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CARDIOLOGY NURSING

HEARTS NORMAL ANATOMY

The heart is located in the LEFT side of the mediastinum Consists of Three layers -

epicardium, myocardium and endocardium.The epicardium covers the outer surface of theheart The myocardium is the middle muscular layer of the heart The endocardium lines the

chambers and the valves.The layer that covers the heart is the PERICARDIUM There are

two parts - parietal and visceral pericardium The space between the two pericardial layers

is the pericardial space

The heart also has four chambers - two atria and two ventricles The Left atrium and theright atrium The left ventricle and the right ventricle.The heart chambers are guarded by

valves The atrio-ventricular valves - tricuspid and bicuspid The semi-lunar valves -

pulmonic and aortic valves.The Blood supply of the heart comes from the Coronary arteries

1. Right coronary artery supplies the RIGHT atrium and RIGHT ventricle, inferior portion

of the LEFT ventricle, the POSTERIOR septal wall and the two nodes - AV (90%) and SAnode (55%). Left coronary artery- branches into the LAD and the circumflex branch The

LAD supplies blood to the anterior wall of the LEFT ventricle, the anterior septum and the

Apex of the left ventricle The CIRCUMFLEX branch supplies the left atrium and the

posterior LEFT ventricle

The CONDUCTING SYSTEM OF THE HEART Consists of the 1. SA node- thepacemaker 2. AV node- slowest conduction 3. Bundle of His branches into the Right and

the Left bundle branch 4. Purkinje fibers- fastest conduction

The Heart sounds 1. S1- due to closure of the AV valves 2. S2- due to the closure of the

semi-lunar valves 3. S3- due to increased ventricular filling 4. S4- due to forceful atrial

contraction.Heart rate Normal range is 60-100 beats per minute Tachycardia is greater than100 bpm Bradycardia is less than 60 bpm Sympathetic system INCREASES HR

Parasympathetic system (Vagus) DECREASES HR.Blood pressure Cardiac output X

peripheral resistance Control is neural (central and peripheral) and hormonal Baroreceptors

in the carotid and aorta Hormones- ADH, aldosterone, epinephrine can increase BP; ANF

can decrease BP.The vascular system consists of the arteries, veins and capillaries Thearteries are vessels that carry blood away from the heart to the periphery The veins are the

vessels that carry blood to the heart The capillaries are lined with squamos cells, theyconnect the veins and arteries. The lymphatic system also is part of the vascular system and

the function of this system is to collect the extravasated fluid from the tissues and returns it

to the blood

Cardiac Assessment

Laboratory Test Rationale 1. To assist in diagnosing MI 2. To identify abnormalities 3. To

assess inflammation

4. To determine baseline value 5. To monitor serum level of medications 6. To assess theeffects of medications

CARDIAC Proteins and enzymes

CK- MB ( creatine kinase)

Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 daysNormal value is 0-7 U/L

Lactic Dehydrogenase (LDH)Elevates in MI in 24 hours, peaks in 48-72 hours

Normally LDH1 is greater than LDH2MI- LDH2 greater than LDH1 (flipped LDH pattern)

Normal value is 70-200 IU/L

Myoglobin

Rises within 1-3 hoursPeaks in 4-12 hoursReturns to normal in a day

Not used aloneMuscular and RENAL disease can have elevated myoglobin

LABORATORY PROCEDURES

Troponin I and T

Troponin I is usually utilized for MI Elevates within 3-4 hours, peaks in 4-24 hours and

persists for 7 days to 3 weeks! Normal value for Troponin I is less than 0.6

ng/mL.REMEMBER to AVOID IM injections before obtaining blood sample! Early andlate diagnosis can be made!

SERUM LIPIDS- Lipid profile measures the serum cholesterol, triglycerides and

lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL. LDH- 130 mg/dLHDL- 30-70- mg/dL NPO post midnight (usually 12 hours)

ELECTROCARDIOGRAM (ECG) A non-invasive procedure that evaluates the electrical

activity of the heart Electrodes and wires are attached to the patient

Holter Monitoring. A non-invasive test in which the client wears a Holter monitor and an

ECG tracing recorded continuously over a period of 24 hours. Instruct the client to resume

normal activities and maintain a diary of activities and any symptoms that may develop

ECHOCARDIOGRAM Non-invasive test that studies the structural and functionalchanges of the heart with the use of ultrasound No special preparation is needed

S Stress Test- A non-invasive test that studies the heart during activity and detects and

evaluates CAD Exercise test, pharmacologic test and emotional test.Treadmill testing is the

most commonly used stress test. Used to determine CAD, Chest pain causes, drug effectsand dysrhythmias in exercise

Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and

avoid smoking, alcohol and caffeine

Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of

breath . Instruct client to avoid taking a hot shower for 10-12 hours after the test

