• Like
  • Save
Cardiovascular & Hematologic System
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

Cardiovascular & Hematologic System

  • 66,292 views
Published

Cardiovascular & Hematologic System

Cardiovascular & Hematologic System

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
No Downloads

Views

Total Views
66,292
On SlideShare
0
From Embeds
0
Number of Embeds
50

Actions

Shares
Downloads
0
Comments
106
Likes
197

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. CARDIOLOGY NURSING
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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%)
  • 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
  • 9.  
  • 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
  • 11.  
  • 12.
    • 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
    The Cardiovascular System
  • 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
  • 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
  • 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
  • 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
  • 17. The Cardiovascular System
    • Cardiac Assessment
  • 18. The Cardiovascular System
    • Laboratory Test Rationale
    • 1. To assist in diagnosing MI
    • 2. To identify abnormalities
    • 3. To assess inflammation
  • 19. The Cardiovascular System
    • Laboratory Test Rationale
    • 4. To determine baseline value
    • 5. To monitor serum level of medications
    • 6. To assess the effects of medications
  • 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
  • 21. The Cardiovascular System LABORATORY PROCEDURES
    • CARDIAC Proteins and enzymes
    • CK- MB ( creatine kinase)
      • Normal value is 0-7 U/L
  • 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
  • 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
  • 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
  • 25. The Cardiovascular System LABORATORY PROCEDURES
    • CARDIAC Proteins and enzymes
    • Myoglobin
    • Not used alone
    • Muscular and RENAL disease can have elevated myoglobin
  • 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
  • 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!
  • 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
  • 29. The Cardiovascular System LABORATORY PROCEDURES
    • SERUM LIPIDS
    • LDH- 130 mg/dL
    • HDL- 30-70- mg/dL
    • NPO post midnight (usually 12 hours)
  • 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
  • 31.  
  • 32.  
  • 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
  • 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
  • 35.  
  • 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
  • 37.  
  • 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
  • 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
  • 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
  • 41. The Cardiovascular System LABORATORY PROCEDURES
    • 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
  • 42. The Cardiovascular System LABORATORY PROCEDURES
    • Pharmacological stress test
    • Use of dipyridamole
    • Maximally dilates coronary artery
    • Side-effect: flushing of face
  • 43. The Cardiovascular System LABORATORY PROCEDURES
    • Pharmacological stress test
    • Pre-test: 4 hours fasting, avoid alcohol, caffeine
    • Post test: report symptoms of chest pain
  • 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
  • 45. The Cardiovascular System LABORATORY PROCEDURES
    • CARDIAC catheterization
    • Used to diagnose CAD, assess coronary atery patency and determine extent of atherosclerosis
  • 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
  • 47. The Cardiovascular System LABORATORY PROCEDURES
    • Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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, 4 th ICS
    • 3. Instruct the client to be relaxed and avoid coughing and straining.
  • 54.  
  • 55. CARDIAC ASSESSMENT
    • ASSESSMENT
    • 1. Health History
    • Obtain description of present illness and the chief complaint
    • Chest pain, SOB, Edema, etc.
    • Assess risk factors
  • 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
  • 57.  
