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Cardiovascular & Hematologic System :: Medical Surgical Nursing :: Review For Nursing Licensure Examination
Slide 2: THE CARDIOVASCULAR SYSTEM HEART’S NORMAL ANATOMY The heart is located in the LEFT side of the
mediastinum Consists of Three layers - epicardium, myocardium and endocardium
Slide 3: THE CARDIOVASCULAR SYSTEM The epicardium covers the outer surface of the heart The myocardium is the
middle muscular layer of the heart The endocardium lines the chambers and the valves
Slide 4: THE CARDIOVASCULAR SYSTEM 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
Slide 5: THE CARDIOVASCULAR SYSTEM The heart also has four chambers - two atria and two ventricles The Left
atrium and the right atrium The left ventricle and the right ventricle
Slide 6: The Cardiovascular System The heart chambers are guarded by valves The atrio-ventricular valves - tricuspid
and bicuspid The semi-lunar valves - pulmonic and aortic valves
Slide 7: The Cardiovascular System 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 SA node (55%)
Slide 8: The Cardiovascular System 2. 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
Slide 10: The Cardiovascular System The CONDUCTING SYSTEM OF THE HEART Consists of the 1. SA node- the
pacemaker 2. AV node- slowest conduction 3. Bundle of His – branches into the Right and the Left bundle branch 4.
Purkinje fibers- fastest conduction
Slide 12: The Cardiovascular System 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
Slide 13: The Cardiovascular System Heart rate Normal range is 60-100 beats per minute Tachycardia is greater than
100 bpm Bradycardia is less than 60 bpm Sympathetic system INCREASES HR Parasympathetic system (Vagus)
DECREASES HR
Slide 14: The Cardiovascular System 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
Slide 15: The Cardiovascular System The vascular system consists of the arteries, veins and capillaries The arteries
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, they connect the veins and arteries
Slide 16: The Cardiovascular System 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
Slide 18: The Cardiovascular System Laboratory Test Rationale 1. To assist in diagnosing MI 2. To identify
abnormalities 3. To assess inflammation
Slide 20: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes CK- MB ( creatine
kinase) Elevates in MI within 4 hours, peaks in 18 hours and then declines till 3 days
Slide 21: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes CK- MB ( creatine
kinase) Normal value is 0-7 U/L
Slide 22: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes Lactic
Dehydrogenase (LDH) Elevates in MI in 24 hours, peaks in 48-72 hours Normally LDH1 is greater than LDH2
Slide 23: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes Lactic
Dehydrogenase (LDH) MI- LDH2 greater than LDH1 (flipped LDH pattern) Normal value is 70-200 IU/L
Slide 24: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes Myoglobin Rises
within 1-3 hours Peaks in 4-12 hours Returns to normal in a day
Slide 25: The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes Myoglobin Not
used alone Muscular and RENAL disease can have elevated myoglobin
Slide 26: The Cardiovascular System 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
Slide 27: The Cardiovascular System LABORATORY PROCEDURES Troponin I and T REMEMBER to AVOID IM injections
before obtaining blood sample! Early and late diagnosis can be made!
Slide 28: The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS Lipid profile measures the serum
cholesterol, triglycerides and lipoprotein levels Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL
Slide 29: The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS LDH- 130 mg/dL HDL- 30-70- mg/dL
NPO post midnight (usually 12 hours)
Slide 30: The Cardiovascular System LABORATORY PROCEDURES ELECTROCARDIOGRAM (ECG) A non-invasive
procedure that evaluates the electrical activity of the heart Electrodes and wires are attached to the patient
Slide 33: The Cardiovascular System LABORATORY PROCEDURES 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
Slide 34: The Cardiovascular System LABORATORY PROCEDURES Holter Monitoring Instruct the client to resume
normal activities and maintain a diary of activities and any symptoms that may develop
Slide 36: The Cardiovascular System LABORATORY PROCEDURES ECHOCARDIOGRAM Non-invasive test that studies
the structural and functional changes of the heart with the use of ultrasound No special preparation is needed
Slide 38: The Cardiovascular System LABORATORY PROCEDURES Stress Test A non-invasive test that studies the heart
during activity and detects and evaluates CAD Exercise test, pharmacologic test and emotional test
Slide 39: The Cardiovascular System LABORATORY PROCEDURES Stress Test Treadmill testing is the most commonly