Pharmacological stress test .Use of dipyridamole Maximally dilates coronary artery Side-

effect: flushing of face

Pre-test: 4 hours fasting, avoid alcohol, caffeine

Post test: report symptoms of chest pain

CARDIAC catheterization

Insertion of a catheter into the heart and surrounding vessels Determines the structure and

performance of the heart valves and surrounding vessels. Used to diagnose CAD, assess

coronary atery patency and determine extent of atherosclerosis

Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight

and height, baseline VS, blood tests and document the peripheral pulses. Fast for 8-12

hours, teachings, medications to allay anxietyIntra-test: inform patient of a fluttery feeling as the catheter passes through the heart;

inform the patient that a feeling of warmth and metallic taste may occur when dye is

administered

Post-test: Monitor VS and cardiac rhythm Monitor peripheral pulses, color and warmth

and sensation of the extremity distal to insertion site Maintain sandbag to the insertion siteif required to maintain pressure Monitor for bleeding and hematoma formation. Maintain

strict bed rest for 6-12 hours Client may turn from side to side but bed should not be

elevated more than 30 degrees and legs always straight Encourage fluid intake to flush out

the dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy

CVP

The CVP is the pressure within the SVC Reflects the pressure under which blood is

returned to the SVC and right atrium. Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O Elevated

CVP indicates increase in blood volume, excessive IVF or heart/renal failure Low CVP

may indicated hypovolemia, hemorrhage and severe vasodilatationMeasuring CVP 1. Position the client supine with bed elevated at 45 degrees 2. Position

the zero point of the CVP line at the level of the right atrium. Usually this is at the MAL,

4th ICS 3. Instruct the client to be relaxed and avoid coughing and straining.

ASSESSMENT ASSESSMENT1. Health History Obtain description of present illness and the chief complaint Chest pain,

SOB, Edema, etc. Assess risk factors

2. Physical examination Vital signs- BP, PP, MAP Inspection of the skin Inspection of the

thorax Palpation of the PMI, pulses Auscultation of the heart sounds

3. Laboratory and diagnostic studies CBC cardiac catheterization Lipid profilearteriography Cardiac enzymes and proteins CXR CVP EEG Holter monitoring Exercise

ECG

CARDIAC IMPLEMENTATION

1.Assess the cardio-pulmonary status VS, BP, Cardiac assessment2. Enhance cardiac output Establish IV line to administer fluids

3. Promote gas exchange Administer O2 Position client in SEMI-Fowlers Encourage

coughing and deep breathing exercises

4. Increase client activity tolerance Balance rest and activity periods Assist in daily

activities5. Promote client comfort Assess the clients description of pain and chest discomfort

Administer medication as prescribed

6. Promote adequate sleep

7. Prevent infection Monitor skin integrity of lower extremities Assess skin site for edema,

redness and warmth Monitor for fever Change position frequently8. Minimize patient anxiety Encourage verbalization of feelings, fears and concerns

Answer client questions. Provide information about procedures and medications

CARDIAC DISEASES

Coronary Artery DiseaseMyocardial Infarction

Congestive Heart Failure

Infective Endocarditis

Cardiac Tamponade

Cardiogenic Shock

VASCULAR DISEASES

Hypertension

Buergers diseaseVaricose veins

Deep vein thrombosis

Aneurysm

CAD

CAD results from the focal narrowing of the large and medium-sized coronary arteries dueto deposition of atheromatous plaque in the vessel wall

RISK FACTORS 1. Age above 45/55 and Sex- Males and post-menopausal females 2.

Family History 3. Hypertension 4. DM 5. Smoking 6. Obesity 7. Sedentary lifestyle 8.Hyperlipedimia

Most important MODIFIABLE factors: Smoking Hypertension Diabetes Cholesterol

abnormalities

PathophysiologyFatty streak formation in the vascular intima T-cells and monocytes ingest lipids in the

area of deposition atheroma narrowing of the arterial lumen reduced coronary

blood flow myocardial ischemiaThere is decreased perfusion of myocardial tissue and inadequate myocardial oxygen

supply If 50% of the left coronary arterial lumen is reduced or 75% of the other coronaryartery, this becomes significant Potential for Thrombosis and embolism

Angina Pectoris

Chest pain resulting from coronary atherosclerosis or myocardial ischemia

Clinical Syndromes Three Common Types of ANGINA

1. STABLE ANGINA The typical angina that occurs during exertion, relieved by rest and

drugs and the severity does not change

2. Unstable angina Occurs unpredictably during exertion and emotion, severity increases

with time and pain may not be relieved by rest and drug3. Variant angina Prinzmetal angina, results from coronary artery VASOSPASMS, may

occur at rest

ASSESSMENT FINDINGS 1. Chest pain- ANGINA The most characteristic symptom

PAIN is described as mild to severe retrosternal pain, squeezing, tightness or burningsensation Radiates to the jaw and left arm

1. Chest pain- ANGINA Precipitated by Exercise, Eating heavy meals, Emotions like

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excitement and anxiety and Extremes of temperature Relieved by REST and Nitroglycerin