  • 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
  • 59. CARDIAC IMPLEMENTATION
    • Assess the cardio-pulmonary status
      • VS, BP, Cardiac assessment
    • 2. Enhance cardiac output
      • Establish IV line to administer fluids
  • 60. CARDIAC IMPLEMENTATION
    • 3. Promote gas exchange
      • Administer O2
      • Position client in SEMI-Fowler’s
      • Encourage coughing and deep breathing exercises
  • 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
  • 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
  • 63. CARDIAC IMPLEMENTATION
    • 8. Minimize patient anxiety
      • Encourage verbalization of feelings, fears and concerns
      • Answer client questions. Provide information about procedures and medications
  • 64. CARDIAC DISEASES
    • Coronary Artery Disease
    • Myocardial Infarction
    • Congestive Heart Failure
    • Infective Endocarditis
    • Cardiac Tamponade
    • Cardiogenic Shock
  • 65. VASCULAR DISEASES
    • Hypertension
    • Buerger’s disease
    • Varicose veins
    • Deep vein thrombosis
    • Aneurysm
  • 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
  • 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
  • 68. CAD
    • RISK FACTORS
    • Most important MODIFIABLE factors:
    • Smoking
    • Hypertension
    • Diabetes
    • Cholesterol abnormalities
  • 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
  • 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
  • 71. Angina Pectoris
    • Chest pain resulting from coronary atherosclerosis or myocardial ischemia
  • 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
  • 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
  • 74. Angina Pectoris: Clinical Syndromes
    • Three Common Types of ANGINA
    • 3. Variant angina
      • Prinzmetal angina, results from coronary artery VASOSPASMS, may occur at rest
  • 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
  • 76. Angina Pectoris
    • ASSESSMENT FINDINGS
    • 1. Chest pain- ANGINA
    • Precipitated by E xercise, E ating heavy meals, E motions like excitement and anxiety and E xtremes of temperature
    • Relieved by REST and Nitroglycerin
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 83.  
  • 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
  • 85. Myocardial infarction
    • Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood supply
  • 86.  
  • 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
  • 88. Myocardial infarction
    • Risk factors
    • 1. Hypercholesterolemia
    • 2. Smoking
    • 3. Hypertension
    • 4. Obesity
    • 5. Stress
    • 6. Sedentary lifestyle
  • 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
  • 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
  • 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
  • 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
  • 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
  • 94.  
  • 95. Myocardial infarction
    • Nursing Interventions
    • 1. Provide Oxygen at 2 lpm, Semi-fowler’s
    • 2. Administer medications
      • Morphine to relieve pain
      • nitrates, thrombolytics, aspirin and anticoagulants
      • Stool softener and hypolipidemics
    • 3. Minimize patient anxiety
      • Provide information as to procedures and drug therapy
  • 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
  • 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
  • 98.  
  • 99. MI
    • Medical Management
    • 1. ANALGESIC
      • The choice is MORPHINE
      • It reduces pain and anxiety
      • Relaxes bronchioles to enhance oxygenation
  • 100. MI
    • Medical Management
    • 2. ACE
      • Prevents formation of angiotensin II
      • Limits the area of infarction
  • 101. MI
    • Medical Management
    • 3. Thrombolytics
      • Streptokinase, Alteplase
      • Dissolve clots in the coronary artery allowing blood to flow
  • 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
  • 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
  • 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
  • 105. CARDIOMYOPATHIES
    • Heart muscle disease associated with cardiac dysfunction
  • 106. CARDIOMYOPATHIES
    • 1. Dilated Cardiomyopathy
    • 2. Hypertrophic Cardiomyopathy
    • 3. Restrictive cardiomyopathy
  • 107. DILATED CARDIOMYOPATHY
    • ASSOCIATED FACTORS
    • 1. Heavy alcohol intake
    • 2. Pregnancy
    • 3. Viral infection
    • 4. Idiopathic
  • 108. DILATED CARDIOMYOPATHY
    • PATHOPHYSIOLOGY
    • Diminished contractile proteins  poor contraction  decreased blood ejection  increased blood remaining in the ventricle  ventricular stretching and dilatation.