used stress test Used to determine CAD, Chest pain causes, drug effects and dysrhythmias in exercise
Slide 40: The Cardiovascular System LABORATORY PROCEDURES Stress Test Pre-test: consent may be required,
adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine
Slide 42: The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test Use of dipyridamole
Maximally dilates coronary artery Side-effect: flushing of face
Slide 43: The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test Pre-test: 4 hours fasting,
avoid alcohol, caffeine Post test: report symptoms of chest pain
Slide 44: The Cardiovascular System LABORATORY PROCEDURES CARDIAC catheterization Insertion of a catheter into
the heart and surrounding vessels Determines the structure and performance of the heart valves and surrounding
vessels
Slide 45: The Cardiovascular System LABORATORY PROCEDURES CARDIAC catheterization Used to diagnose CAD,
assess coronary atery patency and determine extent of atherosclerosis
Slide 46: The Cardiovascular System LABORATORY PROCEDURES Pretest: Ensure Consent, assess for allergy to
seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses
Slide 47: The Cardiovascular System LABORATORY PROCEDURES Pretest: Fast for 8-12 hours, teachings, medications
to allay anxiety
Slide 48: The Cardiovascular System LABORATORY PROCEDURES Intra-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
Slide 49: The Cardiovascular System LABORATORY PROCEDURES 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 site if required to maintain pressure Monitor for bleeding and hematoma formation
Slide 50: The Cardiovascular System LABORATORY PROCEDURES 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
Slide 51: The Cardiovascular System LABORATORY PROCEDURES CVP The CVP is the pressure within the SVC Reflects
the pressure under which blood is returned to the SVC and right atrium
Slide 52: The Cardiovascular System LABORATORY PROCEDURES CVP 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 vasodilatation
Slide 53: The Cardiovascular System LABORATORY PROCEDURES Measuring 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.
Slide 55: CARDIAC ASSESSMENT ASSESSMENT 1. Health History Obtain description of present illness and the chief
complaint Chest pain, SOB, Edema, etc. Assess risk factors
Slide 56: CARDIAC ASSESSMENT 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
Slide 58: CARDIAC ASSESSMENT 3. Laboratory and diagnostic studies CBC cardiac catheterization Lipid profile
arteriography Cardiac enzymes and proteins CXR CVP EEG Holter monitoring Exercise ECG
Slide 60: CARDIAC IMPLEMENTATION 3. Promote gas exchange Administer O2 Position client in SEMI-Fowler’s
Encourage coughing and deep breathing exercises
Slide 61: CARDIAC IMPLEMENTATION 4. Increase client activity tolerance Balance rest and activity periods Assist in
daily activities 5. Promote client comfort Assess the client’s description of pain and chest discomfort Administer
medication as prescribed
Slide 62: CARDIAC IMPLEMENTATION 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 frequently
Slide 63: CARDIAC IMPLEMENTATION 8. Minimize patient anxiety Encourage verbalization of feelings, fears and
concerns Answer client questions. Provide information about procedures and medications
Slide 64: CARDIAC DISEASES Coronary Artery Disease Myocardial Infarction Congestive Heart Failure Infective
Endocarditis Cardiac Tamponade Cardiogenic Shock
Slide 65: VASCULAR DISEASES Hypertension Buerger’s disease Varicose veins Deep vein thrombosis Aneurysm
Slide 66: CAD CAD results from the focal narrowing of the large and medium-sized coronary arteries due to
deposition of atheromatous plaque in the vessel wall
Slide 67: CAD 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
Slide 68: CAD RISK FACTORS Most important MODIFIABLE factors: Smoking Hypertension Diabetes Cholesterol
abnormalities
Slide 69: CAD Pathophysiology Fatty 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
ischemia
Slide 70: CAD Pathophysiology There 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 coronary artery, this becomes
significant Potential for Thrombosis and embolism
Slide 71: Angina Pectoris Chest pain resulting from coronary atherosclerosis or myocardial ischemia
Slide 72: Angina Pectoris: 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
Slide 73: Angina Pectoris: Clinical Syndromes Three Common Types of ANGINA 2. Unstable angina Occurs
unpredictably during exertion and emotion, severity increases with time and pain may not be relieved by rest and
drug
Slide 74: Angina Pectoris: Clinical Syndromes Three Common Types of ANGINA 3. Variant angina Prinzmetal angina,
results from coronary artery VASOSPASMS, may occur at rest
Slide 75: Angina Pectoris ASSESSMENT FINDINGS 1. Chest pain- ANGINA The most characteristic symptom PAIN is
