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MEDICAL SURGICAL NURSING CARDIOVASCULAR DISORDERS

CARDIAC DISORDER
I. DYSRYTHMIAS
are disorders of the formation and/or conduction of the electrical impulses within the heart. These disorders can cause disturbances of the hearts rate, rhythm, or both.

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

MEDICATIONS

A.

SINUS DYSRYTHMIAS A.1 Sinus Bradycardia


- when the sinus node creates an impulse at a slower-thannormal rate

Sinus Node slows because of stimulation of the parasympathetic fibers (vagal nerve).

ECG: Ventricular and Atrial Rate: <60 in Adult, Ventricular and Atrial Rhythm: Regular, QRS Shape and Duration: Usually normal, but maybe regularly abnormal, P Wave: Normal and consistent shape, always in front of the QRS, PR Interval: Consistent interval between 0.12-0.20 s, P:QRS- 1:1

If the decrease in HR results from stimulation of the vagus nerve, such as bearing down during defecation or vomiting, attempts are made to prevent further vagal stimulation

Atropine Sulfate 0.5-1.0 mg/IVP to block vagal stimulation Isoproterenol 1mg/500 mL D5W to stimulate sympathetic response Pacemaker (transcutaneous pacing)

A.2 Sinus Tachycardia


- occurs when the sinus node creates an impulse at a fasterthan-normal rate.

The sympathetic fibers are stimulated thereby, speed up excitation of the SA Node

ECG: Ventricular and Atrial Rate: >100bpm in Adult, Ventricular and Atrial Rhythm: Irregular, QRS Shape and Duration: Usually normal, but maybe regularly abnormal, P Wave: Normal and consistent shape, always in front of the QRS but maybe buried in the preceding T Wave PR Interval: Consistent interval between 0.12-0.20 s, P:QRS- 1:1 ECG: Ventricular and Atrial Rate: 60-100bpm in Adult, Ventricular and Atrial Rhythm: Irregular, QRS Shape and Duration: Usually normal, but maybe regularly abnormal, P Wave: Normal and consistent shape, always in front of the QRS, PR Interval: Consistent interval between 0.12-0.20 s, P:QRS- 1:1

Treat the underlying cause (fever, shock, Fluid and Electrolyte disturbances)

Digitalis Administration Calcium Channel Blockers Beta Blockers

A.3 Sinus Arrythmia


-occurs when the sinus node creates an impulse at an irregular rhythm; the rate usually increases with inspiration and decreases with expiration.

An Irregularity in rhythm which is related to respiratory exchange occurs when the SA Node creates an impulse at an irregular rhythm

Sinus arrhythmia does not cause any significant hemodynamic effect and usually is not treated

No medications given.

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B.

ATRIAL DYSRYTHMIAS B.1 Premature Atrial Complex (PAC)


- An ectopic beat that originates in the atria and is discharged at a rate faster than that of SA Node

Occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node.

ECG: Ventricular and Atrial Rate: Depends on the underlying cause, Ventricular and Atrial Rhythm: Irregular due to early P Waves, creating a PP interval that is shorter than the others. This is sometimes followed by a longerthan-normal PP interval, but one that is less than twice the normal PP interval. This type of interval is called a NONCOMPENSATORY PHASE QRS Shape and Duration: The QRS that follows the early P wave is usually normal, but it maybe abnormal. It maybe absent (blocked PAC) , P Wave: An early and diff. P wave may be seen in the Y-wave, other P waves in the strip are consistent, PR Interval:

If PACs are insufficient, no treatment.

If it increases in frequency (>6/min), Quinidine or Calcium Channel Blocker maybe necessary

CARDIAC DISORDER
I. CORONARY ARTERY DISEASE
-most common is atherosclerosis, which is an abnormal accumulation of lipid, or fatty substances and fibrous tissue in the vessel of the wall. These substances create blockages or narrow the vessel in a way that reduces blood flow to the myocardium.