    • SYSTOLIC DYSFUNCTION
  • 109. HYPERTROPHIC CARDIOMYOPATHY
    • Associated factors:
    • 1. Genetic
    • 2. Idiopathic
  • 110. HYPERTROPHIC CARDIOMYOPATHY
    • Pathophysiology
    • Increased size of myocardium  reduced ventricular volume  increased resistance to ventricular filling  diastolic dysfunction
  • 111. RESTRICTIVE CARDIOMYOPATHY
    • Associated factors
    • 1. Infiltrative diseases like AMYLOIDOSIS
    • 2. Idiopathic
  • 112. RESTRICTIVE CARDIOMYOPATHY
    • Pathophysiology
    • Rigid ventricular wall  impaired stretch and diastolic filling  decreased output
    • Diastolic dysfunction
  • 113. CARDIOMYOPATHIES
    • Assessment findings
    • 1. PND
    • 2. Orthopnea
    • 3. Edema
    • 4. Chest pain
    • 5. Palpitations
    • 6. dizziness
    • 7. Syncope with exertion
  • 114. CARDIOMYOPATHIES
    • Laboratory Findings
    • 1. CXR- may reveal cardiomegaly
    • 2. ECHOCARDIOGRAM
    • 3. ECG
    • 4. Myocardial Biopsy
  • 115. CARDIOMYOPATHIES
    • Medical Management
    • 1. Surgery
    • 2. pacemaker insertion
    • 3. Pharmacological drugs for symptom relief
  • 116. CARDIOMYOPATHIES
    • Nursing Management
    • 1.Improve cardiac output
    • Adequate rest
    • Oxygen therapy
    • Low sodium diet
  • 117. CARDIOMYOPATHIES
    • Nursing Management
    • 2. Increase patient tolerance
    • Schedule activities with rest periods in between
  • 118. CARDIOMYOPATHIES
    • Nursing Management
    • 3. Reduce patient anxiety
    • Support
    • Offer information about transplantations
    • Support family in anticipatory grieving
  • 119. Infective endocarditis
    • Infection of the heart valves and the endothelial surface of the heart
    • Can be acute or chronic
  • 120. Infective endocarditis
    • Etiologic factors
    • 1. Bacteria- Organism depends on several factors
    • 2. Fungi
  • 121. Infective endocarditis
    • Risk factors
    • 1. Prosthetic valves
    • 2. Congenital malformation
    • 3. Cardiomyopathy
    • 4. IV drug users
    • 5. Valvular dysfunctions
  • 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
  • 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
  • 124. Infective endocarditis
    • Assessment findings
    • 5. Osler’s nodes- painful nodules on fingerpads
    • 6. Roth’s spots- pale hemorrhages in the retina
  • 125. Infective endocarditis
    • Assessment findings
    • 7. Heart murmurs
    • 8. Heart failure
  • 126. Infective endocarditis
    • Prevention
    • Antibiotic prophylaxis if patient is undergoing procedures like dental extractions, bronchoscopy, surgery, etc.
  • 127. Infective endocarditis
    • LABORATORY EXAM
    • Blood Cultures to determine the exact organism
  • 128. Infective endocarditis
    • Nursing management
    • 1. regular monitoring of temperature, heart sounds
    • 2. manage infection
    • 3. long-term antibiotic therapy
  • 129. Infective endocarditis
    • Medical management
    • 1. Pharmacotherapy
    • IV antibiotic for 2-6 weeks
    • Antifungal agents are given – amphotericin B
  • 130. Infective endocarditis
    • Medical management
    • 2. Surgery
    • Valvular replacement
  • 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
  • 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
  • 133.  