described as mild to severe retrosternal pain, squeezing, tightness or burning sensation Radiates to the jaw and left
arm
Slide 77: Angina Pectoris ASSESSMENT FINDINGS 2. Diaphoresis 3. Nausea and vomiting 4. Cold clammy skin 5. Sense
of apprehension and doom 6. Dizziness and syncope
Slide 78: Angina Pectoris 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
Slide 79: Angina Pectoris NURSING MANAGEMENT 1. Administer prescribed medications Nitrates- to dilate the
coronary arteries Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP and HR Calcium-channel
blockers- to dilate coronary artery and reduce vasospasm
Slide 80: 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 after THREE tablets seek medical attention
Slide 81: Angina Pectoris 3. 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 activities
Slide 82: Angina Pectoris 5. 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
Slide 84: Angina Pectoris 6. Provide information to family members to minimize anxiety and promote family
cooperation 7. Assist client to identify risk factors that can be modified 8. Refer patient to proper agencies
Slide 85: Myocardial infarction Death of myocardial tissue in regions of the heart with abrupt interruption of
coronary blood supply
Slide 87: Myocardial infarction ETIOLOGY and Risk factors 1. CAD 2. Coronary vasospasm 3. Coronary artery occlusion
by embolus and thrombus 4. Conditions that decrease perfusion- hemorrhage, shock
Slide 88: Myocardial infarction Risk factors 1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress
6. Sedentary lifestyle
Slide 89: Myocardial infarction 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
Slide 90: Myocardial infarction ASSESSMENT findings 1. CHEST PAIN Chest pain is described as severe, persistent,
crushing substernal discomfort Radiates to the neck, arm, jaw and back
Slide 91: Myocardial infarction ASSESSMENT findings 1. CHEST PAIN Occurs without cause, primarily early morning
NOT relieved by rest or nitroglycerin Lasts 30 minutes or longer
Slide 92: Myocardial infarction Assessment findings 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
Slide 93: Myocardial infarction 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
Slide 96: Myocardial infarction 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
Slide 97: Myocardial infarction 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
Slide 99: MI Medical Management 1. ANALGESIC The choice is MORPHINE It reduces pain and anxiety Relaxes
bronchioles to enhance oxygenation
Slide 100: MI Medical Management 2. ACE Prevents formation of angiotensin II Limits the area of infarction
Slide 101: MI Medical Management 3. Thrombolytics Streptokinase, Alteplase Dissolve clots in the coronary artery
allowing blood to flow
Slide 102: Myocardial infarction NURSING INTERVENTIONS AFTER ACUTE EPISODE 1. Maintain bed rest for the first
3 days 2. Provide passive ROM exercises 3. Progress with dangling of the feet at side of bed
Slide 103: Myocardial infarction NURSING INTERVENTIONS AFTER ACUTE EPISODE 4. Proceed with sitting out of bed,
on the chair for 30 minutes TID 5. Proceed with ambulation in the room toilet hallway TID
Slide 104: Myocardial infarction NURSING INTERVENTIONS AFTER ACUTE EPISODE 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
Slide 105: CARDIOMYOPATHIES Heart muscle disease associated with cardiac dysfunction
Slide 107: DILATED CARDIOMYOPATHY ASSOCIATED FACTORS 1. Heavy alcohol intake 2. Pregnancy 3. Viral infection
4. Idiopathic
Slide 108: DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY Diminished contractile proteins poor contraction
decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation.
SYSTOLIC DYSFUNCTION
Slide 110: HYPERTROPHIC CARDIOMYOPATHY Pathophysiology Increased size of myocardium reduced ventricular
volume increased resistance to ventricular filling diastolic dysfunction
Slide 111: 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
Slide 113: CARDIOMYOPATHIES Assessment findings 1. PND 2. Orthopnea 3. Edema 4. Chest pain 5. Palpitations 6.
dizziness 7. Syncope with exertion
Slide 115: CARDIOMYOPATHIES Medical Management 1. Surgery 2. pacemaker insertion 3. Pharmacological drugs
for symptom relief
Slide 116: CARDIOMYOPATHIES Nursing Management 1.Improve cardiac output Adequate rest Oxygen therapy Low
sodium diet
Slide 117: CARDIOMYOPATHIES Nursing Management 2. Increase patient tolerance Schedule activities with rest
periods in between
Slide 118: CARDIOMYOPATHIES Nursing Management 3. Reduce patient anxiety Support Offer information about
transplantations Support family in anticipatory grieving
Slide 119: Infective endocarditis Infection of the heart valves and the endothelial surface of the heart Can be acute
or chronic
Slide 120: Infective endocarditis Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi
Slide 121: Infective endocarditis Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4.