2. Diaphoresis 3. Nausea and vomiting 4. Cold clammy skin 5. Sense of apprehension and

doom 6. Dizziness and syncope

LABORATORY FINDINGS 1. ECG may show normal tracing if patient is pain-free.Ischemic changes may show ST depression and T wave inversion 2. Cardiac catheterization

Provides the MOST DEFINITIVE source of diagnosis by showing the presence of the

atherosclerotic lesions

NURSING MANAGEMENT 1. Administer prescribed medications Nitrates- to dilate thecoronary arteries Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP and

HR Calcium-channel blockers- to dilate coronary artery and reduce vasospasm

2. Teach the patient management of anginal attacks Advise patient to stop all activities Put

one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, take another

tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved afterTHREE tablets seek medical attention3. Obtain a 12-lead ECG

4. Promote myocardial perfusion Instruct patient to maintain bed rest Administer O2 @ 3

lpm Advise to avoid valsalva maneuvers Provide laxatives or high fiber diet to lessen

constipation Encourage to avoid increased physical activities5. Assist in possible treatment modalities PTCA- percutaneous transluminal coronary

angioplasty To compress the plaque against the vessel wall, increasing the arterial lumen

CABG- coronary artery bypass graft To improve the blood flow to the myocardial tissue

6. Provide information to family members to minimize anxiety and promote family

cooperation7. Assist client to identify risk factors that can be modified

8. Refer patient to proper agencies

Myocardial infarction

Death of myocardial tissue in regions of the heart with abrupt interruption of coronaryblood supply

ETIOLOGY and Risk factors 1. CAD 2. Coronary vasospasm 3. Coronary artery occlusionby embolus and thrombus 4. Conditions that decrease perfusion- hemorrhage, shock

Risk factors1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress 6. Sedentary

lifestyle

PATHOPHYSIOLOGY Interrupted coronary blood flow myocardial ischemia

anaerobic myocardial metabolism for several hours myocardial death depressed cardiac function triggers autonomic nervous system response further imbalance of

myocardial O2 demand and supply

ASSESSMENT findings 1. CHEST PAIN Chest pain is described as severe, persistent,

crushing substernal discomfort Radiates to the neck, arm, jaw and back1. CHEST PAIN Occurs without cause, primarily early morning NOT relieved by rest or

nitroglycerin Lasts 30 minutes or longer

2. Dyspnea 3. Diaphoresis 4. cold clammy skin 5. N/V 6. restlessness, sense of doom 7.tachycardia or bradycardia 8. hypotension 9. S3 and dysrhythmias

Laboratory findings

1. ECG- the ST segment is ELEVATED. T wave inversion, presence of Q wave 2.

Myocardial enzymes- elevated CK- MB, LDH and Troponin levels 3. CBC- may show

elevated WBC count 4. Test after the acute stage- Exercise tolerance test, thallium scans,

cardiac catheterization

Nursing Interventions

1. Provide Oxygen at 2 lpm, Semi-fowlers 2. Administer medications Morphine to relieve

pain nitrates, thrombolytics, aspirin and anticoagulants Stool softener and hypolipidemics3. Minimize patient anxiety Provide information as to procedures and drug therapy 4.

Provide adequate rest periods 5. Minimize metabolic demands Provide soft diet Provide a

low-sodium, low cholesterol and low fat diet 6. Minimize anxiety Reassure client and

provide information as needed 7. Assist in treatment modalities such as PTCA and CABG

8. Monitor for complications of MI- especially dysrhythmias, since ventricular tachycardia

can happen in the first few hours after MI 9. Provide client teaching

Medical Management

1. ANALGESIC The choice is MORPHINE It reduces pain and anxiety Relaxes

bronchioles to enhance oxygenation2. ACE Prevents formation of angiotensin II Limits the area of infarction

3. Thrombolytics Streptokinase, Alteplase Dissolve clots in the coronary artery allowing

blood to flow

NURSING INTERVENTIONS AFTER ACUTE EPISODE1. Maintain bed rest for the first 3 days 2. Provide passive ROM exercises 3. Progress with

dangling of the feet at side of bed 4. Proceed with sitting out of bed, on the chair for 30

minutes TID 5. Proceed with ambulation in the room toilet hallway TID.Cardiac

rehabilitation To extend and improve quality of life Physical conditioning Patients who are

able to walk 3-4 mph are usually ready to resume sexual activities

CARDIOMYOPATHIES

Heart muscle disease associated with cardiac dysfunction

1. Dilated Cardiomyopathy 2. Hypertrophic Cardiomyopathy 3. Restrictive

cardiomyopathy

ASSOCIATED FACTORS 1. Heavy alcohol intake 2. Pregnancy 3. Viral infection 4.