  • 134. CHF
    • 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
  • 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
  • 136. New York Heart Association
    • Class 2
    • SLIGHT limitation of ADLs
    • NO symptom at rest
    • Symptom with INCREASED activity
    • Basilar crackles and S3
  • 137. New York Heart Association
    • Class 3
    • Markedly limitation on ADLs
    • Comfortable at rest BUT symptoms present in LESS than ordinary activity
  • 138. New York Heart Association
    • Class 4
    • SYMPTOMS are present at rest
  • 139. CHF
    • PATHOPHYSIOLOGY
    • LEFT Ventricular pump failure  back up of blood into the pulmonary veins  increased pulmonary capillary pressure  pulmonary congestion
  • 140. CHF
    • PATHOPHYSIOLOGY
    • LEFT ventricular failure  decreased cardiac output  decreased perfusion to the brain, kidney and other tissues  oliguria, dizziness
  • 141. CHF
    • PATHOPHYSIOLOGY
    • RIGHT ventricular failure  blood pooling in the venous circulation  increased hydrostatic pressure  peripheral edema
  • 142. CHF
    • PATHOPHYSIOLOGY
    • RIGHT ventricular failure  blood pooling  venous congestion in the kidney, liver and GIT
  • 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
  • 144. LEFT SIDED CHF ASSESSMENT FINDINGS
    • 7. Cool extremities
    • 8. Cyanosis
    • 9. decreased peripheral pulses
    • 10. Fatigue
    • 11. Oliguria
    • 12. signs of cerebral anoxia
  • 145. RIGHT SIDED CHF ASSESSMENT FINDINGS
    • 1. Peripheral dependent, pitting edema
    • 2. Weight gain
    • 3. Distended neck vein
    • 4. hepatomegaly
    • 5. Ascites
  • 146. RIGHT SIDED CHF ASSESSMENT FINDINGS
    • 6. Body weakness
    • 7. Anorexia, nausea
    • 8. Pulsus alternans
  • 147. CHF
    • LABORATORY FINDINGS
    • 1. CXR may reveal cardiomegaly
    • 2. ECG may identify Cardiac hypertrophy
    • 3. Echocardiogram may show hypokinetic heart
  • 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
  • 149. CHF
    • NURSING INTERVENTIONS
    • 1. Assess patient's cardio-pulmonary status
    • 2. Assess VS, CVP and PCWP. Weigh patient daily to monitor fluid retention
  • 150. CHF
    • NURSING INTERVENTIONS
    • 3. Administer medications- usually cardiac glycosides are given- DIGOXIN or DIGITOXIN, Diuretics, vasodilators and hypolipidemics are prescribed
  • 151. CHF
    • NURSING INTERVENTIONS
    • 4. Provide a LOW sodium diet. Limit fluid intake as necessary
    • 5. Provide adequate rest periods to prevent fatigue
  • 152. CHF
    • NURSING INTERVENTIONS
    • 6. Position on semi-fowler’s to fowler’s for adequate chest expansion
    • 7. Prevent complications of immobility
  • 153. CHF
    • NURSING INTERVENTION AFTER THE ACUTE STAGE
    • 1. Provide opportunities for verbalization of feelings
    • 2. Instruct the patient about the medication regimen- digitalis, vasodilators and diuretics
    • 3. Instruct to avoid OTC drugs, Stimulants, smoking and alcohol
  • 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
  • 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
  • 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
  • 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
  • 158. CARDIOGENIC SHOCK
    • LABORATORY FINDINGS
    • Increased CVP
      • Normal is 4-10 cmH2O
  • 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
  • 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
  • 161. CARDIAC TAMPONADE
    • A condition where the heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion)
  • 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
  • 163. CARDIAC TAMPONADE
    • Causative factors
    • 1. Cardiac trauma
    • 2. Complication of Myocardial infarction
    • 3. Pericarditis
    • 4. Cancer metastasis
  • 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
  • 165. CARDIAC TAMPONADE
    • ASSESSMENT FINDINGS
    • 5. Syncope
    • 6. anxiety
    • 7. dyspnea
    • 8. Percussion- Flatness across the anterior chest
  • 166. CARDIAC TAMPONADE
    • Laboratory FINDINGS
    • 1. Echocardiogram
    • 2. Chest X-ray
  • 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
  • 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
  • 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 .
  • 170. HYPERTENSION
    • Types of Hypertension
    • 1. Primary or ESSENTIAL
      • Most common type
    • 2. Secondary
      • Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH
  • 171. HYPERTENSION
    • CLASSIFICATION OF HYPERTENSION by JNC-VII
  • 172.  