IV drug users 5. Valvular dysfunctions
Slide 122: Infective endocarditis 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
Slide 123: Infective endocarditis Assessment findings 1. Intermittent HIGH fever 2. anorexia, weight loss 3. cough,
back pain and joint pain 4. splinter hemorrhages under nails
Slide 124: Infective endocarditis Assessment findings 5. Osler’s nodes- painful nodules on fingerpads 6. Roth’s spots-
pale hemorrhages in the retina
Slide 125: Infective endocarditis Assessment findings 7. Heart murmurs 8. Heart failure
Slide 126: Infective endocarditis Prevention Antibiotic prophylaxis if patient is undergoing procedures like dental
extractions, bronchoscopy, surgery, etc.
Slide 127: Infective endocarditis LABORATORY EXAM Blood Cultures to determine the exact organism
Slide 128: Infective endocarditis Nursing management 1. regular monitoring of temperature, heart sounds 2. manage
infection 3. long-term antibiotic therapy
Slide 129: Infective endocarditis Medical management 1. Pharmacotherapy IV antibiotic for 2-6 weeks Antifungal
agents are given – amphotericin B
Slide 131: CHF A 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
Slide 132: CHF 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 the major ventricular dysfunction- Left or Right
Slide 135: New York Heart Association Class 1 Ordinary physical activity does NOT cause chest pain and fatigue No
pulmonary congestion Asymptomatic NO limitation of ADLs
Slide 136: New York Heart Association Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptom with
INCREASED activity Basilar crackles and S3
Slide 137: New York Heart Association Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms
present in LESS than ordinary activity
Slide 138: New York Heart Association Class 4 SYMPTOMS are present at rest
Slide 139: CHF PATHOPHYSIOLOGY LEFT Ventricular pump failure back up of blood into the pulmonary veins
increased pulmonary capillary pressure pulmonary congestion
Slide 140: CHF PATHOPHYSIOLOGY LEFT ventricular failure decreased cardiac output decreased perfusion to the
brain, kidney and other tissues oliguria, dizziness
Slide 141: CHF PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling in the venous circulation increased
hydrostatic pressure peripheral edema
Slide 142: CHF PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling venous congestion in the kidney, liver
and GIT
Slide 143: 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
Slide 144: LEFT SIDED CHF ASSESSMENT FINDINGS 7. Cool extremities 8. Cyanosis 9. decreased peripheral pulses 10.
Fatigue 11. Oliguria 12. signs of cerebral anoxia
Slide 145: RIGHT SIDED CHF ASSESSMENT FINDINGS 1. Peripheral dependent, pitting edema 2. Weight gain 3.
Distended neck vein 4. hepatomegaly 5. Ascites
Slide 146: RIGHT SIDED CHF ASSESSMENT FINDINGS 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
Slide 148: CHF 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
Slide 149: CHF NURSING INTERVENTIONS 1. Assess patient's cardio- pulmonary status 2. Assess VS, CVP and PCWP.
Weigh patient daily to monitor fluid retention
Slide 150: CHF NURSING INTERVENTIONS 3. Administer medications- usually cardiac glycosides are given- DIGOXIN
or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed
Slide 151: CHF NURSING INTERVENTIONS 4. Provide a LOW sodium diet. Limit fluid intake as necessary 5. Provide
adequate rest periods to prevent fatigue
Slide 152: CHF NURSING INTERVENTIONS 6. Position on semi-fowler’s to fowler’s for adequate chest expansion 7.
Prevent complications of immobility
Slide 154: CHF NURSING INTERVENTION AFTER THE ACUTE STAGE 4. Provide a LOW fat and LOW sodium diet 5.
Provide potassium supplements 6. Instruct about fluid restriction
Slide 155: CHF NURSING INTERVENTION AFTER THE ACUTE STAGE 7. Provide adequate rest periods and schedule
activities 8. Monitor daily weight and report signs of fluid retention
Slide 156: 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
Slide 157: CARDIOGENIC SHOCK 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
Slide 158: CARDIOGENIC SHOCK LABORATORY FINDINGS Increased CVP Normal is 4-10 cmH2O
Slide 159: CARDIOGENIC SHOCK 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
Slide 160: CARDIOGENIC SHOCK 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
Slide 161: CARDIAC TAMPONADE A condition where the heart is unable to pump blood due to accumulation of fluid
in the pericardial sac (pericardial effusion)
Slide 162: CARDIAC TAMPONADE 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
Slide 163: CARDIAC TAMPONADE Causative factors 1. Cardiac trauma 2. Complication of Myocardial infarction 3.
