal arterial branch of the pulmonary artery.

B. Purpose:1. Proximal port: measures RA pressure 2. Distal port:

a. measures PA pressure and PCWP


b. normal values: PA systolic and diastolic less than 20mmHg; PCWP 4-12mmHg

C. Nursing care1. a sterile dry dressing should be applied to site and changed every 24 hours; inspect site daily and report signs of infection2. if catheter is inserted via an extremity, immobilize extremity to prevent catheter dislodgment or trauma.


3. Observe catheter site for leakage4. Ensure that balloon is deflated with a syringe attached except when PCWP is read5. Continuously monitor PA systolic and diastolic pressures and report significant variations6. Irrigate line before each reading of PCWP7. Maintain client in same position for each reading8. Record PA systolic and diastolic readings at least every hour and PCWP as ordered.


CENTRAL VENOUS PRESSURE (CVP)A. Obtained by inserting a catheter into the

external jugular, antecubital, or femoral vein and threading it into the vena cava. The catheter is attached to an IV infusion and H2O manometer by a three way stopcock

B. Purposes:1. Reveals RA pressure, reflecting alterations in the RV pressure


2. Provides information concerning blood volume and adequacy of central venous return3. Provides an IV route for drawing blood samples, administering fluids or medication, and possibly inserting a pacing catheter

C. Normal range is 4-10 cmH20; elevation indicates hypervolemia, decreased level indicates hypovolemia

D. Nursing care1. Ensure client is relaxed


2. Maintain zero point of manometer always at level of right atrium (midaxillary line)3. Determine patency of catheter by opening IV infusion line4. Turn stopcock to allow IV solution to run into manometer to a level of 10-20cm above expected pressure reading5. Turn stopcock to allow IV solution to flow from manometer into catheter; fluid level in manometer fluctuates with respiration


6. Stop ventilatory assistance during measurement of CVP7. After CVP reading, return stopcock to IV infusion position8. Record CVP reading and position of client

EVALUATION

DISORDERS OF THE CARDIOVASCULAR

SYSTEMHEARTCORONARY ARTERY DISEASE (CAD)A. General Information

1. refers to a variety of pathology that cause narrowing or obstruction of the coronary arteries, resulting in decreased blood supply to the myocardium2. major causative factor: Atherosclerosis3. bet 30-50 y.o., men>women4. may manifest as angina pectoris or MI

CORONARY ARTERY DISEASE

5. Risk factors: - family history of CAD - DM- el. Serum lipoproteins - hypertension- cigarette smoking - obesity- el serum uric acid - lifestyle

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

ANGINA PECTORIS

A. Gen. info:1. transient, paroxysmal chest pain produced by insufficient blood flow to the myocardium resulting in myocardial ischemia2. Risk factors:- CAD - 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 adrenergic blocking 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 the neck, jaw, back and arms, relieved by REST2. 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 during exercise

D. Nursing interventions:1. administer oxygen2. give prompt pain relief with nitrates or narcotic analgesics as ordered.

ANGINA PECTORIS

3. Monitor V/S, status of cardiopulmonary function, monitor ECG4. place patient in semi-high Fowler’s position5. provide emotional support, health teachings and discharge instructions.6. Instruct client to notify physician immediately if pain occurs and persists, despite rest and medication administration.

MYOCARDiAL INFARCTiON

A. General information:1. The death of myocardial cells from inadequate oxygenation, often caused by a sudden complete blockage of a coronary artery; characterized by localized formation of necrosis (tissue destruction) with subsequent healing by scar formation and fibrosis.2. Risk factors: - atherosclerotic CAD - DM- thrombus formation - hypertension


B. Assessment findings:1. Pain same as in angina, crushing, viselike with sudden onset; UNRELIEVED by rest or nitrates2. nausea/vomiting, dyspnea3. skin: cool, clammy, ashen4. elevated temperature5. initial increase in BP and pulse, with gradual drop in BP6. Restlessness