  • 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
  • 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
  • 175. HYPERTENSION
    • ASSESSMENT FINDINGS
    • 1. Headache
    • 2. Visual changes
    • 3. chest pain
    • 4. dizziness
    • 5. N/V
  • 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
  • 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
  • 178. HYPERTENSION
    • MEDICAL MANAGEMENT
    • 1. Lifestyle modification
    • 2. Drug therapy
    • 3. Diet therapy
  • 179. HYPERTENSION
    • MEDICAL MANAGEMENT
    • Drug therapy
    • Diuretics
    • Beta blockers
    • Calcium channel blockers
    • ACE inhibitors
    • A2 Receptor blockers
    • Vasodilators
  • 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
  • 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
  • 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
  • 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
  • 184. Vascular Diseases
  • 185. ANEURYSM
    • Dilation involving an artery formed at a weak point in the vessel wall
  • 186. ANEURYSM
    • Saccular= when one side of the vessel is affected
    • Fusiform= when the entire segment becomes dilated
  • 187. ANEURYSM
    • RISK FACTORS
    • Atherosclerosis
    • Infection= syphilis
    • Connective tissue disorder
    • Genetic disorder= Marfan’s Syndrome
  • 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
  • 189. ANEURYSM
    • ASSESSMENT
    • Asymptomatic
    • Pulsatile sensation on the abdomen
    • Palpable bruit
  • 190. ANEURYSM
    • LABORATORY:
    • CT scan
    • Ultrasound
    • X-ray
    • Aortography
  • 191. ANEURYSM
    • Medical Management:
    • Anti-hypertensives
    • Synthetic graft
  • 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
  • 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
  • 194. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
    • Risk factors for Peripheral Arterial occlusive disease
    • Non-Modifiable
    • 1. Age
    • 2. gender
    • 3. family predisposition
  • 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
  • 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
  • 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
  • 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
  • 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
  • 200. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
    • Diagnostic Findings
    • 1. Unequal pulses between the extremities
    • 2. Duplex ultrasonography
    • 3. Doppler flow studies
  • 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
  • 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
  • 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
  • 204. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE
    • Nursing Interventions
    • 3. Promote Home management
    • Encourage lifestyle changes
    • Instruct to AVOID smoking
    • Instruct to avoid leg crossing
  • 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!
  • 206. BUERGER’S DISEASE
    • PATHOPHYSIOLOGY
    • Cause is UNKNOWN
    • Probably an Autoimmune disease
    • Inflammation of the arteries  thrombus formation  occlusion of the vessels
  • 207. BUERGER’S DISEASE
    • 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
  • 208. BUERGER’S DISEASE
    • ASSESSMENT FINDINGS
    • 3. Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances
    • 4. Paresthesia
  • 209. BUERGER’S DISEASE
    • Diagnostic Studies
    • 1. Duplex ultrasonography
    • 2. Contrast angiography
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 216. RAYNAUD’S DISEASE
    • ASSESSMENT FINDINGS 2. tingling sensation
    • 3. Burning pain on the hands and feet
  • 217. RAYNAUD’S DISEASE
    • Medical management
    • Drug therapy with the use of CALCIUM channel blockers
      • To prevent vasospasms
  • 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
  • 219. Venous diseases
  • 220. VARICOSE VEINS
    • THESE are dilated veins usually in the lower extremities