PATHOPHYSIOLOGY
CAD begins as fatty streaks, lipids that are deposited in the intima of the arterial wall. Although, they are thought to be the precursors of atherosclerosis, fatty streaks are common even in childhood. Moreover, not all develop into more advanced lesions. The reason why fatty streaks continue to develop is unknown, although genetic and environment factors are involved. The continued development of CAD involves an inflammatory response. T lymphocytes and monocytes infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate an die; this causes smooth muscle cells within the vessel to proliferate and from a fibrous cap over the dead fatty core. These deposits called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow. If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can

ASSESSMENT FINDINGS
Angina Pectoris Myocardial Ischemia (acute onset of chest pain) Heart Failure

INTERVENTIONS
Controlling Cholesterol Abnormalities CABG Dietary Measures Regulating Physical Activity Promoting cessation of tobacco use

MEDICATIONS
3Hydroxy-3methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statins block cholesterol synthesis, lower LDL and triglyceride levels, and increase HDL levels. Nicotinic acids decrease lipoprotein synthesis, lower LDL and triglyceride Fibric Acid or fibrates decrease synthesis of cholesterol

ECG abnormalities High levels of cardiac enzymes Dysrythmias

ANGINA PECTORIS
clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause

CAD is believed to result from inflammation of the arterial endothelium. C-reactive

Treatment 1. Percutaneous Transluminal Coronary Angioplasty 2. Percutaneous Transluminal Revascularization (PTMR)

Vasodilators (Nitrates) Beta- adrenergic blockers Calcium channel blockers

is usually insufficient coronary blood flow.

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resist the stress from blood flow and vessel movement. If the cap is thin, the lipid core may grow causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop. The thrombus may obstruct blood flow, leading to sudden cardiac death or an cute MI which is the death of heart tissue.

protein (CRP) is a marker for inflammation of vascular endothelium. High blood levels of CRP have been associated with increased coronary artery calcification and risk of an acute cardiovascular event in seemingly healthy individuals. There is interest in using CRP blood levels as an additional risk factor for cardiovascular disease in clinical use and research. An elevated blood level of homocysteine, an amino acid, has also been proposed as an independent risk factor for cardiovascular disease. However, studies have not supported the relationship between mild to moderate elevations of homocysteine and atherosclerosis. No study has yet shown that reducing homocysteine levels reduces the risk for CAD. CLINICAL MANIFESTATIONS Pain described as transient, paroxysmal substernal or precordial pain. Heaviness or tightness of the chest, indigestion, crushing, Radiates down both arms, left shoulder, jaw, neck and back. Precipitated by activity or exertion and relieve by rest or nitroglycerine Diaphoresis Dyspnea Pallor Faintness Palpitations Dizziness Digestive Disturbance due to vagal simulation

3. 4.

Intravascular Stenting Laser therapy

Platelet Aggregation Inhibitors Anticoagulants

Surgical Management: 1. Coronary Artery Bypass Graft (CABG) Nursing Interventions: 1. Diet- Low Na, low fat and low cholesterol, high fiver 2. Avoid saturated fats 3. White meat- chicken without skin, fish are low in saturated fats 4. No restrictions are placed on activity within the patients limitations

Atherosclerosis, hypertension, DM, thromboangitis obliterans, polycythemia vera, aortic regurgitation coronary tissue perfusion myocardial oxygenation anaerobic metabolism lactic acid production (lactic acidosis) angina Several factors are associated with anginal pain: 1. physical exertion which can precipitate an attack by myocardial o2 demand 2. Exposure to cold which can cause vasoconstriction and an elevated BP with O2 demand 3. Eating a heavy meal which blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle 4. Stress which increases the sympathetic response

MYOCARDIAL INFARCTION
formation of localized necrotic areas within the myocardium. Prolonged ischemia lasting more than 35 45 minutes produces irreversible cellular damage and necrosis of the myocardium

Pain Crushing, severe, prolonged, unrelieved by rest or nitroglycerine, often radiating to one or both arms, the neck and back - Characterized by Levines sign Anxiety and Apprehension -feeling of doom, restlessness Shock -systolic pressure below 80mmHg, gray, facial color, lethargy, cold diaphoresis, peripheral cyanosis, Tachycardia/ Bradycardia, weak pulse Oliguria -<30 mL/hr