Idiopathic

PATHOPHYSIOLOGY Diminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and

dilatation. SYSTOLIC DYSFUNCTION

HYPERTROPHIC CARDIOMYOPATHY Associated factors: 1. Genetic 2. Idiopathic

Pathophysiology Increased size of myocardium reduced ventricular volume increased

resistance to ventricular filling diastolic dysfunction

RESTRICTIVE CARDIOMYOPATHY Associated factors 1. Infiltrative diseases like

AMYLOIDOSIS 2. Idiopathic

Slide 112: RESTRICTIVE CARDIOMYOPATHY Pathophysiology Rigid ventricular

wall impaired stretch and diastolic filling decreased output Diastolic dysfunction

Assessment findings 1. PND 2. Orthopnea 3. Edema 4. Chest pain 5. Palpitations 6.

dizziness 7. Syncope with exertion

Laboratory Findings 1. CXR- may reveal cardiomegaly 2. ECHOCARDIOGRAM 3. ECG4. Myocardial Biopsy

Medical Management 1. Surgery 2. pacemaker insertion 3. Pharmacological drugs for

symptom relief

Nursing Management 1.Improve cardiac output Adequate rest Oxygen therapy Low sodium

diet

2. Increase patient tolerance Schedule activities with rest periods in between

3. Reduce patient anxiety Support Offer information about transplantations Support family

in anticipatory grieving

Infective endocarditis

Infection of the heart valves and the endothelial surface of the heart Can be acute or

chronic

Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi

Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4. IV drug

users 5. Valvular dysfunctions

Pathophysiology

Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation erosion of valvular leaflets and

vegetation can embolize

Assessment findings 1. Intermittent HIGH fever 2. anorexia, weight loss 3. cough, back

pain and joint pain 4. splinter hemorrhages under nails 5. Oslers nodes- painful nodules on

fingerpads 6. Roths spots- pale hemorrhages in the retina

7. Heart murmurs 8. Heart failure

Prevention

Antibiotic prophylaxis if patient is undergoing procedures like dental extractions,

bronchoscopy, surgery, etc.

LABORATORY EXAM Blood Cultures to determine the exact organism

Nursing management

1. regular monitoring of temperature, heart sounds 2. manage infection 3. long-termantibiotic therapy

Medical management 1. Pharmacotherapy IV antibiotic for 2-6 weeks Antifungal agents

are given amphotericin B

2. Surgery Valvular replacement

CHFA syndrome of congestion of both pulmonary and systemic circulation caused by

inadequate cardiac function and inadequate cardiac output to meet the metabolic demands

of tissues.Inability of the heart to pump sufficiently The heart is unable to maintain

adequate circulation to meet the metabolic needs of the body Classified according to themajor ventricular dysfunction- Left or Right

Etiology of CHF 1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5.

Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis and cardiac tamponade

PATHOPHYSIOLOGY LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion

decreased cardiac output decreased perfusion to the brain, kidney and other tissues

oliguria, dizziness

CHF PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling in the venous

circulation increased hydrostatic pressure peripheral edema blood pooling

venous congestion in the kidney, liver and GIT

LEFT SIDED CHF ASSESSMENT FINDINGS 1. Dyspnea on exertion 2. PND 3.Orthopnea 4. Pulmonary crackles/rales 5. cough with Pinkish, frothy sputum 6.

Tachycardia 7. Cool extremities 8. Cyanosis 9. decreased peripheral pulses 10. Fatigue 11.

Oliguria 12. signs of cerebral anoxia

RIGHT SIDED CHF ASSESSMENT FINDINGS 1. Peripheral dependent, pitting edema2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites 6. Body weakness 7.

Anorexia, nausea 8. Pulsus alternans

Slide 147: CHF LABORATORY FINDINGS 1. CXR may reveal cardiomegaly 2. ECG

may identify Cardiac hypertrophy 3. Echocardiogram may show hypokinetic heart

LABORATORY FINDINGS 4. ABG and Pulse oximetry may show decreased O2

saturation 5. PCWP is increased in LEFT sided CHF and CVP is increased in RIGHT sided

CHF

NURSING INTERVENTIONS 1. Assess patient's cardio- pulmonary status 2. Assess VS,

CVP and PCWP. Weigh patient daily to monitor fluid retention 3. Administer medications-

usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators

and hypolipidemics are prescribed 4. Provide a LOW sodium diet. Limit fluid intake as

necessary 5. Provide adequate rest periods to prevent fatigue6. Position on semi-fowlers tofowlers for adequate chest expansion 7. Prevent complications of immobility

CHF NURSING INTERVENTION AFTER THE ACUTE STAGE 1. Provide

opportunities for verbalization of feelings 2. Instruct the patient about the medication

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regimen- digitalis, vasodilators and diuretics 3. Instruct to avoid OTC drugs, Stimulants,

smoking and alcohol 4. Provide a LOW fat and LOW sodium diet 5. Provide potassium

supplements 6. Instruct about fluid restriction 7. Provide adequate rest periods and schedule

activities 8. Monitor daily weight and report signs of fluid retention

CARDIOGENIC SHOCK

Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue

perfusion ETIOLOGY 1. Massive MI 2. Severe CHF 3. Cardiomyopathy 4. Cardiac trauma