  • 221. VARICOSE VEINS
    • Predisposing Factors
      • Pregnancy
      • Prolonged standing or sitting
      • Constipation (for hemorrhoids)
      • Incompetent venous valves
  • 222. VARICOSE VEINS
    • Pathophysiology
      • Factors  venous stasis  increased hydrostatic pressure  edema
  • 223. VARICOSE VEINS
    • Assessment findings
      • Tortuous superficial veins on the legs
      • Leg pain and Heaviness
      • Dependent edema
  • 224. VARICOSE VEINS
    • Laboratory findings
      • Venography
      • Duplex scan pletysmography
  • 225. VARICOSE VEINS
    • Medical management
      • Pharmacological therapy
      • Leg vein stripping
      • Anti-embolic stockings
  • 226. VARICOSE VEINS
    • Nursing management
    • 1. Advise patient to elevate the legs
    • 2. Caution patient to avoid prolonged standing or sitting
  • 227. VARICOSE VEINS
    • Nursing management
    • 3. Provide high-fiber foods to prevent constipation
    • 4. Teach simple exercise to promote venous return
  • 228. VARICOSE VEINS
    • Nursing management
    • 5. Caution patient to avoid knee-length stockings and constrictive clothings
  • 229. VARICOSE VEINS
    • Nursing management
    • 6. Apply anti-embolic stockings as directed
    • 7. Avoid massage on the affected area
  • 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
  • 231. DVT- Deep Vein Thrombosis
    • Predisposing factors
      • Prolonged immobility
      • Varicosities
      • Traumatic procedures
  • 232. DVT- Deep Vein Thrombosis
    • Complication
      • PULMONARY thromboembolism
  • 233. DVT- Deep Vein Thrombosis
    • Assessment findings
    • Leg tenderness
    • Leg pain and edema
    • Positive HOMAN’s SIGN
  • 234. DVT- Deep Vein Thrombosis
    • Laboratory findings
    • Venography
    • Duplex scan
  • 235. DVT- Deep Vein Thrombosis
    • Medical management
      • Antiplatelets
      • Anticoagulants
      • Vein stripping and grafting
      • Anti-embolic stockings
  • 236. DVT- Deep Vein Thrombosis
    • Nursing management
    • 1. Provide measures to avoid prolonged immobility
      • Repositioning Q2
      • Provide passive ROM
      • Early ambulation
  • 237. DVT- Deep Vein Thrombosis
    • Nursing management
    • 2. Provide skin care to prevent the complication of leg ulcers
    • 3. Provide anti-embolic stockings
  • 238. DVT- Deep Vein Thrombosis
    • Nursing management
    • 4. Administer anticoagulants as prescribed
    • 5. Monitor for signs of pulmonary embolism
  • 239.  
  • 240. Blood disorders
    • Anemia
    • Nutritional anemia
    • Hemolytic anemia
    • Aplastic anemia
    • Sickle cell anemia
  • 241. ANEMIA
    • A condition in which the hemoglobin concentration is lower than normal
  • 242. ANEMIA
    • Three broad categories
    • 1. Loss of RBC- occurs with bleeding
    • 2. Decreased RBC production
    • 3. Increased RBC destruction
  • 243. Hypoproliferative Anemia
    • Iron Deficiency Anemia
      • Results when the dietary intake of iron is inadequate to produce hemoglobin
  • 244. Hypoproliferative Anemia
    • Iron Deficiency Anemia
      • Etiologic Factors
      • 1. Bleeding- the most common cause
      • 2. Mal-absorption
      • 3. Malnutrition
      • 4. Alcoholism
  • 245. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Pathophysiology
      • The body stores of iron decrease, leading to depletion of hemoglobin synthesis
  • 246. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Pathophysiology
      • The oxygen carrying capacity of hemoglobin is reduced  tissue hypoxia
  • 247. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Assessment Findings
    • 1. Pallor of the skin and mucous membrane
    • 2. Weakness and fatigue
    • 3. General malaise
    • 4. Pica
  • 248. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Assessment Findings
    • 5. Brittle nails
    • 6. Smooth and sore tongue
    • 7. Angular cheilosis
  • 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