7. Occasional findings: rales or crackles; presence of S4; pericardial friction rub; split S1, S2

8. Diagnostic tests:a. elevated WBC, cardiac enzymes (troponin, CPK-MB, LDH, SGOT)b. ECG changes (specific changes dependent on location of myocardial damage and phase of the MI; inverted T wave and ST segment changes seen with myocardial ischemiac. inc. ESR, el. serum cholesterol


C. Nursing interventions:1. establish a patent IV line2. provide pain relief; morphine sulfate IV (poor peripheral perfusion, false + for enzymes)3. Administer O2 as ordered to relieve dyspnea and prevent arrhythmias 4. Provide bed rest with semi fowler’s position 5. Monitor ECG and hemodynamic procedures6. Administer anti-arrhythmias as ordered.


7. Monitor I & O, report if UO <30 ml/hr8. Maintain full liquid diet with gradual increase to soft, low salt9. Maintain quiet environment10. Administer stool softeners as ordered11. Relieve anxiety associated with CCU environment12. Administer anticoagulants, thrombolytics (tpa or streptokinase) as ordered and monitor for S/E


13. Provide client teaching and discharge instruction concerning- effects of MI, healing process and treatment regimen- Medication regimen: name, purpose, schedule, dosage, S/E- Risk factors with necessary lifestyle modification- Dietary restrictions: low salt, low cholesterol, avoidance of caffeine- Resumption of sexual activity as ordered (usually 4-6weeks)


- Need to report the ff. symptoms:* increased persistent chest pain* pain, dyspnea, weakness, fatigue* persistence palpitations, light

headedness- Enrollment of client in a cardiac rehabilitation program

DYSRHYTHMIAS

An arrhythmia is a disruption in the normal events of the cardiac cycle. It may take a variety of forms.

Treatment varies on the type dysrhythmias

SINUS TACHYCARDIAA. General Information:

1. A heart rate of over 100 beats/min, originating in 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 /min2. Rhythm: regular

DYSRHYTHMIAS

3. P wave: precedes each QRS complex with normal contour4. 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 BRADYCARDIAA. General Information:

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 trained athletes

DYSRHYTHMIAS

B. Assessment findings:1. Rate: <60 beats/min2. Rhythm: regular3. P wave: precedes each QRS with a normal contour4. P-R interval: normal5. QRS complex: normal

C. Treatment: usually not needed- if cardiac output is inadequate: atropine and isoproterenol; pacemaker

DYSRHYTHMIAS

ATRIAL FIBRILLATIONA. General information

1. An arrhythmia in which ectopic foci cause rapid, irregular contractions of the heart2. seen in clients with - rheumatic mitral stenosis - thyrotoxicosis- cardiomyopathy - pericarditis- hypertensive heart disease - CHD

DYSRHYTHMIAS

B. Assessment findings:1. Rate: atrial: 350-600 beats/min

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

irregular3. P wave: no definite P wave; rapid undulations called fibrillatory waves4. P-R interval: not measurable5. QRS complex: generally normal

DYSRHYTHMIAS

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

PREMATURE VENTRICULAR CONTRACTIONSA. General Information:

1. Irritable impulses originate in the ventricles2. Caused by:- electrolyte imbalance (hypokalemia)- digitalis drug therapy

DYSRHYTHMIAS

Cont’d: (causes)- stimulants( caffeine, epinephrine, isoproterenol)- hypoxia- CHF

B. Assessment findings:1. Rate: varies according to no. of PVC’s2. Rhythm: irregular because of PVC’s3. P wave: normal; however, often lost in QRS complex

DYSRHYTHMIAS

4. P-R interval: often not measurable5. QRS complex: greater then 0.12secs, wide

C. Treatment: 1. IV push of Lidocaine (50-100mg) followed by IV drip of lidocaine at rate of 1-4 mg/min2. Procainamide, quinidine3. Treatment of underlying cause

DYSRHYTHMIAS

VENTRICULAR TACHYCARDIAA. General information:

1. 3 or more consecutive PVC’s; occurs from repetitive firing of an ectopic focus in the ventricles2. caused by:- MI - CAD- digitalis intoxication - hypokalemia