5. Cardiac tamponade

ASSESSMENT FINDINGS 1. HYPOTENSION 2. oliguria (less than 30 ml/hour) 3.

tachycardia 4. narrow pulse pressure 5. weak peripheral pulses 6. cold clammy skin 7.

changes in sensorium/LOC 8. pulmonary congestion

LABORATORY FINDINGS Increased CVP Normal is 4-10 cmH2O

NURSING INTERVENTIONS 1. Place patient in a modified Trendelenburg (shock )

position 2. Administer IVF, vasopressors and inotropics such as DOPAMINE and

DOBUTAMINE 3. Administer O2

4. Morphine is administered to decreased pulmonary congestion and to relieve pain 5.Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath

and IABP 6. Monitor urinary output, BP and pulses 7. cautiously administer diuretics and

nitrates

CARDIAC TAMPONADEA condition where the heart is unable to pump blood due to accumulation of fluid in the

pericardial sac (pericardial effusion).This condition restricts ventricular filling resulting to

decreased cardiac output Acute tamponade may happen when there is a sudden

accumulation of more than 50 ml fluid in the pericardial sac

Causative factors 1. Cardiac trauma 2. Complication of Myocardial infarction 3.

Pericarditis 4. Cancer metastasis

ASSESSMENT FINDINGS 1. BECKs Triad- Jugular vein distention, hypotension and

distant/muffled heart sound 2. Pulsus paradoxus 3. Increased CVP 4. decreased cardiacoutput 5. Syncope 6. anxiety 7. dyspnea 8. Percussion- Flatness across the anterior chest

Laboratory FINDINGS 1. Echocardiogram 2. Chest X-ray

NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF3. Monitor ECG, urine output and BP 4. Monitor for recurrence of tamponade

Pericardiocentesis Patient is monitored by ECG Maintain emergency equipments Elevate

head of bed 45-60 degrees Monitor for complications- coronary artery rupture,

dysrhythmias, pleural laceration and myocardial trauma

HYPERTENSION

A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg overa sustained period, based on two or more BP measurements.Types of Hypertension 1.

Primary or ESSENTIAL Most common type 2. Secondary Due to other conditions likePheochromocytoma, renovascular hypertension, Cushings, Conns , SIADH

PATHOPHYSIOLOGY Multi-factorial etiology BP= CO (SV X HR) x TPR Any increase

in the above parameters will increase BP 1. Increased sympathetic activity 2. Increased

absorption of Sodium, and water in the kidney3. Increased activity of the RAAS 4. Increased vasoconstriction of the peripheral vessels 5.

insulin resistance

ASSESSMENT FINDINGS 1. Headache 2. Visual changes 3. chest pain 4. dizziness 5.N/V

Risk factors for Cardiovascular Problems in Hypertensive patients Major Risk factors 1.

Smoking 2. Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male and post

menopausal W 6. Family History

DIAGNOSTIC STUDIES 1. Health history and PE 2. Routine laboratory- urinalysis, ECG,lipid profile, BUN, serum creatinine , FBS 3. Other lab- CXR, creatinine clearance, 24-

huour urine protein

MEDICAL MANAGEMENT 1. Lifestyle modification 2. Drug therapy 3. Diet therapyDrug therapy Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2

Receptor blockers Vasodilators

NURSING INTERVENTIONS 1. Provide health teaching to patient Teach about the

disease process Elaborate on lifestyle changes Assist in meal planning to lose weight1. Provide health teaching to the patient Provide list of LOW fat , LOW sodium diet of less

than 2-3 grams of Na/day Limit alcohol intake to 30 ml/day Regular aerobic exercise

Advise to completely Stop smoking

2. Provide information about anti- hypertensive drugs Instruct proper compliance and not

abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct toavoid over-the-counter drugs that may interfere with the current medication

3.. Promote Home care management Instruct regular monitoring of BP Involve family

members in care Instruct regular follow-up 4. Manage hypertensive emergency and

urgency properly

Vascular Diseases

ANEURYSM

Dilation involving an artery formed at a weak point in the vessel wall

ANEURYSM Saccular= when one side of the vessel is affected Fusiform= when the entiresegment becomes dilated

RISK FACTORS Atherosclerosis Infection= syphilis Connective tissue disorder

Genetic disorder= Marfans Syndrome

PATHOPHYSIOLOGY Damage to the intima and media weakness outpouching

Dissecting aneurysm tear in the intima and media with dissection of blood through the

layers

ASSESSMENT Asymptomatic Pulsatile sensation on the abdomen Palpable bruit

LABORATORY: CT scan Ultrasound X-ray Aortography

Medical Management: Anti-hypertensives Synthetic graft

Nursing Management: Administer medications Emphasize the need to avoid increased

abdominal pressure No deep abdominal palpation Remind patient the need for serial

ultrasound to detect diameter changes

PERIPHERAL ARTERIAL OCCLUSIVE DISEASE

Refers to arterial insufficiency of the extremities usually secondary to peripheral

atherosclerosis. Usually found in males age 50 and above The legs are most often affected

Risk factors for Peripheral Arterial occlusive disease

Non-Modifiable 1. Age 2. gender 3. family predisposition

Modifiable 1. Smoking 2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress

ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the hallmark ofPAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently

reproduced with the same degree of exercise or activity

1. INTERMITTENT CLAUDICATION- This pain is RELIEVED by REST This

commonly affects the muscle group below the arterial occlusion 2. Progressive pain on the

extremity as the disease advances 3. Sensation of cold and numbness of the extremities 4.Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position 5.