Pericarditis 4. Cancer metastasis
Slide 164: CARDIAC TAMPONADE ASSESSMENT FINDINGS 1. BECK’s Triad- Jugular vein distention, hypotension and
distant/muffled heart sound 2. Pulsus paradoxus 3. Increased CVP 4. decreased cardiac output
Slide 165: CARDIAC TAMPONADE ASSESSMENT FINDINGS 5. Syncope 6. anxiety 7. dyspnea 8. Percussion- Flatness
across the anterior chest
Slide 167: CARDIAC TAMPONADE NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF 3.
Monitor ECG, urine output and BP 4. Monitor for recurrence of tamponade
Slide 168: 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
Slide 169: HYPERTENSION A systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg over
a sustained period, based on two or more BP measurements.
Slide 173: HYPERTENSION 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 kidney
Slide 174: HYPERTENSION PATHOPHYSIOLOGY Multifactorial etiology BP= CO (SV X HR) x TPR Any increase in the
above parameters will increase BP 3. Increased activity of the RAAS 4. Increased vasoconstriction of the peripheral
vessels 5. insulin resistance
Slide 175: HYPERTENSION ASSESSMENT FINDINGS 1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V
Slide 176: HYPERTENSION 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
Slide 177: HYPERTENSION 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
Slide 178: HYPERTENSION MEDICAL MANAGEMENT 1. Lifestyle modification 2. Drug therapy 3. Diet therapy
Slide 179: HYPERTENSION MEDICAL MANAGEMENT Drug therapy Diuretics Beta blockers Calcium channel blockers
ACE inhibitors A2 Receptor blockers Vasodilators
Slide 180: HYPERTENSION NURSING INTERVENTIONS 1. Provide health teaching to patient Teach about the disease
process Elaborate on lifestyle changes Assist in meal planning to lose weight
Slide 181: HYPERTENSION NURSING INTERVENTIONS 1. 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
Slide 182: HYPERTENSION Nursing Interventions 2. Provide information about anti- hypertensive drugs Instruct
proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct
to avoid over-the-counter drugs that may interfere with the current medication
Slide 183: HYPERTENSION Nursing Intervention 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
Slide 185: ANEURYSM Dilation involving an artery formed at a weak point in the vessel wall
Slide 186: ANEURYSM Saccular= when one side of the vessel is affected Fusiform= when the entire segment becomes
dilated
Slide 187: ANEURYSM RISK FACTORS • Atherosclerosis • Infection= syphilis • Connective tissue disorder • Genetic
disorder= Marfan’s Syndrome
Slide 188: ANEURYSM PATHOPHYSIOLOGY Damage to the intima and media weakness outpouching Dissecting
aneurysm tear in the intima and media with dissection of blood through the layers
Slide 189: ANEURYSM ASSESSMENT • Asymptomatic • Pulsatile sensation on the abdomen • Palpable bruit
Slide 192: ANEURYSM 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
Slide 193: 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
Slide 194: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Risk factors for Peripheral Arterial occlusive disease Non-
Modifiable 1. Age 2. gender 3. family predisposition
Slide 195: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Risk factors for Peripheral Arterial occlusive disease Modifiable
1. Smoking 2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress
Slide 196: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the
hallmark of PAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with
the same degree of exercise or activity
Slide 197: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE ASSESSMENT FINDINGS 1. INTERMITTENT CLAUDICATION- the
hallmark of PAOD This pain is RELIEVED by REST This commonly affects the muscle group below the arterial occlusion
Slide 198: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Assessment Findings 2. Progressive pain on the extremity as
the disease advances 3. Sensation of cold and numbness of the extremities
Slide 199: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Assessment Findings 4. Skin is pale when elevated and
cyanotic/ruddy when placed on a dependent position 5. Muscle atrophy, leg ulceration and gangrene
Slide 200: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Diagnostic Findings 1. Unequal pulses between the extremities
2. Duplex ultrasonography 3. Doppler flow studies
Slide 201: PAOD 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
Slide 202: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE 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 surgery
Slide 203: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Nursing Interventions 2. 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
Slide 204: PERIPHERAL ARTERIAL OCCLUSIVE DISEASE Nursing Interventions 3. Promote Home management
Encourage lifestyle changes Instruct to AVOID smoking Instruct to avoid leg crossing
Slide 205: BUERGER’S DISEASE Thromboangiitis obliterans A disease characterized by recurring inflammation of the
medium and small arteries and veins of the lower extremities Occurs in MEN ages 20-35 RISK FACTOR: SMOKING!