DYSRHYTHMIAS

B. Assessment findings: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 complex4. P-R interval usually not measurable5. QRS complex: greater than 0.12 secs, wide

DYSRHYTHMIAS

C. Treatment:1. IV push of lidocaine (50-100mg), then IV drip of lidocaine 1-4 mg/min2. Procainamide via IV infusion of 2-6 mg/min3. direct current cardioversion4. bretylium, propanolol

PERCUTANEOUS TRANSLUMINAL

CORONARY ANGIOPLASTY (PTCA)

A. General information:1. PTCA can be performed instead of coronary artery bypass graft surgery in various clients with single vessel CAD.2. Aim: revascularize the myocardium

decrease angina – increase survival3. a balloon tipped catheter is inserted into the stenotic, diseased coronary artery. The balloon is inflated with a controlled pressure and thereby decreases 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 CAD2. new supply of blood brought to diseased/occluded coronary artery by bypassing the obstruction with a graft that is attached to the aorta proximally and to the coronary artery distally3. Procedure requires use of extracorporeal circulation (heart-lung machine, cardiopulmonary bypass)


B. Nursing interventions: preoperative1. Explain anatomy of the heart, function of coronary arteries, effects of CAD2. Explain events of the day of surgery3. Orient to the critical and coronary care units and introduce to staff4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc)5. Demonstrate activity and exercise6. Reassure availability of pain medications


C. Nursing interventions: post-operative1. Maintain patent airway2. Promote lung re-expansion3. monitor cardiac status4. maintain fluid and electrolyte balance5. maintain adequate cerebral circulation6. provide pain relief7. prevent abdominal distension


8. Monitor for and prevent the ff. complications:a. Thrombophlebitis / pulmonary

embolismb. Cardiac tamponadec. arrhythmiasd. CHF

9. Provide client teaching and discharge planning concerning:

a. limitation with progressive increase in activities


b. sexual intercourse can usually be resumed by 3rd or 4th week post-op

c. medical regimend. meal planning with prescribed

modificationse. wound cleansing daily with mild soap

and H2O and report for any signs of infectionf. Symptoms to be reported: - fever, dyspnea, chest pain with

minimal exertion

CONGESTIVE HEART FAILURE

A. Gen. Info:- Inability of the heart to pump an adequate supply of blood to meet the metabolic needs of the body

B. Types:1. Left sided heart failure2. Right sided heart failure


1. LEFT SIDED HEART FAILUREa. Left ventricular damage causes blood to back up through the left atrium and into the pulmonary veins. Increased pressure causes transudation into the interstitial tissues of the lungs with resultant pulmonary congestion

b. Caused by:- left ventricular damage (MI, CAD)- hypertension, aortic valve disease (AI, AS)- mitral stenosis, cardiomyopathy


c. Assessment findings:Signs:- easy fatigability, dyspnea on exertion, PND, orthopnea, cough, nocturia, confusion

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


d. Diagnostic tests:- ECG, chest x-ray (cardiomegaly, pleural effusion), echocardiography, cardiac catheterization, dec. PO2, inc. PCO2

2. RIGHT SIDED HEART FAILUREa. weakened RV is unable to pump blood into the pulmonary system; systemic venous congestion occurs as pressure builds up.


b. caused by:- left sided heart failure- RV infarction- atherosclerotic heart disease- COPD, pulmonic stenosis, pulmonary embolism

c. Assessment findings:Symptoms:- easy fatigability, lower extremity swelling, early satiety, RUQ discomfort


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

d. Diagnostic tests:- chest x-ray: reveals cardiac hypertrophy- echocardiography: indicates inc. size of cardiac chambers- elevated CVP, dec. PO2, inc. ALT(SGPT)


C. Medical Management:1. determination and elimination/control of underlying cause2. Drug therapy:- Diuretics: Furosemide, Spironolactone- Dilators: ACE inhibitors, nitrates- Digitalis: digoxin3. Diet: low salt, low cholesterol