Medical Management: 1. Goals a. Prevention of further tissue injury and limitation of infarct size b. Maximize myocardial tissue perfusion and reduce myocardial tissue demands 2. Supplemental O2 by nasal cannula. This increases myocatdial O2 supply and relieves pain 3. Cardiac monitoring to detect dysryhythmias 4. PTCA may be done to reopen an occluded artery 5. Diet: low cholesterol, low salt

Analgesics- Morphine SO4 Thrombolytic Therapy Anticoagulant Beta adrenergic blockers Sedatives

6. Fever-slight elevation of temp. occurs within 24 hours and extends 3-7 days accompanied by leukocytosis and elevated ESR
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MI is usually caused by reduce blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus. Because unstable angina and acute MI are considered to be the same process. Other causes of MI include vasospasm of coronary artery, oxygen supply and demand for O2. In each case, a profound imbalance exists between myocardial supply and demand.

Bed rest is usually prescribed for 2448 hours to o2 demand. Progressive ambulation is implemente4ted ASAP, unless there are complications

Indigestion -gas pains around the heart, nausea and vomiting Acute Pulmonary Edema-sense of suffocation, Dyspnea, orthopnea, gurgling/ bubbling respiration ECG changes - MI causes elevation of ST segment, inversion of T wave and enlargement of the Q wave Elevated CK-MB, LDH, AST

Nursing Management 1. Promote oxygenation and tissue perfusion 2. Promote adequate Cardiac Output 3. Promote Comfort 4. Provide rest 5. Promote gradual in activity 6. Promote Proper Nutrition and Elimination 7. Promote Relief of Anxiety and Feeling of Well-Being 8. Facilitate learning

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CARDIAC DISORDER
II. ACQUIRED VASCULAR DISEASE
MITRAL VALVE PROLAPSE
- formerly known as mitral prolapse syndrome, is a deformity that usually produces no symptoms. Rarely, it progresses and can result in sudden death.

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

MEDICATIONS

IN MVP, a portion of a mitral leaflet balloons back into the atrium during systole. Rarely, the ballooning stretches the leaflet to the point that the valve doesnt remain closed during systole. Blood then regurgitates form the LV back into the LA

Maybe asymtomatic fatigue, shortness of breath light-headedness, dizziness, syncope, palpitations, chest pain and anxiety Physical Examination of the heart discloses an extra heart sound referred as mitral click Symptoms of Heart Failure

Medical Management: 1. Symptomatic 2. Advised to eliminate caffeine and alcohol 3. Stop smoking Surgical Intervention 1. Mitral Valve Repair or Replacement in advanced stages Nursing Management: 1. Health education 2. Instruct patients to take the prescribed medications on time and complete the drug 3. Tell the patients to avoid caffeine and alcohol

Calcium Channel Blockers Beta Adrenergic Blockers

4. 5.

Encourage the patient to read drug labels carefully Explore with the patients possible diet, activity, sleep and other lifestyle

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MITRAL STENOSIS

Normally, the mitral valve opening is as wide as the dm. Of 3 fingers. In cases of marked stenosis, the opening narrows to the width of a pencil. The LA has great difficulty moving blood into the ventricle because of the resistance of the narrowed orifice; it dilates and hypertrophies because of BV it holds. Because there is no valve to protect the pulmonary veins from the backward flow of blood from the atrium, the pulmonary circulation becomes congested. As a result, the RV must contract against an abnormally high pulmonary arterial pressure and is subjected to excessive strain. Eventually the RV fails.

The pulse is weak and often irregularly because of atrial fibrillation. A low-pitched, rumbling, diastolic murmur is heard at the apex. As a result of the increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically unstable, and the patient experiences atrial dysrythmias. Echocardiography is used to diagnose mitral stenosis. ECG and cardiac catherterization with angiography are used to determine the severity of the mitral stenosis.