Muscle atrophy, leg ulceration and gangrene

Diagnostic Findings 1. Unequal pulses between the extremities 2. Duplex ultrasonography

3. Doppler flow studies

PAODMedical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and

improves supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation

and increases vasodilatation 2. Surgery- Bypass graft and anastomoses

Nursing Interventions

1. Maintain Circulation to the extremity Evaluate regularly peripheral pulses, temperature,

sensation, motor function and capillary refill time Administer post-operative care to patient

who underwent surgery2. Monitor and manage complications Note for bleeding, hematoma, decreased urine output

Elevate the legs to diminish edema Encourage exercise of the extremity while on bed Teach

patient to avoid leg-crossing

3. Promote Home management Encourage lifestyle changes Instruct to AVOID smoking

Instruct to avoid leg crossing

BUERGERS DISEASE

Thromboangiitis obliterans A disease characterized by recurring inflammation of themedium and small arteries and veins of the lower extremities Occurs in MEN ages 20-35

RISK FACTOR: SMOKING!

PATHOPHYSIOLOGY

Cause is UNKNOWN Probably an Autoimmune disease Inflammation of the arteries

thrombus formation occlusion of the vessels

ASSESSMENT FINDINGS 1. Leg PAIN Foot cramps in the arch (instep claudication)

after exercise Relieved by rest Aggravated by smoking, emotional disturbance and cold

chilling 2. Digital rest pain not changed by activity or rest

3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as diseaseadvances 4. Paresthesia

Diagnostic Studies 1. Duplex ultrasonography 2. Contrast angiography

Nursing Interventions

1. Assist in the medical and surgical management Bypass graft amputation 2. Strongly

advise to AVOID smoking 3. Manage complications appropriatelyPost-operative care: after amputation Elevate stump for the FIRST 24 HOURS to minimize

edema and promote venous return Place patient on PRONE position after 24 hours Assess

skin for bleeding and hematoma Wrap the extremity with elastic bandage

Medical Management

1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of

O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation and increases

vasodilatation 2. Surgery- Bypass graft and anastomoses

RAYNAUDS DISEASE

A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain and

pallor of the fingertips or toes Cause : UNKNOWN Most commonly affects WOMEN, 16-40 years old

ASSESSMENT FINDINGS 1. Raynauds phenomenon A localized episode of

vasoconstriction of the small arteries of the hands and feet that causes color and

temperature changes. W-B-R Pallor- due to vasoconstriction, then Blue- due to pooling ofDeoxygenated blood Red- due to exaggerated reflow/hyperemia 2. tingling sensation 3.

Burning pain on the hands and feet

Medical management Drug therapy with the use of CALCIUM channel blockers To

prevent vasospasms

Nursing Interventions 1. instruct patient to avoid situations that may be stressful 2. instruct

to avoid exposure to cold and remain indoors when the climate is cold 3. instruct to avoid

all kinds of nicotine 4. instruct about safety. Careful handling of sharp objects

: Venous diseases

VARICOSE VEINS

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THESE are dilated veins usually in the lower extremities

Predisposing Factors Pregnancy

Prolonged standing or sitting Constipation (for hemorrhoids) Incompetent venous valves

Pathophysiology Factors venous stasis increased hydrostatic pressure edema

Assessment findings

Tortuous superficial veins on the legs Leg pain and Heaviness Dependent edema

Laboratory findings Venography Duplex scan pletysmography

Medical management

Pharmacological therapy Leg vein stripping Anti-embolic stockings

Nursing management 1. Advise patient to elevate the legs 2. Caution patient to avoid

prolonged standing or sitting

3. Provide high-fiber foods to prevent constipation 4. Teach simple exercise to promote

venous return 5. Caution patient to avoid knee-length stockings and constrictive clothings

6. Apply anti-embolic stockings as directed 7. Avoid massage on the affected area

DVT- Deep Vein Thrombosis

Inflammation of the deep veins of the lower extremities and the pelvic veins The

inflammation results to formation of blood clots in the area

Predisposing factors Prolonged immobility Varicosities Traumatic procedures

Complication PULMONARY thromboembolism

Assessment findings Leg tendernessLeg pain and edema Positive HOMANs SIGN

Laboratory findings Venography Duplex scan

Medical management Antiplatelets Anticoagulants Vein stripping and grafting Anti-embolic

stockings

Nursing management 1. Provide measures to avoid prolonged immobility Repositioning

Q2 Provide passive ROM Early ambulation

2. Provide skin care to prevent the complication of leg ulcers 3. Provide anti-embolic

stockings 4. Administer anticoagulants as prescribed 5. Monitor for signs of pulmonaryembolism

Blood disorders

Anemia Nu tritional anemia H emolytic anemia Aplastic anemia S ickle cell

anemiaA condition in which the hemoglobin concentration is lower than normal. Three broad

categories 1. Loss of RBC- occurs with bleeding 2. Decreased RBC production 3.