Slide 206: BUERGER’S DISEASE PATHOPHYSIOLOGY Cause is UNKNOWN Probably an Autoimmune disease
Inflammation of the arteries thrombus formation occlusion of the vessels
Slide 208: BUERGER’S DISEASE ASSESSMENT FINDINGS 3. Intense RUBOR (reddish-blue discoloration), progresses to
CYANOSIS as disease advances 4. Paresthesia
Slide 209: BUERGER’S DISEASE Diagnostic Studies 1. Duplex ultrasonography 2. Contrast angiography
Slide 210: BUERGER’S DISEASE Nursing Interventions 1. Assist in the medical and surgical management Bypass graft
amputation 2. Strongly advise to AVOID smoking 3. Manage complications appropriately
Slide 211: 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
Slide 212: BUERGER’S DISEASE Nursing Interventions Post-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
Slide 213: RAYNAUD’S 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
Slide 214: RAYNAUD’S DISEASE ASSESSMENT FINDINGS 1. Raynaud’s phenomenon A localized episode of
vasoconstriction of the small arteries of the hands and feet that causes color and temperature changes
Slide 215: RAYNAUD’S DISEASE W-B-R Pallor- due to vasoconstriction, then Blue- due to pooling of Deoxygenated
blood Red- due to exaggerated reflow/hyperemia
Slide 216: RAYNAUD’S DISEASE ASSESSMENT FINDINGS 2. tingling sensation 3. Burning pain on the hands and feet
Slide 217: RAYNAUD’S DISEASE Medical management Drug therapy with the use of CALCIUM channel blockers To
prevent vasospasms
Slide 218: RAYNAUD’S DISEASE 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
Slide 220: VARICOSE VEINS THESE are dilated veins usually in the lower extremities
Slide 221: VARICOSE VEINS Predisposing Factors Pregnancy Prolonged standing or sitting Constipation (for
hemorrhoids) Incompetent venous valves
Slide 222: VARICOSE VEINS Pathophysiology Factors venous stasis increased hydrostatic pressure edema
Slide 223: VARICOSE VEINS Assessment findings Tortuous superficial veins on the legs Leg pain and Heaviness
Dependent edema
Slide 224: VARICOSE VEINS Laboratory findings Venography Duplex scan pletysmography
Slide 225: VARICOSE VEINS Medical management Pharmacological therapy Leg vein stripping Anti-embolic stockings
Slide 227: VARICOSE VEINS Nursing management 3. Provide high-fiber foods to prevent constipation 4. Teach simple
exercise to promote venous return
Slide 228: VARICOSE VEINS Nursing management 5. Caution patient to avoid knee-length stockings and constrictive
clothings
Slide 229: VARICOSE VEINS Nursing management 6. Apply anti-embolic stockings as directed 7. Avoid massage on
the affected area
Slide 230: 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
Slide 231: DVT- Deep Vein Thrombosis Predisposing factors Prolonged immobility Varicosities Traumatic procedures
Slide 233: DVT- Deep Vein Thrombosis Assessment findings Leg tenderness Leg pain and edema Positive HOMAN’s
SIGN
Slide 234: DVT- Deep Vein Thrombosis Laboratory findings Venography Duplex scan
Slide 235: DVT- Deep Vein Thrombosis Medical management Antiplatelets Anticoagulants Vein stripping and grafting
Anti-embolic stockings
Slide 236: DVT- Deep Vein Thrombosis Nursing management 1. Provide measures to avoid prolonged immobility
Repositioning Q2 Provide passive ROM Early ambulation
Slide 237: DVT- Deep Vein Thrombosis Nursing management 2. Provide skin care to prevent the complication of leg
ulcers 3. Provide anti-embolic stockings
Slide 238: DVT- Deep Vein Thrombosis Nursing management 4. Administer anticoagulants as prescribed 5. Monitor
for signs of pulmonary embolism
Slide 240: Blood disorders Anemia Nutritional anemia Hemolytic anemia Aplastic anemia Sickle cell anemia
Slide 241: ANEMIA A condition in which the hemoglobin concentration is lower than normal
Slide 242: ANEMIA Three broad categories 1. Loss of RBC- occurs with bleeding 2. Decreased RBC production
3. Increased RBC destruction