Medical management 1. Antibiotic prophylaxis therapy 2. Treat CHF Surgical Management: 1. Valvuloplasty 2. Mitral Valve Replacement Nursing Management: 1. Health education 2. Instruct patients to take the prescribed medications on time and complete the drug 3. Tell the patients to avoid caffeine and alcohol 4. Encourage the patient to read drug labels carefully 5. Explore with the patients possible diet, activity, sleep and other lifestyle Medical Management 1. Antibiotic prophylaxis 2. Treat dysrythmias and HF Surgical Management: 1. Aortic valvuloplasty 2. Valve Replacement Nursing Intervention: 1. Health education 2. Instruct patients to take the prescribed medications on time and complete the drug 3. Tell the patients to avoid caffeine and alcohol 4. Encourage the patient to read drug labels carefully 5. Explore with the patients possible diet, activity, sleep and

Prophylactic Antibiotics Anticoagulants - Warfarin (Coumadin)

AORTIC REGURGITATION
is the flow of blood back into the left ventricle from the aorta during diastole. It may be caused by inflammatory lesions that deform the leaflets of the aortic valve, preventing them form completely closing the aortic valve orifice.

Blood from Aorta LV (diastole) LV dilates and hypertrophies arteries try to compensate for the pressure (reflex vasodilation) peripheral arterioles relax peripheral resistance and diastolic BP

A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostals space at the left sternal border. The pulse pressure is considerably widened in patients with aortic regurgitation. One characteristic sign of the disease is the water-hammer pulse, in which the pulse strikes the papating finger with a quick, sharp stroke and then suddenly collapses. Asyymptomatic forceful heart beat marked arterial pulsations that are palpable exertional Dyspnea fatigue progressive signs of LCHF diastolic murmur at the 3rd or 4th ICS at the left sternal border Wide Pulse Pressure WATER hammer pulse Diagnosis confirmed by 8D- Echo, MRI , radionuclide imaging and

Prophylactic Antibiotics

Cardiac catheterization

other lifestyle

AORTIC STENOSIS
aortic valve is narrowing of the orifice between the left ventricle and the aorta.

Progressive narrowing of the valve orifice LV obstruction pressure on LV thickening of the muscle wall heart muscle hypertrophies Heart Failure

Asymtomatic exertional Dyspnea dizziness and syncope angina pectoris Low BP rough-loud systolic murmur is heard in the aortic area systolic crescendo-decrescendo murmur LVH- 12 lead ECG 2D-Echo- diagnose and monitor the progression Pressure tracings form the aorta higher systolic pressure in the LV than the aorta during systole

MEDICAL MANAGEMENT 1. Antibiotic prophylaxis to prevent endocarditis SURGERY: replacement of aortic valve Patients who are symptomatic and are not surgical candidates may benefit form 1 or 2 balloon Percutaneous Valvuloplasty

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CARDIAC DISORDER
III. CADIOMYOPATHY
is a heart muscle disease associated with cardiac dysfunction. It is classified according to the structural and functional abnormalitites of the heart muscle.

PATHOPHYSIOLOGY
Stroke Volume SNS and RAA Systemic Vascular Resistance Na and water retention workload of the heart Heart Failure

ASSESSMENT FINDINGS
stable and asymptomatic signs and symptoms of Heart Failure PND orthopnea fluid retention peripheral edema nausea chest pain palpitations dizziness syncope with exertion sudden death with HCM Tachycardia and extra heart sounds 2D Echo and ECG CXR Cardiac Cath to rule out coronary artery disease as a cause Endomyocardial biopsy

INTERVENTIONS
Medical management: 1. Treat the underlying cause 2. Low Na diet 3. Exercise Rest Regimen 4. Control dysrythmias with medications 5. If there are symptoms of CHF limit fluid intake into 2 L/day 6. Pacemaker Surgical Management 1. Heart Transplantation 2. LVAD 3. Left Ventricular Outflow Tract Surgery Nursing Management 1. Improve CO 2. Increase activity tolerance 3. Reduce anxiety 4. Decrease the sense of powerlessness 5. Promote Self-Care 6. Promote Home and CommunityBased care 7. Continuing Care

MEDICATIONS
Antidysythmic drugs for dysrythmia

V. INFECTIOUS DISEASES OF THE HEART


PERICARDITIS
- refers to an infection of the pericardium, the membranous sac enveloping the heart