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


D. Nursing Interventions:1. Monitor respiratory status and provide adequate ventilation (when CHF progresses to pulmonary edema)2. Provide physical and emotional rest3. Increase cardiac output4. Reduce/eliminate edema5. Provide client teaching and discharge planning

CARDIAC ARREST

A. General Info:- sudden, unexpected cessation of breathing and adequate circulation of blood by the heart

B. Medical management:1. Cardiopulmonary resuscitation (CPR)2. Drug therapy:

a. lidocaine, procainamide, verapamilb. Dopamine, isoproterenol,

Norepinephrine

CARDIAC ARREST

c. Epinephrine to enhance myocardial automaticity, excitability, conductivity, and contractility

d. Atropine sulfate to reduce vagus nerve’s control over the heart, thus increasing the heart rate

e. Sodium bicarbonate: administered during first few moments of a cardiac arrest to correct respiratory and metabolic acidosis

f. Calcium chloride: calcium ions help the heart beat more effectively by enhancing the myocardium's contractile force

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 lidocaine2. If unsuccessful, defibrillation - CPR3. Assist with administration of and monitor effects of emergency drugs

CARDIOPULMONARY RESUSCITATION

A. General info: process of externally supporting the circulation and respiration of a person who has had a cardiac arrest

B. Nursing interventions: unwitnessed cardiac arrest1. Assess LOC

a. Shake victim’s shoulder and shoutb. if no response, summon for help

2. Position victim supine on a firm surface

C P R

3. Open airwaya. Use head tilt, chin lift maneuverb. Place ear nose and mouth- look to see if chest is moving- listen for escape of air- feel for movement of air against facec. If no respiration, proceed to #4

4. Ventilate twice, allowing for deflation between breaths

C P R

5. Assess circulation: if not present, proceed to #66. Initiate external cardiac compressionsa. Proper placement of hands: lower half of the sternumb. Depth of compressions: 1½ - 2 in. for adultsc. One rescuer: 15 compressions (80-100/min) with 2 ventilationsd. Two rescuers: 5 compressions (80-100/min)with 1 ventilation

INFLAMMATORY DISEASES OF THE

HEARTENDOCARDITISA. General Info:

1. Inflammation of the endocardium; platelets and 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 hemolytic streptococcus, gonococcus 3. Precipitating factors: RHD, open heart surgery, GU/OB Gyn surgery, dental extractions

ENDOCARDITIS

B. Medical management:1. Drug therapy:

a. antibiotics specific to sensitivity or organism cultured

b. PenG and streptomycin if org. not known

c. antipyretics2. Cardiac surgery to replace valve

ENDOCARDITIS

C. Assessment findings:1. Fever, malaise, fatigue, dyspnea and cough acute upper quadrant pain, joint pain2. petechiae, murmurs, edema, splenomegaly, hemiplegia and confusion, hematuria3. elevated WBC & ESR, decreased Hgb & Hct.4. Diagnostic tests: positive blood culture for causative organism

ENDOCARDITIS

D. Nursing interventions:1. antibiotics as ordered2. control temperature3. assess for vascular complications and pulm. embolism4. Provide client teaching and discharge planning

- 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 comfort2. Administer analgesics, salicylates, NSAIDS3. Administer O2, provide adequate rest periods4. Limit activities, to dec. workload of heart5. Treat underlying cause6. 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 parietal pericardium2. caused by bacterial, viral, or fungal infection; collagen diseases; trauma; acute MI, neoplasms, uremia, radiation, drugs (procainamide, hydralazine, Doxorubicin HCL)

PERICARDITIS

B. Medical management:1. Determination and elimination/control of underlying cause2. Drug therapya. Medication for pain reliefb. Corticosteroids, *salicylates (aspirin), indomethacin, to reduce inflammation3. Specific antibiotic therapy against the causative organism may be indicated