Slide 243: Hypoproliferative Anemia Iron Deficiency Anemia –Results when the dietary intake of iron is inadequate
to produce hemoglobin
Slide 244: Hypoproliferative Anemia Iron Deficiency Anemia –Etiologic Factors –1. Bleeding- the most common
cause –2. Mal-absorption –3. Malnutrition –4. Alcoholism
Slide 245: Hypoproliferative Anemia IronDeficiency Anemia Pathophysiology –The body stores of iron decrease,
leading to depletion of hemoglobin synthesis
Slide 246: Hypoproliferative Anemia IronDeficiency Anemia Pathophysiology –The oxygen carrying capacity of
hemoglobin is reduced tissue hypoxia
Slide 248: Hypoproliferative Anemia Iron Deficiency Anemia Assessment Findings 5. Brittle nails 6. Smooth and
sore tongue 7. Angular cheilosis
Slide 249: Hypoproliferative Anemia Iron Deficiency Anemia Laboratory findings 1. CBC- Low levels of Hct, Hgb
and RBC count 2. low serum iron, low ferritin 3. Bone marrow aspiration- MOST definitive
Slide 250: Hypoproliferative Anemia Iron Deficiency Anemia Medical management 1. Hematinics 2. Blood
transfusion
Slide 251: Hypoproliferative Anemia Iron Deficiency Anemia Nursing Management 1. Provide iron rich-foods –
Organ meats (liver) – Beans – Leafy green vegetables – Raisins and molasses
Slide 252: Hypoproliferative Anemia Nursing Management 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
Slide 253: Hypoproliferative Anemia Nursing Management 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
constipation
Slide 254: Hypoproliferative Anemia Nursing Management 2. Administer iron IM preparation Administer DEEP
IM using the Z- track method Avoid vigorous rubbing Can cause local pain and staining
Slide 255: APLASTIC ANEMIA Acondition characterized by decreased number of RBC as well as WBC and platelets
Slide 256: APLASTIC ANEMIA CAUSATIVE FACTORS 1. Environmental toxins- pesticides, benzene 2. Certain drugs-
Chemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides 3. Heavy metals 4. Radiation
Slide 257: APLASTIC ANEMIA Pathophysiology Toxins cause a direct bone marrow depression acellualr bone
marrow decreased production of blood elements
Slide 258: APLASTIC ANEMIA ASSESSMENT FINDINGS 1. fatigue 2. pallor 3. dyspnea 4. bruising 5.
splenomegaly 6. retinal hemorrhages
Slide 259: APLASTIC ANEMIA LABORATORY FINDINGS 1. CBC- decreased blood cell numbers 2. Bone marrow
aspiration confirms the anemia- hypoplastic or acellular marrow replaced by fats
Slide 260: APLASTIC ANEMIA Medical Management 1. Bone marrow transplantation 2. Immunosupressant drugs
3. Rarely, steroids 4. Blood transfusion
Slide 261: APLASTIC ANEMIA Nursing management 1. Assess for signs of bleeding and infection 2. Instruct to
avoid exposure to offending agents
Slide 262: 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
Slide 264: Megaloblastic Anemias 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
Slide 265: Megaloblastic Anemias Vitamin B12 deficiency Causative factors 1. Strict vegetarian diet 2.
Gastrointestinal malabsorption 3. Crohn's disease 4. gastrectomy
Slide 266: 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
Slide 267: Megaloblastic Anemias Assessment findings 1. weakness 2. fatigue 3. listless 4. neurologic
manifestations are present only in Vit. B12 deficiency
Slide 268: Megaloblastic Anemias Assessment findings Pernicious Anemia – Beefy, red, swollen tongue – Mild
diarrhea – Extreme pallor – Paresthesias in the extremities
Slide 269: Megaloblastic Anemias Laboratory findings 1. Peripheral blood smear- shows giant RBCs, WBCs with
giant hypersegmented nuclei 2. Very high MCV 3. Schilling’s test 4. Intrinsic factor antibody test
Slide 270: Megaloblastic Anemias 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
Slide 271: Megaloblastic Anemias 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
Slide 272: Hemolytic Anemia: Sickle Cell Asevere chronic incurable hemolytic anemia that results from heritance of
the sickle hemoglobin gene.