Underlying Cause: idiopathic, viral and bacterial infection, disorders of connective tissue, hypersensitivity states, disorders of adjacent structures, neoplastic disease, radiation therapy, trauma, renal failure and uremia, TB accumulation of fluid in the pericardial sac pressure on the heart cardiac tamponade

Pain in the anterior chest, aggravated by coughing, yawning, swallowing, twisting and turning the torso; relieve by upright, leaning forward position Pericardial friction rub Dyspnea Fever, sweating, chills Joint pains Arrhythmias

Medical and Surgical Management: 1. Determine the cause, administer therapy and be alert for cardiac tamponade 2. Pericardiocentesis 3. Pericardictomy Nursing Management: 1. Elevate HOB. Place pillow on the overbed table so that the patient can lan on it 2. Bed rest 3. Administer prescribed pharmacotherapy 4. Assist in pericardiocentesis

Analgesics NSAIDS Cortocosteroids

INFECTIVE ENDOCARDITIS
is the infection of the valves and the endothelium surface of the heart.

The invasion of bacteria produces vegetative growths on the heart valves, the endocardial lining or the endothelium of a blood vessel that may embolize the spleen, kidneys, CNS and lungs

nonspecific and include malaise weakness, anorexia, athralgia, night sweats, chills, valvular insufficiency and intermittent fever for weeks loud regurgitant murmur

Medical and Surgical Management: Supportive treatment- bed rest Surgical valve replacement aortic or mitral valve excision are required Nursing Management: Monitor vital signs Assess signs of organ damage Administer pharmacotherapy Instruct activity restrictions, medications and signs and symptoms of infection Emotional support Coping strategies If patient received surgical management, strict post-op care is observed Medical and Surgical Management: Bed rest Limit sports or strenuous activities for 6 months Physical activity is increased slowly If develops heart failure management is essentially the same Nursing Management: Monitor VS Proper cardiac monitoring Elastic compression stockings Passive and active exercises should be used Instruct the patient not to take aspirin, take caution when taking corticosteroids

Antibiotic therapy Antipyretics

embolization of other vital organs

MYOCARDITIS
- is an inflammatory process involving the myocardium. Myocarditis can cause heart dilation, thrombi on the heart wall, infiltration of circulating blood cells around coronary vessels and between the muscle fibers.

Viral, bacterial, fungal, parasitic, protozoal infection inflammation in one small area and spread throughout the myocardium myocarditis chest pain dysrythmias cardiomegaly faint heart sounds gallop rhythm systolic murmur

Antibiotic therapy corticosteroids Antipyretics

CARDIAC DISORDER
VI. COMPICATIONS FROM HEART DISEASES
CONGESTIVE HEART FAILURE

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS
Left CHF

INTERVENTIONS
Oxygen therapy balanced program of activity and rest Sodium restricted to prevent fluid excess

MEDICATIONS
Digitalis Therapy Diuretic Therapy Vasodilators

Heart Damage, Ventricular Overload, Ventricular Contraction it may lead to Tachycardia, ,ventricular dilatation. Myocardial hypertrophy CO renal perfusion Na retention osmotic pressure ADH water absorption edema heart failure

Dyspnea PND Orthopnea Rales /Crackles Moist cough wheezing blood tinged frothy sputum syncope fatigue weakness anorexia hypokalemia clubbing of fingers polycythemia S3,S4 sounds, pulsus alternans PAO, PWCP, LVEDP

Nursing Management Provide Oxygenation Provide rest and activity Decrease anxiety Facilitate fluid balance Provide skin care Promote proper nutrition Promote elimination Facilitate learning

Right CHF Jugular Vein Engorgement Hepatomegaly Splenomegaly Portal Hpn Ascites Peripheral Edema Jaundice Hemolytic Anemia Internal Hemorrhoids Weight gain Leg Varicosities Cardiac cirrhosis Extra Heart Sounds Elevated CVP reading

If acute pulmonary edema occurs: High Fowlers position Morphine Sulfate Oxygen therapy Aminophylline Rapid digitalization Diuretic therapy Vasodilators Dopamine or dobutamine Monitor serum K

CARDIOGENIC SHOCK (POWER/PUMP FAILURE)

MASSIVE MI Myocardial Contractility CO Hypoperfusion (heart, brain , kidney) Tissue Hypoxia Organ Damage Death

1. 2. 3. 4.