PERICARDITIS

C. Assessment findings:1. chest pain with deep inspiration (relieved by sitting up), cough, hemoptysis, malaise2. tachycardia, fever, pericardial friction rub, cyanosis or pallor, jugular vein distension3. Elevated WBC and ESR, normal or inc. SGOT4. 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 high Fowler’s position2. Monitor hemodynamic parameters 3. Administer medications as ordered and monitor effects4. Provide client teaching and discharge planning:- S/S of pericarditis indicative of recurrence (chest pain intensified by lying down and relieved when sitting up; medication regimen

CONGENITAL HEART DISEASE (CHD)

A. General Info:1. CHDs are structural defects of the heart, great vessels, or both that are present from birth2. 2nd only to prematurity as a cause of death in the first year of life

B. Clinical Classification of Congenital heart disease1. Acyanotic: PDA, ASD, VSD2. Cyanotic: TOF, TGV, Truncus arteriosus3. Obstructive: Coarctation of Aorta, AS, PS

ACYANOTIC CHD (PDA)

ACYANOTIC CHDA. PATENT DUCTUS ARTERIOSUS (PDA)

- results when the fetal ductus arteriosus fails to close completely after birth

1. Pathophysiology- blood flows from the aorta through the PDA and back to the pulmonary artery and lungs, causing inc. LV workload and increase pulmonary vascular congestion

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 characteristic

3. child may have frequent resp. infections4. child may have CHF with poor feeding,

fatigue, hepatosplenomegaly, poor weight gain, tachypnea and irritability

5. 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, PDA sometimes can be closed 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 to atria; results when the atrial septal tissue does not fuse properly during embryonic devt.

1. Pathophysiologya. pressure is higher in the left atrium than the right, causing blood to shunt from left to rightb. the RV and PA enlarge because they are handling more blood

ACYANOTIC CHD (ASD)

2. Assessment findings:a. Clinical manifestations:- most infants tend to be aysmptomatic until early childhood 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

3. Nursing management: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 opening between the right and left ventricles- the degree of this defect vary from a pinhole between the R & L ventricles to an absent septum

1. Pathophysiologya. pressure from the LV causes blood to flow through the defect to RV, resulting in increased pulmonary vascular resistance and right heart enlargement

ACYANOTIC CHD (VSD)

b. RV and PA pressures increase, leading eventually to obstructive pulmonary vascular disease

2. Assessment findings:- symptoms vary with the size of the defect, age and 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)

b. Laboratory and diagnostic study findings:- Echocardiography with Doppler U/S or MRI reveals RVH and possible PA dilatation from the inc. blood flow

- ECG shows RVH

3. Nursing managementa. provide family teaching abt treatment options- some VSDs close spontaneously

- others are closed with a Dacron patch, recommended for large defects, PA hypertension, CHF, recurrent resp. infxns. FTT

CYANOTIC CHD (TOF)

ACYANOTIC CHDACYANOTIC CHDA. TETRALOGY OF FALLOT (TOF)

- consists of 4 major anomalies:a. VSD c. PSb. RVH d. overriding aorta

1. Pathophysiology a. PS impedes the flow of blood to the lungs, causing increased pressure in the RV, forcing deoxygenated blood through the septal defect to the LV

CYANOTIC CHD (TOF)

b. the increased workload on the RV causes hypertrophy. The overriding aorta receives blood from both right and left ventricles.

2. Assessment findings:a. Clinical manifestations: vary, depending on the size of the VSD and the degree of PS.

1. Acute episodes of cyanosis (“tet spells”) and transient cerebral ischemia. “Tet spells” are char. By irritability, 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 oxygenated venous blood from the lower extremities and to inc. SVR, w/c increases pulmonary blood flow and eases respiratory effort)

4. slow weight gain5. clubbing, exertional dyspnea, fainting, or

fatigue slowness due to hypoxia6. a pansystolic murmur may be heard at

the mid-lower left sternal border

CYANOTIC CHD (TOF)

b. Laboratory and diagnostic study findings1. echocardiography and ECG show the

enlarged chambers of the right side of the heart2. echocardiography also demonstrates

the decrease in the size of the PA and the reduced blood flow through the lungs

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

4. CBC reveals polycythemia, ABG demonstrate reduced oxygen saturation

CYANOTIC CHD (TOF)