Increased RBC destruction

Hypoproliferative Anemia Iron Deficiency Anemia Results when the dietary intake of iron is inadequate to produce hemoglobin

Etiologic Factors 1. Bleeding- the most common cause 2. Mal-absorption 3.

Malnutrition 4. Alcoholism

Pathophysiology The body stores of iron decrease, leading to depletion of hemoglobin

synthesis

The oxygen carrying capacity of hemoglobin is reduced tissue hypoxia

Assessment Findings

1. Pallor of the skin and mucous membrane 2. Weakness and fatigue 3. General

malaise 4. Pica5. Brittle nails 6. Smooth and sore tongue 7. Angular cheilosis

Laboratory findings1. CBC- Low levels of Hct, Hgb and RBC count 2. low serum iron, low ferritin 3.

Bone marrow aspiration- MOST definitive

Medical management 1. Hematinics 2. Blood transfusion

Nursing Management

1. Provide iron rich-foods Organ meats (liver) Beans Leafy green vegetables

Raisins and molasses

2. Administer iron Oral preparations tablets- Fe fumarate, sulfate and gluconate Advise to take iron ONE hour before meals Take it with vitamin C Continue taking it

for several months

2. Administer iron Oral preparations- liquid It stains teeth Drink it with a straw

Stool may turn blackish- dark in color Advise to eat high-fiber diet to counteract

constipation2. Administer iron IM preparation Administer DEEP IM using the Z- track method

Avoid vigorous rubbing Can cause local pain and staining

APLASTIC ANEMIA

Acondition characterized by decreased number of RBC as well as WBC and platelets

CAUSATIVE FACTORS 1. Environmental toxins- pesticides, benzene 2. Certain

drugs- Chemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides 3.

Heavy metals 4. Radiation

Pathophysiology Toxins cause a direct bone marrow depression acellualr bone marrow

decreased production of blood elements

ASSESSMENT FINDINGS 1. fatigue 2. pallor 3. dyspnea 4. bruising 5.

splenomegaly 6. retinal hemorrhages

LABORATORY FINDINGS 1. CBC- decreased blood cell numbers 2. Bone marrow

aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats

Medical Management 1. Bone marrow transplantation 2. Immunosupressant drugs

3. Rarely, steroids 4. Blood transfusion

Nursing management 1. Assess for signs of bleeding and infection 2. Instruct to avoid exposure to offending agents

Megaloblastic Anemias

Anemias characterized by abnormally large RBC secondary to impaired DNA synthesis

due to deficiency of Folic acid and/or vitamin B12

Slide 263: Megaloblastic Anemias Folic Acid deficiency Causative factors 1.

Alcoholism 2. Mal-absorption 3. Diet deficient in uncooked vegetables Pathophysiology of Folic acid deficiency Decreased folic acid impaired DNA

synthesis in the bone marrow impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation continues large size

Megaloblastic Anemias Vitamin B12 deficiency Causative factors 1. Strict

vegetarian diet 2. Gastrointestinal malabsorption 3. Crohn's disease 4.

gastrectomy

Megaloblastic Anemias Vitamin B12 deficiency Pernicious Anemia Due to the

absence of intrinsic factor secreted by the parietal cells Intrinsic factor binds with Vit.

B12 to promote absorption

Assessment findings 1. weakness 2. fatigue 3. listless 4. neurologic

manifestations are present only in Vit. B12 deficiency

Assessment findings Pernicious Anemia Beefy, red, swollen tongue Mild diarrhea

Extreme pallor Paresthesias in the extremities

Laboratory findings 1. Peripheral blood smear- shows giant RBCs, WBCs with giant

hypersegmented nuclei 2. Very high MCV 3. Schillings test 4. Intrinsic factor antibody test

Medical Management 1. Vitamin supplementation Folic acid 1 mg daily 2. Diet supplementation Vegetarians should have vitamin intake 3. Lifetime monthly injection

of IM Vit B12

Nursing Management 1. Monitor patient 2. Provide assistance in ambulation 3.

Oral care for tongue sore 4. Explain the need for lifetime IM injection of vit B12

Hemolytic Anemia: Sickle Cell

Asevere chronic incurable hemolytic anemia that results from heritance of the sickle

hemoglobin gene.