Systolic Blood Pressure Oliguria Cod, clammy skin, weak pulse, cyanosis due to circulatory insufficiency mental lethargy, confusion due to poor cerebral perfusion

Medical and Nursing Management 1. Perform hemodynamic monitoring:PAP, PWCP measurements, Intraarterial BP 2. Administer oxygen therapy 3. Correct Hypovolemia 4. Administer IV fluids as ordered 5. Monitor I and O, LOC, arrhythmias 6. Provide psychosocial support 7. Decrease pulmonary edema

Vasodilators Inotrophic Agents Diuretics

8.

Utilize counterpulsation to decrease ventricular work with severe shock

CARDIAC DISORDER
VII. PERIPHERAL VASCULAR DISORDERS
HYPERTENSION

PATHOPHYSIOLOGY

ASSESSMENT FINDINGS

INTERVENTIONS

MEDICATIONS

RISK FACTORS: Family History. Age, High Salt Intake, Low K intake, Obesity, Excess Alcohol Consumption, Smoking, Stress Changes in Arteriolar Bed Systemic Vascular Resistance Afterload Blood Flow to Organs Renal Perfusion, BP, Beta receptor activation Juxtaglomerular cells (Hypovolemia and hyponatremia ) Renin Angitensinogen (ACE) Angiotensin 1 (ACE) Angiotensin II Arteriolar vasoconstriction Peripheral Vascular Resistance

headache. The most characteristic sign epistaxis dizziness tinnitus unsteadiness blurred vision depression nocturia retinopathy,papilledema Maybe asymptomatic

Prevention a. Primary Moderation in Na intake, saturated fats, maintenance of IBW, maintenance of regular pattern of exercise, cessation of cigarette smoking, moderation in alcohol consumption, stress reduction b. Secondary Control of HPN in high risk groups NURSING INTERVENTIONS: 1. Patient teaching and counseling 2. Teaching about medication 3. Prevent non-compliance

1.

Diuretics a. Thiazides b. Loop c. Potassium sparing 2. Adrenergic Inhibitors a. Beta Adrenergic Blockers b. Centrally acting alpha blockers c. Peripherally acting Adrenergic antagonists d. Alpha-1 adrenergic blockers e. Vasodilators f. ACE Inhibitors g. Calcium Channel Blockers 3. ACE inhibitors 4. Angiotensin II receptor blockers

ARTERIOSCLEROSIS The most common direct result of artherosclerosis include narrowing of the lumen, obstruction, aneurysm, ulceration and rupture. Its indirect results are malnutrition and subsequent fibrosis of the organs. All actively functioning tissue cells require an abundant supply of nutrients and oxygen and are sensitive to any reduction in the supply of these nutrients. If such reductions are severe and permanent, the cell undergoes necrosis and is replaced by fibrous tissue, which require lesser blood flow.
Intermittent claudication is an aching, persistent cramplike squeezing pain that occurs after a certain amount of exercise of the affected extremity. It is relieved by rest Coldness or cold sensitivity Color changes Ulceration and gangrene Edema Sexual dysfunction

Primary, Secondary Tertiary Prevention Quit smoking Control serum lipid levels Skin and foot care Low fat, low cholesterol Daily walking program

Vasodilators Antihyperlipidemics

SURGICAL MANAGEMENT 1. Bypass Graft 2. Endarterectomy 3. Endovascular Surgery 4. Balloon angioplasty 5. Laser angioplasty 6. Stent 7. Amputation NURSING INTERVENTION 1. Promote Tissue Perfusion

2. 3. 4.