  • 250. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Medical management
    • 1. Hematinics
    • 2. Blood transfusion
  • 251. Hypoproliferative Anemia
    • Iron Deficiency Anemia
    • Nursing Management
    • 1. Provide iron rich-foods
      • Organ meats (liver)
      • Beans
      • Leafy green vegetables
      • Raisins and molasses
  • 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
  • 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
  • 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
  • 255. APLASTIC ANEMIA
    • A condition characterized by decreased number of RBC as well as WBC and platelets
  • 256. APLASTIC ANEMIA
    • CAUSATIVE FACTORS
    • 1. Environmental toxins- pesticides, benzene
    • 2. Certain drugs- Chemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides
    • 3. Heavy metals
    • 4. Radiation
  • 257. APLASTIC ANEMIA
    • Pathophysiology
    • Toxins cause a direct bone marrow depression  acellualr bone marrow  decreased production of blood elements
  • 258. APLASTIC ANEMIA
    • ASSESSMENT FINDINGS
    • 1. fatigue
    • 2. pallor
    • 3. dyspnea
    • 4. bruising
    • 5. splenomegaly
    • 6. retinal hemorrhages
  • 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
  • 260. APLASTIC ANEMIA
    • Medical Management
    • 1. Bone marrow transplantation
    • 2. Immunosupressant drugs
    • 3. Rarely, steroids
    • 4. Blood transfusion
  • 261. APLASTIC ANEMIA
    • Nursing management
    • 1. Assess for signs of bleeding and infection
    • 2. Instruct to avoid exposure to offending agents
  • 262. Megaloblastic Anemias
    • Anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid and/or vitamin B12
  • 263. Megaloblastic Anemias
    • Folic Acid deficiency
    • Causative factors
    • 1. Alcoholism
    • 2. Mal-absorption
    • 3. Diet deficient in uncooked vegetables
  • 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
  • 265. Megaloblastic Anemias
    • Vitamin B12 deficiency
    • Causative factors
    • 1. Strict vegetarian diet
    • 2. Gastrointestinal malabsorption
    • 3. Crohn's disease
    • 4. gastrectomy
  • 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
  • 267. Megaloblastic Anemias
    • Assessment findings
    • 1. weakness
    • 2. fatigue
    • 3. listless
    • 4. neurologic manifestations are present only in Vit. B12 deficiency
  • 268. Megaloblastic Anemias
    • Assessment findings
    • Pernicious Anemia
      • Beefy, red, swollen tongue
      • Mild diarrhea
      • Extreme pallor
      • Paresthesias in the extremities
  • 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
  • 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
  • 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
  • 272. Hemolytic Anemia: Sickle Cell
    • A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.
  • 273. Hemolytic Anemia: Sickle Cell
    • Causative factor
      • Genetic inheritance of the sickle gene- HbS gene
  • 274. Hemolytic Anemia: Sickle Cell
    • Pathophysiology
    • Decreased O2, Cold, Vasoconstriction can precipitate sickling process
  • 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
  • 276. Hemolytic Anemia: Sickle Cell
    • Assessment Findings
    • 1. jaundice
    • 2. enlarged skull and facial bones
    • 3. tachycardia, murmurs and cardiomegaly
  • 277. Hemolytic Anemia: Sickle Cell
    • Assessment Findings
    • Primary sites of thrombotic occlusion: spleen, lungs and CNS
    • Chest pain, dyspnea
  • 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
  • 279. Hemolytic Anemia: Sickle Cell
    • Medical Management
    • 1. Bone marrow transplant
    • 2. Hydroxyurea
      • Increases the HbF
    • 3. Long term RBC trnasfusion
  • 280. Hemolytic Anemia: Sickle Cell
    • Nursing Management
    • 1. manage the pain
      • Support and elevate acutely inflamed joint
      • Relaxation techniques
      • analgesics
  • 281. Hemolytic Anemia: Sickle Cell