3. Nursing managementa. Provide family teaching about treatment options

1. elective repair is usually performed during the infant’s 1st year of life, but palliative repairs may be warranted for infants who cannot undergo primary repair

2. total repair involves VSD closure, infundibular stenosis resection, and pericardial patch to enlarge RV outflow tractb. Provide preoperative and postoperative care

CYANOTIC CHD (TGV)

B. TRANSPOSITION OF GREAT VESSELS (TGV)- in TGV, the PA leaves the LV and the aorta exits the RV, there is no communication between the systemic and pulmonary circulations

1. Pathophysiologya. this defect results in two separate circulatory patterns; the right heart manages systemic circulation and the left manages pulmonary circulationb. to sustain life, the child must have an associated defect.

CYANOTIC CHD (TGV)

Associated defects such as septal defects or a PDA, permit oxygenated blood into the systemic circulation but cause increased cardiac workload.c. Potential complications include CHF, infective endocarditis, brain abscess, and cerebral vascular accidents resulting from hypoxia or thrombosis.

2. Assessment findings:a. Clinical manifestations vary, depending on associated defects

CYANOTIC CHD (TGV)

1. In infants with minimal communication (no associated defects), severe respiratory depression and cyanosis, will be evident at birth2. In infants with associated defects, there is less cyanosis 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 saturation resulting from the mixing of blood in the chambers

CYANOTIC CHD (TGV)

3. Nursing managementa. Provide family teaching about the treatment options

1. Prostaglandin E is administered to maintain a PDA and further blood mixing.

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

C. TRUNCUS ARTERIOSUS - failure of normal septation and division of the embryonic bulbar trunk into the PA and aorta, resulting in a single vessel that overrides both ventricles

CYANOTIC CHD

1. Pathophysiologya. blood ejected from the ventricles enters the common artery and flows either the lungs or aortic arch.b. pressure in both ventricles is high and blood flow to the lungs is markedly increased.

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

CYANOTIC CHD

2. marked cyanosis, especially on exertion; S/S of CHF; LVH, dyspnea, marked activity intolerance, and retarded growth3. loud systolic murmur best heard at the lower left sternal border and radiating throughout the chest

b. Laboratory and diagnostic study findings:- echocardiography reveals the defect

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

OBSTRUCTIVE CHD (COA)

OBSTRUCTIVE CHDA. COARCTATION OF AORTA (COA)

- a defect that involves a localized narrowing of the aorta

1. Pathophysiology

a. COA is char. by inc. pressure proximal to the defect and decreased pressure distal to itb. restricted blood flow through the narrowed aorta increases the pressure on the LV and causes dilation of the proximal aorta and LVH, w/c may lead to LVF


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

2. Assessment findings:a. Clinical manifestations

1. the child may be asymptomatic or may experience the classic difference in BP and pulse quality between the upper and lower ext. – the BP is elevated 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 leg cramps

3. a systolic murmur may be heard over the left anterior chest and between the scapula posteriorly

4. rib notching may be observed in an older childb. Laboratory and diagnostic findings

1. ECG, echocardiography, and chest x-ray may reveal left sided heart enlargement resulting from back pressure

2. the radiograph may also demonstrate rib notching from enlarged collateral vessels


3. Nursing managementa. 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 the LV outflow of the valve

1. Pathophysiologya. LV pressure inc. to overcome resistance of the obstructed valve and allow blood to flow into the aorta, eventually producing LVH

OBSTRUCTIVE CHD (AS)

b. MI may develop as the inc. O2 demands of the hypertrophied LV go unmet

2. Assessment findings:a. clinical manifestations:

1. faint pulse, hypotension, tachycardia, and poor feeding pattern

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

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

OBSTRUCTIVE CHD (AS)

b. Laboratory and diagnostic study findings:

1. ECG or echocardiography reveals LVH2. cardiac catheterization demonstrates

degree of the stenosis

3. Nursing management:a. if the child’s symptoms warrant, surgical aortic valvulotomy or prosthetic valve replacement is necessary

b. balloon angioplasty can be used to dilate the narrow valve

OBSTRUCTIVE CHD (PS)