Causative factor Genetic inheritance of the sickle gene- HbS gene

Slide 274: Hemolytic Anemia: Sickle Cell Pathophysiology Decreased O2, Cold,

Vasoconstriction can precipitate sickling process Factors cause defective hemoglobin

to acquire a rigid, crystal-like C-shaped configuration Sickled RBCs will adhere to endothelium pile up and plug the vessels ischemia results pain, swelling and fever

Assessment Findings 1. jaundice 2. enlarged skull and facial bones 3. tachycardia,

murmurs and cardiomegaly

Primary sites of thrombotic occlusion: spleen, lungs and CNS Chest pain, dyspnea 1. Sickle cell crises Results from tissue hypoxia and necrosis 2. Acute chest

syndrome Manifested by a rapidly falling hemoglobin level, tachycardia, fever and chest

infiltrates in the CXR

Medical Management 1. Bone marrow transplant 2. Hydroxyurea Increases the HbF

3. Long term RBC trnasfusion

Nursing Management 1. manage the pain Support and elevate acutely inflamed joint Relaxation techniques analgesics 2. Prevent and manage infection Monitor status of

patient Initiate prompt antibiotic therapy3. Promote coping skills Provide accurate information Allow patient to verbalize her

concerns about medication, prognosis and future pregnancy 4. Monitor and prevent

potential complications Provide always adequate hydration Avoid cold, temperature that

may cause vasoconstriction 4. Monitor and prevent potential complications Leg ulcer As eptic technique 4. Monitor and prevent potential complications Priapism S udden

painful erection Instruct patient to empty bladder, then take a warm bath

Polycythemia

Refers to an INCREASE volume of RBCs The hematocrit is ELEVATED to more than 55% Clasified as Primary or Secondary

POLYCYTHEMIA VERA Primary Polycythemia A proliferative disorder in which

the myeloid stem cells become uncontrolled

POLYCYTHEMIA VERA Causative factor unknown

POLYCYTHEMIA VERA Pathophysiology The stem cells grow uncontrollably The bone marrow becomes HYPERcellular and all the blood cells are increased in number

The spleen resumes its function of hematopoiesis and enlarges Blood becomes thick andviscous causing sluggish circulation

Overtime, the bone marrow becomes fibrotic

Assessment findings 1. Skin is ruddy 2. Splenomegaly 3. headache 4. dizziness,

blurred vision 5. Angina, dyspnea and thrombophlebitisLaboratory findings 1. CBC- shows elevated RBC mass 2. Normal oxygen saturation 3

Elevated WBC and Platelets

Complications 1. Increased risk for thrombophlebitis, CVA and MI 2. Bleeding due to

dysfunctional blood cells

Medical Management 1. To reduce the high blood cell mass- PHLEBOTOMY 2.

Allopurinol 3. Dipyridamole 4. Chemotherapy to suppress bone marrow

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Polycythemia Nursing Management 1. Primary role of the nurse is EDUCATOR 2.

Regularly asses for the development of complications 3. Assist in weekly phlebotomy

4. Advise to avoid alcohol and aspirin 5. Advise tepid sponge bath or cool water to

manage pruritus

Leukemia

Malignant disorders of blood forming cells characterized by UNCONTROLLED

proliferation of WHITE BLOOD CELLS in the bone marrow- replacing marrow elements .

The WBC can also proliferate in the liver, spleen and lymph nodes. Theleukemias arenamed after the specific lines of blood cells afffected primarily Myeloid Lymphoid

Monocytic The leukemias are named also according to the maturation of cells ACUTE

The cells are primarily immature CHRONIC The cells are primarily mature or

diferentiated ACUTE myelocytic leukemia ACUTE lymphocytic leukemia

CHRONIC myelocytic leukemia CHRONIC lymphocytic leukemia

ETIOLOGIC FACTORS UNKNOWM Probably exposure to radiation Chemical

agents Infectious agents Genetic

PATHOPHYSIOLOGY of ACUTE Leukemia Uncontrolled proliferation of immaturecells suppresses bone marrow function severe anemia, thrombocytopenia and

granulocytopenia

PATHOPHYSIOLOGY of CHRONIC Leukemia Uncontrolled proliferation of

DIFFERENTIATED cells slow suppression of bone marrow function milder symptoms

Slide 304: Leukemia ASSESSMENT FINDINGS ACUTE LEUKEMIA Pallor

Fatigue Dyspnea Hemorrhages Organomegaly Headache vomiting

ASSESSMENT FINDINGS CHRONIC LEUKEMIA Less severe symptoms

organomegaly

LABORATORY FINDINGS Peripheral WBC count varies widely Bone marrow

aspiration biopsy reveals a large percentage of immature cells- BLASTS Erythrocytes and platelets are decreased

Medical Management 2. Chemotherapy 3. Bone marrow transplantation

Nursing Management 1. Manage AND prevent infection Monitor temperature

Assess for signs of infection Be alert if the neutrophil count drops below 1,000 cells/mm32. Maintain skin integrity 3. Provide pain relief 4. Provide information as to therapy-

chemo and bone marrow transplantation