    • Nursing Management
    • 2. Prevent and manage infection
      • Monitor status of patient
      • Initiate prompt antibiotic therapy
  • 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
  • 283. Hemolytic Anemia: Sickle Cell
    • Nursing Management
    • 4. Monitor and prevent potential complications
      • Provide always adequate hydration
      • Avoid cold, temperature that may cause vasoconstriction
  • 284. Hemolytic Anemia: Sickle Cell
    • Nursing Management
    • 4. Monitor and prevent potential complications
      • Leg ulcer
        • Aseptic technique
  • 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
  • 286. Polycythemia
    • Refers to an INCREASE volume of RBCs
    • The hematocrit is ELEVATED to more than 55%
    • Clasified as Primary or Secondary
  • 287. Polycythemia
    • POLYCYTHEMIA VERA
      • Primary Polycythemia
      • A proliferative disorder in which the myeloid stem cells become uncontrolled
  • 288. Polycythemia
    • POLYCYTHEMIA VERA
    • Causative factor
      • unknown
  • 289. Polycythemia
    • POLYCYTHEMIA VERA
    • Pathophysiology
      • The stem cells grow uncontrollably
      • The bone marrow becomes HYPERcellular and all the blood cells are increased in number
  • 290. Polycythemia
    • POLYCYTHEMIA VERA
    • Pathophysiology
      • The spleen resumes its function of hematopoiesis and enlarges
      • Blood becomes thick and viscous causing sluggish circulation
  • 291. Polycythemia
    • POLYCYTHEMIA VERA
    • Pathophysiology
      • Overtime, the bone marrow becomes fibrotic
  • 292. Polycythemia
    • POLYCYTHEMIA VERA
    • Assessment findings
      • 1. Skin is ruddy
      • 2. Splenomegaly
      • 3. headache
      • 4. dizziness, blurred vision
      • 5. Angina, dyspnea and thrombophlebitis
  • 293. Polycythemia
    • POLYCYTHEMIA VERA
    • Laboratory findings
      • 1. CBC- shows elevated RBC mass
      • 2. Normal oxygen saturation
      • 3 Elevated WBC and Platelets
  • 294. Polycythemia
    • POLYCYTHEMIA VERA
    • Complications
      • 1. Increased risk for thrombophlebitis, CVA and MI
      • 2. Bleeding due to dysfunctional blood cells
  • 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
  • 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
  • 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.
  • 298. Leukemia
    • The leukemias are named after the specific lines of blood cells afffected primarily
      • Myeloid
      • Lymphoid
      • Monocytic
  • 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
  • 300. Leukemia
    • ACUTE myelocytic leukemia
    • ACUTE lymphocytic leukemia
    • CHRONIC myelocytic leukemia
    • CHRONIC lymphocytic leukemia
  • 301. Leukemia
    • ETIOLOGIC FACTORS
      • UNKNOWM
      • Probably exposure to radiation
      • Chemical agents
      • Infectious agents
      • Genetic
  • 302. Leukemia
      • PATHOPHYSIOLOGY of ACUTE Leukemia
      • Uncontrolled proliferation of immature cells  suppresses bone marrow function  severe anemia, thrombocytopenia and granulocytopenia
  • 303. Leukemia
      • PATHOPHYSIOLOGY of CHRONIC Leukemia
      • Uncontrolled proliferation of DIFFERENTIATED cells  slow suppression of bone marrow function  milder symptoms
  • 304. Leukemia
    • ASSESSMENT FINDINGS
    • ACUTE LEUKEMIA
      • Pallor
      • Fatigue
      • Dyspnea
      • Hemorrhages
      • Organomegaly
      • Headache
      • vomiting
  • 305. Leukemia
    • ASSESSMENT FINDINGS
    • CHRONIC LEUKEMIA
      • Less severe symptoms
      • organomegaly
  • 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
  • 307. Leukemia
    • Medical Management
    • Chemotherapy
    • Bone marrow transplantation
  • 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
  • 309. Leukemia
    • Nursing Management
    • 2. Maintain skin integrity
    • 3. Provide pain relief
    • 4. Provide information as to therapy- chemo and bone marrow transplantation