C. PULMONIC STENOSIS (PS)- a defect that involves obstruction of blood flow from the right ventricle

1. Pathophysiologya. RV pressure increases leading to RVH and eventually RV failure may occur

2. Assessment findings:a. Clinical manifestations

1. may be asymptomatic or may have mild cyanosis or CHF


2. a systolic murmur may be heard over the pulmonic area; a thrill may be heard if stenosis is severe

3. in severe cases, decreased exercise tolerance, dyspnea, precordial pain and generalized cyanosis may occur

b. Laboratory and diagnostic findings:1. ECG or echocardiography reveals RVH2. cardiac catheterization demonstrates

the degree of stenosis


3. Nursing managementa. provide family teaching about treatment options

1. Balloon angioplasty techniques are being widely used to treat PS

2. Surgical valvulotomy may be performed (although the need for surgery is uncommon due to the widespread use of balloon angioplasty techniques)b. provide preoperative and postoperative care

THE BLOOD VESSELS

A. HYPERTENSION- persistent elevation of the SBP above 140mmHg and of 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 a gradual onset and prolonged course

HYPERTENSION

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

d. Secondary: elevation of the BP as a result of another disease such as renal parenchymal disease, Cushing’s disease, pheochromocytoma, primary aldosteronism, 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 white men/women

HYPERTENSION

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

B. Medical management:1. Diet and weight reduction (restricted sodium, kcal, cholesterol)2. Lifestyle changes: alcohol moderation, exercise regimen, cessation of smoking3. Antihypertensive drug therapy

HYPERTENSION

C. Assessment findings:1. Pain similar to anginal pain; pain in calves of legs

after ambulation or exercise (intermittent claudication); severe occipital headaches, particularly in the morning; polyuria; nocturia; fatigue; dizziness; epistaxis; dyspnea on exertion

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

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

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

HYPERTENSION

D. Nursing interventions:1. Record baseline BP in 3 positions (lying, sitting,

standing) and in both arms2. Continuously assess BP and report any variables

that relate to changes in BP (positioning, restlessness)3. Administer antihypertensive agents as ordered; monitor

closely and assess for S/E4. Monitor intake and hourly output5. Provide client teaching and discharge planning:

- 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 to blood 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


B. Medical management: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 painc. Anticoagulants to prevent thrombus formation

d. Lipid reducing drug: cholestyramine, colesti[pol Hcl, dextrothyroxine sodium, clofibrate, gemfibrozil (Lopid), niacin, lovastatin (Mevacor), atorvastatin


2. Surgery: bypass grafting, endarterectomy, balloon catheter dilation, lumbar sympathectomy (to increase blood flow), amputation may be necessary

C. Assessment findings:1. Pain both intermittent claudication and rest pain,

numbness or tingling of the toes2. Pallor after 1-2 mins. Of elevating feet, and

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


3. Diagnostic tests: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


2. Administer medications as ordered3. 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 and downward, inward and outward – for 3 minsc. 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: stop cigarette smoking, diet, drug compliance, exercise

THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE)

- Acute inflammatory disorder affecting medium/smaller arteries and veins of the LE. Occurs as focal, obstructive process; results in occlusion of a vessel with 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 effective treatment


B. Assessment findings: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 obliterans except no elevation in serum triglycerides

C. Nursing Interventions:

1. Prepare client for surgery


2. Provide client teaching and discharge planning- drug regimen, avoidance of trauma to the affected extremity, need to maintain warmth esp. during cold weathers, importance of stopping smoking

RAYNAUD’S PHENOMENON

- intermittent episode of arterial spasms, most frequently involving the fingers; most often affects women between the teenage years and age 40; cause unknown

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

A. Medical management: vasodilators, catecholamine-depleting antihypertensive drugs (reserpine, guanethidine monosulfate)

RAYNAUD’S PHENOMENON

B. Assessment findings: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 interventions1. provide client teaching concerning:

- importance of stopping smoking; need to maintain warmth; need to use gloves in handling cold objects; drug regimen

ANEURYSM

- a sac formed by dilation of an artery secondary to weakness and stretching of an arterial wall. The dilation may involve one or all layers of the arterial wall.