Slide 273: Hemolytic Anemia: Sickle Cell 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
Slide 275: Hemolytic Anemia: Sickle Cell Pathophysiology 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
Slide 276: Hemolytic Anemia: Sickle Cell Assessment Findings 1. jaundice 2. enlarged skull and facial bones 3.
tachycardia, murmurs and cardiomegaly
Slide 277: Hemolytic Anemia: Sickle Cell Assessment Findings Primary sites of thrombotic occlusion: spleen, lungs
and CNS Chest pain, dyspnea
Slide 278: Hemolytic Anemia: Sickle Cell Assessment Findings 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
Slide 279: Hemolytic Anemia: Sickle Cell Medical Management 1. Bone marrow transplant 2. Hydroxyurea –
Increases the HbF 3. Long term RBC trnasfusion
Slide 280: Hemolytic Anemia: Sickle Cell Nursing Management 1. manage the pain –Support and elevate acutely
inflamed joint –Relaxation techniques –analgesics
Slide 281: Hemolytic Anemia: Sickle Cell Nursing Management 2. Prevent and manage infection –Monitor status of
patient –Initiate prompt antibiotic therapy
Slide 282: Hemolytic Anemia: Sickle Cell Nursing Management 3. Promote coping skills –Provide accurate
information –Allow patient to verbalize her concerns about medication, prognosis and future pregnancy
Slide 283: Hemolytic Anemia: Sickle Cell Nursing Management 4. Monitor and prevent potential complications –
Provide always adequate hydration –Avoid cold, temperature that may cause vasoconstriction
Slide 284: Hemolytic Anemia: Sickle Cell Nursing Management 4. Monitor and prevent potential complications –
Leg ulcer Aseptic technique
Slide 285: Hemolytic Anemia: Sickle Cell Nursing Management 4. Monitor and prevent potential complications –
Priapism Sudden painful erection Instruct patient to empty bladder, then take a warm bath
Slide 286: Polycythemia Refers to an INCREASE volume of RBCs The hematocrit is ELEVATED to more than 55%
Clasified as Primary or Secondary
Slide 287: Polycythemia POLYCYTHEMIA VERA –Primary Polycythemia –A proliferative disorder in which the
myeloid stem cells become uncontrolled
Slide 289: Polycythemia POLYCYTHEMIA VERA Pathophysiology –The stem cells grow uncontrollably –The bone
marrow becomes HYPERcellular and all the blood cells are increased in number
Slide 290: Polycythemia POLYCYTHEMIA VERA Pathophysiology –The spleen resumes its function of hematopoiesis
and enlarges –Blood becomes thick and viscous causing sluggish circulation
Slide 291: Polycythemia POLYCYTHEMIA VERA Pathophysiology –Overtime, the bone marrow becomes fibrotic
Slide 292: Polycythemia POLYCYTHEMIA VERA Assessment findings –1. Skin is ruddy –2. Splenomegaly –3.
headache –4. dizziness, blurred vision –5. Angina, dyspnea and thrombophlebitis
Slide 293: Polycythemia POLYCYTHEMIA VERA Laboratory findings –1. CBC- shows elevated RBC mass –2. Normal
oxygen saturation –3 Elevated WBC and Platelets
Slide 294: Polycythemia POLYCYTHEMIA VERA Complications –1. Increased risk for thrombophlebitis, CVA and MI
–2. Bleeding due to dysfunctional blood cells
Slide 295: Polycythemia POLYCYTHEMIA VERA Medical Management –1. To reduce the high blood cell mass-
PHLEBOTOMY –2. Allopurinol –3. Dipyridamole –4. Chemotherapy to suppress bone marrow
Slide 296: 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
Slide 297: 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.
Slide 298: Leukemia Theleukemias are named after the specific lines of blood cells afffected primarily – Myeloid –
Lymphoid – Monocytic
Slide 299: Leukemia 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
Slide 300: Leukemia ACUTE myelocytic leukemia ACUTE lymphocytic leukemia CHRONIC myelocytic leukemia
CHRONIC lymphocytic leukemia
Slide 302: Leukemia – PATHOPHYSIOLOGY of ACUTE Leukemia Uncontrolled proliferation of immature cells
suppresses bone marrow function severe anemia, thrombocytopenia and granulocytopenia
Slide 304: Leukemia ASSESSMENT FINDINGS ACUTE LEUKEMIA – Pallor – Fatigue – Dyspnea – Hemorrhages –
Organomegaly – Headache – vomiting
Slide 305: Leukemia ASSESSMENT FINDINGS CHRONIC LEUKEMIA – Less severe symptoms – organomegaly
Slide 306: Leukemia LABORATORY FINDINGS Peripheral WBC count varies widely Bone marrow aspiration biopsy
reveals a large percentage of immature cells- BLASTS Erythrocytes and platelets are decreased
Slide 308: Leukemia 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/mm3
Slide 309: Leukemia Nursing Management 2. Maintain skin integrity 3. Provide pain relief 4. Provide information
as to therapy- chemo and bone marrow transplantation