Maintain Skin Integrity and Prevent Infection Promote Activity Prevent Injury

MEDICAL MANAGEMENT Atheromatous plaques blood flow tissue Ischemia tissue hypoxia necrosis ulceration and gangrene
intermittent Claudication Coldness or cold sensitivity Color changes Ulceration and gangrene Sexual dysfunction Impaired arterial pulsation Edema

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Exercise Program combined with weight reduction and cessation of tobacco and alcohol use

Vasodilators Antihyperlipidemics

SURGICAL MANAGEMENT Bypass Graft Endarterectomy Endovascular Surgery Balloon angioplasty Laser angioplasty Stent Amputation

MEDICAL MANAGEMENT 1. Medications AORTIC ANEURYSM Hypertension Alteration in integrity of its wall irreversible. Localized dilatation of an artery
pulsatile mass over the abdomen Low back pain Lower abdominal pain Flank pain Collapse Shock Possible complication is rupture, causing massive internal hemorrhage, shock and death

Surgery: If greater than 4 cm Teflon/Dacron/gortex graft may be used in a surgical repair NURSING INTERVENTION AFTER SURGERY: 1. Monitor VS and hemodynamic measurements, urine output, BUN creatinine, bowel sounds peripheral pulses 2. Promote Fluid Volume by checking excessive drainage, Hgb and Hct levels MEDICAL MANAGEMENT

Antihypertensives

RAYNAUDS DISEASE

Cold exposure, stress Digital artery Contraction/ Spasm Occlusion of

pallor cyanotic

Avoid exposure to cold Quit smoking Teach effects of smoking

Calcium Channel Blockers

arteries Tissue Ischemia Tissue Hypoxia Tissue Necrosis Tissue Ulceration Gangrene

color sequence: white-blue-red numbness, tingling and burning pain

Teach to avoid exposure to cold Discuss importance of reducing emotional stress Avoid drugs that causes vasoconstriction such as pills, beta blockers and ergotamines

Vasodilators NSAIDS

Surgery
1. Amputation - Sympathectomy to relieve vasospastic symptoms

MEDICAL MANAGEMENT; Bed rest with leg elevation Local moist heat application Compression support stockings THROMBOPHLEBITIS Results form venous thrombosis and inflammation in a superficial vein
pain tenderness palpable induration along the course of vein no edema

NURSING INTERVENTIONS: Prevent venous stasis Prevent recurrence Maintain IBW Alternate standing with sitting at work or at home Regular Patterns of exercise

NSAID Non-narcotic analgesic

MEDICAL MANAGEMENT: Minimize intake of green leafy vegetables DEEP VEIN THROMBOSIS Venous Stasis, Vessel Wall Injury, Hypercoagulability of the Blood DVT
calf pain (+) Homan Sign edema tenderness palpable induartion along the course of the brain

SURGERY: Thromboembolectomy Greenfield vena cava fiber to prevent pulmonary embolism NURSING INTERVENTIONS: Maintaining tissue perfusion Promote comfort MEDICAL MANAGEMENT: Elevation of affected limp for 1530 min at a time. Average of 20 min.] Compression with support

Anticoagulation therapy Thrombolytics

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VARICOSE VEINS

Congenital absence of valves of the veins, hereditary weakness of the valves,

dilated, purplish, tortuous veins leg pain

1.Analgesics as ordered

prolonged sitting or standing, wearing of constricting clothing, obesity, thrombophlebitis, pregnancy, RCHF, liver cirrhosis effects of gravity on venous pressure dilated, prominent veins

leg edema heaviness in the legs

stockings Sclerotherapy Early ambulation

SURGERY: 1. Vein ligation and stripping to relive pain NURSING INTERVENTION 1. Wear elastic stockings during activities requiring long periods of standing or during pregnancy 2. Moderate exercise and elevate the legs during sitting 3. Proper post-operative care Medical Management: 1. eliminate smoking Surgery: 1. Sympathectomy 2. Amputation of ulcerated fingers and toes Nursing Management: 1. during activities requiring long periods of standing or during pregnancy 2. Moderate exercise and elevate the legs during sitting 3. Proper post-operative care
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BUERGERS DISEASE (Thromboangitis Obliterans)

Diffuse inflammation of the small and medium arteries then veins

Intermittent Claudication Skin Cyanosis Pain

Anticoagulants Calcium Channel Blockers

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