Classification1. Fusiform: uniform spindle shape involving the

entire circumference of the artery

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

ANEURYSM

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

4. False: the vessel wall is disrupted, blood escapes into surrounding area but is held in place by surrounding tissue

A. General info:1. an aneurysm, usually fusiform or dissecting, in the

descending, ascending, or transverse section of the thoracic aorta

2. usually occurs in men ages 50-70; caused by arteriosclerosis, infection, syphilis, hypertension

ANEURYSM

B. Medical management:1. control of underlying hypertension2. Surgery: resection of the aneurysm and

replacement with a Teflon/Dacron graft; client will need extracorporeal circulation

C. Assessment findings:1. Often asymptomatic; deep, diffuse chest pain;

hoarseness; dysphagia; dyspnea2. Pallor, diaphoresis, distended neck veins

ANEURYSM

3. Diagnostic tests:a. Aortography shows exact location of the aneurysm

b. X-rays: chest film reveals abnormal widening of aorta; abdominal film may show calcification within walls of aneurysm

4. Nursing interventions: same as in Cardiac surgery

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

B. Medical management: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 or legs, thrombocytopeniab. Warfarin (coumadin): blocks prothrombin synthesis by interfering with vit. K synthesis

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

THROMBOPHLEBITIS

- hypersensitivity: dermatitis, urticaria, pruritus, fever- other: transient hair loss, burning sensation of feet, bleeding complications.

2. Surgerya. Vein ligation and strippingb. venous thrombectomy: removal of a clot in the iliofemoral regionc. plication of the inf. vena cava: insertion of an umbrella-like prosthesis into the lumen of the vena cava to filter incoming clots

THROMBOPHLEBITIS

C. Assessment findings:1. Pain in the affected extremity2. Superficial vein: tenderness, redness, induration

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

tenderness over involoved vein, (+) Homan’s sign4. Elevated WBC and ESR5. Diagnostic tests:

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

THROMBOPHLEBITIS

b. Doppler ultrasonography: impairment of blood flow ahead of thrombusc. Venous pressure measurements: high in affected limb until collateral circulation is developed

D. Nursing interventions1. Provide bed rest, elevating involved extremity2. Apply continuous warm, moist soaks to dec.

lymphatic congestion3. Administer anticoagulants as ordered

THROMBOPHLEBITIS

a. Heparin1. monitor PTT, use infusion pump to administer IV heparin2. 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

notify physician immediately if bleeding or signs of bleeding occurs

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

THROMBOPHLEBITIS

4. monitor for chest pain or SOB (possible pulmonary embolism)

5. Provide client teaching and discharge planning:a. need to avoid standing, sitting for long periods; constrictive clothing; crossing legs at the knees; smoking; oral contraceptivesb. importance of adequate hydration c. use of elastic stockings when ambulatoryd. importance of planned rest with elevation of feete. importance of weight reduction and exercise

VARICOSE VEINS

A. General info:1. Dilated veins that occur most often in the lower

extremities and trunk. As the vessel dilates, the valves become stretched and incompetent with resultant venous pooling/edema

2. most common between ages 30-503. predisposing factor: congenital weakness of the veins,

thrombophlebitis, pregnancy, obesity, heart disease

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

VARICOSE VEINS

C. Assessment findings:1. Pain after prolonged standing (relieved by elevation)2. Swollen, dilated, tortuous skin veins3. Diagnostic tests:

a. Trendelenburg test: varicose veins distend very quickly (less than 35 secs)b. Doppler U/S: decreased or no blood flow heard after calf or thigh compression

D. Nursing interventions:1. Elevate legs above heart level

VARICOSE VEINS

2. Apply knee length elastic stockings3. Provide adequate rest4. 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 edemac. apply elastic bandages and stockings,

which should 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